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Biomedical subjects

M Goldman

Publications and source records attributed to M Goldman.

At least 451 records · Page 25Linked to original sources
PubMed1989

[Autoimmune syndrome associated with host versus graft reaction in the mouse].

The neonatal injection of semi-allogeneic spleen cells in mice induces a state of tolerance which can be demonstrated in mixed lymphocyte culture by the inability of T lymphocytes to proliferate, to secrete interleukin-2 and to generate cytolytic activities towards the injected alloantigens. Tolerant animals develop an autoimmune syndrome characterized by an antibody-mediated glomerulonephritis associated with high levels of IgE, IgG1 and anti-DNA antibodies. This syndrome is linked to the activation of B cells injected at birth by host T cells which escape tolerance induction. Interleukin 4 is one of the mediators of these lymphocytic interactions, which suggests that Th2 cells play an important role in this experimental model of autoimmune glomerulonephritis.

Animals↗
PubMed1989

[Glomerulonephritis by glomerular anti-basement membrane antibodies after renal transplantation].

Glomerulonephritis (GN) due to antiglomerular basement membrane (GBM) antibodies after kidney transplantation may be classified into two groups: 1. Recurrent GN are very rare provided circulating anti-GBM antibodies are absent at grafting. If present, linear fixation along the GBM occurs but does not lead to GN in some cases. 2. De novo anti-GBM diseases have been rarely reported. They developed in 8 patients with Alport's syndrome and in at least 3 additional patients in whom hereditary nephritis was not the original disease. A prospective and retrospective study was performed in 54 transplanted patients with hereditary nephritis: circulating anti-GBM antibodies were detected in only one case; linear fixation along the GBM was found but no evidence of GN. The risk of anti-GBM disease after kidney transplantation is low in patients with hereditary nephritis but this complication must be rapidly identified. Its occurrence is probably related to the defect in GBM antigenicity involving the Goodpasture antigen, found in some patients with Alport's syndrome or related hereditary nephritis.

Antibodies↗
PubMed1989

Dentinal bonding after chemomechanical caries removal--effect of surface topography.

A study was carried out to determine whether or not the topography of the dentinal surface that is left after caries removal affects bond strength. The caries was removed either by a rotating instrument and a bur or by the chemomechanical method using D,L,2-aminobutyric acid. The bond strength appeared to be enhanced on those specimens treated by the chemomechanical removal since the surface was characterized by lack of a smeared layer and by open dentinal tubules and numerous undercuts.

Aminobutyrates↗
PubMed1989

Prospective and retrospective data compared in patients with PTFE femoropopliteal bypass grafts.

Twenty-four patients with PTFE, femoropopliteal grafts were studied using two different methods. A prospective study was carried out as part of a clinical trial and later the same patients were identified as part of a retrospective study. Comparison of the details obtained independently showed marked differences in patients' ages, indications for surgery, angiographic runoff, operative detail, risk factors and subgroup patency.

Age Factors↗
PubMed1988

The global impact of the Chernobyl reactor accident.

Radioactive material was deposited throughout the Northern Hemisphere as a result of the accident at the Chernobyl Nuclear Power Station on 26 April 1986. On the basis of a large amount of environmental data and new integrated dose assessment and risk models, the collective dose commitment to the approximately 3 billion inhabitants is calculated to be 930,000 person-gray, with 97% in the western Soviet Union and Europe. The best estimates for the lifetime expectation of fatal radiogenic cancer would increase the risk from 0 to 0.02% in Europe and 0 to 0.003% in the Northern Hemisphere. By means of an integration of the environmental data, it is estimated that approximately 100 petabecquerels of cesium-137 (1 PBq = 10(15) Bq) were released during and subsequent to the accident.

Accidents↗
PubMed1988

Human gastric perfusion: evidence for non-uniformity of blood flow.

Post-mortem injection studies have demonstrated marked differences in the course and distribution of arterioles in the stomach, but evidence of differential perfusion in man is lacking. Using the non-invasive laser Doppler technique, we studied 38 patients referred for gastroscopy for dyspeptic symptoms. Flux measurements were made at nine sites: distal oesophagus, cardia, mid-body and antrum on lesser and greater curves, and pre- and post-pylorus. In all cases the stomach was macroscopically normal. Flux in the proximal stomach was significantly greater than that in the antrum, (P less than 0.001, Student's t test). This in vivo study demonstrates a flow gradient related to the previously demonstrated anatomical differences.

Blood Flow Velocity↗
PubMed1988

Inflammatory demyelinating polyradiculoneuropathy associated with human immunodeficiency virus infection.

