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Biomedical subjects

J H Herman

Publications and source records attributed to J H Herman.

At least 55 records · Page 3Linked to original sources
PubMed1988

Identification of Bakb, a new platelet-specific antigen associated with posttransfusion purpura.

Baka is a platelet alloantigen whose putative allele, Bakb, has not been identified previously. By using a serum, "Har," obtained from a patient with posttransfusion purpura, we describe the platelet alloantigen Bakb. The Har serum reacted with an NP-40-extractable platelet membrane protein of 142 kd with mobility similar to platelet glycoprotein IIb alpha. We found that the antigen recognized by the Har serum is inherited in an autosomal dominant mode with an apparent gene frequency of .39. Chi-square analysis of observed and expected phenotype frequencies indicated that serum Har recognizes Bakb, the anticipated allele of Baka. Our findings provide new evidence for polymorphism of glycoprotein IIb and for the association of posttransfusion purpura with alloimmunization to determinants on this glycoprotein.

Antigens, Human Platelet↗
PubMed1987

Modulation of cartilage destruction by select nonsteroidal antiinflammatory drugs. In vitro effect on the synthesis and activity of catabolism-inducing cytokines produced by osteoarthritic and rheumatoid synovial tissue.

Non-enzymatic factors produced by synovial tissue can potentially mediate cartilage destruction by inducing the synthesis and release of matrix-degrading proteinases from chondrocytes. Pharmacologic control of this process is of potential clinical relevance. The in vitro effect of therapeutic concentrations of select nonsteroidal antiinflammatory drugs on the synthesis and activity of catabolism-inducing cytokines produced by 6-day explant cultures of osteoarthritic and rheumatoid synovial tissue was studied. Piroxicam regularly suppressed such factor synthesis by both types of tissue without significantly affecting total protein synthesis. This did not occur using sodium salicylate or indomethacin in osteoarthritis tissue cultures and was observed only occasionally in rheumatoid arthritis cultures. None of the nonsteroidal antiinflammatory drugs studied consistently blocked catabolism-inducing activity in osteoarthritis tissue, whereas piroxicam more consistently inhibited activity produced by rheumatoid arthritis tissue. Results suggest that the catabolism-inducing factors produced by the 2 tissue sources may differ.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1987

Red cell Th activation: biochemical studies.

The peanut agglutinin from Arachis hypogea is a lectin that reacts with red blood cells expressing the Th antigen. The Th antigen has been said to be qualitatively similar to the T antigen, a well-defined antigen due to desialylation of glycophorin A and B that also reacts with the peanut agglutinin. We examined Th activated red blood cells from two patients with Fanconi's anaemia using 125I radiolabelled peanut agglutinin as a probe in Western blotting of red blood cell membrane proteins. We also probed the surface of intact Th activated red blood cells for structures related to the T antigen using [3H]sialic acid and a purified sialyltransferase. Neither of these techniques found antigens on the Th activated red blood cells that were similar to the antigen found on T activated red blood cells. These results show that the Th antigen in Fanconi's anaemia is qualitatively different to the antigen found in T activation.

Anemia, Aplastic↗
PubMed1987

Immunologic modulation of cartilage metabolism.

Preservation of the structural integrity of cartilage requires that metabolic homeostasis be maintained between chondrocyte anabolic and catabolic functions. This critical balance is perturbed in osteoarthritis (OA) in which synovial tissue and subchondral intratrabecular marrow often contain a focal and at times more diffuse mononuclear cell infiltration. Cytokines derived from T lymphocytes and monocytes have a capacity to: a) cause qualitative changes in and reversibly suppress chondrocyte proteoglycan, collagen, and non-collagen protein synthesis, and b) induce the synthesis and release of chondrocyte proteinases. Factors having comparable metabolic regulatory activity are produced by synovial tissue derived from idiopathic and secondary forms of OA.

Biological Products↗
PubMed1987

Platelet transfusion. Current techniques, remaining problems, and future prospects.

