Jerome B. Jacobs
St Vincent Hospital
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Publication
Featured researches published by Jerome B. Jacobs.
Journal of Laryngology and Otology | 1983
John G. Batsakis; Jerome B. Jacobs; Alexander C. Templeton
A case of a hemangiopericytoma of the nasal cavity in a 79-year-old woman is presented. Ultrastructural examination confirmed the pericytic origin of the tumor. Most of the reported hemangiopericytomas of the sinonasal tract are histologically low-grade and their biologic course is in concert with their appearance.
British Journal of Haematology | 1981
L. M. Snyder; N. Sauberman; H. Condara; J. Dolan; Jerome B. Jacobs; I. Szymanski; Normand L. Fortier
Summary. Osmotically resistant red cells associated with some haemolytic anaemias, including hereditary xerocytosis, sickle‐cell disease and β thalassaemia minor, are more sensitive than normal red cells to exogenous in vitro hydrogen peroxide (H2O2). This sensitivity is manifested by a rapid loss of intracellular potassium, shape change, protein aggregation, and methaemoglobin formation at lower concentrations of H2O2 (225 μm.) than are required to induce similar effects in normal red cells (450 μm). Malonyldialdehyde (MDA) formation occurs later than the other effects and can be inhibited by the antioxidant, butylated hydroxytoluene (BHT), without affecting protein aggregation or potassium leak. Incubation of normal red cells directly with MDA induces protein aggregation, but only after 1 h of incubation. Although nystatin‐sucrose treated normal cells which are dehydrated with altered cation content, and therefore osmotically resistant, do not display abnormal H2O2 hypersentitivity as manifested by excessive potassium permeability, they do show an increase in methaemoglobin formation and protein aggregation similar to xerocytes. These data indicate that membrane protein cross‐linking occurring immediately following H2O2 exposure seems independent of either the sulfhydryl or MDA mechanisms, and that the membrane permeability of the abnormal red cells predisposes them to oxidative damage.
British Journal of Haematology | 1985
L.Michael Snyder; Grant Fairbanks; Jane Trainor; Normand L. Fortier; Jerome B. Jacobs; Laszlo Leb
Summary We have presently demonstrated morphologic differences between young and senescent red cells following 18 h of metabolic depletion in vitro. Young and old red cells both form echinocytes, whereas only young cells demonstrated myelin forms or microspheres. Furthermore, vesicles were released in greater quantities into the cell‐free supernatant from young cells. Isolated vesicles from both young and old red cells contained lipids, intrinsic membrane proteins (especially band 3), and haemoglobin, and they were also enriched in acetylcholinesterase (AChE). Young cells produced more vesicles than old cells but the composition of the low density vesicles was similar except that haemoglobin‐spectrin complex was found exclusively in vesicles from young cells. Oxidation of young red cells prior to metabolic depletion prevented both myelin formation and vesicle release.
Virchows Archiv | 1981
Joseph Alroy; Danica Roganovic; Barbara F. Banner; Jerome B. Jacobs; Frederick B. Merk; Angelo A. Ucci; Paul Kwan; John S. Coon; Alexander W. Miller
Neoplastic and non-neoplastic tissue specimens from ten patients with primary adenocarcinoma of the urinary bladder were examined. Most of these tumors were associated with either foci of transitional cell carcinoma and/or with glandular metaplasia of the bladder epithelium. The mucin produced by the neoplastic cells was PAS, alcian blue, mucicarmine, PB/KOH/PAS, and RPB/KOH/PAS-positive. ABH isoantigens of these tumors were not always deleted. Ultrastructurally, the neoplastic cells resembled goblet cells. Their plasma membrane had numerous microvilli with prominent glycocalyx. Proliferation and attenuation of tight junctions were noted. The gap junctions were few and small. Two types of desmosomes were found. The ultrastructural features of the neoplastic cells were attributed in part to the malignant transformation and in part to the direction of their differentiation. We have not observed any distinctive morphologic, histochemical, immunologic or ultrastructural features that might be diagnostic for these adenocarcinomas.
Cancer Research | 1976
Jerome B. Jacobs; Masayuki Arai; Samuel M. Cohen; Gilbert H. Friedell
Cancer Research | 1976
Samuel M. Cohen; Jerome B. Jacobs; Masayuki Arai; Sonny L. Johansson; Gilbert H. Friedell
Cancer Research | 1977
Frederick B. Merk; Bendicht U. Pauli; Jerome B. Jacobs; Joseph Alroy; Gilbert H. Friedell; Ronald S. Weinstein
Journal of Supramolecular Structure | 1976
Charles W. Boone; Jerome B. Jacobs
Cancer Research | 1975
Jerome B. Jacobs; L. M. Edelstein; L. M. Snyder; N. Fortier
Journal of the National Cancer Institute | 1976
Jerome B. Jacobs; Masayuki Arai; Samuel M. Cohen; Gilbert H. Friedell