syncfusion pdf viewer mvc

pdfsharp html to pdf mvc

asp. net mvc pdf viewer

mvc display pdf in partial view

asp.net mvc pdf generation, generate pdf using itextsharp in mvc, asp.net mvc web api pdf, asp.net pdf viewer free, asp.net mvc generate pdf from view, how to open pdf file on button click in mvc, asp.net pdf viewer control free, how to show .pdf file in asp.net web application using c#, asp.net pdf viewer annotation, how to open a .pdf file in a panel or iframe using asp.net c#, asp.net pdf viewer annotation, how to generate pdf in mvc 4, mvc display pdf from byte array, asp.net pdf viewer devexpress, mvc export to pdf

.net code 39 reader, .net pdf viewer component, c# split multi page tiff, ssrs qr code, winforms pdf preview, libtiff.net convert tiff to jpeg, download pdf in mvc 4, pdf to jpg converter android online, asp.net mvc generate qr code, crystal reports upc-a barcode

gates may be toxic to neurons, either directly or in their proto brillary form (a situation similar to that suggested for the toxicity of synuclein in Parkinson disease) The situation is, however, likely to be more complex, since the bulk of huntingtin deposition is found in cortical neurons, whereas the neuronal loss is predominantly striatal One theory, based on experimental data, supports the concept that the polyglutamine expansion renders certain cell types unduly sensitive to glutamate-mediated excitotoxicity; another notion is that it creates an insuf ciency of trophic in uences directed to the caudate from the cortex; yet another theory relates the polyglutamine expansion to the acetylation of histones, which leads to cell death This nding has led to trials of inhibitors of histone deacetylases and other therapies that modify gene expression in transgenic mouse models of Huntington disease Other theories implicate mitochondrial dysfunction As importantly, since polyglutamine expansions are implicated in several neurodegenerative diseases (reviewed below), treatments that block their effect on cellular function may be broadly effective in several degenerative diseases Diagnostic Problems Once the disease has been observed in its fully developed form, its recognition requires no great clinical acumen The main dif culty arises with patients who lack a family history but who display the progressive chorea, emotional disturbance, and dementia with onset in adult life This dif culty has been largely overcome since the mutation causing Huntington disease was identi ed It is now possible to con rm or exclude the diagnosis by analysis of DNA from a blood sample The presence of greater than 39 to 42 CAG repeats at the Huntington locus essentially con rms its presence; lesser numbers leave room for equivocation Sometimes it is learned later that the family history was incomplete or falsi ed or that an illness in a parent had been misinterpreted Chorea that begins in late life, with only mild or questionable intellectual impairment and without a family history of similar disease, is another source of dif culty; referring to it as senile chorea does not solve the problem Indeed, senile chorea may have more than one cause We have seen it appear with infections, drug therapy, and thyrotoxicosis, only to disappear after a few weeks A few times we have been confronted with the problem of an older patient who displays orolingual dyskinesias that are most characteristic of exposure to neuroleptic drugs but in whom there was no such history of exposures; testing disclosed Huntington disease Chorea in early adult life always raises the question of a late form of Sydenham chorea, of lupus erythematosus with antiphospholipid antibodies, or of cocaine use, but neither familial occurrence nor mental deterioration is part of these processes A benign inherited chorea, transmitted as an autosomal dominant trait without prolongation of a triplet sequence, has been traced to chromosome 14q It is differentiated from Huntington disease by onset before age 5, progressing little and having no associated mental deterioration (Breedveld et al) Other progressive neurologic disorders inherited as autosomal dominant traits and beginning in adolescence or adult life (eg, polymyoclonus with or without ataxia, acanthocytosis with progressive chorea, and dentatorubropallidoluysian degeneration) can closely mimic Huntington disease, as described further on; sometimes only the genetic and pathologic ndings settle the matter There are several other rare degenerative disorders with chorea, some of which have already been mentioned A midlife progressive chorea without dementia (after more than 25 years follow-.

