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Biomedical subjects

A Carter

Publications and source records attributed to A Carter.

At least 73 records · Page 4Linked to original sources
PubMed1995

Factor V Leiden gene mutation and thrombin generation in relation to the development of acute stroke.

To determine the prevalence of the factor V Leiden gene mutation in relation to the phenotypes of cerebral infarction and cerebral hemorrhage, we studied 386 randomly selected cases of acute stroke and 247 control subjects. Factor V genotype was determined by amplification of a 267-bp sequence of exon/intron 10 of the factor V gene. Levels of prothrombin fragment F(1 + 2), a marker of thrombin generation, were determined in both acute and convalescent stroke and related to factor V genotype. Prothrombin fragment F(1 + 2) was assessed by using an enzyme-linked immunosorbent assay. Sixteen stroke cases (4.1%) were identified as having the mutation compared with 14 (5.6%) control subjects. Prothrombin fragment F(1 + 2) levels were estimated in 191 cases and found to be elevated both acutely and after 3 months, but they were not related to factor V genotype. Prothrombin fragment F(1 + 2) is elevated in acute stroke and requires further evaluation in relation to cerebrovascular disease. These results suggest that the factor V Leiden gene mutation is not a risk factor for arterial thrombosis causing stroke.

Base Sequence↗
PubMed1994

Respective effects of soluble interleukin-1 receptor and tumour necrosis factor receptor on IL-1 and TNF-alpha-induced DNA synthesis of common acute lymphoblastic leukaemia blasts in vitro.

This study investigates the capacity of human recombinant interleukin-1 alpha (IL-1 alpha), IL-1 beta and tumour necrosis factor-alpha (TNF-alpha) to induce DNA synthesis of highly purified blasts from nine adult common acute lymphoblastic leukaemias (cALL) in 7 d liquid culture. IL-1 alpha, IL-1 beta and TNF-alpha stimulated 3H-TdR uptake in leukaemic blasts in a dose-dependent fashion. The IL-1-induced DNA synthesis of cALL cells could not be prevented by the addition of neutralizing antibodies against IL-3, GM-CSF, IL-6 or TNF-alpha. Similarly, the TNF-alpha-stimulated 3H-TdR incorporation of leukaemic blasts was not affected by the addition of antibodies towards IL-1 alpha, IL-1 beta, IL-3, GM-CSF or IL-6. These observations suggest that IL-1 as well as TNF-alpha stimulated growth could not be attributed to the endogenous production of factors, corresponding to the antibodies used in these experiments. Both IL-1 as well as TNF-alpha mediate their action through interaction with specific cell surface receptors. Recently two distinct types of IL-1 receptors (IL-1-Rs), IL-1R(p80) and IL-1-R(p65), as well as two distinct types of TNF-receptors (TNF-Rs), TNF-R (p55) and TNF-R (p75) have been identified. Both types of TNF-Rs exist also in soluble forms (sTNF-Rs), while soluble IL-1-Rs (sIL-1-Rs) have not yet been found naturally. In this study we show that sIL-1-R as well as sTNF-R modulate the effects of their corresponding cytokine in a dose-dependent bimodal fashion; at lower concentrations they augmented while at higher concentrations they inhibited the cytokine-stimulated DNA synthesis of cALL blasts in vitro. It may therefore be concluded from this study that soluble receptors for both IL-1 and TNF, at least in vitro, are functional and interfere with their corresponding cytokine bioactivity.

Cell Division↗
PubMed1994

Effects of soluble interleukin-1 receptor and tumor-necrosis factor receptor, respectively, on the IL-1- and TNF-alpha-induced DNA synthesis of acute myeloblastic leukemia blasts in vitro.

This study demonstrates that soluble interleukin-1 receptor and tumor necrosis factor receptor modulate their corresponding cytokine-induced DNA synthesis of acute myeloblastic leukemia (AML) blasts in a dose-dependent, bimodal fashion; at lower concentrations they enhanced, while at high concentrations they inhibited, the cytokine-mediated effects. Furthermore, the concentrations of endogenously produced IL-1 beta and TNF-alpha were found to be significantly (p < 0.01) higher in supernatants of AML cells cultured in the presence of corresponding soluble receptors compared to their levels in supernatants of cells growing in the absence of these molecules. Our data might suggest that the attenuation of the spontaneous decay of IL-1 beta as well as TNF-alpha activities by soluble receptors may account for their ability to augment some of their effects.

Adolescent↗
PubMed1993

Quantifying social development in autism.

OBJECTIVE: This study was concerned with the development of quantitative measures of social development in autism. METHOD: Multiple regression equations predicting social, communicative, and daily living skills on the Vineland Adaptive Behavior Scales were derived from a large, normative sample and applied to groups of autistic and nonautistic, developmentally disordered children. Predictive models included either mental or chronological age and other relevant variables. RESULTS: Social skills in the autistic group were more than two standard deviations below those predicted by their mental age; an index derived from the ratio of actual to predicted social skills correctly classified 94% of the autistic and 92% of the nonautistic, developmentally disordered cases. CONCLUSIONS: The findings are consistent with the idea that social disturbance is central in the definition of autism. The approach used in this study has potential advantages for providing more precise measures of social development in autism.

Adolescent↗
PubMed1992

Effect of interleukin-1, tumor necrosis factor-alpha, and interferon-alpha on the blast cells of acute myeloblastic leukemia.

