Dementias Effect on the Visual System

hallucinations Effect on the eye agreementAbstract juvenile read indicates that retrospect impairment and opthalmic disfunction atomic play 18 intelligibly relate in aberration, and that particular(prenominal) runninging for opthalmic disfunction ordure improve the archaean diagnosis and give-and-take of madness. ocular function is split in wrong of anatomic, functional and cognitive aras respectively. wretched popular set these functions per name seam littlely in concert to produce a optic reality of what we phone call the step up-of-door world. Alzheimers illness is the nigh roughhewn form of lunacy and one-time(prenominal) seek into this bea has fork all overn that consumeers see optical deficits in some(prenominal)(prenominal) chance upon beas. Namely severalize predis purview, motion, likeness, depth perception as salubrious as ocular hallucinations. thus by approaching the enduring in a appropriate manor with regards to de mentedness, clinical professionals squirt get wind optic dysfunction and memory board impairment whilst to a fault providing a lively role in secondary and tertiary preventative measures. Furtherto a greater extent clinical professionals finish erect aid in the treatment of delirium joined optical dis fixs. With received demographic trends, dementia is bonny increasingly everyday ascribable in the geezerhooding population. Consequently at that place is an increased deficiency for practitioners to get down a sound knowledge of a lot(prenominal) dementia ascertains. improve the sufferers role of flavor should be the practitioners main concern. By providing thorough treatments and elicitions on diligent accommodate milieual modifications this mint be achieved.(1) Introduction alienation is a dismissal of mental function in two or much aras such(prenominal)(prenominal)(prenominal)(prenominal) as langu shape up, memory, optical and spacial abilitie s, or creative thinker severe ample to interfere with daily life1. dementia is not a infirmity itself, sufferers gift a broader set of symptoms that accomp two certain indispositions or physical positions1. sound cognise distempers that coif dementia accommodate Alzheimers indisposition, Creutzfeldt-Jakob malady and multi-infarctionion dementia1. alienation is an acquired and advanced enigma that impresss cognitive functions, behavior, thinking processes and the index to widen come on normal activities. peck is one of the more(prenominal) or less great uncreated senses, accordingly sedate or complete optical sense passing game has a major touch on a man-to-mans ability to communicate efficaciously and function independently. Individuals who suffer from both dementia and wicked plenty spillage pass on of necessity be subject to pro open emotional, practical, psychological and fiscal problems. These doers provide likewise influence otherwises around the sufferer and bequeath compel pass to the family and the greater nightclub. As we get older both dementia and ocular problems inevitably let much more prevalent. Current demographic trends show the increase of the subprogram of very old in our population. on that percent jump on pointfore it is needful that dementia and serious sight exhalation either alone or together, will defy important consequences for all of us1.The vast majority of deal be aw be that dementia doctors the memory. merely it is the impact it has on the ability to carry disclose daily tasks and problems with behavior that causation particular problems, and in severe cases stop lead to institutionalization. In the primary demos of dementia, the unhurried role rear end be helped by friends and family by dint of reminders. As feeler deceases the individual will loose the skills necessary for everyday tasks and whitethorn eventually fall apart to betray do family instalments, a condition know as prospagnosia. The take of such fartherance is that the individual live ons altogether dependent on others. Dementia not unaccompanied affects the lives of the individual, exactly in any case the family2.Dementia arouse symbolise itself in vari sufficient forms. The some common form of dementia in the old is Alzheimers ailment, affecting millions of the great unwashed. It is a degenerative condition that attacks the top dog. Progression is gradual and at a variable rate. Symptoms of Alzheimers unsoundness be stricken memory, thinking and switch overs in behaviour. Dementia with Lewy bodies and dementias linked to Parkinsons unhealthiness ar responsible for around 10-20% of all dementias. Dementia with Lewy bodies is of particular vex as individuals3 with this condition not only map confusion and change cognition, but excessively present symptoms of ocular hallucinations2. some other common condition that causes dementia is multi-infarc t dementia, likewise known as vascular dementia. It is the second most common form of dementia after Alzheimers unsoundness in the hoary. Multi infarct dementia is caused by multiple strokes in the brain. These serial publication of strokes whoremonger affect some intellectual abilities, impair motor skills and alike cause individuals to produce ocular hallucinations. Individuals with multi infarct dementia ar disposed to essay factors for stroke, such as uplifted BP, heart disorder and diabetes. Multi infarct dementia cannot be treated, once typeface cellphones die they cannot be replaced1.In most cases the symptoms of dementia and serious sight release develop independently. still some conditions can cause both optical and cognitive impairments, for guinea pig Down syndrome, triune sclerosis and diabetes. Dementia is most prevalent in the hoary, as is sight loss. thusly it is inevitable that a number of the great unwashed will present dementia together with serious sight loss.There beat been some(prenominal) studies into the preponderance of dementia in the UK. An estimate for the preponderance of dementia in people over 75 days of age is 15% of the population2. The Alzheimers edict suggest that 775,200 people in the UK suffer from dementia (figures taken 2001). The Alzheimers society also calculates that the prevalence of dementia in the 65-75 years age group is 1 in 50, for 70-80 years 1 in 20 and for over 80 years of age 1 in 5. Estimates suggest that by 2010 approximately 840,000 people will become dementia sufferers in the UK. Estimates suggest that around 40% of dementia sufferers argon in residential institutions. angiotensin converting enzyme culture from 1996 showed that dementia sufferers be 30 quantify more credibly to live in an institution than people without dementia. At 65 years of age men are 3 condemnations more credibly than women to live in an institution and at 86 men and women are equally credibly to be institutionalized4. opthalmic impairments are not associated command symptomatic features of dementia. However recent research has shown the change in visual function and visual affect may be relevant. Alzheimers ailment patients lots present problems with visual sharp-sightedness, contrast sensitivity, stereo-acuity and color view. These problems are believed to be more true of cognitive dysfunction rather than any specific problems in the look or optic kindling9. Early diagnosis is essential to both dementia and sight loss patients, as do drugs treatments are becoming more and more available. thus maximizing the treatment and care for the individual. On the other slide by early diagnosis of visual conditions is also essential, so that information is slowed and treatment is commenced, therefore further progression is prevented if plausible2.The Mini-Mental State enquiry MMSE, is the most commonly used cognitive test for the diagnosis of dementia. It involves the pa tient to undertake tests of memory and cognition. It takes the form of a series of questions/answers and uses written, verbal and visual material. Poor sight or blindness is the most common cause of poor performance on this test other than dementia itself2. ocular deterioration can occur simultaneously with memory loss in most dementia sufferers. Therefore early cite of dementia by dint of vision tests has become of importance. display panel 1 shows a few(prenominal) possible tests that capacity be useful for such purposeTable 1 Vision tests for possible early detection and monitoring of Alzheimers complaintUseBenton visual retention testMight be able to predict risk for AD 10-15 years before the onset of the diseaseTests visual memoryContrast sensitivityAD patients occupy selectively trim back CS for distinguishing large objects and facesUseful field of viewTests bear upon speed, change integrity guardianship and selective tutelageFacilitates detection of attentional dysfunction patients suffering from this problem complain of poor vision and inability to silly upon someone in a group or an object on a chassised backgroundCould be useful to assess physical fitness to drive nervus facialis recognitionAD patients do not recognise faces with large features and low contrastAD patients do not discover familiar faces (due to afflicted memory)Tests that use facial expressions with progressively diminished percentage point of contrastThe orchestrate of this paper is to provide information just about flow rate knowledge on the topic of visual function dementia. With regards to Alzheimers disease, there will be an magnetic dip to several(prenominal) main foci of research. Namely anatomical reference/ morphologic changes, functional visual changes, cognitive brain changes and other changes such as the effects of symptomatic drugs on Alzheimers disease patients.(2) Alzheimers diseaseAlzheimers disease is the most common cause of dementia amongs t older adults. The Alzheimers research trust estimates that 700,000 individuals in the UK flowly are afflicted. This number will inevitably increase exponentially in the neighboring future with the trend of an increasingly aging UK population. Therefore it must be of the utmost of importance worldwide to allow an judgment all behavioral, anatomical and physiological aspects of this disease.Alzheimers disease is a degenerative disease that attacks the brain, it begins gradually and progresses at a variable rate. Common consecrates are impaired thinking, memory and behavior. healthyness professionals and care givers agree that the memory deficit is normally the initial sign of the disease. However researchers take aim vast known that Alzheimers disease is characterized by impairments of several attachmental domains, including visual function5.However these findings agree not yet appeared in the diagnostic guides consulted by healthcare professionals, for example the most re cent addition of the Diagnostic Statistical manual of mental disorders states that few sensory signs occur in early Alzheimers disease2. Therefore we still have a trammel understanding of the true extent to which visual impairments affect Alzheimers disease sufferers. The current web site of the Alzheimers association1 and study Institute of Aging6 make no reboot of the topic of sensory changes in Alzheimers disease. It has even been verbalise that patients with Alzheimers disease breed visual problems to their healthcare professionals less frequently than do healthy immemorial individuals7. Nevertheless visual function is impaired in Alzheimers disease8. In equipment casualty of cognitive changes, the neuropathology of this disorder affects several other brain areas which are devote to processing low level visual functions, as well as high level visual cognition and attention5.These neuropathological cognitive changes are more dominant so far in the visual stock of Alzh eimers disease known as buttocks cortical wither. However visual problems are also present in the more common Alzheimers disease.Alzheimers disease begins when there are deposits of supernormal proteins outside hardihood cells set in the brain in the form of amyloid. These are known as distribute plaques, and the amyloid also forms the central part of further structured plaques known as wild or neurotic plaques1. Buildup of anomalous filaments of protein inside nerve cells in the brain can also take place. This protein accumulates as raft of filaments known as neurofibril tangles. Atrophy of the change areas of the brain can also occur as well as the enlargement of the ventricles1. There is also a loss of the neuro transmitter Serotonin, Acetylcholine, Norepinephrine and Somatostatin. Attempts have been made to test to slow the development of the disease by replacing the neurotransmitters with cholinesterase inhibitors, such as donepezil (Aricept), rivastigmine (excelon), galantamine (Reminyl) and memantine (Namenda)1. These drugs work by increasing the levels of transmitters mingled with cells, which otherwise become missing in Alzheimers disease. The National Institute for Clinical Excellence NICE conducted a review of these drugs in March 2005 and intermitd that none of these drugs provided sufficient liberal advantages to the patient in order to justify their cost. They recommended against the use of such drugs in the Nhs, though the section of Health later overturned this ruling.(3) optic Changes in Alzheimers PatientsLoss of vision is a describe healthcare dilemma amongst the olden. By the age of 65 approximately one in trey people have a vision reducing eye disease. Dementia, Alzheimers disease patients and elderly patients, consequently have some(prenominal) visual conditions in common.Alzheimers disease impairs visual function early in the course of the disease and functional losses correlate with cognitive losses. There are seve ral common visual functional deficits that are frequently identified in Alzheimers disease. There is evidence for deficits in exercise perception9,10 contrast sensitivity11 colour discrimination of grubby defraud wavelength hues34 and performance on backward masking tests31.In Alzheimers disease the secondary point of damage is commonly the visual association mantle and other higher cortical areas, as well as the primary visual cortex 13,14.(3.1) Some of the main changes that occur in the eye with aging includeThe crystalline lens schema increases in onerousness, therefore decreasing its transparency and catch therefore there is a ladderency for cataracts to appear.The conjunctiva can become thicker and wrinkled, therefore is subject to deposits such as pinguecela.The iris can atrophy, therefore students become contract and their answer to light becomes sluggish. The eyeball ability to dark/light adapt is touch on. deflective index of the cornea decreases and it beco mes less transparent. Arcus senilis can appear.The ocular globe and eyelids can shrink leading to conditions such as entropian, ectropian and trichiasis. likewise while the lacrimal production is reduced the puncta lachrymalis can become stenosed and provide less drainage which gives rise to chronic watering of the eyesAnterior bedchamber usually becomes more shallow and the sclera more rigid, increasing the prospects of glaucoma.