Detection of HIV-1 DNA sequences in pre-ejaculatory fluid.
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Biomedical subjects
Publications and source records attributed to P Baron.
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Proteolipid protein (PLP), the major myelin protein in the central nervous system (CNS), is also made by Schwann cells (SC) in the peripheral nervous system (PNS) but is not incorporated into the SC myelin sheath. We analyzed several PLP cDNA clones isolated from a rat sciatic nerve cDNA library and found that their coding sequences were identical to PLP cDNAs previously isolated from the CNS. In addition, we have discovered an unusual form of PLP message, present in both brain and sciatic nerve RNA, that is likely formed by alternative splicing within the 3' untranslated region of the primary PLP transcript. The absence of PLP from the SC myelin sheath thus cannot be explained by an alteration in its amino acid sequence. Steady-state levels of PLP mRNA in SC cultures treated with the cAMP analogue dibutyryl cAMP (dBcAMP) were not increased, whereas dBcAMP increased steady-state levels of mRNA encoding the major myelin protein, P0. We have also shown that expression of PLP, unlike that of P0, is regulated in SC in vitro at a posttranscriptional level. Finally, the steady-state levels of P0 mRNA are much more dramatically reduced than those of PLP mRNA during Wallerian degeneration of the peripheral nerve. Thus PLP expression in the PNS is probably controlled by different molecular mechanisms from P0, and may not be part of the coordinate program of myelin gene expression. In contrast to its expression in the PNS, transcription of PLP in the CNS is coordinately regulated along with the other myelin protein genes, suggesting there may be differences in the cis-acting elements and transacting factors involved in the regulation of PLP transcription in SC and oligodendrocytes (OC). Consistent with this notion, we have found that most PLP transcripts are initiated at the more proximal of two start sites in the PNS, while in the CNS proportionally more PLP transcripts are initiated from the distal start site. We propose that the proximal site, utilized predominantly in SC, is responsible for maintenance expression of PLP and is not inducible, while the distal site is responsible for the rapid, inducible increase of PLP message during brain development.
A multicentre, double-blind, between-patient study was carried out to evaluate the efficacy and tolerability of oxiracetam (800 mg tablet), in comparison with placebo, each given twice daily for 12 weeks to patients suffering from primary degenerative, multi-infarct or mixed dementia. Efficacy was assessed by a neuropsychological battery (simple reaction time, controlled associations, short story, Raven's Progressive Matrices, token test, digit span, word list learning), administered at the beginning and at the end of the study, and by a quality of life scale, administered at entry and after 6 and 12 weeks treatment. Sixty-five patients (28 men, 37 women, mean age 71 yrs) were enrolled; 58 completed the study: 2 on oxiracetam were withdrawn because of poor tolerability, 2 (one in each group) were withdrawn for poor compliance, one (on oxiracetam) for the occurrence of a transient ischaemic attack (defined as not related to the treatment) and 2 for administrative reasons. A significantly (p < 0.01) different effect in favour of oxiracetam was observed on the quality of life scale, and confirmed by significant (defined according to the Bonferroni technique) differences in some neuropsychological tests (e.g. controlled associations, short story). Four patients in the oxiracetam group complained of a total of 5 unwanted effects, and 1 on placebo complained of 3 unwanted effects, but none of them was withdrawn from the study.
The phenotypic (morphologic and antigenic) properties and mitotic index of cultured Schwann cells obtained by dissecting nerves from six diabetic patients were studied. These features were compared with those of Schwann cells cultured in vitro from six normal control nerves. Preservation of the specific antigenic properties of cells, identified with rabbit antiserum as bovine protein S-100, was documented by immunofluorescence with monoclonal antibodies against laminin, fibronectin, histocompatibility antigens HLA-A, B, C and -DR, HNK-1 antigen and the human receptor for nerve growth factor. The cell proliferation index was assessed by incorporation of bromodeoxyuridine. The results of the study showed that the mitotic capacities of Schwann cells from diabetic nerves cultured in vitro remained comparable with those of normal control cells. As regards phenotypic characteristics, no modifications were detectable by immunofluorescence. These findings suggest that the phenomena of demyelination and remyelination, sometimes with onion bulb features, which can be observed in some cases of diabetic neuropathy, are not due to a primary dysfunction of the Schwann cells but are secondary to axonal degeneration.
