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Biomedical subjects

M Fisher

Publications and source records attributed to M Fisher.

At least 505 records · Page 28Linked to original sources
PubMed1983

Platelet activation and mitral valve prolapse.

Mitral valve prolapse (MVP) is a predisposing factor for cerebral ischemia, especially in young adults. Cerebral embolization of intracardiac thrombi is the probable mechanism in many cases. Platelets play a key role in the development of thrombi. We found that platelet factor 4, a marker protein of platelet activation, was elevated in 12 of 33 MVP patients (36%) without a history of stroke. This finding indicates that platelets are frequently activated in asymptomatic MVP patients and may allow identification of a subgroup of MVP patients with activated platelets who are at increased risk for emboli.

Adolescent↗
PubMed1983

Carotid occlusion in cysticercosis.

A man without orthostatic hypotension had transient ischemic attacks that were initiated by upright posture. CT showed a cystic mass in the interhemispheric fissure and basilar cisterns. Cerebral angiography demonstrated supraclinoid occlusion of the right internal carotid artery. At frontal craniotomy, cysticercosis cysts were found adherent to a pulseless right internal carotid artery. This is the first antemortem documentation of a large artery occlusion directly related to Cysticercosis racemosus.

Adult↗
PubMed1983

Suppression of lymphocyte proliferative responses: characterization of the suppressor and kinetics of suppression.

Culturing spleen cells for 2 or more days in the absence of mitogenic stimulation results in the generation of suppressor cells that can effectively inhibit the proliferative responses of freshly prepared spleen cells to mitogen or alloantigen stimulation. Suppression does not appear to be mediated by prostaglandins nor other soluble factors produced during the preculture period. The suppressor cell is described as a plastic-adherent Thy-1.2-, IgM-, FcR+ macrophage-like cell. Significant suppression of Con A responses can be detected at suppressor to target ratios as low as 1:100. The plastic-adherent suppressor is capable of terminating Con A-induced proliferation of spleen cells whether added at the onset of the Con A response or added as late as 48 hr after mitogenic stimulation. The suppressed spleen cell population displays an absence of large blast cells and a decrease in surface density of Thy-1.2 determinants.

Animals↗
PubMed1983

Analysis of the effects of Streptomyces hyaluronidase on formation of the neural tube.

Chick embryos at stages 8 to 9 were treated in ovo with Streptomyces hyaluronidase (SH) to determine whether neurulation occurs normally in embryos depleted of hyaluronic acid, a major component of the extracellular matrix. Open neural tube defects occurred in 60-94% (depending on the particular enzyme batch) of the embryos treated with SH and examined after an additional 24 h of incubation. Defects were confined mainly to the spinal cord. The neural folds underwent elevation in defective regions but failed to converge and fuse across the dorsal midline. The extracellular matrix of embryos treated with SH was depleted consistently, as determined with sections stained with Alcian blue. Control experiments were done to ensure that neural tube defects were not caused by non-specific protease contamination of SH, or by digestion products of hyaluronic acid. We propose several plausible and testable mechanisms through which the extracellular matrix might influence the complex developmental process of neurulation.

Animals↗
PubMed1983

Focal cerebral ischemia and mitral valve prolapse in monozygotic twins.

Mitral valve prolapse (MVP) is a common frequently inherited cardiac valvular disorder. Ischemic cerebrovascular disease (ICVD) is an apparent complication of MVP. We report the concordance of MVP and ICVD in a pair of monozygotic twins. This occurrence reinforces the concepts that MVP is highly concordant in monozygotic twins and that it can be the cause of familial ICVD.

Brain Ischemia↗
PubMed1983

Suppression of lymphocyte proliferative responses: demonstration of two stages occurring in the in vitro generation of suppressor macrophages.