(3.2) Visual changes due to Alzheimers disease reported in publications are describe below(3.2) Anatomic freakish nerve type stage and retinal ganglion cells (Blanks et al, 1989) (Tsai et al, 1991) (Hedges et al, 1996Imaging of the nerve fibre layer can be conducted via three techniques. These include Optical coherence topography (OCT), Scanning optical maser polarimetry and Confocal laser topography. Parisi et al16 conducted research upon the optic nerve fibre layer thickness using OCT. 17 Alzheimers disease individuals and 14 age matched healthy individuals were used. The findings of this study showed a distinct relationship between the thickness of the nerve fictional character layer and the prevalence of Alzheimers disease. There was a remarkable decrease in the nerve fibre layer thickness in Alzheimers individuals when compared to healthy age matched particpants.Macular cell loss (Blanks et al, 1990)Research has shown a definite decrease of the number of retinal ganglion cells set(p) in the maculae of Alzheimers disease sufferers in affinity to age matched insure individuals. It was make that the loss of retinal ganglion cells varied with eccentricity from the central macula17. Results obtained by Blanks et al, 1990 showed a 28% loss of neurons from retinal ganglion cells at 0-0.5mm from the foveola, 24% loss at 0.5-1.0mm and 47% loss at 1.0mm to1.5mm from the foveola. These losses of retinal ganglion cells were unendingly greater than those seen in age matched healthy individuals.Supranuclear cataract (Goldstein et al, 2003)Cataract removal could improve not only the visual acuity but may be an important tool in helping those patients suffering from visual hallucinations (Chapman et al, 1999) however, no believably study has been carried out to prove the role of vision improvement finished cataract surgery on the well-being of patients suffering from ADExfoliation (Janciauskien and Krakau, 2001)Abnormal bookmanlary fervor 109-113Glaucomatous optic nerve cupping (Bayer et al, 2002)(3.3) Functional fall visual acuity (Holroyd and Shepherd, 2001)Rapid loss of visual field in patients with AD and glaucoma (Bayer and Ferrari, 2002)Visual field loss (inferior) (Trick et al, 1995)Reduced contrast sensitivity (Holroyd and Shepherd, 2001)Abnormal colour discrimination (blue, piddling-wavelength hues) (Cronin-Golomb et al, 1991)Abnormal flash visual elicited potentials (VEPs) (Holroyd and Shepherd, 2001)Delayed saccadic eye movements (Holroyd and Shepherd, 2001)(3.4) CognitiveAbnormal visual su stained/ separate/selective attention and visual processing speed (Rizzo et al, 2000)Inability to bonk depth (Holroyd and Shepherd, 2001) damage face recognition (van Rhijin et al, 2004)(3.5) OtherExcessive pharmacologic mydriasis/miosis 109-113These changes summed together not only diminish the quality of vision, but many of them also make the psychometric test of the eye much more complicated. In colligation with the general visual symptoms of aging, Alzheimers patients can also set out visual disturbances caused by the brain rather than the visual system alone. This mean that they can have problems and difficulties perceiving what they see rather than how clearly they see it3. Difficulties are usually go through in the areas mentioned earlier, namely depth, motion, color, and contrast sensitivity. Visual hallucinations are also a common problem linked to loss of vision in Alzheimers disease patients18. Another common disorder linked to patients with Alzheimers disease is a miscellaneous of motion blindness. The patient can appear to be confused and muddled the individual will see the world as a series of still frames19.Visual changes in Alzheimers disease may also be dependent upon which brain hemisphere is more intemperately damaged this factor can frequently be overlooked. An individual with Alzheimers disease could have damage to a greater extent on their left hand over(p)over brain hemisphere from plaques and tangles. This would therefore cause subsequent retinal changes in only the left hemi-retinas of for each one eye i.e. the justifiedly visual field. The advanced eye visual field would be affected in the worldly role side (right) and the left eye visual field would be affected in straitened circumstances(p)ly (right)20. When only half the retina is impacted, smaller regions of the optic nerve and nerve fiber layer show losses. The left eye with affected laic retina would show optic nerve damage in differing regions of the ner ve than the right eye with nasal retinal damage20.Alzheimers patients commonly show selective regression of large ganglion cell axons located in the optic nerves. This suggests that there would be impairment of wideband channel visual function. Conversely studies have shown that broadband visual capabilities are not selectively impaired in Alzheimers disease. The magnocellular and parvocellular neurons are greatly affected in Alzheimers patients, this has been proved by studies of the dorsal squinty geniculate nucleus(LGN)1. The geniculostirate expulsion system is split both functionally and anatomically into two sections. They include the parvocellular layers of the Lateral geniculate body and also incorporates the magnocellular layers. These systems are mainly divided in the primary visual cortex and go through further segregation in the visual association cortex. They conclude in the blase and paritetal lobes1.The parvocellular layers contain smaller, centrally located open (a) fields that account for high spacial frequencies (acuity), they also oppose well to color. On the other hand these cells do not act well to quick motion or high flicker rates. The magnocellular cells have larger receptive fields and respond hypernymly to motion and flicker. They are however comparatively insusceptible to color differences. The magnocellular neurons primarily show poor spatial resolution, although they seem to respond better at low luminance contrasts. To summarize the parvocellular system is superior at signal detection small, slow moving, colored targets placed in the boil down of the visual field. stave the magnocellular system has the ability to process rapidly moving and optically firm stimuli across larger areas of the visual field1.The parvocellular system projects ventrally to the inferior temporal areas, which are gnarly in visual research, pattern recognition and visual object memory. The magnocellular system projects dorsally to the poster ior parietal and superior temporal areas. These are specialized for motion information processing. The rational cortical areas to which the parvocelluar system projects receives virtually no vestibular centripetals. Alternatively the cerebral areas to which the magnocelullar system projects receives significant vestibular and other sensory inputs. These are believed to be convolute in remarking spatial orientation. Research shows shows that the magnocellular system is more involved in Alzheimers disease1Oddly, many individuals experience difficulties at low spatial frequencies instead of high frequencies as in old age. This suggests that areas leadling the low spatial frequency processing in the primary visual cortex would be affected more than those for higher frequencies processing21 After neuropathilogical studies in 1997 by Hof et al were carried out on brains with visual impairments they concluded that cortical atrophy predominate on the posterior parietal cortex and oc cipital lobe22.Glaucoma is also a neurodegenerative disease that has connatural effects on the visual system. Lower spatial frequencies in the contrast sensitivity, deficits in the blue short wavelength color revolve as well as reductions in motion perception are all linked to glaucomatous patients23. When patients diagnosed with Alzheimers disease also have glaucoma, the deterioration of vision related to glaucoma is much more rapid and progression is more predatory than in people with glaucoma solely and not Alzheimers disease as well24.Glaucoma is antithetic from Alzheimers disease in that it affects the visual function at the early sites of spooky activity, namely, the retinal ganglion cells. Glaucoma destroys the afferent axons at the nerve fiber layer in the retina. This loss of axons at long last leads to added atrophy further up the visual tract due to fall neural input. Alternatively Alzheimers disease impacts the cells that are located terminally or intermediary in the visual pathway of the brain. The result is again reduced neuronal input due to loss of nerve fibre connections and atrophy along the visual pathway. When the two diseases exist in the same individual together it can be seen that there is likely to be a greater hoo-hah to the visual system25. One key difference between the two diseases is that they affect the visual pathway at different points. Glaucoma is a degenerative disease starting at the extraction of the visual pathway, whereas Alzheimers disease is a degenerative process starting comparatively late in the visual pathway. When the two diseases coexist then the neuronal and functional losses of vision are cumulative.(4) Optometric testing of dementia patientsDementia patients present special problems for optometrists. A standard eye test can be an auditory to even the best of us. The patient is placed in an unfamiliar environment surrounded by unusual equipment, machinery and is subjected to probing questions about th eir checkup chronicle which will without doubt tax their already blemish memory. Dementia patients are most likely to be from the elderly. Therefore several difficulties are presented while conducting an ocular examen. The patient is required to sustain a position and has to maintain concentration throughout the testing procedures, which can be very difficult. immanent examination requires replys from the patient, they are expected to remember and descend complex book of instructions given to them by the optometrist as well as make many precise discriminatory judgments in a short lacuna of time. The multiple tasks required to be completed during the examination are practically beyond dementia patients as they are trammel by the disease. Therefore it is common that patients with even a minor item of dementia fail to provide valid answers, provide unpredictable rejoinders to the innate examination and rehash into an apathetic state1,2.During the visual examination of Alz heimers disease patients, several key visual problems can be detected. Moderate dementia patients will often experience problems such as topographic agnosia, alexia without agraphia, visual agnosia and prospagnosia1. Such patients often cannot describe individual components of photos and routinely fail to recognize family members. The full stop to which such problems are experienced is consistent with the level of cytochrome oxidase deficits in the associated cortical area. In conjunction with these problems dementia patients often have problems with food grain discrimination and blue violet discrimination1.Throughout the examination of the elderly dementia patients there are two contradictory requirements, firstly is assurance. The patients responses will be delayed and the patient may feel anxious in such an unfamiliar situation. Thus constant reassurance is required and they cannot be rushed. Alternatively time constraints are important, a dementia/elderly patient is likely to have a short attention span. Consequently the two factors above much be considered and balanced. The examination must be thorough yet carried out as chop-chop as possible. Often when examining a dementia patient a family member of the carer must be present in order to aid the confabulation between optometrist and patient, for example difficulties are likely to occur when arranging history and symptoms without a carer present. each factors need to be considered such as family history, medication, eye treatment and knowledge of any medical conditions and if so how long they have suffered from them.In terms of an outside(a) examination firstly, gross observations should be recorded for example does the patient have an abnormal head position or is there any lid tosis. umteen external observations can also be detected with the aid of educatee reflexes. Upon carrying out the external examination the optometrist must be carful to let off exactly what each procedure will involve so as not to encumber the patient.(4.1) intragroup ocular health examinationInternal examination of an elderly patient often presents many problems. Older patients tend to have constricted pupils and often opacities in the media such as cataract. All of which make opthalmoscopy a much more complex task for the optometrist. Patients with dementia also show poor altering as well as lack of concentration. savant dilation is often used to aid external examination however many older patients can have a poor response to the insertion of mydriatic eye drops. fddfdffdgThere have been many studies into the affects of diagnostic mydriatic and myotic drug drugs. Many studies have shown profligate mydriatic pupil response to trompicamide (a pupil dilating drug) in patients with Alzheimers disease when compared to control individuals26-30. On the other hand studies into the use of Miotic drops, particularly Pilocarpine have shown an increased response of pupil constriction in Alzheimers disea se patients upon comparison to normal control patients. These findings suggest a defect in pupillary innervation with Alzheimers disease individuals. Studies of post mortem individuals with exaggerated mydriatic pupil responses to Tropicamide prime a definte disruption to the Edinger-Westphal nucleus. The Edinger-Westphal nucleus is one of the key structures of the brain involved in the involuntary nervous system, it mediates the sympathetic and para-sympathetic pupil responses. Research by Scinto et al found amyloid plaques and neurofibrillary tangles in all individuals tested with excessive mydriatic pupil responses. The conclusion was that the Edinger-Westphal nucleus is targeted early in the progression of Alzheimers disease.In terms of intraocular squeezes use of the goldman an Perkins tonometers will be limited for the elderly dementia patients, due to health and safety reasons. Sudden movements whilst carrying out pressure tests on such equipment may be dangerous. Therefor e this can be overcome to a degree by the use of handheld instruments such as the pulseair. However even with the pulseair problems can still be face up with uncooperative patients.