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Biomedical subjects

C Carter

Publications and source records attributed to C Carter.

At least 199 records · Page 11Linked to original sources
PubMed1988

The relationship of isolated sleep paralysis and panic disorder to hypertension.

An hypothesis is proposed that there exists a subgroup of African-American hypertensive patients whose hypertension could have been prevented by the early detection and treatment of easily recognizable symptoms that signal the initiation of the pathophysiologic processes that lead to essential hypertension.A pilot study of 31 patients with elevated blood pressure revealed that 41.9 percent had isolated sleep paralysis, 35.5 percent had panic attacks, and 9.7 percent had panic disorder. These proposed hyperadrenergic phenomena may be related to the development of hypertension in certain individuals.

Adult↗
PubMed1987

Peripheral type benzodiazepine binding sites are a sensitive indirect index of neuronal damage.

The effects of excitotoxic lesions on the neuronal marker enzymes choline acetyltransferase and glutamate decarboxylase and on the levels of 'peripheral type' benzodiazepine binding sites (PTBBS) (a putative glial marker) have been compared to see whether PTBBS provide a suitable if indirect quantitative index of neuronal damage. Intrastriatal injection of excitotoxic compounds provoked a dose-dependent increase in the levels of PTBBS. The potency order was the following: kainate greater than AMPA greater than N-methyl-D-aspartate (NMDA) greater than quisqualate. The maximal increases in this parameter were 400, 470, 320 and 210% for kainate (12 nmol), AMPA (100 nmol), NMDA (500 nmol) and quisqualate (250 nmol), respectively. 2-Amino-5-phosphonovalerate (100 nmol)--an antagonist of the NMDA receptor subtype--completely blocked the increase in PTBBS induced by NMDA (250 nmol), but was without effect against the other excitotoxins. Increases in binding levels were in general mirrored by a decrease in choline acetyltransferase and glutamate decarboxylase activity. However, PTBBS were a more sensitive indirect index of neuronal damage than neuronal enzymes because the alterations in binding were statistically significant at doses of excitotoxins lower than those causing a loss of marker enzymes. It is concluded that PTBBS are a suitable and sensitive means of detecting discrete neurotoxic changes and that its measurement will help in the study of other pathological and experimental models.

Animals↗
PubMed1987

Lack of effect of a 24-hour infusion of iloprost in intermittent claudication.

24 hour infusion of iloprost was compared with placebo infusion in 19 patients with stable intermittent claudication using a double blind, balanced crossover design. Despite significant inhibition of platelet aggregation to ADP and collagen (p less than 0.001) and the typical cardiovascular and gastrointestinal side effects, there was no significant effect on treadmill exercise times at any time up to 6 weeks after infusion. The 95% confidence limits indicated that an improvement of more than 25% was unlikely to occur. No significant changes in B thromboglobulin, platelet aggregate ratio, bleeding time, whole blood viscosity and euglobulin clot lysis time were demonstrated.

Aged↗
PubMed1987

Association of reovirus proteins with the structural matrix of infected cells.

The interaction of reovirus with the cytoskeleton was investigated. The soluble components of infected cells were extracted with the nonionic detergent NP-40 in a physiological buffer, and a cytoskeletal extract was prepared from the detergent-insoluble fraction. We observed a selective association of viral-specified products with the cytoskeleton that was temporally controlled. Viral dsRNA appeared first on the framework but after several hours was found also in the soluble phase, encapsidated in mature virions. The initial viral translation products were associated exclusively with the soluble fraction, but concomitant with the appearance of dsRNA, viral proteins microNS and sigma 3 were detected on the cytoskeleton. Several hours later, all viral proteins were detected on the framework. Viral polypeptide microNS exhibited unique spatial distribution patterns that correlated with viral assembly: Before dsRNA replication, it appeared as diffusely distributed protein; a few hours later, it was detected in punctate foci interconnected by tiny filaments; several hours later, it appeared as an extensive fiber network that traversed the foci. The other viral proteins were detected only within viral foci. MicroNS remained bound to the matrix fraction after treatment with DNase, Mg2+, and high salt, treatments that released other viral proteins. This distribution pattern was virus-directed because passage of virus at high multiplicity of infection induced mutations that prevented assembly of the microNS-coated filament organization. A small fraction of the viral-specified products that included polypeptide microNS, but not viral dsRNA, was coprecipitated from cytoskeletal extracts with proteins of mol wt approximately 55K by monoclonal antibodies that recognized tubulin and vimentin. Disruption of this interaction by long exposure to colchicine did not prevent association of viral proteins or RNA with the matrix, indicating that viral products were not transported through these interactions. The results indicate that reovirus morphogenesis includes temporal and spatial controls not described previously.