The suppressor macrophages generated by in vitro culture of spleen cells are shown to be derived from nonadherent splenic precursors. The induction of suppressor macrophage generation requires the presence of both plastic-adherent and plastic-nonadherent spleen cells during the first 24 to 48 hr of culture. After this induction period, the primed nonadherent cells can continue to generate suppressor macrophages through several serial transfers. The primed nonadherent spleen cell population is predominantly comprised of cFcR+ cells (40 to 50%) and Thy-1+ cells (40%), many of which appear to be undergoing blastogenesis. The generation of suppressor macrophages appears to proceed in two stages. The first stage is radiosensitive and has a minimum duration of 1 to 2 days. Although this stage initially coincides with the inductive period, it is also required for the continuous propagation of the suppressor macrophages upon serial transfer of the nonadherent spleen cells. The second stage is radioresistant and has a maximum duration of 2 to 3 days. The in vitro events thus bear similarities to events occurring during in vivo differentiation and activation of effector macrophages. It is suggested that the in vitro generation of suppressor macrophages may be one component of syngeneic mixed lymphocyte responses when spleen cells are used as the responding population, and that the suppressors represent part of a regulatory system controlling lymphocyte and macrophage differentiation and activation.

Animals↗
PubMed1982

Influence of time, temperature and coagulation on the measurement of C3, C3 split products and C4.

Quantitative and qualitative immunoelectrophoretic analyses of circulating C3, C3 split products and C4 were performed in matched EDTA plasma and serum obtained from 5 normal subjects and stored for up to 48 h at room temperature (18 degrees C-22 degrees C) and 4 degrees C. Fluctuations in apparent levels of C3 were greater in serum than plasma stored at room temperature, a fall in levels seen by 24 h being followed by a significant increase. By contrast, levels of C3 did not alter if stored at 4 degrees C. C4 levels in both EDTA plasma and serum remained unchanged for 24 h, a slight decrease being seen at 48 h. Levels of C4 remained constant if samples were stored at 4 degrees C. Crossed immunoelectrophoresis revealed a significant progressive decrease in C3 levels and a simultaneous increase in C3c occurring after 4 h in serum and 8 h in EDTA plasma, stored at room temperature. In studies conducted at 4 degrees C, similar but delayed fluctuations were seen. A progressive and significant increase in C3d levels was seen in both plasma and serum samples stored at room temperature, levels rising to 276% (plasma) and 308% (serum) of levels seen at zero time. At 4 degrees C marginal increases in C3d levels only were observed. These results suggest that in vitro degradation of C3 and C4 are readily facilitated by temperature, time and coagulation, and that conditions of collection and storage of samples must be optimized for the accurate definition of activation of the complement cascade.

Adult↗
PubMed1982

Marker proteins of platelet activation in patients with cerebrovascular disease.

Platelet activation is assumed to occur in many patients with strokes of transient ischemic attacks (TIAs). Determination of this activity can now be measured by assaying the platelet-specific proteins, platelet factor 4 and beta-thromboglobulin. These proteins are platelet specific and are released during irreversible aggregation. The plasma level of these proteins was measured in patients with strokes and TIAs and both groups had significantly greater values than healthy control subjects. These markers of platelet activation may provide further understanding of the role of platelets in the etiology, diagnosis, and treatment of cerebrovascular disease.

Adolescent↗
PubMed1982

Hemolytic uremic syndrome and metastatic malignancy.

We report a case of hemolytic uremic syndrome (HUS) with advanced renal failure and metastatic adenocarcinoma of the prostate. The HUS rapidly improved after treatment with blood transfusions, Plasmanate infusions, aspirin and dipyridamole, and hemodialysis for uremia. No cancer chemotherapy was given. This case illustrates that, in adults, HUS may have an excellent prognosis even with advanced renal failure, and that the presence of metastatic cancer does not necessarily imply a relationship between the two diseases.

Acute Kidney Injury↗
PubMed1982

Late unheralded pacemaker pocket infection due to Staphylococcus epidermidis: a new clinical entity.

Late pacemaker pocket infections in the absence of predisposing factors such as multiple pacemaker related procedures, skin erosion, chest wall trauma or generalized sepsis have been rarely reported. In the past year, we have seen three late pocket infections (18, 32 and 47 months post-implantation) due to Staphylococcus epidermidis (S. epidermidis). All three patients with late S. epidermidis infections presented with painless swelling over the pulse generator site and had been well until shortly before admission. The patients denied febrile illnesses or chest trauma in the preceding year and no skin erosion was evident. All had been seen regularly in clinic and bimonthly transtelephonic recordings had shown normal pacemaker function. Local drainage, antibiotics and removal of the pacing system was successful in all three patients. We conclude that late pacemaker pocket infections due to S. epidermidis may become an important clinical problem in this era of long-lasting pulse generators. In light of the insidious nature of S. epidermidis infections, regular inspection of the pocket area by both patient and physician is mandatory.