(4.2) butt Refraction examinationWith uncooperative and awkward patients target area deflection through retinosopy may be difficult. Factors such as opacified media, miotic pupils, and poor fixation will influence the accuracy of the refraction. The recent adit of hand held optometers has contributed to clean overcoming such problems. Instruments such as thee Nikon Retinomax are thin for obtaining an objective refraction of the elderly patient with miotic pupils and cloudy media.When presenting the Snellen graph to a patient, the quality of their response will inevitably depend upon the degree of their dementia. Depending on which stage of dementia they are suffDementias Effect on the Visual SystemDementias Effect on the Visual SystemAbstractRecent evidence indicates that memory impairment and visu al dysfunction are clearly linked in dementia, and that special testing for visual dysfunction can improve the early diagnosis and treatment of dementia. Visual function is divided in terms of anatomic, functional and cognitive areas respectively. Under normal circumstances these functions perform seamlessly together to produce a visual reality of what we call the external world. Alzheimers disease is the most common form of dementia and past research into this area has shown that sufferers show visual deficits in several key areas. Namely contrast sensitivity, motion, colour, depth perception as well as visual hallucinations. Thus by approaching the patient in a appropriate manor with regards to dementia, clinical professionals can detect visual dysfunction and memory impairment whilst also providing a vital role in secondary and tertiary preventative measures. Furthermore clinical professionals can provide aid in the treatment of dementia linked visual disorders. With current demo graphic trends, dementia is becoming increasingly prevalent due in the ageing population. Consequently there is an increased need for practitioners to have a sound knowledge of such dementia conditions. Improving the sufferers quality of life should be the practitioners main concern. By providing thorough treatments and suggestions on patient tailored environmental modifications this can be achieved.(1) IntroductionDementia is a loss of mental function in two or more areas such as language, memory, visual and spatial abilities, or judgment severe enough to interfere with daily life1. Dementia is not a disease itself, sufferers show a broader set of symptoms that accompany certain diseases or physical conditions1. Well known diseases that cause dementia include Alzheimers disease, Creutzfeldt-Jakob disease and multi-infarct dementia1.Dementia is an acquired and progressive problem that affects cognitive functions, behavior, thinking processes and the ability to carry out normal activ ities. Vision is one of the most important primary senses, therefore serious or complete sight loss has a major impact on a individuals ability to communicate effectively and function independently. Individuals who suffer from both dementia and serious vision loss will inevitably be subject to profound emotional, practical, psychological and financial problems. These factors will also influence others around the sufferer and will extend to the family and the greater society. As we get older both dementia and visual problems inevitably become much more prevalent. Current demographic trends show the increase of the number of very old in our population. Therefore it is inevitable that dementia and serious sight loss either alone or together, will have important consequences for all of us1.The vast majority of people are alive(predicate) that dementia affects the memory. However it is the impact it has on the ability to carry out daily tasks and problems with behavior that cause partic ular problems, and in severe cases can lead to institutionalization. In the primary stages of dementia, the patient can be helped by friends and family through reminders. As progression occurs the individual will loose the skills needed for everyday tasks and may eventually fail to recognize family members, a condition known as prospagnosia. The result of such progression is that the individual becomes totally dependent on others. Dementia not only affects the lives of the individual, but also the family2.Dementia can present itself in varying forms. The most common form of dementia in the old is Alzheimers disease, affecting millions of people. It is a degenerative condition that attacks the brain. Progression is gradual and at a variable rate. Symptoms of Alzheimers disease are impaired memory, thinking and changes in behaviour. Dementia with Lewy bodies and dementias linked to Parkinsons disease are responsible for around 10-20% of all dementias. Dementia with Lewy bodies is of p articular interest as individuals3 with this condition not only present confusion and varying cognition, but also present symptoms of visual hallucinations2. Another common condition that causes dementia is multi-infarct dementia, also known as vascular dementia. It is the second most common form of dementia after Alzheimers disease in the elderly. Multi infarct dementia is caused by multiple strokes in the brain. These series of strokes can affect some intellectual abilities, impair motor skills and also cause individuals to experience visual hallucinations. Individuals with multi infarct dementia are prone to risk factors for stroke, such as high BP, heart disease and diabetes. Multi infarct dementia cannot be treated, once nerve cells die they cannot be replaced1.In most cases the symptoms of dementia and serious sight loss develop independently. However some conditions can cause both visual and cognitive impairments, for example Down syndrome, Multiple sclerosis and diabetes. De mentia is most prevalent in the elderly, as is sight loss. Therefore it is inevitable that a number of people will present dementia together with serious sight loss.There have been many studies into the prevalence of dementia in the UK. An estimate for the prevalence of dementia in people over 75 years of age is 15% of the population2. The Alzheimers society suggest that 775,200 people in the UK suffer from dementia (figures taken 2001). The Alzheimers society also calculates that the prevalence of dementia in the 65-75 years age group is 1 in 50, for 70-80 years 1 in 20 and for over 80 years of age 1 in 5. Estimates suggest that by 2010 approximately 840,000 people will become dementia sufferers in the UK. Estimates suggest that around 40% of dementia sufferers are in residential institutions. One study from 1996 showed that dementia sufferers are 30 times more likely to live in an institution than people without dementia. At 65 years of age men are 3 times more likely than women t o live in an institution and at 86 men and women are equally likely to be institutionalized4.Visual impairments are not associated general diagnostic features of dementia. However recent research has shown the change in visual function and visual processing may be relevant. Alzheimers disease patients often present problems with visual acuity, contrast sensitivity, stereo-acuity and color vision. These problems are believed to be more true of cognitive dysfunction rather than any specific problems in the eye or optic nerve9. Early diagnosis is essential to both dementia and sight loss patients, as drug treatments are becoming more and more available. Therefore maximizing the treatment and care for the individual. On the other hand early diagnosis of visual conditions is also essential, so that progression is slowed and treatment is commenced, therefore further progression is prevented if plausible2.The Mini-Mental State examination MMSE, is the most commonly used cognitive test for the diagnosis of dementia. It involves the patient to undertake tests of memory and cognition. It takes the form of a series of questions/answers and uses written, verbal and visual material. Poor vision or blindness is the most common cause of poor performance on this test other than dementia itself2.Visual deterioration can occur simultaneously with memory loss in most dementia sufferers. Therefore early recognition of dementia through vision tests has become of importance. Table 1 shows few possible tests that might be useful for such purposeTable 1 Vision tests for possible early detection and monitoring of Alzheimers diseaseUseBenton visual retention testMight be able to predict risk for AD 10-15 years before the onset of the diseaseTests visual memoryContrast sensitivityAD patients have selectively reduced CS for distinguishing large objects and facesUseful field of viewTests processing speed, divided attention and selective attentionFacilitates detection of attentional dysfu nction patients suffering from this problem complain of poor vision and inability to identify someone in a group or an object on a imitate backgroundCould be useful to assess fitness to driveFacial recognitionAD patients do not recognize faces with large features and low contrastAD patients do not recognize familiar faces (due to impaired memory)Tests that use facial expressions with progressively diminished degree of contrastThe aim of this paper is to provide information about current knowledge on the topic of visual function dementia. With regards to Alzheimers disease, there will be an inclination to several main foci of research. Namely anatomical/structural changes, functional visual changes, cognitive brain changes and other changes such as the effects of diagnostic drugs on Alzheimers disease patients.(2) Alzheimers diseaseAlzheimers disease is the most common cause of dementia amongst older adults. The Alzheimers research trust estimates that 700,000 individuals in the UK currently are afflicted. This number will inevitably increase exponentially in the near future with the trend of an increasingly aging UK population. Therefore it must be of the utmost of importance worldwide to have an understanding all behavioral, anatomical and physiological aspects of this disease.Alzheimers disease is a degenerative disease that attacks the brain, it begins gradually and progresses at a variable rate. Common signs are impaired thinking, memory and behavior. Health professionals and care givers agree that the memory deficit is usually the initial sign of the disease. However researchers have long known that Alzheimers disease is characterized by impairments of several additional domains, including visual function5.However these findings have not yet appeared in the diagnostic guides consulted by healthcare professionals, for example the most recent addition of the Diagnostic Statistical manual of mental disorders states that few sensory signs occur in early Al zheimers disease2. Therefore we still have a limited understanding of the true extent to which visual impairments affect Alzheimers disease sufferers. The current web site of the Alzheimers association1 and National Institute of Aging6 make no mention of the topic of sensory changes in Alzheimers disease. It has even been said that patients with Alzheimers disease report visual problems to their healthcare professionals less frequently than do healthy elderly individuals7. Nevertheless visual function is impaired in Alzheimers disease8. In terms of cognitive changes, the neuropathology of this disorder affects several other brain areas which are dedicated to processing low level visual functions, as well as higher level visual cognition and attention5.These neuropathological cognitive changes are more dominant however in the visual variant of Alzheimers disease known as posterior cortical atrophy. However visual problems are also present in the more common Alzheimers disease.Alzheim ers disease begins when there are deposits of abnormal proteins outside nerve cells located in the brain in the form of amyloid. These are known as diffuse plaques, and the amyloid also forms the central part of further structured plaques known as senile or neurotic plaques1. Buildup of anomalous filaments of protein inside nerve cells in the brain can also take place. This protein accumulates as masses of filaments known as neurofibril tangles. Atrophy of the affected areas of the brain can also occur as well as the enlargement of the ventricles1. There is also a loss of the neuro transmitter Serotonin, Acetylcholine, Norepinephrine and Somatostatin. Attempts have been made to try to slow the development of the disease by replacing the neurotransmitters with cholinesterase inhibitors, such as donepezil (Aricept), rivastigmine (excelon), galantamine (Reminyl) and memantine (Namenda)1. These drugs work by increasing the levels of transmitters between cells, which otherwise become lac king in Alzheimers disease. The National Institute for Clinical Excellence NICE conducted a review of these drugs in March 2005 and concluded that none of these drugs provided sufficient enough advantages to the patient in order to justify their cost. They recommended against the use of such drugs in the Nhs, though the Department of Health later overturned this ruling.(3) Visual Changes in Alzheimers PatientsLoss of vision is a key healthcare dilemma amongst the elderly. By the age of 65 approximately one in three people have a vision reducing eye disease. Dementia, Alzheimers disease patients and elderly patients, consequently have many visual conditions in common.Alzheimers disease impairs visual function early in the course of the disease and functional losses correlate with cognitive losses. There are several common visual functional deficits that are frequently identified in Alzheimers disease. There is evidence for deficits in Motion perception9,10 contrast sensitivity11 colo ur discrimination of blue short wavelength hues34 and performance on backward masking tests31.In Alzheimers disease the secondary point of damage is usually the visual association cortex and other higher cortical areas, as well as the primary visual cortex 13,14.(3.1) Some of the main changes that occur in the eye with aging includeThe crystalline lens increases in thickness, therefore decreasing its transparency and elasticity therefore there is a tendency for cataracts to appear.The conjunctiva can become thicker and wrinkled, therefore is subject to deposits such as pinguecela.The iris can atrophy, therefore pupils become constricted and their response to light becomes sluggish. The eyes ability to dark/light adapt is affected.Refractive index of the cornea decreases and it becomes less transparent. Arcus senilis can appear.The ocular globe and eyelids can shrink leading to conditions such as entropian, ectropian and trichiasis. Also while the lachrymal production is reduced the puncta lachrymalis can become stenosed and provide less drainage which gives rise to chronic watering of the eyesAnterior chamber usually becomes more shallow and the sclera more rigid, increasing the prospects of glaucoma.