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S Sinclair

Publications and source records attributed to S Sinclair.

16 recordsLinked to original sources
PubMed1991

Cellular and metabolic requirements for induction of macrophage procoagulant activity by murine hepatitis virus strain 3 in vitro.

The cellular basis for the variation in induction of monocyte procoagulant activity (PCA) by murine hepatitis virus strain 3 (MHV-3) was examined using a set of recombinant inbred strains of mice derived from the resistant (A/J) and susceptible C57B1/6J (B) progenitors. Induction of PCA by MHV-3 required live virus and host protein and RNA synthesis. Absolute restriction for induction of PCA was observed at the level of the macrophage. Peritoneal macrophages from resistant parental A/J and RI strains (AXB5) could not be induced to express PCA when stimulated by MHV-3 alone or in the presence of lymphocytes from susceptible and H-2 compatible RI mice (AXB3) although they did respond to endotoxin (LPS). In contrast, macrophages from both susceptible (AXB3) and semisusceptible (AXB1) RI strains of mice expressed a similar increase in PCA after stimulation with MHV-3 in the absence of lymphocytes. The levels of PCA expressed by macrophages in the presence of Thy-1.2+ lymphocytes correlated with susceptibility to disease. Thy-1.2+ lymphocytes from susceptible RI AXB3 mice could induce levels of PCA in macrophages from semisusceptible RI AXB1 mice equivalent to that seen in cultures of macrophages and lymphocytes from susceptible mice. Further subfractionation of Thy-1.2+ cells demonstrated that L3T4+ cells instructed macrophages to produce PCA. Thy-1.2+ cells from MHV-3 immunized resistant AXB5 mice, but not from non-immunized mice, were able to suppress induction of PCA. This suppressor cell activity could be detected 4 days after immunization, reaching maximal activity at day 7 with significant suppression even at 28 days. The PCA was shown to have direct prothrombin cleaving activity (prothrombinase) by ELISA and immunofluorescence staining using the mAb 3D4.3. These results demonstrate that induction of a unique PCA (prothrombinase) is restricted at the level of the macrophage and define a regulatory role for T lymphocytes in its induction.

Animals↗
PubMed1990

Fulminant hepatitis.

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Blood Coagulation Disorders↗
PubMed1990

Eicosanoids and the liver.

Prostaglandins and leukotrienes are ubiquitous mediators of a wide variety of physiologic and immunologic effects in liver function and disease. Although the biochemical, synthetic and catabolic pathways of these compounds from arachidonic acid are well known, their cellular mechanisms of action are less well understood. Numerous studies have demonstrated the role for leukotrienes in the pathogenesis and the protective action of PG in experimental animal models of liver injury. These have included models of liver cell damage due to ischemia, galactosamine, carbon tetrachloride, and lipopolysaccharide. More importantly, the results of these studies have led to the demonstration of protective properties of 16, 16 dimethyl PGE2 (dm PGE2) in a mouse model of viral hepatitis. These results have led to the use of IV PGE1 in the treatment of patients with fulminant viral hepatitis, where 71% overall survival was observed as well as in the setting of primary non function and recurrent hepatitis B following liver transplantation. While the mechanisms of prostaglandin hepatic protection are not well understood, it has been demonstrated that dm PGE2 abrogates the induction of tumour necrosis factor, leukotriene B4 (LTB4) and procoagulant activity by macrophages as well as attenuating the expression of major histocompatibility class antigens on the surface of hepatocytes, and may inhibit viral replication. Finally, prostaglandins are known to play a role in the renal dysfunction associated with cirrhosis and fulminant hepatic failure, and therefore further studies of these agents in the pathophysiology and treatment of liver diseases and their complications are warranted.

Animals↗
PubMed1977

Prevalence of Echinococcus granulosus and other cestodes in dogs on the Navajo reservation in Arizona and New Mexico.

Fecal specimens from 429 dogs purged with arecoline hydrobromide at 131 rural camps on the Navajo Reservation in Arizona and New Mexico were examined for cestodes. Echinococcus granulosus was found in feces from 3 dogs at 3 different camps. Other cestodes present were Taenia hydatigena--45.5%, Taenia pisiformis--21.0%, Taenia serialis--11.9%, and Taenia ovis--1.6%.

Animals↗
PubMedDate not supplied

Blood lead levels of children with pica and surma use.

Blood lead levels of 253 Delhi children were estimated by dithizone method. In 82 (controls) children with no symptoms mean blood lead level was 9.6 micrograms/dl (+/- SD 6.8: median 10 micrograms); only 6 had high levels between 30-33 micrograms/dl. In 88 children with pica, the mean blood lead level was 23.0 micrograms/dl (+/- SD 13.82; median 17 micrograms) which was significantly higher than the control; 26 had high levels between 30-92 micrograms/dl. Sixteen children with pica and surma-use and 46 children suspected of lead poisoning showed lead level patterns like the pica group. However, 21 surma-using children without pica resembled the control group. Children with pica were significantly more anemic than the controls and showed higher prevalence of abdominal-neurological symptoms. Because, in India, blood lead cannot be estimated in most of the hospitals, it is suggested that children with severe pica, anemia, abdominal-neurological symptoms and exposure to surma or lead, be suspected of lead poisoning, kept in lead-free environment with corrected nutrition, and be given a short cautious therapeutic trial with oral penicillamine.

Adolescent↗