Animals↗
PubMed1987

Monoclonal antibody definition of multiple polymorphic epitopes on human leukocyte antigen-DRw52.

Monoclonal antibodies have revealed complexity within the human leukocyte antigen class II antigens. We have studied epitopes present on a DR3 homozygous B-lymphoblastoid cell line using five polymorphic monoclonal antibodies produced and characterized in our laboratory. Serological analysis on a panel of B-cell lines revealed that the antibodies have different, but related, specificities (NDS9-anti-DR3, NDS10-anti-DR5, less than 3, less than w6, NDS11-anti-DR3, 5, w6, NDS12-anti-DR3, 5, w6, w8, NDS13-anti-DR3, 5, w6, w8+). Competitive radioimmunoassays and two-dimensional gel analyses demonstrated that whereas the epitopes recognized by the broadly reactive antibodies NDS10, 11, 12, and 13 reside on the same molecule, the epitope detected by NDS9 is present on a molecule with different electrophoretic mobility. Thus, using polymorphic monoclonal antibodies, we have defined multiple epitopes associated with DR3, which have different distributions at the population level.

Antibodies, Monoclonal↗
PubMed1987

Clinical impact of neonatal thrombocytopenia.

In a 1-year prospective study, the outcome in infants with a platelet count less than 100 X 10(9)/L (n = 97) was compared with the outcome in an age-, weight-, and disease-matched nonthrombocytopenic control group (n = 80). The hemostatic impact of the thrombocytopenia was assessed by modified template bleeding time, hemorrhage score, and determination of the presence and extent of intraventricular hemorrhage (IVH) in thrombocytopenic infants weighing less than 1500 at birth (n = 39) compared with all nonthrombocytopenic infants less than 1500 g (n = 122) admitted during the study period. The development outcome in infants less than 1500 g was compared at 12 months after delivery. Neonatal thrombocytopenia had a major impact on hemostatic integrity: bleeding time was inversely related to platelet count (r = -0.56, P less than 0.001) and became prolonged when the platelet count fell to less than 100 X 10(9)/L. In addition, many infants (40%) had evidence of platelet dysfunction with prolonged bleeding times despite only moderately reduced platelet counts (75 to 150 X 10(9)/L). The hemorrhage score was greater in the thrombocytopenic infants compared with the sick control infants, and increased as the platelet count fell (r = -0.58, P less than 0.001). The incidence of IVH in thrombocytopenic infants less than 1500 g was 78%, compared with 48% in the nonthrombocytopenic infants (P less than 0.01). In addition, the more severe grades of IVH were more frequent in the thrombocytopenic infants. The serious neurologic morbidity for the surviving infants less than 1500 g was 41% in the thrombocytopenic infants and 7% in the nonthrombocytopenic infants. Thus, on the basis of three indices of abnormal bleeding, thrombocytopenic infants are at greater risk for bleeding than equally sick nonthrombocytopenic infants. The thrombocytopenia itself may have contributed to the high mortality and neurologic morbidity.

Bleeding Time↗
PubMed1987

Linkage analysis of British and Indian families with Von Recklinghausen neurofibromatosis.