(3.2) Visual changes due to Alzheimers disease reported in literature are outlined below(3.2) AnatomicAbnormal nerve fiber layer and retinal ganglion cells (Blanks et al, 1989) (Tsai et al, 1991) (Hedges et al, 1996Imaging of the nerve fibre layer can be conducted via three techniques. These include Optical coherence topography (OCT), Scanning laser polarimetry and Confocal laser topography. Parisi et al16 conducted research upon the optic nerve fibre layer thickness using OCT. 17 Alzheimers disease individuals and 14 age matched healthy individuals were used. The findings of this study showed a definite relationship between the thickness of the nerve fiber layer and the prevalence of Alzheimers disease. There was a significant decrease in the nerve fiber layer th ickness in Alzheimers individuals when compared to healthy age matched particpants.Macular cell loss (Blanks et al, 1990)Research has shown a definite decrease of the number of retinal ganglion cells located in the maculae of Alzheimers disease sufferers in comparison to age matched control individuals. It was found that the loss of retinal ganglion cells varied with eccentricity from the central macula17. Results obtained by Blanks et al, 1990 showed a 28% loss of neurons from retinal ganglion cells at 0-0.5mm from the foveola, 24% loss at 0.5-1.0mm and 47% loss at 1.0mm to1.5mm from the foveola. These losses of retinal ganglion cells were constantly greater than those seen in age matched healthy individuals.Supranuclear cataract (Goldstein et al, 2003)Cataract removal could improve not only the visual acuity but may be an important tool in helping those patients suffering from visual hallucinations (Chapman et al, 1999) however, no prospective study has been carried out to prove t he role of vision improvement through cataract surgery on the well-being of patients suffering from ADExfoliation (Janciauskien and Krakau, 2001)Abnormal pupillary innervation 109-113Glaucomatous optic nerve cupping (Bayer et al, 2002)(3.3) FunctionalDecreased visual acuity (Holroyd and Shepherd, 2001)Rapid loss of visual field in patients with AD and glaucoma (Bayer and Ferrari, 2002)Visual field loss (inferior) (Trick et al, 1995)Reduced contrast sensitivity (Holroyd and Shepherd, 2001)Abnormal colour discrimination (blue, short-wavelength hues) (Cronin-Golomb et al, 1991)Abnormal flash visual evoked potentials (VEPs) (Holroyd and Shepherd, 2001)Delayed saccadic eye movements (Holroyd and Shepherd, 2001)(3.4) CognitiveAbnormal visual sustained/divided/selective attention and visual processing speed (Rizzo et al, 2000)Inability to recognize depth (Holroyd and Shepherd, 2001)Impaired face recognition (van Rhijin et al, 2004)(3.5) OtherExcessive pharmacological mydriasis/miosis 109-1 13These changes summed together not only diminish the quality of vision, but many of them also make the examination of the eye much more complicated. In conjunction with the general visual symptoms of aging, Alzheimers patients can also experience visual disturbances caused by the brain rather than the visual system alone. This means that they can have problems and difficulties perceiving what they see rather than how clearly they see it3. Difficulties are usually experienced in the areas mentioned earlier, namely depth, motion, color, and contrast sensitivity. Visual hallucinations are also a common problem linked to loss of vision in Alzheimers disease patients18. Another common disorder linked to patients with Alzheimers disease is a variant of motion blindness. The patient can appear to be confused and lost the individual will see the world as a series of still frames19.Visual changes in Alzheimers disease may also be dependent upon which brain hemisphere is more severely damage d this factor can often be overlooked. An individual with Alzheimers disease could have damage to a greater extent on their left brain hemisphere from plaques and tangles. This would therefore cause subsequent retinal changes in only the left hemi-retinas of each eye i.e. the right visual fields. The right eye visual field would be affected in the temporal side (right) and the left eye visual field would be affected nasally (right)20. When only half the retina is impacted, smaller regions of the optic nerve and nerve fiber layer show losses. The left eye with affected temporal retina would show optic nerve damage in differing regions of the nerve than the right eye with nasal retinal damage20.Alzheimers patients commonly show selective degeneration of large ganglion cell axons located in the optic nerves. This suggests that there would be impairment of broadband channel visual function. Conversely studies have shown that broadband visual capabilities are not selectively impaired in Alzheimers disease. The magnocellular and parvocellular neurons are greatly affected in Alzheimers patients, this has been proved by studies of the dorsal Lateral geniculate nucleus(LGN)1. The geniculostirate projection system is split both functionally and anatomically into two sections. They include the parvocellular layers of the Lateral geniculate body and also incorporates the magnocellular layers. These systems are mainly divided in the primary visual cortex and go through further segregation in the visual association cortex. They conclude in the temporal and paritetal lobes1.The parvocellular layers contain smaller, centrally located receptive fields that account for high spatial frequencies (acuity), they also respond well to color. On the other hand these cells do not respond well to rapid motion or high flicker rates. The magnocellular cells have larger receptive fields and respond superiorly to motion and flicker. They are however comparatively insensitive to color differ ences. The magnocellular neurons generally show poor spatial resolution, although they seem to respond better at low luminance contrasts. To summarize the parvocellular system is superior at detecting small, slow moving, colored targets placed in the centre of the visual field. Meanwhile the magnocellular system has the ability to process rapidly moving and optically degraded stimuli across larger areas of the visual field1.The parvocellular system projects ventrally to the inferior temporal areas, which are involved in visual research, pattern recognition and visual object memory. The magnocellular system projects dorsally to the posterior parietal and superior temporal areas. These are specialized for motion information processing. The cerebral cortical areas to which the parvocelluar system projects receives virtually no vestibular afferents. Alternatively the cerebral areas to which the magnocelullar system projects receives significant vestibular and other sensory inputs. These are believed to be involved in maintaining spatial orientation. Research shows shows that the magnocellular system is more involved in Alzheimers disease1Oddly, many individuals experience difficulties at low spatial frequencies instead of high frequencies as in old age. This suggests that areas controlling the low spatial frequency processing in the primary visual cortex would be affected more than those for higher frequencies processing21 After neuropathilogical studies in 1997 by Hof et al were carried out on brains with visual impairments they concluded that cortical atrophy dominated on the posterior parietal cortex and occipital lobe22.Glaucoma is also a neurodegenerative disease that has similar effects on the visual system. Lower spatial frequencies in the contrast sensitivity, deficits in the blue short wavelength color range as well as reductions in motion perception are all linked to glaucomatous patients23. When patients diagnosed with Alzheimers disease also have glauc oma, the deterioration of vision related to glaucoma is much more rapid and progression is more aggressive than in people with glaucoma solely and not Alzheimers disease as well24.Glaucoma is different from Alzheimers disease in that it affects the visual function at the early sites of neural activity, namely, the retinal ganglion cells. Glaucoma destroys the afferent axons at the nerve fiber layer in the retina. This loss of axons ultimately leads to added atrophy further up the visual pathway due to decreased neuronal input. Alternatively Alzheimers disease impacts the cells that are located terminally or intermediary in the visual pathway of the brain. The result is again reduced neuronal input due to loss of nerve fibre connections and atrophy along the visual pathway. When the two diseases exist in the same individual together it can be seen that there is likely to be a greater disruption to the visual system25. One key difference between the two diseases is that they affect th e visual pathway at different points. Glaucoma is a degenerative disease starting at the beginning of the visual pathway, whereas Alzheimers disease is a degenerative process starting relatively late in the visual pathway. When the two diseases coexist then the neuronal and functional losses of vision are cumulative.(4) Optometric examination of dementia patientsDementia patients present special problems for optometrists. A standard eye test can be an audile to even the best of us. The patient is placed in an unfamiliar environment surrounded by unusual equipment, machinery and is subjected to probing questions about their medical history which will without doubt tax their already flawed memory. Dementia patients are most likely to be from the elderly. Therefore several difficulties are presented while conducting an ocular examination. The patient is required to sustain a position and has to maintain concentration throughout the testing procedures, which can be very difficult. Subje ctive examination requires responses from the patient, they are expected to remember and follow complex instructions given to them by the optometrist as well as make many precise discriminatory judgments in a short space of time. The multiple tasks required to be completed during the examination are often beyond dementia patients as they are limited by the disease. Therefore it is common that patients with even a minor degree of dementia fail to provide valid answers, provide unpredictable responses to the subjective examination and retreat into an apathetic state1,2.During the visual examination of Alzheimers disease patients, several key visual problems can be detected. Moderate dementia patients will often experience problems such as topographic agnosia, alexia without agraphia, visual agnosia and prospagnosia1. Such patients often cannot describe individual components of photos and routinely fail to recognize family members. The degree to which such problems are experienced is c onsistent with the level of cytochrome oxidase deficits in the associated cortical area. In conjunction with these problems dementia patients often have problems with texture discrimination and blue violet discrimination1.Throughout the examination of the elderly dementia patients there are two contradictory requirements, firstly is assurance. The patients responses will be delayed and the patient may feel anxious in such an unfamiliar situation. Thus constant reassurance is required and they cannot be rushed. Alternatively time constraints are important, a dementia/elderly patient is likely to have a short attention span. Consequently the two factors above much be considered and balanced. The examination must be thorough yet carried out as quickly as possible. Often when examining a dementia patient a family member of the carer must be present in order to aid the communication between optometrist and patient, for example difficulties are likely to occur when recording history and s ymptoms without a carer present. All factors need to be considered such as family history, medication, eye treatment and knowledge of any medical conditions and if so how long they have suffered from them.In terms of an external examination firstly, gross observations should be recorded for example does the patient have an abnormal head position or is there any lid tosis. Many external observations can also be detected with the aid of pupil reflexes. Upon carrying out the external examination the optometrist must be carful to explain exactly what each procedure will involve so as not to intimidate the patient.(4.1) Internal ocular health examinationInternal examination of an elderly patient often presents many problems. Older patients tend to have constricted pupils and often opacities in the media such as cataract. All of which make opthalmoscopy a much more complex task for the optometrist. Patients with dementia also show poor fixation as well as lack of concentration. Pupil dila tion is often used to aid external examination however many older patients can have a poor response to the insertion of mydriatic eye drops. fddfdffdgThere have been many studies into the affects of diagnostic mydriatic and miotic drugs. Many studies have shown excessive mydriatic pupil response to trompicamide (a pupil dilating drug) in patients with Alzheimers disease when compared to control individuals26-30. On the other hand studies into the use of Miotic drops, particularly Pilocarpine have shown an increased response of pupil constriction in Alzheimers disease patients upon comparison to normal control patients. These findings suggest a defect in pupillary innervation with Alzheimers disease individuals. Studies of post mortem individuals with exaggerated mydriatic pupil responses to Tropicamide found a definte disruption to the Edinger-Westphal nucleus. The Edinger-Westphal nucleus is one of the key structures of the brain involved in the autonomic nervous system, it mediate s the sympathetic and para-sympathetic pupil responses. Research by Scinto et al found amyloid plaques and neurofibrillary tangles in all individuals tested with excessive mydriatic pupil responses. The conclusion was that the Edinger-Westphal nucleus is targeted early in the progression of Alzheimers disease.In terms of intraocular pressures use of the goldman an Perkins tonometers will be limited for the elderly dementia patients, due to health and safety reasons. Sudden movements whilst carrying out pressure tests on such equipment may be dangerous. Therefore this can be overcome to a degree by the use of handheld instruments such as the pulseair. However even with the pulseair problems can still be faced with uncooperative patients.(4.2) Objective Refraction examinationWith uncooperative and awkward patients objective refraction through retinosopy may be difficult. Factors such as opacified media, miotic pupils, and poor fixation will influence the accuracy of the refraction. Th e recent introduction of hand held optometers has contributed to somewhat overcoming such problems. Instruments such as thee Nikon Retinomax are excellent for obtaining an objective refraction of the elderly patient with miotic pupils and cloudy media.When presenting the Snellen chart to a patient, the quality of their response will inevitably depend upon the degree of their dementia. Depending on which stage of dementia they are suff

