1,721,079 research outputs found
HIV-1 DNA in brains in AIDS and pre-AIDS: Correlation with the stage of disease
No full textSeventeen asymptomatic individuals positive for human immunodeficiency virus type 1 (HIV-1) and 16 patients with acquired immunodeficiency syndrome (AIDS), all with polymerase chain reaction evidence of HIV-1 DNA, were selected for quantitative analysis to correlate the levels of HIV-1 DNA in brain tissue with the stage of infection. The AIDS patients either were clinically asymptomatic or presented various abnormalities. Neuropathological lesions were assessed by morphological and immunohistochemical methods. To determine the level of HIV-1 DNA, semiquantitative nested polymerase chain reaction was applied using a digoxigenin-labeled primer and chemiluminescence. Serial dilutions of standard HIV DNA. were run in parallel with brain DNA samples. Among the 16 AIDS brains studied, 9 showed changes characteristic of HIV encephalitis/leukoencephalopathy while 1 showed focal pontine leukoencephalopathy and 6 showed no obvious neuropathological lesions. Abnormalities in pre-AIDS individuals included meningitis, microgliosis, and astrogliosis. Copy numbers of HIV-1 DNA in the brains of AIDS patients were higher than those in asymptomatic individuals (median, 135 vs 45 copies/150,000 cells). However, there was some degree of overlapping between the two groups, with some AIDS patients showing low figures while 3 asymptomatic individuals had high copy numbers. This suggests that the use of HIV-1 DNA load in the central nervous system as an indicator of progression of the disease should be restricted to large series and not single patients
IMMUNOHISTOCHEMICAL STUDY OF LEWYS BODIES AND NEUROFIBRILLARY TANGLES WITH A MONOCLONAL-ANTIBODY AGAINST PHOSPHORYLATED EPITOPES OF NEUROFILAMENTS IN DIFFERENT CLINICAL CONDITIONS
No full textPCR detection of HIV proviral DNA (gag) in the brains of patients with AIDS: comparison between results using fresh frozen and paraffin wax embedded specimens.
No full textAIMS:
To adapt the polymerase chain reaction (PCR) technique of HIV detection to paraffin wax embedded brain tissue and to compare the results with those obtained using frozen tissue.
METHODS:
HIV antigen and HIV proviral DNA were detected in specimens of frontal lobe using immunohistochemistry and PCR, respectively. DNA was extracted from fresh tissue using standard methods whereas the technique for extracting DNA from paraffin wax embedded tissue was partly modified.
RESULTS:
Twenty cases were examined. HIV DNA was detected in 16 cases in frozen specimens. Of these, 15 were also positive when paraffin wax embedded material was analysed.
CONCLUSIONS:
This study shows that HIV proviral DNA can be detected in formalin fixed, paraffin wax embedded brain tissue by PCR. The results obtained from paraffin wax embedded specimens showed a similar degree of reliability to those from fresh frozen brain. Factors such as fixative, fixation time, and delay in performing post mortem examinations did not seem to influence PCR amplification as positive results were obtained with specimens left in fixative for up to eight months, as well as in cases where post mortem examinations had been delayed for up to four days
Inhibition of sensory neuron apoptosis and prevention of loss by NT-3 administration following axotomy
No full textFollowing permanent transection of their peripheral axons, a proportion of adult rat dorsal root ganglion neurons undergo programmed cell death (apoptosis) over a period of months. The underlying causes of this neuron loss are unclear, but may involve the interruption of the supply of target-derived neurotrophic factors, the replacement of which could prevent this loss from occurring. To investigate whether the administration of neurotrophic factors can prevent the dorsal root ganglion neuron death in adults, a 1 mg/ml solution of ciliary neurotrophic factor or of NT-3 was applied via a silicon reservoir to the proximal stump after unilateral sciatic transection at mid-thigh level. The incidence of apoptotic neurons and neuronal loss in the L4 and L5 ganglia ipsilateral to sciatic nerve transection when compared with the contralateral ganglia was then measured 1 month later. This was assessed by examining serial sections of ganglia for neurons undergoing apoptosis and expressing the total counted as a percentage of the total number of neurons estimated using a stereological neuron counting technique. Our results show that NT-3 administration significantly reduced the incidence of apoptotic neurons and prevented neuron loss, while CNTF had no effect on either parameter. (C) 1999 Academic Press
Relationship between accumulation of beta-APP and neuropsychological abnormalities in HIV encephalitis
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Spatz-Lindenberg disease: a rare cause of vascular dementia
No full textSpatz-Lindenberg disease should be considered in the differential diagnosis of vascular dementia. Additional studies of its pathogenesis are required to determine appropriate treatment
Axotomy-induced apoptosis in adult rat primary sensory neurons
No full textNeuronal death following unilateral axotomy of a sensory nerve has long been inferred from neuronal counts of dorsal root ganglion neurons, using the contralateral ganglia as a control. The counting methods used usually involved the counting of neuronal nucleoli and made assumptions about them which could conceivably be flawed. Very few studies have used direct observations of dying or degenerating neurons to address questions concerning the duration of the period of neuronal death or the mechanisms involved in this process. Here we describe a morphological, morphometric and histochemical study into the nature and duration of sensory neuron death following transection and ligation of the sciatic nerve at mid-thigh level in the adult rat. We show that at least some of this neuronal loss occurs by apoptosis as defined by morphological criteria and in situ end-labelling of damaged DNA. Absolute numbers of apoptotic neurons were counted from serial paraffin sections of ganglia and estimates of neuronal numbers obtained by disector analysis at 1, 2, 3 and 6 months after axotomy. Using this approach we show that axotomy-induced apoptosis begins at around 1 week and continues up to at least 6 months after axotomy
Detection and localisation of HIV-1 in fixed adult AIDS brain tissue by in situ amplification
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