Aged↗
PubMed1982

Nonenzymatic glucosylation of low-density lipoprotein alters its biologic activity.

Human low-density lipoprotein (LDL) was glucosylated by incubation in vitro with glucose (20-80 mM) with or without addition of cyanoborohydride. The incorporation of covalently bound glucose was linear over time, and amino acid analysis showed the presence of glucosyllysine residues. The glucosylated LDL (glc LDL) moved more rapidly than normal LDL on agarose electrophoresis. The rate of degradation of 125I-labeled glucosylated LDL (glc LDL) by cultured human fibroblasts was reduced compared with that of native I-LDL, the difference increasing with extent of glucosylation. Effects were seen with blockage of as few as 6-15% of the LDL lysine residues; high-affinity degradation was completely lost when one-third of the lysine residues were blocked. Conjugation of LDL with glucose-6-phosphate also blocked high-affinity uptake and degradation. Whereas native LDL uptake inhibited the activity of beta-hydroxy-beta-methylglutaryl coenzyme A reductase and stimulated acyl coenzyme A:cholesterol acyltransferase activity, glc LDL had no effects on these enzymes. The fractional catabolic rate of glc LDL in guinea pigs was reduced. Degradation of glc LDL by mouse peritoneal macrophages was not significantly faster than that of native LDL. Finally, the presence of glc LDL in human plasma was demonstrated. Preliminary data show that 1.3% of lysine residues in normal LDL and 2-5.3% of lysines in diabetic LDL were glucosylated. Since, like other plasma proteins, LDL undergoes glucosylation in diabetes, its turnover and sites of catabolism may differ from normal and this may be relevant to the accelerated atherosclerosis of diabetes.

Amino Acids↗
PubMed1982

Nonenzymatic glucosylation of high-density lipoprotein accelerates its catabolism in guinea pigs.

Nonenzymatic glucosylation of lysine residues of high-density lipoprotein (HDL) was shown to occur in vitro. Most of the incorporated glucose was localized to apoprotein A-I, but other apoproteins were glucosylated as well. Glucosylated high-density lipoproteins (glcHDL) had enhanced electrophoretic mobility on agarose. With increasing amounts of glucose incorporated there was a proportionate increase in the rate of clearance of glcHDL when injected intravenously into guinea pigs. When 60% of lysines were derivatized, clearance of glcHDL was 60% faster than that of control HDL. When as few as 2% of lysines were glucosylated, there was still an 8% increase in the rate of clearance. Uptake of glcHDL by macrophages was not increased. The accelerated clearance of glcHDL from plasma may be relevant to the decreased HDL levels observed in diabetic subjects.

Animals↗
PubMed1981

The role of mRNA levels and cellular localization in controlling sn-glycerol-3-phosphate dehydrogenase expression in tissues of the mouse.

sn-Glycerol-3-phosphate dehydrogenase (glycerol-P dehydrogenase, EC 1.1.1.8) activity levels in seven tissues of adult mice vary approximately 100-fold from a low of 0.1 unit/mg of protein in the cerebral cortex to a high of 8 units/mg of protein in the brown fat of cold-adapted mice; the brown fat accounts for approximately 1% of the total tissue protein. This high degree of variation in the quantitative expression of an enzyme in different tissues has provided us with a system for analyzing the mechanism by which tissue specific variation for a given gene product is controlled. To this end we have measured the amount of immunoreactive enzyme and the level of translatable glycerol-P dehydrogenase mRNA and have localized the glycerol-P dehydrogenase-positive cells by immunocytochemistry. We have found that the amount of enzyme protein in a tissue is strongly correlated with the level of its translatable mRNA (correlation coefficient = 0.996) and that in several cases the differences among tissues can be explained by differences in the numbers of glycerol-P dehydrogenase-positive cells.

Adipose Tissue, Brown↗