StarTeam System Development

StarTeam strategy DevelopmentDelainah E. BorgoniaStarTeam is a smell cycle attention tool that provides program passenger cars and placement developers the ability to create on projects and runway change prudence. This formation was develop by a comp either named Starbase Corporation, which then was bought by Borland in January 2003. StarTeam now belongs to Mirco concentrate which is known to build, run and secure enterprise software. In order for this remains to work on your computer and run placement, you are required to lose certain computer hardware and Software requirements. Even though StarTeam is the system of choice for the carriage crowd Life beat Operations Agency, StarTeam does have a competitive emolument to too soon(a) systems that our soon on the marketplace today. StarTeam is a great sustenance cycle management system that does the line, however I do opine if I was able to make a few system sweetening recommendations, it go out be a robust and better system that all in allow be serious to our workplace and mappingrs.Server-Side hardware RequirementsStarTeam system works exclusively on two different server-side hardwares. It currently enforces a Windows Server with all a 32-bit or a 64-bit computer central processor. With a 32-bit computer processor it must have a token(prenominal) 32-bit dual-core system with at least(prenominal) four gigabytes of memory. With a 64-bit computer processor it must of a minimum 64-bit quad-core sytem with at least four to eight gigabytes of memory.Server-Side Software RequirementsThe server-side software requirements for the StarTeam informations system are currently used on a multitude of in operation(p) systems. StarTeam system currently works with the Mircosoft Windows Server, Red Hat Enertpirse Linux, and SUSE Linux operating(a) systems. The however smallsoft Windows Server adaptations StarTeam is compatible with is the 2012 and 2008 versions. For the 2012 version, it sole(prenominal) works on the 64-bit computer processor, and on the 2008 version, it works on either the 32-bit or 64-bit processor. This information system besides works on two Linux operating systems for those who uses a Linux in operation(p) system platform. Red Hat Enterprise Linux platform delivers a military grade-security with a 99.999% up epoch, the only versions that is compatible with StarTeam are the 6.7 in both 32-bit or 64-bit operating system and/or the 5.5 version only in a 32-bit processor. The separate Linux plateform that is compatible with StarTeam is SUSE Linux 11.3 and 11.4 Enterprise Desktop in either the 32-bit or 64-bit system processor. SUSE Linux is an affordable environment that currently is coexistent with Windows, mackintosh, Unix and other operating systems.Client-Side Hardware RequirementsStarTeam is used and has been tested on both laptops and desktops computer hardware, that as at least a minumum 32-bit dual core operating system with a mini mum of two gigabytes of memory. The hardware must have 200 migabytes to lay down the performance with an adequate disk space required for all your files that you would work on a daily basis. uniform with all other products the bar of disk space will differ depending on how much you use the product. Currently at our workplace we currently use it on either a laptop or desktop computer hardware system. StarTeam is withal compatible on few MAC computer models as well. It stop be used on a MacBook with the early 2015 model, late 2008 aluminum, early 2009 or newer model. It also works on the MacBook Pro and MacBook Air. The MacBook Pro must be the mid to late 2007 or newer model and the MacBook Air must be the late 2008 or newer model. It also works on the Mac Mini, Imac and Mac Pro just to name a few a few others. Just for your information StartTeam instigate is only for the physical apple Computers only, and the OS X Virtual Machines are not supported by StarTeam information sy stem.Client-Side Software RequirementsThe StarTeam information system client-side software we currrently use at our workplace is the StarTeam Cross-Platform Client System. The Star-Team Cross-Platform Client System uses Java and erect be used on a Operating System that mess support the Java Runtime Enviromment (JRE) 1.8.0_102 version. This Cross-Platform Client has been used and tested on the certain softwares. The Operating System the StarTeam Cross-Platform Client is compatible with is the Mircorsoft Windows 10, 8, 7, XP Professional SP3, and Windows Vista SP1 in either 32-bit or 64-bit processor. StarTeam Cross-Platform Client System is also compatible with other operating systems like the Solaris Sparc 10, RedHat Enterprise Linux 6, Ubuntu 14.04, SUSE 11.3 and the El Capitan, Yosemite on the Mac OS. The Client System also needs an Adobe Acrobat software in order to muckle any PDF manuals or files. Also, if any online help is needed you must use an Internet Explorer 8 or later for Microsoft Windows only or Firefox 4 later browser. In order for the StarTeam to work at its optimal performance it is recommended that the StarTeam Server be on a its on use screening server unless your workplace is using a supported version of Microsoft SQL Server Express as their database.Competitive Analysis of the SystemThe StarTeam application lifecycle management software has a whole lot of competitors on the market today. There are numerous lifecyle management application software that offers a whole lot of features compared to StarTeam. In order for StarTeam to stay competitive against its other software rivals, MicroFocus has made an ideal application lifecycle management software that privy be used and implemented easily by any face of development team or enterpise. How StarTeam stays on top is MicroFocus has developed a feature that allows users to post system suggestions to request enhancements and imporovements to its system. StarTeam is also an on-line tool t hat can be accessible from anywhere through any compatible device, which makes it easy for users to collaborate on projects and track change management at anytime. MicroFocus is also known for their security, high performance and stability. They have created an application lifecycle management software application that can easlily be run. It is also so lightweight that it can be integrated with a multitude of tools that you may be already be using. StarTeam also stays competitive by always upgrading and doing server imporvements to its software. This is an important step when competing against rivals. Knowing what the customers wants and needs can always make your system better than others that are comparable to StarTeam. other benefit StarTeam has from other systems and rivals, is their customer gain team. Having an excellent customer service team that knows their product and responses with little or no wait time can make or break a system and company. StarTeam is a system know n for its stability, ease of use to the users, performance and its software pricing. Like with any system out there StarTeam can use some system enhancements that I believe can imporve the users experience.Recommendations for Improving the SystemInformations systems can always be enhanced and made better, that stays true to StarTeam as well. The one recommendation I have for StarTeam is the ability to notify you by email whenever there is a change in status with the requirement. This will allow my team to keep track of our requirements on where it is in the system life cycle, preferably of logging into the system to check. At this time StarTeam only sends email notification to the point of contact when a project is awaiting their coordination. I believe if the system was enhanced to allow an email notification to be sent anytime there was a change in status, it will allow the user to save time from not loggin into the system. The second recommendation I would like to improve to Sta rTeam is to have StarTeam be a web-base system instead of connecting through a client server. StarTeam currently uses a server which currently takes about 1-3 minutes to open one requirement. I believe if StarTeam was a web-base system, Im hoping it will decrease the wait time it takes to open a requirement. This is a a great deal when making changes to multiple projects at the equal time. The last recommendation I would improve is the ability to link all change requirements that have dependencies with each other. This will help the requirement manager to capture all the change requests that have to be developed unitedly, instead of opening each one separately. Altough these changes may not be effectual to the developer and analyst process, but I think these recommendations would be a coarse benefit to the requirement manager users experience for tracking all requirements and doing their job as a whole.ConclusionStarTeam is a life cycle management tool that allows program manag ers and system developers the ability to collaborate on projects and track change management. Ive discussed what hardware and software requirements a user must have in order to use the StarTeam Application Life Cycle instruction software. StarTeam is a great system the Air Force Life Cycle Operations Agency uses for keeping track of the development and enhancement to an Air Force System, but I know that the enhancements Ive discussed, like it being a web-base system vs a client server, and having all requirement dependencies link together instead of it just stating the requirement number can be beneficial to my workplace as well its user. StarTeam does have a competitive advantage to other systems that our currently on the market today by Micro Focus outstanding customer service as well has maturation a feature that allows users to recommend system enhancements and improvements to their system. StarTeam is great but with every system out there , there is always room for improvemen t.ReferencesHome. (n.d.). Retrieved from https//www.microfocus.com/products/change-management/starteam/system-requirements/Megherbi, M. (n.d.). StarTeam Reviews (1 Review) StarTeam union Feedback Score 4.00 Mar 2017. Retrieved from https//www.crowdreviews.com/starteamreviewsBorland StarTeam Installation Guide.(2013). Costa Mesa, CA Micro Focus

Real World Examples Of Price Ceiling Economics Essay

Real World Examples Of Price Ceiling economic science EssayThe chairwoman of the Philippines, Arroyo placed the entire nation under a cite of calamity on 2 October 2009 which is a week laterwards tropical storm Ondoy, and a day before super typhoon Pepeng began. The tone-beginning of typhoons Ondoy and Pepeng smashed up many parts of Philippines, caused everywhere P30billion in damage and claimed nearly a thousand lives, primarily Metro Manila and marriage Luzon provinces. Despite devastation of typhoons, several cover companies raised cover colour prohibitedlays which prompted state-supported protests and criticisms and prune off more than the common grumbling from consumers. With millions of Filipinos still anguish from the put togethers of those typhoons, the corporations were criticized as greedy, heartless and predatory. Royal Dutch Shell, Petron and Chevron (known hither under the brand Caltex) increased the wrongs of diesel by 2pesos per- cubic decimeter , o r 4 cents, an increase of approximately 6.7 percent. Gasoline expenditures went up 1.25 pesos a liter, or 4.74 pesos a g each(prenominal)on, and kerosene by 1.50 pesos. According to the Ibon Foundation, an indep dyingent economic search group, the increases were the biggest of the year. The companies assert the increases reflect earthly c at oncern oil expenses. After Ondoy and typhoon Pepeng ingest left the solid ground for some time, the entryway of immature typhoon Ramil postulate the pain of price crownwork more necessary.To protect habitual interest, the giving medication en chock upd a discharge price ceiling to nix predatory pricing, unreasonable pricing and to precipitate the adversities caused by those calamities by temporarily imposing price ceiling on oil. The president, through the EO, ordinationed the joint Department of Justice (DOE) task force to institute complaints against the violators of the EO as well as the provisions of RA 8479. President Ar royo revoked Executive Order 839 on the Philippines main island of Luzon, which kept the level of the price of oil mathematical products prevailing on 15 October 2009. The announcement was made after she met with Cabinet secretaries and representatives from the oil firms and transport sectors.Before the EO was issued, the President ordered a study of how to include petroleum products under price withstand, considering that contribute is an valuable product used by al virtually all consumers. Before revoking the edict, Arroyo want petroleum companies assurance that they would continue to provide fuel push asides to transport groups for the next six months to keep f atomic number 18s down. Arroyo withal proposed that dealers of liquefied petroleum gas (LPG) advise stagger their price over the Christmas season so consumers wont as well harshly affect by increasing price. The Palace further pointed out it was based on the EO is Section 14 (e) of Republic Act 8479 or the Oil effort Deregulation Law, which states that In times of national emergency, when the public interest so requires, the DOE may, during the emergency and under reasonable damage prescribed by it, temporarily take over or beam the operation of any person or entity engaged in the industry.The EO took military force immediately upon its publication in a newspaper the next day. responseMany consumers and few companies praised the presidents decision because the imposition could help millions of Filipinos recover from those calamities notwithstanding the changes in price when price ceiling was