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Biomedical subjects

J Weiss

Publications and source records attributed to J Weiss.

At least 415 records · Page 23Linked to original sources
PubMed1982

Presence of intact and gonadectomized juveniles and the reduction of fighting between adult male rats.

Research is reported which investigated the aggressive interactions between adult male rats in the presence of 17-27 day old juvenile conspecifics. Following a brief exposure to an inaccessible juvenile male, juvenile female, estrous adult female, or empty compartment, the males of Experiment 1 were allowed to interact with another adult male. Results were that the presence of both genders of juveniles reduced fighting between the adult males, and pre-pubertal females were particularly effective as an aggression-inhibitor. The hormonal bases for those sex differences were examined in Experiment 2 using juveniles gonadectomized on Postnatal Day 10. Adult males were more aggressive following exposure to intact juvenile males than to castrated juvenile males; the latter males, intact juvenile females, and ovariectomized juvenile females provoked similar and low rates of fighting between adult males. These data suggest that the sexual dimorphism is a function of testicular hormones present during the juvenile stage which modify the stimulus characteristics of a pre-pubertal male rat.

Aggression↗
PubMed1982

Melanoma of the male urethra: surgical approach and pathological analysis.

Primary urethral melanoma in male subjects is rare and optimum therapy has not been established. We described a male patient with a primary urethral melanoma that arose in a precursor nevus and was treated by excision, bilateral groin dissections and postoperative radiation therapy. Urinary and sexual functions have been maintained. We review the previously reported cases of urethral melanoma in male subjects. The biologic relationship of melanoma to precursor lesions in mucosal sites is discussed.

Adult↗
PubMed1982

Toxic shock syndrome or toxic epidermal necrolysis? Case reports showing clinical similarity and histologic separation.

A case of toxic shock syndrome and a case of drug-induced toxic epidermal necrolysis with renal involvement are described. The two patients had similar early clinical manifestations and therefore posed a difficult differential diagnosis. Diagnostic distinction is important because therapy differs considerably. A skin biopsy in each case proved helpful in establishing the correct diagnosis, since there appears to be a different histologic pattern for each condition: superficial perivascular dermatitis for toxic shock syndrome and an interface dermatitis for toxic epidermal necrolysis.

Adult↗
PubMed1982

Perforating folliculitis in association with hemodialysis.

Five patients developed pruritic, keratotic, perforating follicular papules and nodules within 2 months of starting maintenance hemodialysis. Clinically and histologically, the papules and nodules showed the features of perforating folliculitis with superimposed prurigo nodularis, a condition not previously described in patients on maintenance dialysis. The patients with perforating folliculitis constituted 10% of our patients on dialysis during the period of this study. Notably, all five patients were black and had chronic renal failure secondary to diabetic nephropathy. The precise pathogenesis of perforating folliculitis in these patients is unclear at this time.

Adult↗
PubMed1982

Nutrition-related factors in acutely injured patients.

Parameters thought to reflect nutritional status were assessed in 25 critically ill postoperative patients who had been acutely injured. Results were compared with those fom a group of 28 critically ill postoperative patients who had not sustained trauma. The anthropometric measures were significantly better preserved in the previously healthy and presumably well-nourished trauma patients, but striking abnormalities were observed in both groups in albumin and transferrin levels, in the lymphocyte count, and in skin test reactivity. The latter findings suggest the influence of non-nutritional factors at least in the acutely injured patient. Anergy, although frequently observed in both groups of patients, was not predictive of mortality nor did the 44 surviving patients differ significantly in any of the other measured parameters from the nine patients who died. We conclude that, at present, the need for nutrition therapy for the acutely injured patient is best determined on traditional clinical grounds.

Adolescent↗
PubMed1982

Sensitivity of K1-encapsulated Escherichia coli to killing by the bactericidal/permeability-increasing protein of rabbit and human neutrophils.

