Biomedical subjects
Publications and source records attributed to M Szewczyk.
The authors presented symptoms of botulism, diagnostics and treatment. In this case there was a necessity of urgent tracheotomy. The authors had good results because of early treatment with serum antibotulism A+B+C and symptomatic treatment. Decannulation was only after 45 days because the paralytic symptoms declined very slowly.
The aim of the study was to compare 2 hours postdose concentration (C2) of CyA in stable patients receiving ketoconazole concomitantly late after heart transplantation (OHT) with patients not receiving ketoconazole. Routine C2 and C1 (1 hour postdose concentration) of CyA monitoring (FPIA, AxSYM, Abbott) along with C0 (trough level) were performed in 64 elective patients. The KETO group consisted of 29 patients receiving 200 mg of ketoconazole daily along with CyA; the remaining 35 patients were included into the control group. Patient characteristics (KETO vs control group) were as follows: age, 49 +/- 11 versus 48 +/- 12 years; percentage of male patients, 93 versus 80; follow-up post-OHT, 4.3 +/- 2 versus 5.3 +/- 2 years. Target C0 of CyA was 175 to 225 ng/mL; CyA doses remained stable for at least 1 month. We compared maintenance doses of CyA, C0, C1, C2 of CyA, number of biopsy-proven acute cellular rejection (AR) during the one year and after the first year post-OHT, and creatinine in both groups. Statistical significance was assessed using Mann-Whitney U test. Results were as follows (KETO versus control group): CyA dose, 53 +/- 30 versus 216 +/- 69 mg, P <.000001; C0, 181 +/- 77 versus 160 +/- 53 ng/mL, NS; C1, 406 +/- 78 versus 803 +/- 317 ng/mL, P =.000001); C2, 397 +/- 174 versus 689 +/- 284 ng/mL, P =.000001, AR during the first year after OHT, 2.8 +/- 1.9 versus 2.3 +/- 1.6, NS; AR beyond first year after OHT, 0.2 +/- 0.5 versus 0.7 +/- 0.9, P =.03); creatinine, 181 +/- 50 versus 160 +/- 114 micromol/L NS. In conclusion; C2 monitoring in stable heart transplant recipients receiving cyclosporine and ketoconazole concomitantly late after procedure does not seem to be sufficient to estimate the immunosuppressive effect of this combination.
Basing on literature and own experience authors have presented possibilities and advantages this method. During 1994-1997 3239 patients were hospitalized, 249 because of larynx diseases. 88 (35.34%) from them were operated by Kleinssaser tool kit with control by surgical microscope. Between these patients in histological examination were found in 30 patients--changes of hypertrophy, in 23 patients--polypus vocal fold, in 17 patients cancer of larynx--early shape, in 12 patients--vocal nodulus and 2 patients--Reincke oedema, 2--laryngeal papillomas and 2--cysts of larynx. Patients with cancer of larynx were treated by partial laryngectomy. Other patients had return full function of larynx.
The question of the physician's liability, both that of civil as well as penal law nature--is always emotionally approached. Dynamic development of medical and biological sciences as well as technics is the cause of progress but it also gives rise to the increase of hazards or abuses in medical therapy. If we speak of the therapeutic intervention being originally legal we mean that it is carried out in compliance with the principles of medical art. In such circumstances, even though the intervention resulted in negative effects, the intervening physician cannot be made penally liable. Civil law liability, in its turn, may have either ex contractu or ex delictu basis. When the general prerequisites of this kind of liability are present, the intervening physician (Art. 353 or 415 of Civil Code) or the State Treasury (Art. 417 of Civil Code) may be made liable for causing damage, joint and several liability of the physician and the Treasury being also possible (Art. 420 of Civil Code). The carrying out of therapeutic intervention without the law required consent of the patient may lead--on the basis of Polish law--to the physician's civil law liability for the infringement of the patient's personal interests even though the intervention ended in success (Articles 23 and 24 of Civil Code). From the point of view of Polish penal law such situation may cause the physician's penal liability for the offence against freedom (Art. 192 of Penal Code). The euthanatic homicide should be, and in Polish law, is an offence. Considering the potential abuses arising from making the euthanasia legal, penal law whose major function is that of the guarantee nature, must ensure safeguards vis-à-vis life to the utmost limit. Polish Legislator shows, however, full understanding of the extremely difficult and conflict-generating situation in which the individual committing euthanatic homicide may find himself. Hence, in section 2 of Art. 150 of Penal Code the Legislator declared that "in exceptional, particularly justified cases, the Court may apply extraordinary mitigation of penalty or even depart at all from meeting out the penalty". Law regulations cannot however solve problems whose moral and ethical dimension exceeds sometimes that limited to law only. Hence in plenty of cases the physicians are left to themselves with the "verdicts" produced by their own conscience. And indeed, these verdicts may many a time be more severe than the decision of the Court because the physicians cannot appeal from them.
