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Biomedical subjects

M Mirowski

Publications and source records attributed to M Mirowski.

At least 19 recordsLinked to original sources
PubMed1992

The automatic implantable cardioverter-defibrillator. Long-term clinical experience and outcome at a hospital without an open-heart surgery program.

From November 1982 through April 1989, 111 patients with refractory sustained ventricular tachycardia/fibrillation had the automatic cardioverter-defibrillator implanted at our institution, the first community hospital involved in implantation of such a device. We have reviewed our long-term clinical experience to assess the feasibility, learning curve, and efficacy of device implantation in a facility with cardiac electrophysiology expertise but without open-heart surgery facilities. All patients were considered inoperable or at high risk for other concomitant surgery. Eighty-six patients (77%) underwent uneventful implantation. Nine patients (8%) died prior to hospital discharge. Operative mortality declined from 10.9% to 5.4% during the first half (55 patients; November 1982 through September 1986) and second half (56 patients; October 1986 through April 1989) of the experience. Other postoperative complications occurred in 16 patients (14%), 12 of whom experienced complications during the first half of the experience. At 22 +/- 20 (mean +/- SD) months' follow-up, 78 (76%) of 102 patients discharged were alive, and 24 patients (24%) had died. Fifty patients (49%) had experienced at least one automatic cardioverter-defibrillator discharge associated with hypotensive symptoms. The actuarial incidence of sudden death at 1, 2, and 3 years was 1.2%, 5.5%, and 6.2%, respectively. We concluded that the automatic implantable cardioverter-defibrillator is an effective therapy for refractory ventricular tachycardia/fibrillation and that device implantation at community hospitals with an experienced cardiac electrophysiology team is both feasible and practical.

Adult↗
PubMed1992

Purification and characterization of a 65-kDa tumor-associated phosphoprotein from rat transplantable hepatocellular carcinoma 1682C cell line.

We have isolated a homogeneous tumor-associated phosphoglycoprotein of about 65 kDa (p65) by ammonium sulfate precipitation of proteins from conditioned medium containing the rat transplantable hepatocellular carcinoma 1682C cell line, followed by high-performance liquid chromatography on molecular-sieving and phenyl hydrophobic interaction columns. The protein was concentrated in a Rotofor isoelectric focusing cell and finally separated by isoelectrofocusing followed by SDS--polyacrylamide gel electrophoresis. We achieved a purification of approximately 11,000-fold after the Rotofor concentration step. This protein migrated as a single band upon electrophoresis in SDS-PAGE and had a pI of 5.8 in isoelectrofocusing gels. The carbohydrate content of the blotted phosphoglycoprotein was analyzed by probing the blots with biotinylated lectins; a positive reaction was detected with concanavalin A, wheat-germ agglutinine, and Ricinus communis agglutinine. To confirm the tumor origin of this molecule, hepatocellular carcinoma cells were labeled in vivo using [32P]orthophosphate as well as [35S]methionine and cell culture medium was analyzed for the presence of radioactive band that corresponds with our protein. Phosphoamine acid analysis by thin-layer chromatography showed the presence of phosphotyrosine, phosphothreonine, and phosphoserine, which was later confirmed by analysis of the amino acid composition. Using the method described by Marchalonis and Weltman for comparative analysis of protein structure and evolution, we compared the protein isolated by us with other tumor markers and proteins showing similar properties and found no significant similarities.

Animals↗
PubMed1991

[Plasminogen activator inhibitors from neoplastic tissues].

This article contains a survey of works, published in the last few years on plasminogen activators inhibitors in neoplastic tissues. These inhibitors belong to a heterogenous group of proteins, having different molecular weights and specific ways of acting. They exemplify immunological relationship to known inhibitors of fibrinolysis from normal tissues--i.e. the inhibitors from endothelial cells--(PAI-1) and placental inhibitor--(PAI-2). To PAI-1 type belong: acid-stabile inhibitor of fibrinolysis with Mr 50,000 from HTC hepatoma cells in rats, acid-labile inhibitor Mr 42,770 produced by HepG2 human hepatoma cells; the inhibitor with Mr 54,000 from HT 1080 human cells from fibrosarcoma and single-chain acid-stabile inhibitor with Mr 50,000 from MJZJ melanoma cells. In PAI-2 type we can mention the inhibitor with Mr 47,000 from U-937 histiocytic lymphoma cells.

Animals↗
PubMed1990

Fibrinolytic activity of rat plasma during development of Guerin epithelioma.

Fibrinolytic activity in the blood of rats during the development of Guerin epithelioma was studied. It was measured by means of radiometric method, based on the amount of plasmin degradation products released from 125I-fibrin, as well as by means of amidolytic technique with the use of Chromozym PL. During the initial phase of epithelioma development the fibrinolytic activity of plasma, determined after inactivating plasma proteinase inhibitors, increases. It also increases in the euglobulin fraction. Simultaneously, the content of fibrin(ogen) degradation products (FDP) increases in the blood. During the stage of the intensive development of neoplastic disease fibrinolytic activity as well as plasminogen activator activity become inhibited, whereas the concentration of FDP retains the level observed in healthy animals. Inhibition of fibrinolytic activity in the later phase of the disease coincides with the appearance of low-molecular weight antifibrinolytic factor in the blood of rats loaded with epithelioma.