Neurofibromatosis type 1 (NF-1, von Recklinghausen's disease) is characterized by the focal accumulation of Schwann-like cells (SLC) to form subcutaneous and plexiform neurofibromas and schwannomas. The aim of the present study was to determine whether NF-SLC are competent to differentiate in the presence of axons. Five dermal neurofibromas from five patients with NF-type 1 were enzymatically dissociated and the resultant cells were co-cultured with fetal rat dorsal root ganglion neurons. The cultures were studied by indirect immunofluorescence microscopy using antibodies against galactocerebroside (galC), P0 glycoprotein, human nerve growth factor receptor (NGFR) and human myelin-associated glycoprotein (MAG). SLC were strongly NGFR+ but galC- and MAG-SLC for the 2 weeks of coculture. After 3 weeks in vitro, SLC-NGFR was down-regulated but some of the spindle shaped cells had become galC+. MAG-SLC first appeared after 5 weeks in vitro but P0 glycoprotein was never detected when studied up to 6 weeks. Our data demonstrate that axons induce SLC to down-regulate surface NGFR and to express some myelin components in a qualitatively normal fashion.
Oxygen free radicals damage kidneys and accumulate during the period of preservation prior to transplantation. We hypothesized that a perfusate containing either an oxygen free radical scavenger such as ceruloplasmin, or an iron-chelating agent such as deferoxamine, would improve kidney preservation. Thirty-eight mongrel dogs underwent autotransplantation of the left kidney after 30 min of warm ischemia and 48 hr of machine perfusion (MOX-100, Water Instruments, Rochester, MN) at 5 degrees C and pH of 7.4. The right kidney was removed at the time of autotransplantation. Four blind code-labeled preservation solutions were tested. SGF-I was used for the control group (Group 1, n = 13), and the remaining animals were transplanted with kidneys preserved with one of three solutions modified from the basic SGF-I solution: Group 2, SGF-I plus deferoxamine (656 mg/liter), n = 8; Group 3, SGF-I ceruloplasmin enriched (72 mg/dl), n = 8; and Group 4, SGF-I ceruloplasmin reduced (3.4 mg/dl), n = 9. Serum creatinine levels were measured daily for 2 weeks and survival curves for each of the four groups were estimated by the Kaplan-Meier method. Peak mean serum creatinine levels +/- standard errors in Groups 1 through 4 were 12.6 +/- 1.97, 7.8 +/- 0.90, 7.1 +/- 1.26, and 8.2 +/- 1.09, respectively. Repeated measures analysis of variance showed statistically significant differences between the groups with respect to their serum creatinine profiles (Wald's test x2 with 3 df = 22.39, P value less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
Anti-p24 reactions in sera from 42 human immunodeficiency virus type 1 (HIV-1)-infected and 36 uninfected people with indeterminate Western blot antibody tests for HIV-1 were studied. Anti-p24 reactivity in HIV-1-infected people was completely blocked by HIV-1 recombinant p24 antigen, whereas the reaction in uninfected individuals with indeterminate patterns was inhibited partly or not at all. In contrast to infected individuals, anti-p24 reactivity from uninfected individuals could not be detected by an inhibition ELISA for HIV-1 p24 antibody. These results suggest a practical way to distinguish anti-p24 reactivity in sera from patients with HIV-1 infection from that seen in uninfected patients with indeterminate Western blot reactions.
An ELISA-inhibition assay based on commercially available HIV-1 p24 antigen tests was developed for detecting p24 antibodies. The test is specific and simple. p24 antibody was detectable in all p24 antigen negative Western blot positive sera, but was detectable infrequently in antigen positive sera. Sera from patients with indeterminate HIV-1 reactions (individuals without evidence of HIV-1 infection who nevertheless had p24 antibody) were p24 antigen negative and p24 antibody negative in the ELISA-inhibition reaction.
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The 3rd of 4 communications on metal concentrations in human body media deals with mercury. Publications obtained from a comprehensive data bank search from January 1980 to April 1984 are listed in tables; study groups have been assigned to the following categories: normal, exposed; and exposed, exhibiting adverse health effects. Quality and strength of evidence of analytical procedures and reported data are discussed, particularly in light of adverse health effects. General methods and individual analytical procedures were presented in the 1st communication, a summary of mean exposure levels, critically elevated levels, and references will be published in the 4th communication.
The last of 4 communications on metal concentrations in human body media deals with lead. It includes also a summary of mean exposure levels, critically elevated levels, and references. Publications obtained from a comprehensive data bank search from January 1980 to April 1984 are listed in tables; study groups have been assigned to the following categories: normal; exposed; and exposed, exhibiting adverse health effects. Quality and strength of evidence of analytical procedures and reported data are discussed, particularly in light of adverse health effects. General methods and individual analytical procedures were presented in the 1st communication.