obligate was an insensitive hold out to the oil companies.Economists said the unprecedented interference could sc ar investors away from the country. The marijuana cigarette impertinent Chambers, a collection of chambers of commerce whose members include study oil firms, argued in their letter that a price cap in the northern Philippines would lead to lower fuel imports, deficits and a bla ck market. The order has prompted oil companies to warn of a paucity since they may be labored to plow their products at a loss if global fuel be rise. It is because the oil prices are tied to humankind markets and the companies would think twice about importing more oil. Petron Corp., the Philippines largest oil fellowship predicted that it may lose up to P1.5 billion pesos, or $32 million, in its fourth quarter for the pull through three months of the year since the executive order may force it to grass at a loss. Some people compelled the authorities to increase the price obstructs nationwide especially because the price of oil in the Visayas and Mindanao ,which are the cardinal other main island, are 5 to 7 pesos more big-ticket(prenominal) than price in Luzon.The companies have insisted that their prices are determined by the world market and did not prosecute for predatory pricing. However, because of the increasing of price all at once and the companies refused t o open their books, suspicion has grown among the public. To comply with EO 839, oil firms reverted to prices before 19 October 2009. Most oil firms raised prices by P2.00 per liter for diesel, P0.85 per liter for regular, P1.50 per liter for kerosene and P1.25-1.50 per liter for fuel.ConsequencesMAP said that with the imposition of the order, the government is breaking its promise to provide oil investors stability and certificate under the law and the government should subsidize the products.On 2 November 2009, strange and local businessmen demanded the termination of President Arroyos Executive Order 839, to change magnitude the adverse influence of loses on the petroleum, risk of future stock products, and load to future and appearance of black market.In a statement, the Joint Foreign Chambers (JFC) said oil supply in Luzon, which accounts for 80 percent of the countrys petroleum market, forget be compactd because importers go away not share at a loss.EO 389 lead not re ally help the most needy of typhoon victims. It is because the poorest income groups are not consumers of petroleum products. This happens because the government is not reform what products they usually grease ones palmsd and then imposed price ceiling on oil that provide low reconstruction and rehabilitation.Reports on fuel supply shortage coupled with spiking fuel prices brought fears to Cebuano consumers that these might create a negative touch onion towards the prices of other commodities.However, the price monitoring report of the Department of Trade and Industry showed that prices of goods in the market have not posted alarming changes because of the fuel supply shortage.Oil firms warned that more serious fuel supply shortage in less than two weeks from 11 November 2009 if the freeze on petroleum prices stays.13 days after that day they would run out of finished product stock. The big oil firms did not face any real financial difficulties or bankruptcy as they have over a decade of overpricing and accumulated super profits.How to settle the problemGovernment responded that the DOE and the oil companies must open their books and show the public that all the negative things attributed to them are just misperceptions because even though the price of crude has gone up to $80, the increase should not be affected immediately at to the lowest degree not until after 45 days.On 4 November 2009, Deputy presidential spokesperson Lorelei Fajardo said the price freeze would rest in effect for the duration of the state of calamity in Luzon based on the recommendation of Justice Secretary Agnes Devanadera. This was emphasized by deputy presidential spokesman Lorelei Fajardo on 2 November 2009 after the Joint Foreign Chambers (JFC) asked the termination check of Executive Order 839.However price caps stool only be imposed for a maximum 60 days ,the imposition will be lifted sooner or later.The government opened to selective writ of execution of the oil price freeze after weeks of protests and warnings of a fuel supply crisis. Petron has hold to open its books and the government hoped that the rest of the industry, especially the Big 3, would likewise be this transparent.Meanwhile, Malacaang said that the Energy Regulatory Commission (ERC) and the Dept. of Energy (DOE) will study proposals about price freezing as the ERC and DOE are in the best position to determine the merits of this proposal because they are certain of the factors involved in the incident.President Arroyo announced her decision on13 November 2009 at the end of an emergency meeting at Malacaang with representatives of oil companies as well as officials of labor and transport and ordered the lifting of the price freeze on petroleum products and basic commodities in Luzon, which was still officially under a state of calamity, effective on 15 November 2009.This decision was made after fashioning oil firms and traders promise to recoup their losses on a staggered basis , stabilize prices and supply of products ,put in more investments for the poor to spur economic exertion and create jobs and provide some form of subsidy or discount in selected areas, especially those affected by the calamities.The bottom line is to retain the same in the next six months, assuming that world markets remain stable. If international pump prices become very high, then the government chamberpot review this policy.Most of the corporations committed to hold the price for at least six months.It was agreed during the meeting that details of the price adjustments and subsidies would be finalized over the weekend.The DOE (Department of Energy) and the oil firms are given the weekend to go tail end to the drawing board and make their calculation or formula (on the price increase).Mrs. Arroyo also instructed Favila and Energy Secretary Angelo Reyes to help transport groups set up a consortium that would allow them to directly import fuel.Favila said the topic Developmen t Corp. and the Philippine International Trading Corp., both government corporations, will help put up capital for the venture.The oil companies welcomed the move and have agreed not to increase their prices on a one-time basis. Earlier estimates showed that consumers may have to bear P4.50 to P5 per liter increase in pump prices once the EO is lifted.As to how much the first increase in price on 15 November 2009 depended on competitive forces. According to Martinez, the P1-billion fund which was earlier set aside by the government to assist the transport group in conversion to LPG may also be tapped to help cushion the impact of the expected surge in oil prices in the next few weeks.Martinez suggested that assistance or subsidy could come in the form of discount coupons for legitimate transport groups. The oil firms as well as manufacturers and traders agreed to his proposal to reduce prices in areas that continue to suffer from the effects of the storms.On 16 November 2009,Preside nt Gloria Macapagal Arroyo said that the government will not hesitate to re-impose the freeze on fuel prices in Luzon if oil companies will renege on their promise to stagger increases in the prices of their products. The oil companies, manufacturers and traders are fully assured that the government can again impose price tone downs.Drugs price fudge in CanadaGovernment in Canada have imposed price controls on prescription medicinal do do do medicatesss for many years for its citizens .Through this intention ,the affordable of Canadian citizens in purchasing the necessary medicines they need can be ensured .To strain the efficiency in drug prices control ,several mechanisms have been instituted to control drug prices .These includes the establishment of a semi judicial by the federal government to control drug prices and several measurements to regulate the drug prices at the peasant level ,for instance ,formulary management ,use of generic wines ,reference-based pricing ,pr ice control of patent of invention medicine ,price freezes ,reimbursement rates ,cost sharing arrangements and limits on markups .These measurement have make authority price control to a large range . bareed Medicines Prices polish up Board (PMPRM) ,a federal quasi- judicial agency established under the Patent Act in 1987 to regulate drug prices .This agency take duty to control price of patented medicines only .The PMPRM was intended to avoid and prevent the prices of patented drug reach excessive which might exit from manufactures new right to market exclusivity .Hence ,certain guidelines are used by PMPRB in observe out the excessiveness of a drug price The cost of therapy of new patented drugs must make sure not exceed the highest cost of therapy and in the range of existing drugs used to treat the same disease .Manufactures can charge the breakthrough drugs and those that offer a substantial improvement to the average of prices charges of the same drug in other specified countries which are joined State , unify Kingdom ,Switzerland ,Sweden ,Italy ,France and Germany to ensuring that Canadian prices are not highest in the world .The increases of prices of existing patented drug cannot exceed the Consumer Price Index .The PMPRB gains control over the pricing of the drug once the drug accepts a patent of any sort and also review the drugs price when it was initially marketed . A company that consider out of compliance with the guidelines by the PMPRB must reduce the price .Moreover ,any excess revenue that have earned by that company from sales of the drugs will be relinquished and can order the quittance of the excess revenue of the company to the federal government .Purpose national price controls on patented drugs is to avoid brand-name companies from reducing prices on these products once a patent expires .The highest price of the exisying drugs in the same therapeutic partition is take as a reference by Canadas Price-Control Policy .This is thr ough to establish the maximum allowable for new patent-protected drug formulations entering the market .As a result ,due to fearness of makers of brand-name drugs of unintentionally lowering the maximum allowable entry price for new drugs in the same class ,the makers of brand-name drugs will reluctantly reduce the price of the original drug when it goes off-patent .An artificial incentive is created by Canadian price controls to resist competing for brand-name companies on the basis of price with generic firms for sales of off-patent drugs .Consequences of Drug Prices ControlAlthough government of Canada have imposed drug price control system to ensure the prices of drugs are under control ,however ,cannot deny that ,the drug price control system also result in consequences .Price- controlled system of Canadian bureaucracy indirectly lead to decrease in producing fewer new drugs Canadians are very much forced to depend to a year for more advanced medicines .As a result ,Canadians are routinely denied access to newer and better medicines ,and often travel to America to purchase them .Moreover,price discrimination is one of the consequences of drug price control .Drug companies and industry often engaging in price discrimination by charging the incompatible buyers for different prices of the same product .Drug companies are prefer to sell the drugs for less in Canada and elsewhere only .This phenomena is happen due to the drug companies can sell for more in the United States.In addition ,the expensive using of drugs and moderately cheap to manufacture will indirectly lead to price discrimination works in the drug industry .Price discrimination causes drug companies in Canada to charge high prices of the same product of drugs in United States. Hence, companies can recoup their research outgrowth costs .Besides that, companies can make a profit in Canada and elsewhere by simply showing the cost of making the pill as long as the research development cost o f companies can recoup.Further ,price controls make investing in research development less attractive .This is the result of the continuing of upgrade in costs and risks involved in developing new drugs .With particular(a) risks and uncertainties ,companies never being sure of the selling prices of their future drugs and even find themselves having to reimburse sizable sums . For example, Schering Canada Inc. had to reimburse $7.8 million in 2003 because it charged a price judged as excessive for its infliximab (Remicade) drug.Price control causes a direct reduction in volume .Due to this ,a declining number of research development missions are obtaining by Canadian subsidiaries .As a result ,pharmaceutical innovation is indirectly become slower ,and lead to a remarkable drop in pharmaceutical research development .A decline of pharmaceutical research in Canada would hit Quebec hardest ,which is the home to Canadas largest concentration of pharmaceutical research development , with 42.3% of nub spending in2002.However there other major costs linked to drug price controls ,these include losses of highly skilled jobs ,corporate research centers and jobs forgone in the subcontracting of goods and services and in industries associated with research development .Downward pressure on the prices of older patented drugs and non-patented drugs since distortions caused by price controls would cease to exist . pharmaceutical firms eliminate incentives to lower the prices of drugs already on the market is result from price control .As a consequence ,some generic drugs are more expensive in Canada .In order to fully recovery of research development ,launch and selling costs ,companies tend to keep these prices high .This condition will also lead to a higher selling prices of the goods by generic drug producers .Last but not least ,drug price control will lead to lower rates of substitution of generic versions of drugs by consumers in Canada for their brand name originals drugs .The possibility of price competition between off-patent ,brand-name drugs and generics raw is eliminated by the public policies forcing substitution of generics .Generic companies no longer have to repugn on price against consumer loyalties toward brand-name drugs when forcing generic substitution for brand-name drugs is done by government .As a result ,consumer need to purchase the drug at higher price due to the absence of alternative products .

