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Biomedical subjects

M Hussain

Publications and source records attributed to M Hussain.

At least 253 records · Page 14Linked to original sources
PubMed1984

Differential effects of complement activation induced by cobra venom factor on pulmonary transvascular fluid and protein exchange.

Sheep were prepared with lung lymph fistulas for assessment of the effects of complement activation on pulmonary transvascular fluid and protein exchange in the intact animal. Cobra venom factor (CVF 200 +/- 46 U/kg) was injected intravenously for activation of the complement system. In some animals (n = 6), pulmonary lymph flow (Qlym) and pulmonary arterial pressure (Ppa) increased without a change in the lymph-to-plasma protein concentration ratio (L/P) or in pulmonary blood flow (QL), indicating an increase in pulmonary vascular permeability to proteins. In another group (n = 6), Qlym and the L/P did not change, and there were also no changes in Ppa and QL following a similar injection of CVF. Morphologic evidence showed that leukocytes were trapped in pulmonary vessels and interstitium of both groups. Pulmonary edema was also present in both groups. Complement activation does not uniformly increase pulmonary lymph flow despite pathologic evidence of leukocyte sequestration and pulmonary edema. The lack of change in lymph flow in some animals may be due to lymphatic insufficiency, or lack of generation of humoral mediators, and/or a decrease in pulmonary capillary pressure.

Animals↗
PubMed1983

Hemodynamic comparison of primary venous or arteriolar dilatation and the subsequent effect of furosemide in left ventricular failure after acute myocardial infarction.

The hemodynamic effect of venous dilatation (intravenous isosorbide dinitrate [ISDN]) and arteriolar dilatation (intravenous hydralazine), both as firstline treatment and then combined with intravenous furosemide, were evaluated in a randomized, between-group comparison in 20 men with severe acute left-sided cardiac failure after myocardial infarction (MI). Both ISDN (50 to 200 micrograms/kg/hour) (Group 1) and hydralazine (0.15 mg/kg) (Group 2) reduced systemic arterial pressure (p less than 0.05) and vascular resistance (p less than 0.05). Pulmonary artery occluded pressure was reduced (p less than 0.01) only by ISDN, whereas heart rate (p less than 0.01), cardiac output (p less than 0.01) and stroke volume (p less than 0.05) were increased only after hydralazine. After ISDN, furosemide (1 mg/kg) decreased left-sided cardiac filling pressure by 1 mm Hg (p greater than 0.05), whereas after hydralazine, furosemide in a similar dose reduced pulmonary artery occluded pressure by 5 mm Hg (p less than 0.01). In both groups of patients, furosemide transiently increased systemic arterial pressure (p less than 0.05). Cardiac output was reduced (p less than 0.05) and systemic vascular resistance increased (p less than 0.05) in Group 1 patients after furosemide. Similar changes in both variables in Group 2 patients did not attain statistical significance. In conclusion, ISDN-induced venous dilatation is preferable to primary arteriolar dilatation by hydralazine as first-line treatment in acute left-sided cardiac failure. However, hydralazine and furosemide in combination were equally effective in reducing pulmonary artery occluded pressure and increasing cardiac output. The influences of each regimen on prognosis await further investigation.

Adult↗
PubMed1983

Bacillus cereus 569/H beta-lactamase I: cloning in Escherichia coli and signal sequence determination.

The gene, penPC, for beta-lactamase I of Bacillus cereus 569/H has been cloned and its expression studied in Escherichia coli. The protein product from the in vitro translation of penPC was shown by gel electrophoresis to have an Mr of 36 000 which is larger than the in vivo products found in B. cereus and E. coli. The DNA sequence of the signal region was determined. It revealed that the smallest known mature form present in B. cereus culture fluids is preceded by 45-48 amino acids in pre-beta-lactamase I, considering that there are 3 initiation codons in the same reading frame, one or more of which might be initiating translation. Unlike the Bacillus licheniformis 749/C beta-lactamase, which has a membrane-bound thioether lipoprotein form, the single Cys residue in the B. cereus beta-lactamase I signal sequence is unmodified and a single processed form of the enzyme is present in E. coli cells carrying penPC.