In this study, we further established the role of interleukin-1 alpha (IL-1 alpha), interleukin-1 beta, tumor necrosis factor-alpha (TNF-alpha), and interferon-alpha (IFN-alpha) as regulators of proliferation of acute myeloid leukemia (AML) cells. AML cells from 8 of 15 patients incorporated high levels of 3H-thymidine (3H-TdR) in the absence of exogenous growth factors. The spontaneous DNA synthesis could be abrogated with monospecific antibodies directed toward IL-1 alpha, IL-1 beta, or TNF-alpha, as well as with antigranulocyte-macrophage colony-stimulating factor (GM-CSF). Human recombinant GM-CSF reversed the inhibitory action of each of these antibodies and reinduced DNA synthesis in AML cells. Thus, in these cases, constitutively produced IL-1 or TNF-alpha had stimulated the synthesis of GM-CSF, which resulted in GM-CSF-dependent proliferation of AML blasts. Exogenous IL-1 up-regulated the endogenous production of GM-CSF, suggesting a positive regulation of autocrine growth factor production. We also present evidence that TNF-alpha may exert both stimulative as well as inhibitory effects on DNA synthesis in AML cells. The enhancing effect of TNF-alpha was mediated through the induction of GM-CSF production, as stimulation of DNA synthesis in AML blasts could be abrogated with anti-GM-CSF antibody. A concentration-dependent inhibitory effect of TNF-alpha on 3H-TdR incorporation into AML blasts was observed only when these cells were grown in the absence of GM-CSF. Finally, we show that human recombinant IFN-alpha is a potent inhibitor of AML cell proliferation in vitro.

Adolescent↗
PubMed1992

Medieval example of metastatic carcinoma: a dry bone, radiological, and SEM study.

An elderly male skeleton from medieval Canterbury displayed evidence of DISH and metastatic carcinoma. The dry bone findings, SEM, and radiography suggest a primary focus in the prostate. A review of the palaeopathological literature has shown that such a finding is extremely rare in archaeological remains. This is the first reported case of prostatic carcinoma from medieval England.

Bone Neoplasms↗
PubMed1992

The hinged shoulder spica cast for management after shoulder surgery.

A shoulder spica cast is often required after major surgery to the shoulder. This type of cast is usually heavy and awkward. A lightweight fiberglass spica has proven to be useful after repair of the deltoid origin, repair of complete rupture of the rotator cuff, and shoulder arthrodesis. Hinges have been incorporated in the spica at the elbow and shoulder to permit maximum motion appropriate to the surgery. This cast is light and well tolerated. Elbow and shoulder stiffness is reduced by the hinges, which may be fabricated out of stock devices heretofore used in knee orthoses.

Adolescent↗
PubMed1990

The role of interleukin-1 and tumour necrosis factor-alpha in human multiple myeloma.

This study investigates the capacity of interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) to induce interleukin-6 (IL-6) production in freshly isolated myeloma cells (MC) and bone marrow-derived stromal cells (MSC). Recombinant human (rh) IL-1 alpha, IL-1 beta and TNF-alpha augmented production of IL-6 in human MC. IL-6 was determined on a factor-dependent Cess cell line. This activity was completely abrogated by anti-IL-6 antibodies. Prior incubation of IL-1 alpha, IL-1 beta and TNF-alpha with their respective antibodies inactivated the ability of recombinant cytokines to stimulate the release of IL-6 from myeloma cells. IL-1 alpha, IL-1 beta and TNF-alpha enhanced 3H-TdR uptake in myeloma cells through IL-6, as antibodies to IL-6 completely abolished the DNA synthesis induced by culture supernatants of MC exposed to these cytokines. rhIL-6 reversed the inhibitory action of anti-IL-6 antibodies and reinduced DNA synthesis in MC. Next we found that IL-1 alpha, IL-1 beta and TNF-alpha induced MSC to produce IL-6. In contrast, supernatants of unstimulated MSC did not contain detectable IL-6 biologic activity. Further data demonstrated that human MC were able to induce IL-6 production in MSC. The stimulatory activities of MC appeared to be mediated through endogenously released IL-1, as the addition of antibodies towards IL-1 at the initiation of cocultures completely abrogated the IL-6 production. We conclude from our data that IL-1 and TNF-alpha may play an important role in the pathogenesis of human multiple myeloma.

Bone Marrow↗
PubMed1989

Expression of a novel 3.5-kb macrophage colony-stimulating factor transcript in human myeloma cells.

Macrophage CSF (M-CSF) induces proliferation of monocyte/macrophage progenitor cells and can also activate some functions of mature cells. Three different human M-CSF cDNA (4.0, 3 to 3.5, and 1.5 kb) which are the result of alternative splicing of the single M-CSF gene have been cloned. Each of these cDNA encode a biologically active M-CSF. M-CSF transcripts are expressed in normal fibroblasts and other mesenchymal cells, and also in some hematopoietic cells such as monocytes. Normal human cells examined to date express only the 4.0-kb transcript. In contrast, a 3.5-kb M-CSF transcript was continuously expressed in two multiple myeloma cell lines (RPMI 8226 and U266/AF10) and in a bone marrow specimen of a patient with multiple myeloma. The myeloma cell lines secreted biologically active M-CSF. Resting and activated normal B lymphocytes and other B cell neoplasms examined did not express the 3.5-kb transcript, but could be induced to express the 4.0-kb transcript and to secrete M-CSF. Myeloma cells appear to be unique among hematopoietic cells in their expression of the 3.5-kb M-CSF transcript.

B-Lymphocytes↗