The presence of K1 capsular polysaccharides increases the resistance of Escherichia coli to killing by serum and phagocytosis by polymorphonuclear leukocytes (PMNs). To determine whether K1 capsule impedes the action of intracellular bactericidal systems of PMNs, we compared the sensitivity of several K1-encapsulated and non-encapsulated strains of E. coli to killing by the bactericidal/permeability-increasing protein (BPI) isolated from rabbit and human PMNs. BPI appears to be the principal bactericidal agent of PMNs toward E. coli and other gram-negative bacteria (Weiss et al., J. Clin. Invest. 69:959-970, 1982). The presence of K1 capsule was monitored by sensitivity to K1-specific bacteriophages. The non-encapsulated strains used represent both random bacteremic isolates and non-encapsulated derivatives of K1-encapsulated strains obtained by selection for resistance to K1-specific phages. We found little or no difference in the sensitivity of K1-encapsulated and non-encapsulated E. coli to killing by neutralized acid extracts of rabbit PMNs. Bacterial killing by these crude fractions can be attributed to the action of BPI because: (i) bacterial killing was blocked by immune (anti-BPI) immunoglobulin but not by preimmune immunoglobulin and (ii) comparison of the dose-response curves of bacterial killing by crude extracts and by purified BPI showed that the bactericidal activity of crude fractions corresponded closely to the BPI content. Human and rabbit BPIs exhibited similar bactericidal potency toward K1-encapsulated E. coli; i.e., <5 mug of either protein killed >90% of 2.5 x 10(7) bacteria. Thus, the potent bactericidal action of BPI toward E. coli is not impeded by K1 capsule, suggesting that the virulence of K1-encapsulated E. coli is a consequence of extracellular survival but not of resistance to intracellular killing.

Animals↗
PubMed1982

Extracellular K+ accumulation during myocardial ischemia in isolated rabbit heart.

Double-barreled valinomycin K+-sensitive electrodes were used to record extracellular K+ activity ([K+]o) in the isolated arterially perfused rabbit interventricular septum under conditions of global ischemia. During ischemia a triphasic pattern of [K+]o accumulation was observed consisting of an initial rise, a plateau phase, and a second rise. The initial rise (0.5-1 mM/min) was homogeneous throughout the preparation, reversible, and reproducible. It was augmented by increases in heart rate, contractility, and temperature. The level of the plateau phase (onset 12.3 +/- 3.1 min) was dependent on temperature and heart rate. Hyperkalemia, acidosis, or catecholamine release did not appear to be responsible for the plateau. The second rise in [K+]o (onset 24.2 +/- 4.6 min) was inhomogeneous and always associated with the development of rest tension and irreversible damage to the preparation. Cellular K+ influx mechanisms appeared to be at least partially intact throughout the plateau phase. K+ loss during ischemia could not be attributed to acidosis or catecholamine release, but substrate depletion may play a contributory role.

Anaerobiosis↗
PubMed1982

[K+]o accumulation and electrophysiological alterations during early myocardial ischemia.

Double-barreled valinomycin K+-sensitive electrodes and floating microelectrodes were used to monitor extracellular K+ concentration ([K+]o) and intracellular potential, respectively, in the isolated arterially perfused rabbit interventricular septum, under conditions of global ischemia without collateral flow and hypoxia with maintained flow. During ischemia [K+]o reproducibly increased at rates of 0.5-1 mM/min, usually in a triphasic pattern, and was accompanied by shortening of the action potential duration (APD) and an increase in conduction time (CT). Hyperkalemia, equivalent to that occurring during ischemia, in combination with respiratory acidosis (pH 6.2-6.5) and catecholamines reproduced quantitatively the ischemia-induced changes in APD and CT. None of these factors alone produced quantitatively comparable electrophysiological changes. Faster heart rates increased [K+]o accumulation during ischemia and accentuated the changes in APD and CT during ischemia. These findings suggest that local hyperkalemia, intracellular acidosis, and catecholamines release during early ischemia may account for electrophysiological changes predisposing to the development of reentrant arrhythmias.

Acidosis, Respiratory↗
PubMed1982

Killing of gram-negative bacteria by polymorphonuclear leukocytes: role of an O2-independent bactericidal system.