Amino Acid Sequence↗
PubMed1983

Accumulation of glyceride-modified pre-penicillinase of Bacillus licheniformis in Escherichia coli treated with globomycin.

The membrane penicillinase of Bacillus licheniformis is a glyceride-cysteine lipoprotein whose NH2 terminus is analogous to the major outer membrane lipoprotein of Escherichia coli. When E. coli cells producing B. licheniformis penicillinase were treated with the antibiotic, globomycin, a precursor of the penicillinase, pre-penicillinase, accumulated in the cell. It could be immunoprecipitated with anti-penicillinase antibodies; it contained palmitate; and one of its two cysteine residues was modified by glycerol. The action of globomycin, probably indirectly, also activates protease which acts differently on the pre-penicillinase than does the signal peptidase. The results strongly indicate that the pre-penicillinase is processed by the globomycin-sensitive signal peptidase in E. coli, and the modification of precursor by lipid precedes removal of the signal peptide as it does with the membrane lipoproteins of E. coli.

Anti-Bacterial Agents↗
PubMed1983

Haemodynamic advantages of isosorbide dinitrate over frusemide in acute heart-failure following myocardial infarction.

The immediate haemodynamic effects of intravenous frusemide (1 mg/kg) and intravenous isosorbide dinitrate (50-200 micrograms/kg/h) were compared in a prospective, randomised, between-group study in 28 men with radiographic and haemodynamic evidence of left ventricular failure following acute myocardial infarction. The diuresis induced by frusemide reduced the left heart filling pressure and cardiac output and transiently raised systemic blood-pressure. In contrast, isosorbide dinitrate was accompanied by a reduction in systemic blood-pressure and peripheral resistance with the result that the cardiac output was not decreased despite a large fall in the pulmonary vascular and left heart filling pressures. These results indicate that reduction of excessive preload by venodilatation may be haemodynamically superior to that induced by diuresis in terms of both reducing myocardial oxygen consumption and maintaining peripheral perfusion. The influence of these contrasting treatments on the prognosis of these high-risk patients warrants further study.

Acute Disease↗
PubMed1983

Haemodynamic effects of frusemide and its influence on repetitive rapid volume loading in acute myocardial infarction.

The haemodynamic effects of intravenous frusemide (1 mg/kg) were studied in 22 male patients with left ventricular failure following acute myocardial infarction. Radiographic pulmonary oedema was present in all patients and their average left heart filling pressure was 20 mmHg. Bolus injection of the drug was followed by immediate increases in systemic arterial pressure (P less than 0.05) and heart rate (less than 0.05); these declined to pre-injection values after 60 min. Following frusemide there were progressive reductions in left heart filling pressure (P less than 0.01), thermodilution cardiac output (P less than 0.01) and stroke volume (P less than 0.05) and a progressive increase in the derived systemic vascular resistance (P less than 0.05). There was an average diuresis of 860 ml during the 90 min following the frusemide injection. The influence of frusemide on left ventricular performance was studied by comparing the circulatory effects of passive leg raising in the control period with those at 30, 60 and 90 min after the drug. In the control period this manoeuvre increased left heart filling pressure, but not heart rate, cardiac output, stroke volume or systemic vascular resistance. Ninety minutes after frusemide, but not before, passive leg raising resulted in a significant increase in cardiac output (P less than 0.01) and stroke volume at a similar increment in filling pressure and a significant reduction in the systemic vascular resistance (P less than 0.05). These circulatory actions of intravenous frusemide are compatible with initial arteriolar constriction and venodilatation followed by depletion of blood volume with subsequent change in left ventricular pumping performance.

Adult↗
PubMed1983

Haemodynamic dose-response effects of i.v. penbutolol in angina pectoris.