Linkage analysis has been undertaken in two British and three South African Indian families with Von Recklinghausen neurofibromatosis. Eleven polymorphic DNA probes were studied, including both random DNA sequences and candidate oncogenes. Although no evidence for linkage of these probes to the disease was detected, substantial exclusion regions were established on six of the chromosomes studied.

Genetic Linkage↗
PubMed1987

Exclusion of linkage of loci on chromosome 19 with multiple endocrine neoplasia, type 2.

Linkage between seven loci on chromosome 19 and multiple endocrine neoplasia type 2a (MEN2A) was examined in a single large Swedish pedigree. A total of 50 cM was excluded from the male genetic map by pairwise analysis and an estimated 63 cM by multipoint analysis. Using existing data on the likelihood of different marker-marker distances and taking into account current exclusions on other chromosomes, the probability that the gene for MEN2A segregating in this pedigree could still be located on chromosome 19 is approximately 0.28%.

Chromosome Mapping↗
PubMed1987

Variations in hospital malpractice costs, 1983-1985.

The rapid increase in the costs of hospital liability in recent years has focused attention on the present and future ability of hospitals to offer complex, high-risk procedures. In this study of the costs of malpractice coverage and their rates of increase between 1983 and 1985, we found that the rapid increases in the costs of liability insurance are largely accounted for by the fact that hospitals are purchasing more coverage. Their costs per dollar coverage remained constant over the two-year period. Although malpractice cost differences are narrowing among the nine U.S. census regions, our analyses suggest that there will be significant inequities in what Medicare allows in its prospective payment formula for malpractice insurance costs.

Costs and Cost Analysis↗
PubMed1987

Presynaptic alpha-2 adrenoceptors play a major role in the effects of idazoxan on cortical noradrenaline release (as measured by in vivo dialysis) in the rat.

Transcortical dialysis in awake unrestrained rats has been used to evaluate the functional role of differently located alpha-2 adrenoceptors in mediating the action of the alpha-2 adrenoceptor antagonist idazoxan on cerebral noradrenaline release. Basal efflux of noradrenaline collected by a cortically implanted dialysis fiber was stable over a period of 4 days. Systemic injections of idazoxan (20 mg/kg i.p.) increased cortical noradrenaline efflux. This effect was potentiated by pretreatment with the noradrenaline uptake blocker desipramine (20 mg/kg i.p.). Local cortical infusion of (10(-4) M idazoxan which provides a theoretical extracellular administration of 4 to 48 microM) via the dialysis fiber, thus eliminating the potential contribution of somatodendritic alpha-2 adrenoceptors, also elevated cortical noradrenaline efflux. Desipramine (20 mg/kg i.p.) potentiated this effect. Four days after lesioning cortical cell bodies with ibotenic acid (20 min infusion of 10(-4) M ibotenic acid via the dialysis fiber), both systemic injections and local cortical infusions of idazoxan were still effective in increasing cortical noradrenaline efflux. Lesion of serotonergic afferents to the cerebral cortex (by i.c.v. injection of 5,7-dihydroxytryptamine) or of cortical cholinergic afferents (by bilateral electrocoagulation of the nucleus basalis magnocellularis) did not affect the ability of cortical idazoxan infusion to stimulate noradrenaline efflux. The results suggest that the effects of idazoxan on cortical noradrenaline release are mediated primarily by alpha-2 adrenoceptors on noradrenergic nerve terminals, rather than by those located postsynaptically, somatodendritically or on the terminals of other neuronal inputs to the cerebral cortex.

5,7-Dihydroxytryptamine↗
PubMed1986

Frequency and mechanism of neonatal thrombocytopenia.