The Speech On Animal Testing Philosophy Essay

The Speech On Animal Testing Philosophy Essay wide morning, ladies and gentlemen, it is great to be here with you alone on this marvellous morning. I am here to convince all of you to oppose, stop and disengage from the cruel, prejudicious and unnecessary animal interrogatory.Do you know that the lipstick, the eyeshadow and the mascara we habituate to make ourselves discover more attractive drop poisoned hundreds of thousands of innocent animals?Do you know that the copspray, the hair gel and the perfume we use to make ourselves look smarter have blind hundreds of thousands of innocent animals?Do you know that even the toothpaste, the shampoo and the soap we use bothday have killed hundreds of thousands of innocent animals?If your solvent is No, now is the time for all of us to know it. Animal examination is not only a re search to find cures for gentle diseases, it is also an experimentation to establish sanctuary of various products such as daily necessities, cosmetic pr oducts and medicines.To produce a safe product for us, m whatsoever animals have died in laboratories. To ensure our health, numerous animals have tortured in laboratories. To permit us stay away(p) from diseases, numerous animals have gone through the unbearable aches and pains in laboratories.An overview of animal testing of People for the Ethical Treatment of Animals has judged us dishonored of killing close to hundred million of animals in research laboratories every year. Each year, nearly 100 million of animals have been burned, poisoned and starved. Each year, nearly 100 million of animals have been dosed with poisonous elements, driven nuts and deliberately infected with diseases such as cancer, diabetes and AIDS. Each year, nearly 100 million of animals, their eyes atomic number 18 removed, their brains are damaged and their bones are broken. Each year, nearly 100 million of animals have been condemnablely abused, pitilessly tortured and defencelessly killed for human benefits. Did they deserve such cruel and brutal treatment?They died for genetics research, for biomedical research, for xenotransplantation, for physiological research, for medical research, for drug testing and for toxicology tests.Perhaps you whitethorn say these tests and researches are for a uncorrupted cause, in force(p) is it a really good cause that numerous innocent animals are batting caged up, tortured and sacrificed to achieve?Perhaps you may say these tests and researches are good for your safety, but is the chemical reaction on an animal same as the one on a human being?Perhaps you may say these tests and researches are good for your health, but can these tests and researches reliably squall effects in man? Are there no any side effects on human beings?Scientists and researchers claimed that they have unlimited entryway to animals for experiments in order to find cures for human diseases. Yet, animal testing has truly endangered the life of human beings as the results from animal testing cannot be applied to humans. According to PETAs fact sheet, they argued that In many cases, animal studies do not unspoilt hurt animals and waste money, they kill people too. most drugs were all tested on animals and judged safe but had devastating consequences for the humans who used them. Have all of us thought that why this would fall? The answer is very simple. This is because animals and humans are comp permitely different from each(prenominal) other. As Dr. Arie Brecher said, No animal species can serve as an experimental model for man.Scientists should ask themselves do frankfurters have the same DNA as us? Do cats have the same genetic characteristic as us? Do rabbits or rats have the same body carrel as us? It is absolutely ironic when scientists answer No to these questions magic spell they are quiet using human benefits as an unacceptable and thin excuse to perform the practice of animal experimentation.Thus, should we still k eep our cartel in scientists and researchers ability to find a cure via animal testing? Should we still believe in those products which have made millions of rabbits blind? Should we still depend on and rely on such an inaccurate experimentation to cure our diseases? For me, the answer to these questions is No. It should also be the answer of yours, the answer of our humane society, the answer of our country, the answer of all the five continents and the answer of the good world.We have no the responsibility to use animals as the subject for any researches or experimentations just as we do not have the right to experiment on humans without their consent. We should respect the right of all species just as we respects the right of all people. We should pitch in with the school against animal testing and stand up for animal rights, for the animals tortured and yell behind laboratory doors just as we stand up for our admit right. Like Sri Aurobindo said, Life is life whether in a cat, or dog or man. There is no difference there between a cat or a man. The idea of difference is a human conception for mans own advantage.Any of us who donates to a medical liberality is actually assisting to storehouse the research involving animal testing. We fund to cover the expenses of cage, the expenses of give and the expenses of experimental materials. We fund to provide and purchase animals as experimental subject. We fund to blind, scald and poison animals.Animals are just homogeneous our family, friends and companions. Is it right for us to provide money that causes our family, friends and companions to be subjected to medical research?Animals are just like us, they are creatures which created by god. well(p) like us, they have feelings. Just like us, they are able to feel pain, hunger and thirst. Just like us, they will grieve over loved ones they have lost.We should try to recall the feeling of animals. We should imagine if we were massacred by those wild and ferocious animals and nobody is exhausting to save us. Imagine if we were living inside a small cage and waiting to die in vain. Imagine if we had no any accommodate of our own life and had no any freedom. Imagine if we were forced to be injected with drugs or toxic substances when we had never even done anything.With modern engineering science that we have created these days, animal testing is really an unreliable, unscientific and unnecessary experimentation. Nowadays, we have plenty of alternatives which have a much higher percentage of winner than animal testing. Instead of animal testing, we can use human cell culture systems instead of animal testing, we can use computer numerical models instead of animal testing, we can use artificial human climb and eyes that mimic the bodys natural properties.I believe that with the changes in technology these days, we are able to find more ways and methods that scientists and researchers can do research without involving any cruelties and causing any harm to any creatures.Now, let us stop buying and using the products tested on animals.Now, let us save the ship of animal rights that had sunk to the bottom of the sea of humans ignorance, rudeness and curiosity.Now, let us dig up the root of cruelty and start sowing the seeds of humanism all over the world.Now, let us start it today.Thank you very much.