The use of platelet transfusions to stop or to prevent bleeding in patients with thrombocytopenia or platelet dysfunction has accelerated in the past decade. Platelet counts and bleeding times, performed in conjunction with careful clinical evaluation of the patient, are appropriate guides in assessing the need for platelet transfusion. Complications of platelet transfusions are similar to those of red cell transfusions, with some additional concerns. Pooled random donor or single-donor apheresis concentrates, either randomly or selectively matched, are the major platelet products available. In most cases, transfusion requirements can be satisfied by use of random donor units. Proper evaluation of the effectiveness of transfused platelets is essential in determining the dose and frequency of future platelet transfusions. Refractoriness to random donor platelets eventually occurs in many recipients. This is most commonly associated with alloimmunization to histocompatibility antigens, but other platelet alloantigens may play a role. Many in vitro tests for platelet antibodies have been developed, and the clinical utility of these assays in selecting compatible platelets is now under evaluation. Strategies and different approaches to the management of thrombocytopenic patients with hypoplastic bone marrow states are also reviewed.

Bleeding Time↗
PubMed1987

Hereditary complement (C6) deficiency associated with systemic lupus erythematosus, Sjögren's syndrome and hyperthyroidism.

Results of clinical, serologic and histologic studies documenting an association between hereditary C6 deficiency and a connective tissue disease are provided. The propositus had systemic lupus erythematosus with prominent discoid features, Sjögren's syndrome and hyperthyroidism. Serum C6 was undetectable by radial immunodiffusion and hemolytic assays. Serologic and typing studies performed on 9 family members suggested an autosomal codominant transmission. No correlation with a specific HLA phenotype was established.

Complement C6↗
PubMed1986

Cartilage metabolism and anti-inflammatory drugs in osteoarthritis.

The issue of selecting nonsteroidal anti-inflammatory drugs (NSAIDs) for the management of osteoarthritis based upon their direct effect on normal cartilage metabolism and their ability to modulate mechanisms that disturb such metabolism is addressed. This article provides an overview of the anatomic and biochemical changes that occur in diseased synovial tissue and cartilage, and the pathophysiologic mechanisms presumed to function in the induction and perpetuation of cartilage failure. Studies using experimental animal models of osteoarthritis are reviewed to evaluate the natural history of the disease, as well as the direct effect of NSAIDs on anabolic and catabolic cartilage function. Experimental evidence strongly indicates that NSAIDs of different classes, as well as members within a given class, function differently and manifest activity in addition to cyclo-oxygenase inhibition.

Animals↗
PubMed1986

In utero cerebral hemorrhage in alloimmune thrombocytopenia.

Central nervous system hemorrhage is a well-recognized complication of neonatal alloimmune thrombocytopenia attributed to perinatal trauma from passage through the birth canal. That central nervous system (CNS) hemorrhage can occur in utero is not as well recognized, and congenital CNS lesions have only circumstantially been linked to thrombocytopenia. We report two cases of intrauterine CNS hemorrhage shown to have occurred prenatally, resulting in porencephaly. The second case is unique in that the necropsy finding of a porencephalic cyst arising from an old hemorrhagic site pathologically confirms that the etiology of congenital CNS lesions in alloimmune thrombocytopenia is due to hemorrhage. This second case received close prenatal monitoring and yet died as a result of hemorrhage that was not detected until emergency operative delivery. A review of the literature revealed 10 cases, including two other pairs of siblings, who had CNS damage attributable to intrauterine hemorrhage. These findings indicate that congenital CNS lesions in alloimmune thrombocytopenia are due to intrauterine hemorrhage that careful obstetric and prenatal care may not identify or prevent. This fact should be included when genetic counseling is offered to alloimmunized mothers.

Blood Platelets↗
PubMed1986

The resolution of platelet serologic problems using Western blotting.