Animals↗
PubMed1990

Plasminogen activator (PA) in Guerin epithelioma. Additional PA inhibitor in plasma of rats bearing the epithelioma.

The presence of plasminogen activator (PA) with a Mr of about 35,000 was detected by SDS-PAGE in extract from Guerin epithelioma. The activator, which is a serine proteinase, was partially purified on Sephadex G-50 followed by Lys-Sepharose. Rat plasma, both of healthy and epithelioma-bearing animals, inhibited the activity of such isolated PA. However, the difference between these plasmas in their antiactivator action was observed after inactivation of plasma proteinase inhibitors. In such conditions, the control plasma lost the ability to inhibit the examined PA, whereas the plasma of epithelioma bearing rats retained this ability.

Aniline Compounds↗
PubMed1989

Low molecular weight fibrinolytic inhibitor from Guerin epithelioma.

Antifibrinolytic activity of the extract from Guerin epithelioma, a highly metastatic tumour implanted to rats, was determined by fibrinolytic and zymographic methods. The extract exhibits antifibrinolytic activity which is thermostable (60-100 degrees C) and pH-stable (pH 2.7-12). It contains a fibrinolytic inhibitor, with Mr about 7000, with antiplasmin properties, bound to lys-Sepharose and heparin-Sepharose. The molecular weight, physicochemical properties and antiplasmin action of the epithelioma inhibitor prove its identity with the low molecular weight antifibrinolytic factor appearing in the plasma of rats during the development of this tumour.

Animals↗
PubMed1989

Fibrinolytic inhibitors from the experimental rat epithelioma.

Guerin epithelioma, a highly metastatic tumour implanted to Wistar rats contains two inhibitors of fibrinolysis which can be detected with the use of zymographic techniques. The first one--with Mr about 48000 forms SDS-stable complex with urokinase. The second--with Mr about 7000 inhibits fibrinolytic and amidolytic activity of plasmin.

Aniline Compounds↗
PubMed1989

[Fast-acting plasminogen activator inhibitor in the plasma].

This study contains a survey of papers published in the last few years on the specific inhibitor of plasminogen activation (PA-inhibitor, or antiactivator) discovered in plasma in 1983. Molecular weight of the PA-inhibitor is ranging from 40,000 to 50,000; the antiactivator is present in very small concentration in plasma. Most probably it originates from the endothelial cells. The antiactivator inhibits both tissue plasminogen activator and urokinase, forming complexes in molar ratio 1:1 with them. Possibly, it is the main plasmic inhibitor of plasminogen activators. Its increased content in plasma of patients with tendency to develop thromboembolic disease points to a relationship between lowered fibrinolytic activity and increased concentration of the PA-inhibitor in blood.

Blood Coagulation↗
PubMed1988

Impending sudden cardiac death: treatment with myocardial revascularization and the automatic implantable cardioverter defibrillator.

Myocardial revascularization and implantation of the automatic implantable cardioverter defibrillator (AICD) have individually been shown to improve survival in patients after sudden cardiac death. Their combined role has not been well defined. Twenty-three survivors of sudden death underwent revascularization and AICD implantation at an average age of 59 years. The initial arrest was caused by ventricular fibrillation in 15 and ventricular tachycardia in 8. Exercise stress tests, ambulatory ECGs, and electrophysiological monitoring with programmed electrical stimulation were done preoperatively and postoperatively. Follow-up averaged 24 months with a two-year survival of 91%. Eight patients (35%) required AICD resuscitation an average of 8 months postoperatively, and electrophysiological testing did not accurately predict arrhythmia recurrence. The addition of AICD implantation to revascularization substantially improves survival of patients with sudden cardiac death.

Adult↗
PubMed1988

Implantation of the automatic implantable cardioverter defibrillator.

Since February 1980 the automatic implantable cardioverter defibrillator has been implanted in over 1,500 patients. Sudden death rates have been reduced to 2%-4% annually. This report reviews the implantation techniques, their indications, and our clinical experience in 200 patients.

Arrhythmias, Cardiac↗
PubMed1987

Success of chronic defibrillation and the role of antiarrhythmic drugs with the automatic implantable cardioverter/defibrillator.

Because the automatic internal cardioverter defibrillator's long-term ability to reduce arrhythmic mortality in patients with ventricular tachycardia/fibrillation is unknown, it is important to determine whether the threshold for defibrillation changes over time. Serial defibrillation thresholds were measured in 23 patients over a mean replacement time of 24.8 +/- 7.5 months. In all cases the lead system was a superior vena cava coil to a left ventricular epicardial patch. The defibrillation threshold for the entire group increased from 12.3 +/- 4.7 J to 16.9 +/- 5.9 J (p less than 0.05). Striking increases in the defibrillation threshold were seen in the subgroup of patients taking amiodarone (from 10.9 +/- 4.3 J at implantation to 20.0 +/- 4.7 J at replacement, p less than 0.05). Defibrillation threshold decreased in patients taking no antiarrhythmic drugs or taking class I agents. Thus, the increase in mean defibrillation threshold was the result of an increase in the patients taking amiodarone. These data suggest that at initial implantation lead systems associated with the lowest defibrillation threshold should be used and the defibrillation threshold should be measured at generator change to guarantee an adequate margin of safety.

Aged↗