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Biomedical subjects

J Weinstein

Publications and source records attributed to J Weinstein.

At least 91 records · Page 5Linked to original sources
PubMed1985

Demonstration of an extensive trans-tubular network continuous with the Golgi apparatus stack that may function in glycosylation.

Sialyltransferase (Gal beta 1,4GlcNAc alpha 2,6 sialyltransferase) was localized by immunoelectron microscopy in rat liver hepatocytes using affinity-purified antibodies. Immunoreactivity for sialyltransferase was found in the Golgi apparatus, where it was restricted to an interconnected system consisting of the trans-cisternae and the trans-tubular network. This region of the Golgi apparatus exhibited both TPPase and CMPase activity and was the intracellular site where sialic acid residues bound to glycoprotein were detected using the Limax flavus lectin. Sialyltransferase and sialic acid residues were not detected in medial and cis-cisternae of the Golgi apparatus. These findings suggest that in rat hepatocytes sialylation of N-linked glycoproteins occurs in the complex formed by the trans-cisternae and the trans-tubular network of Golgi apparatus.

Animals↗
PubMed1984

Biosynthesis of a disialylated sequence in N-linked oligosaccharides: identification of an N-acetylglucosaminide (alpha 2----6)-sialyltransferase in Golgi apparatus from rat liver.

Rat liver Golgi apparatus are shown to have a CMP-N-acetylneuraminate: N-acetylglucosaminide (alpha 2----6)-sialyltransferase which catalyzes the conversion of the human milk oligosaccharide LS-tetrasaccharide-a (NeuAc alpha 2----3Gal beta 1---- 3GlcNAc beta 1----3Gal beta 1----4Glc) to disialyllacto -N- tetraose containing the terminal sequence: (formula: see text) found in N-linked oligosaccharides of glycoproteins. The N-acetylglucosaminide (alpha 2----6)-sialyltransferase has a marked preference for the sequence NeuAc alpha 2----3-Gal beta 1---- 3GlcNAc as an acceptor substrate. Thus, the order of addition of the two sialic acids in the disialylated structure shown above is proposed to be first the terminal sialic acid in the NeuAc alpha 2----3Gal linkage followed by the internal sialic acid in the NeuAc alpha 2---- 6GlcNAc linkage. Sialylation in vitro of the type 1 branches (Gal beta 1---- 3GlcNAc -) of the N-linked oligosaccharides of asialo prothrombin to produce the same disialylated sequence is also demonstrated.

Animals↗
PubMed1983

The international registry to support approval of intracoronary streptokinase thrombolysis in the treatment of myocardial infarction. Assessment of safety and efficacy.

The data from 224 cases of acute myocardial infarction treated with intracoronary streptokinase plus standard coronary care unit management and 178 cases of acute myocardial infarction treated solely with standard coronary care unit management were reviewed to assess the efficacy and safety of the intracoronary administration of streptokinase during evolving myocardial infarction. Successful recanalization of the occluded infarct-related coronary artery was achieved in 176 of 224 streptokinase-treated cases (79%). The incidence of in-hospital postinfarction complications was lower and the mean left ventricular ejection fraction was improved in the successfully reperfused group. The in-hospital cardiac mortality in the reperfused patients was 4.5%. The intervention with coronary angiography and intracoronary streptokinase was generally well tolerated. Adverse reactions were relatively infrequent and were controlled with standard treatment.

Cardiac Catheterization↗
PubMed1982

Purification of a Gal beta 1 to 4GlcNAc alpha 2 to 6 sialyltransferase and a Gal beta 1 to 3(4)GlcNAc alpha 2 to 3 sialyltransferase to homogeneity from rat liver.