Figure 39-4 The upper CT scan is from a 54-year-old mildly demented woman with a 10-year history of Huntington chorea The bulge in the inferolateral border of the lateral ventricle, normally created by the head of the caudate nucleus (lower scan from a patient of the same age for comparison), has been obliterated There is also a diffuse enlargement of the lateral ventricles

FIGURE 11-9

font code 39 para excel, image to pdf converter software free download for windows 10, generate code 128 barcode in excel, pdf split and merge software free download 64 bit, code 39 barcode font excel, how to create barcodes in excel 2010 free

neurotransmitters (norepinephrine, glutamic acid decarboxylase, choline acetyltransferase, GABA, acetylcholine, and somatostatin), but the signi cance of these biochemical disturbances is unknown Viewed from the molecular perspective, the pathogenesis of this disease is a direct but still poorly understood consequence of the aforementioned expansion of the polyglutamine region of huntingtin (the protein product of the Huntington gene) It has been shown that the expansion predisposes the mutant huntingtin protein to aggregate in the nuclei of neurons Moreover, the protein accumulates preferentially in cells of the striatum and parts of the cortex affected in Huntington disease Evidence, particularly that given by Wetz (cited in the review by Bates), suggests that these aggre-

.

up) that does not display the Huntington genotype has been reported In at least one family in which this clinical picture is dominantly inherited, the fundamental defect is a mutation in the gene encoding the light chain (L chain) of ferritin (Curtis) Affected individuals have axonal changes in the pallidum with swollen, ubiquitin- and tau-positive aggregates; serum ferritin levels may be depressed The implication of this mutation is that perturbations of iron metabolism may be toxic to neurons, a feature that also characterizes Hallervorden-Spatz disease (page 832) Dentatorubropallidoluysian atrophy (DRPLA), often misdiagnosed clinically as Huntington chorea, was described in four European families by Warner and associates and is discussed further on in the section on cerebellar degenerations The extrapyramidal manifestations include chorea, myoclonus, and rigidity Adultonset chorea and dementia has been described with propionic acidemia; propionic acid is elevated in the plasma, urine, and CSF This disorder must be added to other metabolic diseases described in Chap 37 as causes of chorea and dyskinesia such as glutaric acidemia, keratin sulfaturia, calci cation of basal ganglia, phenylketonuria, and Hallervorden-Spatz disease (Hagberg et al) Other problems in differential diagnosis include bilateral thalamic degeneration with dementia and chorea, referred to earlier; paroxysmal choreoathetosis (page 68); Wilson disease (page 830); acquired hepatocerebral degeneration (page 975); and, most often and especially, tardive dyskinesia (page 94) Many drugs in addition to the toxic effects of L-dopa and antipsychotic medications occasionally cause chorea (amphetamines, cocaine, tricyclic antidepressants, lithium, isoniazid) Treatment The dopamine antagonist haloperidol, in daily doses of 2 to 10 mg, is probably the most effective agent in suppressing the movement disorder Because of the danger of superimposing tardive dyskinesia on the chronic disorder, the chorea should be treated only if it is functionally disabling, using the smallest possible dosages Haloperidol may also help alleviate abnormalities of behavior or emotional lability, but it does not alter the progress of the disease The authors have not been impressed with the therapeutic effectiveness of other currently available drugs Levodopa and other dopamine agonists make the chorea worse and, in the rigid form of the disease, evoke chorea Drugs that deplete dopamine or block dopamine receptors such as reserpine, clozapine, and tetrabenazine suppress the chorea to some degree, but their side effects (drowsiness, akathisia, and tardive dyskinesia) outweigh their desired effects The juvenile (rigid) form of the disease is probably best treated with antiparkinsonian drugs Preliminary studies of the transplantation of fetal ganglionic tissue into the striatum achieved mixed results The psychologic and social consequences of the disease require supportive therapy, and genetic counseling is essential Huntington disease pursues a steadily progressive course and death occurs as mentioned, on average 15 to 20 years after onset, sometimes much earlier or later.

September 2008 42U 787 inches (2,000 mm) H 24 inches (613 mm) W 397 inches (1,015 mm) D 1,350 lbs (614 kg) 137 kW 48,000 BTU/ hour

.

FIGURE 11-10

convert pdf to docx using java, javascript ocr api, .net core barcode reader, .net core qr code reader