Five patients infected with immunodeficiency virus who were suffering from chronic polyradiculoneuropathy were investigated during evolution of the disease. Four of them were immunodeficient. The prominent neurological feature was distal and symmetrical weakness of the legs. After 5 months only one patient had improved. All patients had an increased protein level in the cerebrospinal fluid and pleocytosis. Electrodiagnostic studies and sural nerve biopsies indicated demyelination. Sural nerve viral cultures, including human immunodeficiency virus, were negative. The presence of circulating anti-peripheral nerve antibodies and of immunoglobulin deposits in nerve biopsy specimens was investigated by immunofluorescence techniques but failed to demonstrate any immunoreactivity.

Acquired Immunodeficiency Syndrome↗
PubMed1988

Acute effects of aspartic acid on ventilation of male and female rats.

The effects of aspartic acid (aa) on ventilation were evaluated in awake male and female rats prior to and 15, 30, and 45 minutes after saline, 100 mg/kg or 580 mg/kg aa was injected subcutaneously. Subsequently, rats were exposed to hypoxic and hypercapnic gas challenges. In males, 100 mg/kg aa increased ventilation (VE) by increasing inspiratory flow rate (VT/TI), tidal volume (VT), and frequency of breathing (f) by 30 minutes, whereas in females VT was increased above saline levels only at 15 minutes. VE did not decrease over time. A dose of 580 mg/kg aa depressed ventilation in males for 2 hours by decreasing VT, VT/TI and f. In contrast, female rats exhibited a decreased ventilation only at 15 minutes which then began to return to saline levels by 45 minutes. Neither male nor female rats treated with either dose of aa showed a depressed response to hypoxia or hypercapnia. These data indicate that aa at two doses can affect the pattern of ventilation differently in male and female rats. One mechanism responsible for the differences noted between the two groups is the effect aspartic acid may have on testosterone production. An additional study comparing ventilatory responses of sham operated and castrated males to various doses of aa indicated that testosterone was not necessary to show the 'male' pattern of response.

Animals↗
PubMed1988

Endothelial cell adhesion to vascular prosthetic surfaces.

Improving the long term patency of small diameter prosthetic grafts remains an important but elusive objective in vascular surgery. In pursuit of a non-thrombogenic surface, we have cultured human-adult endothelial cells, examined their adhesive properties and their ability to colonize the inner surface of a Dacron graft. To examine cell adhesion, endothelial cells were labelled with 111In-oxine and inoculated onto prosthetic wells previously prepared with either cold insoluble globulin (CIG), 1% gelatin, alginate or left untreated as a control. At 100 min, mean percentage adhesion to CIG and gelatin precoated wells was 86.0 +/- 9.9% (+/- SD) and 81.6 +/- 2.9% respectively, whereas alginate at 57.5 +/- 7.5% and the control well at 48.3 +/- 9.9% showed significantly less adhesion. Further experiments examined the adhesion of Indiumoxine labelled endothelial cells to Dacron graft (2 cm X 6 mm ID) placed in an in vitro arterial circuit. An immediate loss of approximately 20% of the cells occurred within the first 30 s, whereafter, a stable population were adherent to the graft material. By 102 min, 73.4 +/- 1.8% of cells remained attached when exposed to tissue culture medium, but only 64.1 +/- 6.9% after exposure to blood. Cultured human adult endothelial cells adhere most effectively to prosthetic surfaces precoated with CIG or gelatin, and remain attached following exposure to shear forces.

Alginates↗
PubMed1988

SCE induction in Chinese hamster ovary cells (CHO) exposed to G agents.

Cultured Chinese hamster ovary (CHO) cells were exposed to two neurotoxic organophosphates, either sarin (GBI, GBII) at 1.4 X 10(-3) M or soman (GD) at 1.1 and 2.2 X 10(-3) M for 1 h, grown and their metaphase chromosomes scored for sister-chromatid exchanges (SCE). No cytotoxicity was seen with either agent at any dose level tested. Since histograms of SCE per cell showed that they were non-symmetrically arrayed around the mean, the number of SCEs were analyzed by using the nonparametric tests, Mann-Whitney and Kruskall-Wallis. Agents GBI and GBII did not show any significant increase in SCE over baseline. On the other hand, GD demonstrated a statistically significant increase in SCE with and without metabolic activation. Ethyl methanesulfonate (EMS) alone at 5 X 10(-3) M and cyclophosphamide (CP) at 10(-4) M in the presence of rat microsomes (S9) induced a 3- and 8-fold increase in SCE per cell, respectively.

Animals↗
PubMed1988

Toxicity of an acute dose of agent VX and other organophosphorus esters in the chicken.