A Gal beta 1 to 4GlcNAc alpha 2 to 6 sialyltransferse and a Gal beta 1 to 3(4)GlcNAc alpha 2 to 3 sialyltransferase have been purified 23,000- and 860,000-fold to homogeneity from Triton CF-54 extracts of rat liver membranes. The two enzymes were concentrated by affinity chromatography on CDP-hexanolamine-agarose and resolved by NaCl gradient elution from the same adsorbent. Final purification of the Gal beta 1 to 4GlcNAc alpha 2 to 6 sialytransferase, the most abundant enzyme, was achieved by specific elution from CDP-agarose with CDP. The Gal beta 1 to 3(4)GlcNAc alpha 2 to 3 sialyltransferase was also purified further by CDP elution from CDP-agarose, but final purification required affinity chromatography on an adsorbent prepared by coupling asialoprothrombin to cyanogen bromide-activated agarose. Asialoprothrombin contains the terminal sequence Gal beta 1 to 3GlcNAc on N-linked oligosaccharides and is the best acceptor substrate of the enzyme (Km congruent to 6 microM). The Gal beta 1 to 3(4)GlcNAc alpha 2 to 3 sialyltransferase was found to bind to asialoprothrombin-agarose in the presence of CDP and could be eluted with a solution containing 0.2 M lactose and no CDP. Sodium dodecyl sulfate-gel electrophoresis of the Gal beta 1 to 4GlcNAc alpha 2 to 6 and Gal beta 1 to 3(4)GlcNAc alpha 2 to 3 sialyltransferases revealed a single major protein band for each enzyme with apparent molecular weights of 40,500 and 44,000, respectively. Rabbit antibodies raised to the Gal beta 1 to 4GlcNAc alpha 2 to 6 sialyltransferase inhibit its enzymatic activity greater than 99% but caused little or no inhibition of Gal beta 1 to 3(4)GlcNAc alpha 2 to 3 sialytransferase. Moreover, the Gal beta 1 to 4GlcNAc alpha 2 to 6 sialyltransferase quantitatively bound to a column containing antibody adsorbed to Protein A-agarose, while the Gal beta 1 to 3(4) GlcNAc alpha 2 to 3 sialyltransferase did not bind. This demonstrated that the two sialyltransferases are antigenically unrelated and formed the basis for removal of contaminating Gal beta 1 to 4GlcNAc alpha 2 to 6 sialyltransferase from solutions of the Gal beta 1 to 3(4)GlcNAc alpha 2 to 3 sialyltransferase. Enzymatic characterization of the two sialyltransferases suggests that their major biological roles are in the terminal glycosylation of N-linked oligosaccharides of glycoproteins. (Weinstein, J., de Souza-e-Silva, U., and Paulson J. C. (1982) J. Biol. Chem. 257, 13845-13853. The alpha 2 to 6 sialyltransferase efficiently forms the NeuAc alpha 2 to 6Gal beta 1 to 4GlcNAc sequence, and the alpha 2 to 3 sialyltransferase forms the NeuAc alpha 2 to 3Gal beta 1 to 3GlcNAc and NeuAc alpha 2 to 3Ga; beta 1 to 4GlcNAc sequences.

Animals↗
PubMed1982

Newcastle disease virus contains a linkage-specific glycoprotein sialidase. Application to the localization of sialic acid residues in N-linked oligosaccharides of alpha 1-acid glycoprotein.

Newcastle disease virus sialidase was found to exhibit strict specificity for hydrolysis of the NeuAc alpha 2 leads to 3Gal linkage contained in glycoprotein oligosaccharides both N-linked to asparagine and O-linked to threonine or serine under conditions that left oligosaccharides containing the NeuAc alpha 2 leads to 2 leads to 6Gal and NeuAc alpha 2 leads to 6GallNAc linkages intact. This was determined, in part, by examining the viral sialidase for its ability to hydrolyze glycoprotein oligosaccharides derivatized with purified sialyltransferases to contain the [14C]NeuAc alpha 2 leads to 3Gal, [14C]NeuAc alpha 2 leads to 6GalNAc, and [14C]NeuAc alpha 2 leads to 6Gal linkages. The viral sialidase was also tested for hydrolysis of the NeuAc alpha 2 leads to 3Gal and NeuAc alpha 2 leads to 6Gal linkages on the N-linked oligosaccharides of alpha 1-acid glycoprotein. Selective hydrolysis of the NeuAc alpha 2 leads to 3Gal linkage was shown by periodate oxidation and by 500-MHz 1H-NMR spectroscopy of native and sialidase-treated glycopeptides. The NMR spectra, together with composition data, further indicated that the NeuAc alpha 2 leads to 3Gal and NeuAc alpha 2 leads to 6Gal linkages were localized to specific branches of the major tri- and tetraantennary oligosaccharides of alpha 1-acid glycoprotein. The results indicate that the Newcastle disease virus sialidase can initiate the selective degradation of N-linked oligosaccharide branches containing the NeuAc alpha 2 leads to 3Gal linkage.