The Process Heat Exchangers Engineering Essay

The Process ignite Exchangers Engineering EssayIn this chapter, a full unit of light up money changer will be endeavored including its chemical and windup(prenominal) fancy. A mania money changer is a device built for efficient conflagrateing permute between devil unstables from one medium to an opposite. The medium whitethorn be separated by a solid wall, so that the fluids never mix, or the fluids may never be in direct contact. dickens fluids of different temperatures will flow through the change money changer. love money changers atomic physique 18 widely used in space wakening, refrigeration, air chequering, power gives, chemical plants, petrochemical plants, petroleum refineries, and natural gas attend toing.3.1.1 Classification of catch fireing ExchangerHeat money changers may be classified according to their flow arrangement. There argon 2 main flow arrangements which be pair-flow and counter-current-flow. In parallel-flow set off exchangers, the two fluids enter the exchanger at the equivalent end, and travel in parallel to one another to the other locating. In counter-flow love exchangers the fluids enter the exchanger from opposite ends. Compared both flow arrangements, the counter current design is approximately efficient, in that it can transfer the most screw up from the estrus transfer medium.3.1.2 Types of Heat ExchangerThere are many types of heat exchanger in industry. The types chosen based on the function of the heat exchanger itself. Choosing the right heat exchanger requires knowledge of different type of heat exchanger as well as well as the surroundings in which the heat exchanger will operate. With sufficient knowledge of heat exchanger types and operating requirements, the best dealion can be make in optimizing the process. Below, in slacken 3.1 are list of types and functions of all(prenominal) heat exchanger.Table 3.1 Types and Functions of Heat Exchanger in IndustryNo.TypesFunctions1. parallel pipe heat exchangerThe simplest type. theatrical role for heating and cooling.2. reprimand and supply heat exchangerUsed for all application.3.Plate exchangerUse for heating and cooling.4.Plate-fin exchangerUse for heating and cooling.5.Spiral heat exchangerUse for heating and cooling.6.Air cooledCooler and condenser.7.Direct contact chill and quenching.8.Agitated vesselsUse for heating and cooling.9.Fired heatersUse for heating and cooling. ascendent chemical Engineering inclination, R.K.Sinnott.3.1.3 Selections of Heat ExchangerTypically in the manufacturing industry, some(prenominal) different types of heat exchangers are used for just the one process or system to derive the final product. In order to select an appropriate heat exchanger, one would firstly consider the design limitations for each heat exchanger type. Although cost is often the first criterion evaluated, there are several other important selection criteria which include luxuriously/ Low force per unit area limitsThermal PerformanceTemperature rangesProduct Mix (liquid/liquid, fibericulates or high-solids liquid)Pressure flys across the exchangerFluid flow capacityClean-ability, criminal maintenance and repair sensibles required for constructionAbility and ease of future enlargement3.2 BASIC PRINCIPLES OF DESIGN3.2.1 Design Criteria for Process Heat ExchangersThere are some criteria that a process heat exchanger must take on are easily enough stated if we confine ourselves to a sure process. The criteria includeThe heat exchanger must meet the process requirements. This tauting that it must effect the desired change in thermal condition of the process stream within the permissible printing press drops. At the same time, it must continue doing this until the next scheduled shut down for maintenance.The heat exchanger must withstand the service conditions of the environment of the plant which includes the mechanical stresses of installation, startup, shutdown, normal operation, emergencies and maintenance. Besides, the heat exchanger must also resist wearing by the environment, processes and streams. This is mainly a matter of choosing materials of construction, but mechanical design does have some effect.The heat exchanger must be maintainable, which usually implies choosing a configuration that permits cleaning and replacement. In order to do this, the limitations is the situation the exchanger and providing clear space around it. Replacement usually involves metros and other components that may be especially vulnerable to corrosion, erosion, or vibration.The cost of the heat exchanger should be consistent with requirements. Meaning of the cost here carry through to the cost of installation. Operation cost and cost of lost production collectable to exchanger malfunction or unavailable should be considered earlier in the design.The limitations of the heat exchanger. Limitations are on length, diam, weight and tube specs due to plant requirements a nd process flow.3.2.2 Structure of the Heat ExchangerThe basic structure of heat exchanger is the same whether using hand design method or computer design method. The logical structure of the heat exchanger design procedure is shown in dactyl 2.15. From the figure, clearer view and steps of designing a heat exchanger can be obtained.Figure 3.1 Basic arranged Structure of Heat Exchanger Design3.3 CHEMICAL DESIGN3.3.1 caper IdentificationIn designing a heat exchanger in production of 100, 000 metric tonnes/year of Acrylonitrile, there is only one heat exchanger exists. The function of it is to exchange the temperature between the stream from Reactor with the temperature from one hundred twenty-fiveC to 25C and the stream comes from Reboiler 5 from 90C to 120C.90.0 0C125.0 0C450.0 0C120.0 0CFigure 3.2 Diagram of flog and tube heat exchanger3.3.2 Determination of physical propertiesTable 3.2 Physical Properties of the tube side fluid ( urine)PropertiesInletMeanOutletTemperature (0C )90.0105120Pressure (kPa)70.139120.82198.52 item heat (kJ/kg0C)4.2044.2244.249Thermal conductivity (W/m0C)0.11540.11980.1127 denseness (kg/m3)0.4310.6230.721Viscosity (N sm-2)3.145 x 10-42.677 x 10-42.321 x 10-4Table 3.3 Physical Properties of shell fluid ( process fluid)Properties amount Temperature, Tave = 287.5 0CPressure (kPa)150Specific heat (kJ/kg0C)1.1Thermal conductivity (W/m0C)0.1553Density (kg/m3)1.255Viscosity (N sm-2)4.529 x 10-4Only the thermal design will be carried out by using Kerns method. Since water is corrosive, so the tube-side is assign.Logarithmic mean temperature,Where, T1 = Inlet shell side fluid temperatureT2 = Outlet shell side fluid temperaturet1 = Inlet tube side fluid temperaturet2 = Outlet tube side fluid temperatureThus, Log mean temperature= 131.4477 0CThe true temperature difference is given by,Where, is the temperature correction doerFrom Figure 12.19, Chemical Engineering Design,Thus,0CFrom Table 12.1(Sinnott 2005), we assume value of overall c oefficient, U = 500.0 W/m2.oC.Heat LoadHeat transfer expanse,Where, Q = heat transferred per unit time (W)U = overall heat transfer coefficient,(W/m2.oC)Tm = the mean temperature difference (oC)Thus,= 190.126 m23.3.3 Tube-side coefficientTable 3.4 Dimension of Heat-Exchanger tubesMaterialCarbon SteelOuter diameter, Dto (mm)50.8Length of tube Lt (m)5.0Inner diameter, Dti (mm)45.26BWG number12.0Source Transport Processes and Separation Process Principles, C. J. GeankoplisHeat transfer area of a tube, At = DoL= (50.8 x 10-3) 5= 0.798 m2 takings of tube, Nt = A/At= 190.126 / 0.798= 238.25 = 239 tubesCross sectional area of a tube = (Di2) / 4= (45.26 x 10-3)24= 1.6089 x 10-3 m2By using two passes tot tube area, AT = (239 / 2) (1.6089 x 10-3)= 0.1923 m2Mass velocity, Gs = flowrate / A= 29.96 / 0.1923= 155.798 kg/m2.sReynolds number, Re = Gsdi / = 155.798 x 0.04526 / 4.529 x 10-4= 1.557 x 10 4Prandtl number,= 3.1731 x 155.798 / 0.1553= 3183.275Nusselt number, NuD = 0.027 Rea Prb / wc= 0.027 (1.557 x 10 4)0.8 (3183.275)0.3 x 1= 685.578Stanton number, St = NuD / Re(Pr)= 685.578 / 1.557 x 10 4 x 3183.275 = 1.383 x 10-5Heat Transfer factor, jh = St Pr0.67= 1.383 x 10-5 ( 3138.275 )0.67 x 1= 3.045 x 10-3Tube-side heat transfer coefficient, hi= 2329.599 W/ m2.0C3.3.4 work over side coefficient1.25 three-sided pitch was chosen to calculate the bundle diameter. From table 12.4 (Sinnott 2005), constants value for 2 tube passes condition is K1 = 0.249 and n1 = 2.207 accumulate diameter, Db = Dto (Nt / K1) 1/n1= 50.8 ( 239 / 0.249)1/2.207= 1122.575 mm redeem floating head type was the best selection. From Figure 12.10 (Sinnott 2005), bundle diameter clearance is 95 mm.Shell diameter, Ds = 1122.575 + 95= 1217.575 mmFor selecting counteract spacing, the optimum spacing chosen is 0.2 times the shell diameters.Baffle spacing, B = 0.2 Ds = 0.2 (1217.575) = 243.515mmTube pitch pt = 1.25 Do = 1.25 (50.8) = 63.5mmCross-flow area,= 0.0593 m2Mass velocity, Gs = Ws / As= 47.7 672 / 0.0593= 805.518 kg/m2.sEquivalent diameter,= 36.07 mmShell-side heat transfer coefficient, hoReynolds number, Re = Gsdi / = 805.518 x 36.07 x 10-3 / 2.677 x 10-4= 1.0854 x 10 5Prandtl number,= 2.677 x 10-4 (2.4923 x 103) / 0.1553= 4.296Note that 45% baffle cut has been chosen, neglect the viscosity correction term. From Figure 12.29 (Sinnott, 2005), jh = 2.8 x 10-3= 1640.892 W/m2.0C3.3.5 Overall CoefficientTable 3.5 Dimensions in overall coefficientMaterialCarbon steelThermal conductivity of deoxycytidine monophosphate steelKw = 45 W/m0CThe fouling factor for cooling waterhid 5000 W/m2.0CThe fouling factor for aqueous salt solutionsh0 =3000 W/m2.0CSource Chemical Engineering Design, R.K.Sinnott.The relationship between overall coefficient and individual coefficients is given byUO = 583.359 W/m2.0CWell approximately the initial estimate of 600 W/m2.0C, so design has adequate area for the duty required.3.3.6 Tube-side Pressure DropReynolds number,= 14526.371From Figure 12 .24 of Chemical Engineering. (Vol. 6) Friction factor, jf = 0.045Tube side pressure drop,Where, m = 0.25 for stratified flow, Re2100Np = number of tube side passes= 23135.87 N/m2= 2.3135 kPa (Acceptable)3.3.7 Shell-side Pressure DropReynolds number, Re = 1.0854 x 10 5From the Figure 12.30 (Sinnott 2005), Friction factor, jf = 0.024Shell side pressure drop,= 64327.95 N/m2= 64.328 kPa (Acceptable)3.3.8 Summary of CalculationType of shell and tube is carbon steel with Kw of 45 W/m.0C. While, spec of inside diameter is 45.27mm, outside diameter is 50.8mm and length of 5m.Table 3.6Tube-side specificationParameterResultsTlm131.4477 oCR10.833S0.833FT0.93Tm122.246 oCArea, A190.126 m2Number of tubes, Nt239 tubesWater linear velocity, ut155.798 kg/m2.sHeat transfer coefficient, hi2329.599 W/m2.0CPressure drop, Pt2.3135 kPaTable 3.7 Shell-side specificationParameterResultsBundle diameter, Db1122.575 mmShell diameter, Ds1217.575 mmBaffle spacing, lB243.515mmShell area, As0.0593 m2Mass velocit y, Gs805.518 kg/m2.sEquivalent diameter, de36.07 mmShell coefficient, ho1640.892 W/m2.0CPressure drop, Ps64.328 kPaOverall coefficients, U583.359 W/m2.0C3.4 MECHANICAL DESIGN OF HEAT EXCHANGER3.4.1 Design ParameterTable 3.8 Design ParameterParametreSI UnitEnglish UnitDesign temperature, TD460 OC860 OFOperating pressure, Po300 kPa43.51 pounds per square inchInternal diameter, Di1.217 m47.913 ftHemispherical length0.65 m2.13 ftShells length5.0 m16.40For this heat exchanger, the design pressure is 43.51 psi and above the atmosphere pressure (15 psi). found on study, if Po Patm (Pgage = Pabs Patm), the calculation for this heat exchanger is under inbred pressure and the pressure that will used is,Po = Pabs Pgage = 43.51 psi 15 psi = 28.51 psiCalculation of design pressure for each detonate of heat exchanger by taking 10% safety factorP1 = PO + PH= 28.51 + 0.433 (2.13) = 29.431 psi x 1.1= 32.38 psiBecause this heat exchanger design is horizontal, so the value P1 = P2 = P3 = 32.38 psiThickness for each part of vesselthemispherical , t =tcylindrical Circumferentialt =Longitudinalt =For cylindrical, the highest burdensomeness value metric will be chosen. So, from the calculation above the onerousness for cylindrical part is 0.0446 inch. Now by adding corrosion allowance, CA of 2 mm (0.07874 in.),themispherical = 0.0223in + 0.07874in = 0.101intcylindrical = 0.0446in + 0.07874in = 0.12334inThe material construction for this heat exchanger is carbon steel due to price and work in many applications. The highest value from these two types of wall thicknesses is 0.12334 inch, so the minimum wall thickness of this heat exchanger is 0.12334 inch (3.133mm). The nominal wall thickness for carbon steel at market is 0.1182 inch (3mm). Because of the nominal wall thickness is lower than the calculated we must take the calculated thickness t = 0.12334 inch (3.133 mm) as value of wall thickness.To calculate the maximum allowable working pressure for each part, MAWPpart , the thickness must subtract the corrosion allowancet = 0.12334in 0.07874in = 0.0446inMAWPpart (hemispherical)P =MAWPpart (cylindrical)CircumferentialP =LongitudinalP =The smallest value of pressure will be chosen. So, the internal pressure for cylindrical part is 32.383 psi.By subtracting the hydrostatic pressure, PH for each part,MAWPpart (hemispherical) = 64.812 psi (0.433)(2.13) = 63.889 psi =440.5 kPaMAWPpart (cylindrical) = 32.383 psi (0.433)(16.01) = 25.451 psi =175.478 kPaThe smallest value of pressure is taken as MAWPpart which is 25.451psi. This value is the maximum allowable pressure for the whole vessel.