Serologic identification of anti-PLAl and other platelet specific antibodies is difficult because other platelet reactive antibodies (e.g. anti-HLA) are commonly found in the samples. We have developed and evaluated a method using Western blotting to identify platelet specific antibodies. Since anti-PLAl is the most frequently encountered antibody, we used this antibody to validate the method. The PLAl antigen was found on a 95,000 Dalton protein, confirmed as glycoprotein IIIa by two-dimensional electrophoresis. The usefulness of Western blotting in resolving difficult platelet serologic problems was compared to a radiolabeled antiglobulin test using intact platelets. Our results showed that all sera with anti-PLAl identified by serology were confirmed by Western blotting. In addition, one anti-PLAl was detectable only by the proposed method. Western blotting was also as useful as a serologic method to PLAl type platelets. HLA antibodies were not demonstrable by this technique. In summary, Western blotting is a highly specific and sensitive way of identifying anti-PLAl in a variety of clinical situations. This approach may be used to identify antibodies to other platelet specific antigens and to standardize platelet antigen typing sera.

Antibody Specificity↗
PubMed1986

Multiple cholesterol emboli syndrome simulating systemic necrotizing vasculitis.

The multiple cholesterol emboli syndrome associated with severe atherosclerotic vascular disease may clinically simulate systemic necrotizing vasculitis. Widespread visceral infarctions in conjunction with potential leukocytosis, eosinophilia, thrombocytopenia, hypocomplementemia and an elevated sedimentation rate may be present. It frequently occurs after intraarterial procedures such as cardiac catheterization and aortography. Diagnosis is made by biopsy of involved tissue. It is essential to establish a proper diagnosis to avoid inappropriate use of steroid and cytotoxic treatment measures.

Arteriosclerosis↗
PubMed1986

Studies on the pathophysiology of posttransfusion purpura.

Posttransfusion purpura typically occurs in PLA1 negative blood recipients who have been previously immunized to the PLA1 antigen. Following transfusion, severe thrombocytopenia develops with the formation of anti-PLA1. Since the patients' platelets lack the PLA1 antigen, one would not expect this antibody to destroy autologous platelets. In this study we show that PLA1 antigen exists in stored blood and can absorb to PLA1 negative platelets making them PLA1 reactive. Incubating PLA1 (-) platelets with ultracentrifuged plasma from PLA1 (+) blood donors allowed anti-PLA1 to bind to PLA1 (-) platelets. Control plasma from PLA1 (-) blood donors did not lead to anti-PLA1 binding. Using an inhibition assay, we showed that stored blood contains PLA1 material that was not removed by ultracentrifugation. The material absorbing to PLA1 (-) platelets represented the PLA1 antigen, which was confirmed by Western blotting. After incubating plasma containing PLA1 antigen with PLA1 (-) platelets, reactivity at 95,000 D was observed. Native PLA1 (+) platelets showed a similar band. When PLA1 (-) platelets were incubated with plasma from a PLA1 (-) donor, this band was not present. These studies show that a soluble form of PLA1 antigen exists in stored blood that can absorb to PLA1 (-) platelets. Consequently, anti-PLA1 can bind to these platelets leading to thrombocytopenia. These observations may explain the autologous destruction of platelets in posttransfusion purpura.

Antigens, Human Platelet↗
PubMed1986

The in vitro effect of select classes of nonsteroidal antiinflammatory drugs on normal cartilage metabolism.

The in vitro effect of piroxicam, a newer nonsteroidal antiinflammatory drug (NSAID), on normal cartilage metabolism has been studied and response contrasted to indomethacin and sodium salicylate. Therapeutic levels of piroxicam has no effect on cartilage glycosaminoglycan (GAG), collagen or noncollagen protein synthesis by porcine weight bearing articular cartilage explants. Salicylate consistently suppressed GAG and protein synthesis, whereas indomethacin had no consistent effect on GAG production but suppressed protein synthesis. NSAID studied had no effect on proteoglycan catabolism. The potential significance of the effect of NSAID on cartilage metabolism is discussed and placed in perspective as regards selection of these agents for human use.

Animals↗
PubMed1984

Nonsteroidal anti-inflammatory drugs and modulation of cartilaginous changes in osteoarthritis and rheumatoid arthritis. Clinical implications.