On the basis of 72 reports in the literature and own case, the authors described new theories on the pathogenesis of congenital cholesteatoma. They present differentiation of congenital and acquired cholesteatoma by cyto-, histochemical and immunohistochemical methods. They discuss methods of diagnosis and therapy. Attention has been called to diagnosis by CT and MR examinations.
Common mood disorders that are seen in women in primary care are major depression, dysthymic disorder, adjustment reaction with depressed mood, and premenstrual syndrome. This article reviews the diagnosis and treatment of major depression, which also are applicable in many ways to other mood disorders. Specifics about other mood disorders that are encountered frequently in women are discussed subsequently.
Heparin cofactor II (HC) is a plasma serine proteinase inhibitor (serpin) that inhibits alpha-thrombin in a reaction that is dramatically enhanced by heparin and other glycosaminoglycans/polyanions. We investigated the glycosaminoglycan binding site in HC by: (i) chemical modification with pyridoxal 5'-phosphate (PLP) in the absence and presence of heparin and dermatan sulfate; (ii) molecular modeling; and (iii) site-directed oligonucleotide mutagenesis. Four lysyl residues (173, 252, 343, and 348) were protected from modification by heparin and to a lesser extent by dermatan sulfate. Heparin-protected PLPHC retained both heparin cofactor and dermatan sulfate cofactor activity while dermatan sulfate-protected PLPHC retained some dermatan sulfate cofactor activity and little heparin cofactor activity. Molecular modeling studies revealed that Lys173 and Lys252 are within a region previously shown to contain residues involved in glycosaminoglycan binding. Lys343 and Lys348 are distant from this region, but protection by heparin and dermatan sulfate might result from a conformational change following glycosaminoglycan binding to the inhibitor. Site-directed mutagenesis of Lys173 and Lys343 was performed to further dissect the role of these two regions during HC-heparin and HC-dermatan sulfate interactions. The Lys343----Asn or Thr mutants had normal or only slightly reduced heparin or dermatan sulfate cofactor activity and eluted from heparin-Sepharose at the same ionic strength as native recombinant HC. However, the Lys173----Gln or Leu mutants had greatly reduced heparin cofactor activity and eluted from heparin-Sepharose at a significantly lower ionic strength than native recombinant HC but retained normal dermatan sulfate cofactor activity. Our results demonstrate that Lys173 is involved in the interaction of HC with heparin but not with dermatan sulfate, whereas Lys343 is not critical for HC binding to either glycosaminoglycan. These data provide further evidence for the determinants required for glycosaminoglycan binding to HC.
Review of literature and the own case was presented. The symptoms, diagnosis and treatment were described.
Fifty-seven of 159 rural elementary school students had an explosive spread of pruritus and rash--a rarely described manifestation of epidemic hysteria. In a sample of 13 children (23%), each child examined had irregular, macular, erythematous lesions that were excoriated and actively changed during examination. Rash occurred only at sites readily accessible to hands. The symptoms disappeared promptly when the children left school and recurred each morning when they returned. There were no secondary family cases in sample children. School-wide attack rates were higher in girls and younger children. The outbreak resolved after two to three weeks, with identification of its nature and resumption of normal activities. Academic stresses were circumstantially linked to the outbreak.
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The insect myotropic octapeptide leucopyrokinin Glp-Thr-Ser-Phe-Thr-Pro-Arg-Leu-amide (LPK or Lem-PK) (1) and its truncated analogues without the first N-terminal amino acids [2-8]-LPK (2) as well as devoid of the first, second and third N-terminal amino acids [4-8]-LPK (3) were prepared together with a series of the following modified [2-8]-LPK heptapetides such as: [Ala2] (4)-, [Ala3] (6)-, [D-Phe4] (7)-, [Ala5] (8)-, [D-Ala5] (9)-, [D-Thr5] (10)-, [Ser5] (11)-, [D-Pro6] (12)-, [Ala6] (13)- and [D-Arg7]-[2-8]-LPK (14) and [Pro1]-LPK (5). Bioassays were carried out by means of a hot-plate and a tail immersion tests in rats after i.c.v. and i.p. injections. Peptides 1 and 2 revealed prolonged high antinociceptive effects, while other peptides were practically inactive. [2-8]-LPK (2) probably crosses the blood-brain barrier in rats.