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We describe a technique for the preparation of highly purified populations of Schwann cells (SC) from human fetal nerves. Cultures were prepared by chemical and mechanical dissociation of human fetal sciatic nerves by modification of the method of Kreider et al. developed for newborn rat nerve. A time course analysis of some SC-associated markers at different times in vitro was performed employing immunofluorescence (IF) and immunoperoxidase (IP) to determine the percentage of SC in culture and to evaluate the maintenance of specific SC characteristics. We compared this method with that of Askanas et al. which produces enriched SC cultures by utilizing successive re-explantation of the original nerve explant. After 48 h, approximately 90% of the cells were bipolar and S-100+ and over the next two weeks about 70-80% of cells were SC by cytologic and immunocytologic criteria. At 35 days, 35% were SC, whereas less than or equal to 2.5% of 35-day-old multi-explant cultures were SC. The SC obtained by this method displayed the typical morphological and immunological characteristics: they expressed surface laminin and nerve growth factor receptors, whereas fibronectin, which is localized on fibroblast surface, was absent.
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The present review covers 208 papers dealing with determination of the metals arsenic, cadmium, lead and mercury in human biologic material. A comprehensive data bank survey of the literature from January 1980 to April 1984 was conducted and supplemented by review of some earlier publications. As shown by comparison of the results from a number of papers, the various state-of-the-art methods for determining metal content in biologic materials (e.g., atomic absorption spectrophotometry, neutron activation analysis, and x-ray fluorescent analysis) appear to be equally sensitive and reliable. These detection methods are suited to determination of the above metals in the following media: arsenic in urine, hair; cadmium in blood, urine, hair, renal cortex; lead in blood, hair; mercury in blood, urine, hair. To permit better comparison of the results presented in various publications, agreement must be reached on use of uniform concentration units and participation in quality control programs. Safe levels of chronic biological exposure overlap with concentrations which cause health effects or measurable impairment of body function over a wide range. Individual sensitivity to biological exposure varies. In a number of studies, metal concentrations are measured in symptom-free persons which cause symptoms in persons examined in other studies. Due to differences in the sensitivity of detection of symptoms, the range of minimum levels of biological exposure considered to be associated with deleterious health effects (levels of critical exposure) is unacceptably broad. Minimum levels of critical exposure should protect against development of early symptoms of toxicity. If the lowest published critical levels of biological exposure are taken as a cutoff, then a sizable portion of the persons currently revealing metal exposure in any of the reported media exceeds such levels. Symptoms of detrimental effects should be detectable in such persons and should be investigated. In establishing and evaluating current minimum levels of critical chronic metal exposure, there is a general need for a quantitative increase in determinations and for a qualitative increase in the sensitivity of detection of symptoms and other health effects--in order to avoid dependence on reports of acute toxicity. When detected levels of a given metal are in a range held to be normal, exclusion of toxic effects and poisoning requires additional consideration of clinical findings.
The 2nd of 4 communications on metal concentrations in human body media deals with cadmium. Publications obtained from a comprehensive data bank search from January 1980 to April 1984 are listed in tables; study groups have been assigned to the following categories: normal; exposed; and exposed, exhibiting adverse health effects. Quality and strength of evidence of analytical procedures and reported data are discussed, particularly in light of adverse health effects. General methods and individual analytical procedures were presented in the 1st communication, a summary of mean exposure levels, critically elevated levels, and references will be published in the 4th communication.
High speed grinding of gray iron castings long has been associated with excessive exposure to crystalline silica. Not all workers engaged in these operations are protected by conventional ventilation techniques. Dust in the air that has been entrained by the spinning grinding wheel and not captured in the grinder hood has been postulated to be a major exposure source. A pilot grinding operation was constructed, and the size distribution and concentration of airborne particles were measured with the aerodynamic particle sizer (APS). Various control measures proved effective in reducing the respirable dust concentration: increased exhaust ventilation, and installation of baffles and/or the use of an air jet to deflect the entrained air stream. The concentration of respirable dust is the breathing zone was reduced approximately 20-fold through the combined use of increased ventilation, interior baffles, and an air jet. The air jet and baffle utilized at the base ventilation rate reduced the respirable dust concentration by a factor of three to four, whereas the baffle alone halved the concentration.