Carbohydrate Conformation↗
PubMed1982

Identification of a Gal beta 1 goes to 3GlcNAc alpha 2 goes to 3 sialyltransferase in rat liver.

Rat liver Golgi was found to contain a sialyltransferase activity which would convert lacto-N-tetraose (Gal beta 1 goes to 3GlcNAc beta 1 goes to 3Gal beta 1 goes to 4Glc) to LS-tetrasaccharide a (NeuAc alpha 2 goes to 3Gal beta 1 goes to 3GlcNAc beta 1 goes to 3Gal beta 1 goes to 4Glc). The enzyme has been partially purified by affinity chromatography on CDP-hexanolamine agarose. Of the glycoprotein substrates examined, it utilizes the Gal beta 1 goes to 3GlcNAc sequence found on the asparagine-linked oligosaccharides of prothrombin as its preferred acceptor substrate, and thus has been tentatively designated a Gal beta 1 goes to 3GlcNAc alpha 2 goes to 3 sialyltransferase. The partially purified enzyme has an acceptor specificity distinct from other purified mammalian sialyltransferases which synthesize the NeuAc alpha 2 goes to 3Gal beta 1 goes to 3 GalNAc and NeuAc alpha 2 goes to 6 GalNAc sequences common to oligosaccharides O-linked to threonine or serine and the NeuAc alpha 2 goes to 6Gal beta 1 goes to 4GlcNAc sequence found on oligosaccharides N-linked to asparagine.

Animals↗
PubMed1982

Treatment of angina pectoris with pindolol: the significance of intrinsic sympathomimetic activity of beta blockers.

Although all beta blockers have been found to be effective in the symptomatic relief of angina pectoris, the importance of intrinsic sympathomimetic activity (ISA) has not been studied extensively. In a randomized, double-blind study, we administered equipotent doses of propranolol (10, 20, and 40 mg four times a day) and pindolol (2.5, 5, and 10 mg four times a day), a beta blocker with significant ISA, to 52 patients with angina. Both agents were found to be effective in the treatment of angina. At peak dose, propranolol reduced the number of angina attacks per 2 weeks from 29.29 +/- 4.79 to 18.0 +/- 4.4 (p = 0.021) (a 39% reduction) and increased the exercise tolerance on the treadmill from 7.55 +/- 0.67 METS to 9.36 +/- 0.58 (p = 0.002). Pindolol decreased the number of anginal attacks per 2 weeks from 16.48 +/- 2.63 to 8.65 +/- 2.46 (p = 0.0027) (a 48% reduction) and increased exercise tolerance from 7.95 +/- 0.56 METS to 9.40 +/- 0.57 (p = 0.0245). At the end of the maximum tolerated exercise, propranolol decreased the heart rate from 110.00 +/- 3.41 to 99.71 +/- 3.74 (p = 0.0015). Pindolol also decreased the heart rate at the maximum tolerated exercise from 113.59 +/- 3.24 to 108.12 +/- 3.16 (p = 0.0102). At rest, however, propranolol induced a more pronounced (p = 0.0066) decrease in heart rate (from 69.00 +/- 1.85 to 61.50 +/- 1.99; p = 0.0018), whereas pindolol did not significantly affect the resting heart rate (65.37 +/- 1.47 to 65.5 +/- 1.44; p = 0.9392). In addition propranolol decreased echocardiographically determined ejection fraction from 0.57 +/- 0.02 to 0.15 +/- 0.01 (p = 0.04) and increased the left ventricular end-diastolic volume from 71.8 +/- 3.2 to 92.2 +/- 1.9 ml (p = 0.003), whereas pindolol did not affect the ejection fraction and caused a less pronounced (p = 0.03) increase in end-diastolic volume (from 70.8 +/- 1.8 to 80.2 +/- 2.8; p = 0.02). The data indicate that both propranolol and pindolol are effective in the treatment of angina pectoris and that pindolol decreases the resting heart rate and ejection fraction and increases the left ventricular end-diastolic volume to a lesser extent than propranolol.