The haemodynamic dose-response effects of intravenous penbutolol, a newer beta-adrenoceptor antagonist with intrinsic sympathomimetic activity but without cardioselectivity, were evaluated in 10 patients with angiographically documented coronary artery disease. Following four logarithmetically cumulative i.v. boluses (0.5-4 mg dosage range) there was a log linear increase in plasma penbutolol concentration; the levels achieved (51 +/- 8 to 219 +/- 19 ng/ml) were in the therapeutic range (12 to 250 ng/ml). Penbutolol resulted in a linear decrease in heart rate (maximum delta HR - 4 beats/min; P less than 0.01); there was a small increase in pulmonary artery occluded pressure which reached its maximum at the lower doses (maximum delta PAOP + 1 mm Hg; P less than 0.01). The resting cardiac output, blood pressure and calculated systemic vascular resistance were unchanged. During 4 min steady-state supine bicycle exercise there was attenuation of exercise cardiac output (delta C.I. - 0.6 1 min-1 m-2; P less than 0.01) and systolic pressor response (delta SBP - 13 mm Hg; P less than 0.01) compared with control observations without change in other measured or derived variables. The haemodynamic profile of penbutolol compared favourably with other beta-adrenoceptor antagonists previously evaluated under similar conditions in patients with ischaemic heart disease. Over the i.v. dose-range evaluated penbutolol attenuated exercise-induced angina with a relatively modest depression of cardiac performance; the small change induced in resting haemodynamic variables may, in part, have been contributed to by the intrinsic sympathomimetic activity of penbutolol.

Adult↗
PubMed1983

Mycosis fungoides: subcutaneous and visceral tumors, orbital involvement, and ophthalmoplegia.

A patient with advanced severe mycosis fungoides presented several unusual features, including prominent lesions of the palate and tongue and an orbital tumor with exophthalmos and ophthalmoplegia. A hitherto undescribed feature was the development of multiple, massive subcutaneous tumors unrelated to the dermis or to lymph nodes, and large tumors in the connective tissues of the buttock, flank, and retroperitoneum. The usual sites of extracutaneous dissemination of mycosis fungoides--lymph nodes, spleen, liver, lungs, and blood--were not demonstrably involved. This may be a new pattern of dissemination for this disease. Of practical importance is the immediate and complete relief of exophthalmos and ophthalmoplegia that was obtained with emergency radiotherapy.

Aged↗
PubMed1983

Natural killer and suppressor T-cell chronic lymphocytic leukemia.

A patient with low-grade lymphocytosis, splenomegaly, and neutropenia, but adequate myeloid leukogenesis, was found to have chronic lymphocytic leukemia, which represented a clonal proliferation of a distinct T-lymphocyte subset. The lymphocytes did not form E rosettes but had an OKT3+, OKT4+, OKT6+, OKT8+, OKT11+, HNK-1+, HNK-36+, OKIa1+, OKM1+ phenotype and functionally had suppressor and natural killer activity. Morphologically, they were large granular lymphocytes, which were strongly acid phosphatase positive and nonspecific esterase negative. They did not respond to mitogens, or to allogeneic cells. Initially, the spleen appeared to be the most involved organ and, judging from the high proportion of leukemic splenic lymphocytes in the S and G2/M phases of the cell cycle, was also the organ of origin of the leukemic cells. Only a few leukemic cells in the blood and bone marrow were in S and G2/M phases. After splenectomy, the lymphocyte count rose considerably and the bone marrow became progressively more infiltrated by tumor nodules. One year after diagnosis, the patient was started on chemotherapy because of progressive anemia. He responded to the chemotherapy by normalization of the hemoglobin and neutrophil count and had a moderate decrease in the bone marrow involvement and peripheral lymphocytosis.

Antibodies, Monoclonal↗
PubMed1983

Haemodynamic dose-response effects of intravenous labetalol in acute myocardial infarction.