We performed a 1-year prospective study of 807 consecutive infants admitted to a regional neonatal intensive care unit to determine the frequency, natural history, mechanism(s), and cause of thrombocytopenia. Thrombocytopenia developed in 22% of the infants. The platelet count nadir usually occurred by day 4 and resolved by day 10. Possible mechanisms responsible for the thrombocytopenia were assessed by comparing mean platelet volume, platelet-associated IgG (PAIgG), and coagulation test results in those infants whose platelet count fell below 100 X 10(9)/L (n = 97) with values in age-, weight-, and disease-matched control infants without thrombocytopenia (n = 80). In some thrombocytopenic infants, 111In-labeled-platelet survival, an estimate of megakaryocyte number in bone marrow biopsy specimens obtained at autopsy, and response to platelet infusions were also assessed. The thrombocytopenia was caused by increased platelet destruction, as shown by short 111In-labeled-platelet survival (12 to 128 hours), a rising mean platelet volume during the first week of life, normal numbers of megakaryocytes, and a poorer than predicted response to platelet infusions. A potential cause for the thrombocytopenia could be found in the majority of infants: 52% had elevated levels of PAIgG, 21% had laboratory evidence of disseminated intravascular coagulation, and 12% had had exchange transfusions. In contrast, the control infants had normal coagulation assay results, and only 15% had elevated levels of PAIgG. Birth asphyxia was identified as an associated risk factor for thrombocytopenia. This study demonstrates that transient, destructive thrombocytopenia develops in a large proportion (22%) of infants admitted to a neonatal intensive care unit, and that birth asphyxia is an important risk factor.

Asphyxia Neonatorum↗
PubMed1986

A labile inhibitor blocks immunoglobulin kappa-light-chain-gene transcription in a pre-B leukemic cell line.

The murine pre-B leukemic cell line 70Z/3 contains both an unrearranged immunoglobulin kappa-light-chain gene and a functionally rearranged but silent kappa-light-chain gene. Mitogenic stimulation of growing 70Z/3 cells with bacterial lipopolysaccharide (LPS) activates kappa-light-gene transcription and results in a 10- to 20-fold increase in cytoplasmic kappa-light-chain mRNA. The induction of kappa gene expression by LPS was probed by using an inhibitor of protein synthesis. Concomitant treatment of 70Z/3 cells with LPS and cycloheximide failed to block kappa-light-chain mRNA accumulation, indicating that new protein synthesis is not required for the activation of kappa-gene expression. Treatment of 70Z/3 cells with cycloheximide alone resulted in kappa-mRNA induction equivalent to those produced by LPS alone. The kappa mRNA synthesized in the presence of cycloheximide was intact and able to direct the synthesis of kappa light chains. Nuclear transcription assays revealed that cycloheximide, like LPS, activated kappa-gene transcription. These findings indicate that the trans-acting factors necessary for kappa-light-chain-gene transcription are present in pre-B cells, but their activity is blocked by short-lived inhibitory proteins.

Animals↗
PubMed1986

The tyrosine phosphorylation substrate p36 is developmentally regulated in embryonic avian limb and is induced in cell culture.

The 36-kD protein-tyrosine kinase substrate p36 has been variously postulated to be involved in membrane-cytoskeletal interactions, membrane traffic, and the regulation of phospholipase A2, and its phosphorylation may play some role in malignant transformation by avian sarcoma viruses. Because embryonic tissues are resistant to transformation by avian sarcoma viruses, we have examined the expression of p36 in the developing avian embryonic limb. The level of p36 increased progressively from day 5 to day 14 of development. It was largely absent from day-5 mesenchyme, and was induced during the differentiation of mesenchymal cells into connective tissue and cartilage, but was not induced in differentiating muscle. In contrast, p36 was detected in ectodermal cells at all developmental stages examined. When day-5 limbs were dissociated and cultured, p36 was induced in all adherent cells, beginning at 2-4 h after plating, and reaching levels comparable to those observed with intact day-14 limb tissue within 48 h. The accumulation of p36 in culture was dependent on substratum adherence, suggesting that its stability is regulated by cell attachment or spreading. These findings are consistent with a structural or mechanical role for p36.

Age Factors↗