Adult↗
PubMed1982

Treatment of myocardial infarction with intracoronary streptokinase: efficacy and safety data from 209 United States cases in the Hoechst-Roussel registry.

Efficacy and safety data from 209 U.S. cases in the Hoechst-Roussel intracoronary streptokinase (STK) registry were analyzed. Successful recanalization was achieved in 76% of infarct-related occluded coronary arteries. Postinfarction complications (i.e., malignant arrhythmia, heart block, and pump failure) were substantially less frequent after successful recanalization compared to the recanalization failures. Cardiac in-hospital mortality was 2.5% in the recanalized group and 18% in the group in which recanalization failed. Several severe hemorrhagic complications occurred in patients who were heparinized. The data suggest that myocardial reperfusion following STK coronary recanalization during evolving myocardial infarction may salvage myocardium. Except for excessive bleeding associated generally with heparinization, side effects and adverse reactions were readily controlled.

Adult↗
PubMed1980

Synovial fluid leukocytosis associated with intracellular lipid inclusions.

A unique case of an inflammatory monoarthritis associated with intracellular lipid inclusions in synovial fluid leukocytes is described. In contrast to previous reports, these lipid inclusions were uniformly intracellar, not associated with articular destruction, and not visible under ordinary light but readily seen under polarized light microscopy.

Arthritis↗
PubMed1980

Cronkhite-Canada syndrome: report of a case with bacteriologic, immunologic, and electron microscopic studies.

A case of Cronkhite-Canada syndrome is presented. The patient developed protein-losing enteropathy, generalized gastrointestional polyposis, skin pigmentation, onychodystrophy, and alopecia. This patient also exhibited certain unusual features such as: fluctuating dermal manifestations, sclerodermalike skin changes, elevated levels of carcinoembryonic antigen, retinal detachment, cataracts, and cerebellar atrophy. Bacteriologic studies of small intestinal fluid, chromosomal analysis, immunologic investigations, and morphologic studies failed to provide any etiologic clues.

Adult↗
PubMed1979

Lateral diffusion of surface immunoglobulin, Thy-1 antigen, and a lipid probe in lymphocyte plasma membranes.

Fluorescence photobleaching recovery was used to measure the lateral diffusion coefficient and mobile fraction of surface immunoglobulin (sIg), Thy-1 antigen, and a lipid probe in the plasma membrane of mouse lymphocytes. The lipid probe (3,3'-dioctadecylindocarbocyanine) had a mean (+/-SD) diffusion coefficient of (1.7 +/- 0.3) x 10(-8) cm(2)/sec, with essentially all of the probe mobile in the membrane. We detected little or no effect on the diffusion of this probe due to the presence of microvilli. Its diffusion was slightly restricted in capped regions. No differences in lipid probe mobility were detected between T and B cells. Fifty to 90% of the detectable sIg and Thy-1 antigen was free to move in the plane of the membrane with diffusion coefficients of approximately 3 x 10(-10) cm(2)/sec; the remainder was immobile. Crosslinking of sIg with anti-Ig antibodies (in the presence of azide to inhibit capping) completely immobilized sIg at high concentrations but failed to do so at low concentrations. Thy-1 antigen could not be immobilized with an IgG rabbit anti-mouse brain reagent without an additional layer of crosslinking antibody. In parallel labelings (in the absence of azide), capping of sIg and Thy-1 antigen was observed only under crosslinking conditions sufficient to immobilize the membrane antigen. Sodium azide, colchicine, and cytochalasin B had no measurable effect on lipid probe, sIg, or Thy-1 diffusion.

Animals↗