The haemodynamic consequences of combined alpha- and beta-adrenoceptor blockade with intravenous labetalol were evaluated in 21 males with either high (n = 6), normal (n = 9) or low (n = 6) systemic arterial pressure, 4-17 hours after acute myocardial infarction without heart failure. Labetalol 190 +/- 18 mg (range 62-300 mg) infusion resulted in dose-related falls in systolic (P less than 0.01) and diastolic (P less than 0.05) arterial pressure in all patients. The rate of pressure reduction per mg of infused labetalol was directly proportional to the control systolic arterial pressure. Cardiac output (thermodilution) was reduced (P less than 0.05) with low dose labetalol (39 +/- 5 mg) without change on continued infusion. Left heart filling pressure (pulmonary artery occluded pressure) was unchanged throughout infusion in all patients. In conclusion, the vasodilating properties of labetalol appeared to offset the beta-blocker induced depression of cardiac function. The increased sensitivity to the effects of labetalol in those patients with hypertension may be related to excessive alpha-adrenoceptor mediated vasoconstriction in this patient group.

Dose-Response Relationship, Drug↗
PubMed1983

Management of acute heart failure following myocardial infarction: hemodynamic advantages of isosorbide dinitrate over frusemide.

The immediate hemodynamic effects of intravenous frusemide (1 mg/kg) and intravenous isosorbide dinitrate (50-200 micrograms/kg/h) were compared in a prospective, randomized, between-group study in 28 men with radiographic and hemodynamic evidence of left ventricular failure following acute myocardial infarction. The diuresis induced by frusemide reduced the left-heart filling pressure and cardiac output and transiently raised systemic blood pressure. In contrast, isosorbide dinitrate was accompanied by a reduction in systemic blood pressure and peripheral resistance, with the result that the cardiac output was not decreased despite a large fall in the pulmonary vascular and left-heart filling pressures. The results indicate that reduction of excessive preload by venodilatation may be hemodynamically superior to that induced by diuresis in terms of both reducing myocardial oxygen consumption and maintaining peripheral perfusion. The influence of these contrasting treatments on the prognosis of these high-risk patients warrants further study.

Adult↗
PubMed1983

Invasive thymoma: unique presentation as an anterior chest wall mass.

A 57-year-old white woman presented with pericardial effusion and an anterior superior mediastinal mass protruding through the sternum. The diagnosis of thymoma was established by the light and electron microscopic features of a biopsy specimen and a pericardial aspirate. The tumour was a thymic carcinoma, a recently described variant characterized by cellular atypia, enhanced invasiveness, and a higher incidence of metastases. Presentation as an anterior chest wall mass has not been described. Response to radiotherapy was slow and incomplete, and tumour progression occurred during treatment with cisplatin. The chemotherapy of thymoma is reviewed: some apparent responses to agents that are primarily lympholytic may represent the elimination of non-neoplastic lymphocytes from the tumour mass, with spurious radiological improvement and theoretically a risk of tumour enhancement.

Antineoplastic Agents↗
PubMed1982

An improved method of isolation of rat pancreatic prokallikrein. Characterization of the zymogen and of the kallikrein produced by trypsin activation.

A prokallikrein was purified 1600-fold from rat pancreatic tissue in an overall yield of 40% by a simple four-stage procedure. The final and crucial step was immunoaffinity chromatography utilizing antibody raised to a very small amount of prokallikrein. Both the pure zymogen and the active kallikrein generated from it by trypsin activation are single chain species with Mr values of 38400 +/- 300 and 35500 +/- 400, respectively. Valine is the N-terminal amino acid residue of prokallikrein. The zymogen was comparatively stable both to autoactivation and denaturation with respect to temperature and pH. The kallikrein produced by trypsin activation of the zymogen was similar in some of its catalytic properties to the kallikrein purified from autolyzed rat pancreas but the two species differed in their susceptibility to substrate activation.

Amino Acid Sequence↗
PubMed1982

Mechanism of signal peptide cleavage in the biosynthesis of the major lipoprotein of the Escherichia coli outer membrane.