The neurotoxicities of single doses of a chemical warfare agent VX [phosphonothioic acid, methyl-S-(2-[bis(1-methylethyl)amino/ethyl) O-ethyl ester], a metabolite of the agricultural chemical parathion, paraoxon, PO (phosphonothioic acid, diethyl paranitrophenyl ester), and the known neuropathic agents DFP] phosphorofluoridic acid, bis(1-methylethyl) ester] and TOCP (phosphoric acid, tri-o-tolyl ester) were compared in the chicken. Single injections (subcutaneous, sc) of VX as high as 150 micrograms/kg (5 times the LD50, intramuscular, im) were tolerated by laying tens if atropine and 2-pralidoxime were used as antidotes before and immediately after injection. The 150 of VX for inhibition of chicken brain acetylcholinesterase was approximately 5 X 10(-10). Plasma acetylcholinesterase, but not butyrylcholinesterase, was depressed 2 h after injections of 2-20 micrograms VX/kg im without antidotes. Levels of plasma enzymes such as creatine kinase, indicative of tissue damage, were increased after exposure to both VX and PO. Injections of up to 150 micrograms/kg of VX with antidotes did not cause locomotor or histological signs of organophosphorus-induced delayed neuropathy, but single injections of 400 mg TOCP/kg did.

Acetylcholinesterase↗
PubMed1988

Toxicity of repeated doses of organophosphorus esters in the chicken.

Hens were repeatedly exposed to paraoxon (PO, phosphonothioic acid, diethyl paranitrophenyl ester), the chemical warfare agent VX/phosphorofluoridic acid, methyl-S-(2-[bis(1-methylethyl)amino/ethyl)O-ethyl ester], or the neuropathic DFP [phosphorofluoridic acid, bis(1-methylethyl)ester] as evidence was sought for nerve or other tissue damage following long-term treatments at high dose levels. Thirty-day and 90-d trials were performed in which each bird was injected 3 or 5 times per week with atropine as protection, weighed, their eggs collected, and their blood enzymes (cholinesterases creatine kinase, and lactic dehydrogenase) and locomotion periodically examined. Muscle and brain enzymes were assayed at the end of the experiments. Doses of PO and VX were at or above LD50 levels. DFP doses were lowered with each run to estimate a no-observable-effect level for organophosphate-induced delayed-neuropathy (OPIDN). No abnormalities attributable to repeated exposures to either PO or VX were found, even though acute, short-term symptoms of toxicity appeared after each injection. No evidence for OPIDN was obtained with repeated exposures to PO and VX under conditions where OPIDN was caused by DFP. Histological signs of OPIDN appeared in the spinal cord without gross symptoms of ataxia following repeated treatments of 25 mg/kg of DFP. The results of one experiment suggested that exposure to protective injections of atropine delays the appearance of the locomotor symptoms of the DFP-induced neuropathy.

Animals↗
PubMed1988

Autoimmunity and glomerulonephritis after neonatal induction of lymphoid chimerism in mice: role of donor B cells and host T cells.

Balb/c mice neonatally injected with semiallogeneic (A/J x Balb/c) F1 or (C57 BL/6 x Balb/c) F1 hybrid spleen cells develop autoantibodies, marked increase in serum levels of IgG1 and IgE, lymphoid hyperplasia, and immune-complex glomerulonephritis. F1 donor B cells play a dominant role in the pathogenesis of this autoimmune disease since B-cell chimerism is required for the occurrence of immunopathology, donor-specific allotype is expressed on serum anti-DNA antibodies, and substantial amounts of donor-derived immunoglobulins are present in the kidney eluate of chimeric mice. In vitro experiments indicate that T cells from diseased Balb/c mice induce activation of F1 donor B cells with secretion of anti-DNA antibodies. These findings suggest that a host-versus-graft reaction between recipient T cells and donor F1 B cells is responsible for the secretion of pathogenic antibodies in this model.

Animals↗
PubMed1988

Osteoarticular amyloidosis associated with haemodialysis: an immunoultrastructural study.

Osteoarticular amyloidosis occurred in a patient receiving long term haemodialysis. Histological examination showed that the amyloid deposit was surrounded by inflammatory cells and macrophages filled with haemosiderin. Electron microscopy showed that the amyloid fibrils were in close contact with cytoplasmic expansions, or located in intracytoplasmic pockets of the infiltrating cells. Immunohistological and immunoultrastructural observations confirmed that beta 2-microglobulin was a major constituent of amyloidosis associated with dialysis. Amyloid P component was also detected within the amyloid deposits. These findings suggest that amyloid P component, iron overload, or macrophage derived factors could have a role in the polymerisation of beta 2-microglobulin into amyloid deposit.

Amyloid↗