Nonsteroidal anti-inflammatory drugs have a potential for modifying the complex pathophysiologic events leading to cartilage destruction in various forms of arthritis. Following an evaluation of basic mechanisms in the pathogenesis of cartilaginous destructive lesions, the effects of nonsteroidal anti-inflammatory drugs on normal chondrocyte metabolism are discussed. Their capacity to modulate cartilage and bone lesions in experimental forms of arthritis is addressed, as is the manner in which they may modify the pathophysiology of cartilage destruction in human forms of arthritis. Different classes of nonsteroidal anti-inflammatory drugs produce different effects in certain in vivo or in vitro settings.

Animals↗
PubMed1984

Cytokine modulation of chondrocyte proteinase release.

Nonenzymatic, trypsin sensitive cytokines derived from lectin stimulated normal human mononuclear cells have been shown to induce release of proteoglycan and collagen degrading proteinase activity from chondrocytes in cartilage organ and isolated suspension culture systems. Active chondrocyte protein and RNA synthesis were required to induce activity. Cytokines responsible were of both monocyte and T cell origin. Direct monokine catabolic induction and monokine/lectin-triggered lymphokine inducing activity could be demonstrated. Cyclooxygenase inhibitors and direct or indirect modulation of mononuclear cell or chondrocyte cAMP levels had no effect on factor synthesis or activity. Hydrocortisone abrogated the effect. Cytokines responsible were heat labile, unaffected by reduction/alkylation or neuraminidase exposure, and stable over a pH range of 3-10.

Biological Products↗
PubMed1984

Cytokine modulation of chondrocyte metabolism--in vivo and in vitro effects of piroxicam.

Changes in the macromolecular proteolycan (PG) and collagen of the cartilage matrix may culminate in irreparable tissue destruction. Molecular modifications appear to result from: (A) exogenous proteinases, (B) endogenous chondrocyte proteinases whose synthesis and release is modulated by exogenous non-enzymatic cytokines (CKs) and (C) quantitative and/or qualitative alterations in chondrocyte PG and collagen synthesis which are potentially induced by exogenous CKs. Studies have recently been initiated to determine the effect of piroxicam on the synthesis and activity of such metabolic regulatory CKs in patients with rheumatoid arthritis and osteoarthritis, and in age-, sex-, and race-matched controls. Therapeutic doses of piroxicam alone had no effect on the anabolic or catabolic function of chondrocytes. Current studies concern the effect of piroxicam on: (a) spontaneous and lectin-driven production by peripheral blood monocytes and T-cells of trypsin-sensitive, heat-labile CKs (interleukin 1, lymphokine) which, in a protein- and RNA-synthesis-dependent manner, induce a concentration and duration of substrate exposure dependent release of chondrocyte PG- and collagen- degrading neutral proteinases in cartilage organ and chondrocyte suspension culture systems; (b) spontaneous and lectin-driven synthesis by peripheral blood T-cells of lymphokines capable of suppressing chondrocyte PG, glycosaminoglycan, protein, collagen and nucleic acid synthesis in a quantitatively reversible manner; (c) pathological synovial membrane synthesis of such catabolic-inducing and anabolic-modulatory CKs. These experimental model system are reviewed together with preliminary data on the effect of piroxicam.

Anti-Inflammatory Agents↗
PubMed1984

Evidence for a directional correspondence between eye movements and dream imagery in REM sleep.

We examined the relationship between eye movement direction in REM sleep recorded by electrooculograph (EOG) and gaze direction in dream imagery. In a double-blind protocol, carefully screened and trained subjects were awakened subsequent to direct coupled EOG activity that was either predominantly horizontal or vertical. Following a target eye movement that fulfilled predetermined amplitude and directional criteria, a brief period of ocular quiescence was allowed to transpire before the subject was awakened. The dream narratives and EOG activity occurring prior to the REM awakenings were each reduced to a series of quantitatively scaled ratings. Analyses of variance demonstrated that when the confidence level of the experimenters' prediction is taken into account, statistically significant relationships exist between the number and direction of shifts of gaze in the dream report and scaled measurements of the corresponding EOG. When given dream narratives and the corresponding EOG recordings in sets of four, judges were unable to match them correctly better than by chance. However, in the above matching, judges significantly paired the dream narratives with EOG recordings that were in the same axis of gaze.

Adult↗