On treatment of Escherichia coli cells with globomycin, a glyceride-containing precursor of the major outer membrane lipoprotein accumulates in the cytoplasmic membrane (Hussain, M., Ichihara, S., and Mizushima, S. (1980) J. Biol. Chem. 255, 3707-3712). When the envelope fraction from such cells was incubated in a suitable buffer, this precursor could be processed to the mature lipoprotein. The processing involved removal of the signal peptide and subsequent acylation of the NH2 terminus thus bared. Two types of peptidase and an acylation enzyme(s) were found to be involved in these processes. The enzyme that cleaves the signal peptide, called signal peptidase in this paper, had many unique properties: being highly resistant to high temperature, having a wide optimum pH range, and being highly sensitive to detergents. The other peptidase(s), called signal peptide peptidase in this paper, was assumed to be responsible for the digestion of the signal peptide that had been cleaved from the precursor lipoprotein. This enzyme was rather heat-sensitive. Thus the processing from the precursor to the mature lipoprotein at a high temperature resulted in accumulation of a peptide that was most probably the intact signal peptide. The third enzyme(s) involved in the processing was the one that is responsible for acylation of the newly bared NH2 terminus of the lipoprotein. The enzyme activity was also lost at 80 degrees C. In the light of these findings, the biosynthetic pathway of the lipoprotein is discussed.

Cell Membrane↗
PubMed1982

Mechanism of export of outer membrane lipoproteins through the cytoplasmic membrane in Escherichia coli. Binding of lipoprotein precursors to the peptidoglycan layer.

Upon treatment of Escherichia coli cells with globomycin, precursors of Braun's lipoprotein, a peptidoglycan-associated lipoprotein (PAL) and several new species of lipoproteins accumulated in the cell envelope (Hussain, M. Ichihara, S., and Mizushima, S. (1980) J. Biol. Chem. 255, 3707-3012; and Ichihara, S., Hussain, M., and Mizushima, S. (1981) J. Biol. Chem. 256, 3125-3129). The precursors of the Braun's lipoprotein and PAL thus accumulated were able to interact with the peptidoglycan layer. A considerable fraction of the precursor of Braun's lipoprotein was covalently bound to the peptidoglycan layer through its COOH-terminal lysine residue in the same manner as in the mature form. The manner of interaction of the precursor of PAL with the peptidoglycan layer was also the same as that of its mature form in which the central to COOH-terminal region of the lipoprotein is important for the interaction. Both precursors were localized in the cytoplasmic membrane when the outer and cytoplasmic membranes were separated after digestion by lysozyme of the peptidoglycan layer. When the cell envelope fraction was incubated, these precursors were chased to the corresponding mature forms. These results indicate that these proteins can be exported through the cytoplasmic membrane while they still retain the signal peptide that is most probably held in the cytoplasmic membrane.

Anti-Bacterial Agents↗
PubMed1982

Signal peptide digestion in Escherichia coli. Effect of protease inhibitors on hydrolysis of the cleaved signal peptide of the major outer-membrane lipoprotein.

Upon incubation of the envelope fraction of Escherichia coli a precursor of the major outer membrane lipoprotein that accumulates in the cytoplasmic membrane of the globomycin-treated cell is processed to the mature form [Hussain, M., Ichihara, S., and Mizushima, S. (1980) J. Biol. Chem. 255, 3707-3712; (1982) J. Biol. Chem. 257, 5177-5182]. When this precursor-containing envelope fraction was incubated in the presence of protease inhibitors such as antipain, leupeptin, chymostatin and elastatinal, a new peptide appeared on a polyacrylamide gel at the position where the signal peptide was expected to appear. This was proved to be the signal peptide of the lipoprotein from the following facts: (a) its appearance is in proportion to the appearance of the lipoprotein and disappearance of the precursor; (b) when the cleavage of the signal peptide from the precursor was inhibited by globomycin, the peptide did not appear on the gel; and (c) the results of labeling of the peptide with [3H]leucine, [35S]methionine and [3H]arginine were consistent with the amino acid composition of the signal peptide. The signal peptide thus accumulated in the envelope fraction was hydrolyzed by an enzyme named 'signal peptide peptidase' when the envelope fraction was washed to remove the inhibitors. The hydrolysis was inhibited by re-addition of these inhibitors. The signal peptide peptidase hydrolyzed the signal peptide only after its cleavage from the lipoprotein precursor.

Bacterial Proteins↗