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Biomedical subjects

J Sugarman

Publications and source records attributed to J Sugarman.

At least 73 records · Page 4Linked to original sources
PubMed1991

Regulation of c-fos and c-jun protooncogene expression by the Ca(2+)-ATPase inhibitor thapsigargin.

Thapsigargin, a non-phorbol-ester-type tumor promoter, discharges intracellular Ca2+ stores by specific inhibition of the endoplasmic reticulum Ca(2+)-ATPase. We used this drug to analyze the involvement of Ca2+ and Ca(2+)-ATPases in the control of growth- and transformation-related genes. Here we show that treatment of mouse NIH 3T3 fibroblasts with thapsigargin induced rapid expression of the c-fos and c-jun protooncogenes. Inhibition or depletion of protein kinase C partially diminished the c-fos but not the c-jun response. Furthermore, thapsigargin could synergize with the tumor promoter phorbol 12-myristate 13-acetate to induce c-fos but not c-jun. However, thapsigargin had no effect on basal or phorbol ester-induced protein kinase C activity. Our results indicate that Ca2+ is a potent second messenger that controls expression of growth- and transformation-related genes. Since inhibition of the endoplasmic reticulum Ca(2+)-ATPase results in a strong induction of these genes, our data suggest that this Ca2+ pump may act as a negative regulator of cell growth.

Animals↗
PubMed1990

Pulmonary embolism and splenic infarction in a patient with sickle cell trait.

A 43 year-old black man with sickle cell trait documented by hemoglobin electrophoresis presented with severe pleuritic chest pain and hypoxemia three weeks after discharge following abdominal surgery. A pulmonary embolus was diagnosed by angiography and he was treated with heparin; the minimum arterial pO2 was 55 torr while O2 was being administered at a rate of 3 L/min. During this therapy, he developed abdominal pain. Computerized tomography suggested splenic infarction, which was documented by radionuclide liver-spleen scan and magnetic resonance imaging (MRI); the patient's spleen had been normal at exploratory laparotomy three weeks previously. No source for emboli was identified in the deep venous system by MRI. Although splenic infarction has been reported in patients with sickle cell trait at high altitude, this is the first reported case of splenic infarction secondary to the hypoxemia of pulmonary embolism in a patient with sickle cell trait. The spleen is subject to infarction in sickle cell trait because blood flow is slow through a hypoxemic and acidemic environment. The additional hypoxemia due to pulmonary embolism is presumed, in our patient, to have created a local splenic environment which permitted infarction to occur.

Adult↗
PubMed1989

Prevalence of diabetes in a Navajo Indian community.

The age- and sex-adjusted prevalence of non-insulin-dependent diabetes mellitus (NIDDM) of 494 (76 per cent) Navajo adults living in a reservation community was 10.2 per cent, approximately 60 per cent greater than the estimated prevalence (6.4 per cent) in the general US population. The screening protocol utilized likely underestimates the prevalence of NIDDM in this population. A high proportion of Navajo people were overweight when compared to the general US population.

Adult↗
PubMed1987

Striking memories of medical education: a glimpse of three physician writers.

Each of these three works focused on indelible memories of its writer's medical education. Thomas Browne spoke about autopsies, medical theories, religion. Tobias Smollett exposed the horrendous conditions aboard naval vessels and some of the problems facing young physicians. John Brown depicted surgery before anesthesia and antisepsis. Uniformly, the events and circumstances that seemed to have affected them were on the forefront of medical and social history. Religio Medici, Roderick Random, and "Rab and His Friends" were each the first major literary work of the authors discussed; each achieved instant success, yet somehow their popularity waned. Perhaps, the evolution of medicine has eclipsed what was once sensational, disturbing, interesting, and marketable, leaving only the dry and lifeless bones of stories--remnants of what once they were.

Education, Medical↗
PubMed1986

Structural and functional differences between decay-accelerating factor and red cell acetylcholinesterase.

The abnormal erythrocytes in paroxysmal nocturnal hemoglobinuria, both PNH II (the moderately abnormal cells) and PNH III (the markedly abnormal cells), lack both acetylcholinesterase (AChE) activity and decay-accelerating factor (DAF) activity. Both of these activities are found on glycoprotein molecules with a molecular weight of about 70 Kd. To demonstrate that these two activities are in fact on different proteins, we have shown that binding to normal red cells of antibody to DAF does not inhibit the subsequent binding of monoclonal antibody to AChE nor AChE activity. Inhibition of DAF activity by polyclonal antibody increases the susceptibility of normal erythrocytes to lysis by complement but inhibition of AChE activity by antibody does not. The rate of decay of the C3 convertase complex of the classical pathway of complement activation was inhibited by DAF added in the fluid phase but not by AChE. When DAF was exhaustively immunoprecipitated from a solution of the erythrocyte membrane proteins, AChE remained and vice versa. These studies indicate that acetylcholinesterase and decay-accelerating factor are two different proteins, both of which are lacking on PNH II and PNH III erythrocytes.

Acetylcholinesterase↗