Previous studies have suggested that a cationic bactericidal/permeability-increasing protein (BPI) present in both rabbit and human polymorphonuclear leukocytes is the principal O2-independent bactericidal agent of these cells toward several strains of Escherichia coli and Salmonella typhimurium (1978. J. Biol. Chem. 253: 2664--2672; 1979. J. Biol. Chem. 254: 11000--11009). To further evaluate the possible role of this protein in the killing of gram-negative bacteria by polymorphonuclear leukocytes, we have measured the bactericidal activity of intact rabbit peritoneal exudate leukocytes under aerobic or anaerobic conditions and of intact human leukocytes from a patient with chronic granulomatous disease. Anaerobic conditions were created by flushing the cells under a nitrogen stream. Effective removal of oxygen was demonstrated by the inability of nitrogen-flushed leukocytes to mount a respiratory burst (measured as increased conversion of 1-[14C]glucose leads to 14CO2 or by superoxide production) during bacterial ingestion. At a bacteria/leukocyte ratio of 10:1, killing of gram-positive, BPI-resistant, Staphylococcus epidermidis is markedly impaired in the absence of oxygen (76.4 +/- 3.3% killing in room air, 29.2 +/- 8.2% killing in nitrogen). Essentially all increased bacterial survival is intracellular. In contrast, both a nonopsonized rough strain (MR-10) and an opsonized smooth strain (MS) of S. typhimurium 395 are killed equally well in room air and nitrogen. A maximum of 70--80 MR-10 and 30--40 MS are killed per leukocyte either in the presence or absence of oxygen. There is no intracellular bacterial survival in either condition indicating that intracellular O2-independent bactericidal system(s) of rabbit polymorphonuclear leukocytes can at least match the leukocyte's ingestive capacity. Whole homogenates and crude acid extracts manifest similar bactericidal capacity toward S. typhimurium 395. This activity can be accounted for by the BPI content of these cell fractions and is virtually eliminated by immune (anti-BPI), but not by preimmune goat IgG-rich fractions. Opsonization of smooth MS, required for bacterial killing by intact leukocytes, does not alter bacterial sensitivity to BPI in crude or purified form. Leukocytes of a patient with chronic granulomatous disease killed ingested S. typhimurium 396 MS nearly as well as did normal leukocytes. The bactericidal activity toward E. coli (J5) of crude acid extracts of the CGD and normal human leukocytes was virtually the same and was nearly completely inhibited by anti-BPI IgG-rich fractions, but not by preimmune IgG-rich fractions. These findings suggest that the killing of gram-negative bacteria such as S. typhimurium by intact polymorphonuclear leukocytes may also be attributed to the action of BPI.

Aerobiosis↗
PubMed1982

Purified tumour angiogenesis factor enhances proliferation of capillary, but not aortic, endothelial cells in vitro.

Purified tumour angiogenesis factor (TAF) obtained from rat Walker 256 carcinoma and found to induce neovascularization in vivo was examined for its effect on endothelial cell cultures of capillary (CBEC), cow aorta (CAEC) and pig aorta (PAEC) in vitro. Treatment with TAF increased the growth of capillary but not aortic endothelial cells, and then only when the cells were growing on a native collagen substratum. These data show an important growth difference between endothelial cells, in that the ability to proliferate in response to TAF depends not only on the substratum used but also on the vascular origin of the cells.

Angiogenesis Inducing Agents↗
PubMed1982

[Combined drug/hormone therapy in metastatic breast cancer with vincristine, adriamycin, cyclophosphamide and high dose medroxyprogesterone acetate--VAC-MAP. Preliminary results of a phase II study of the German Cancer Society's Internal Medicine Oncology Task Force].

In a study of the AIO 67 patients with metastatic breast cancer were treated with VAC-MAP--a combination of chemo- and hormonal therapy consisting of vincristine 1 mg/m2 day 1, i.v.; adriamycin 40 mg/m2 day 1, i.v.; cyclophosphamide 200 mg/m2 day, 3-6, p.o. and medroxyprogesteroneacetate 1500 mg daily (day 1-42), 500 mg daily from day 42 until relapse. At present, 50 patients are evaluable. Remission rates of all patients correspond with those described in the literature for VAC, i.e. 58%. In CMF-resistant cases remissions were obtained in 50% of the patients and even 78.6% in hormone receptor positive tumors. Only 2 patients did not respond to the therapy. It appears that with a maintenance therapy of 500 mg MAP daily remission duration cannot be prolonged, apparently due to too low a dosage. MAP should improve the subjective tolerance of chemotherapy and bone marrow tolerance towards cytostatic drugs.

Adult↗
PubMed1982

[Histochemical and biochemical investigations of the hippocampus and neocortex of the wistar rat. III. Electron-microscopic investigations on the localization of non-specific esterases in the hippocampus (author's transl)].

This report describes the ultrastructural localization of the non-specific esterases in the pyramidal cells of the CA3-region of rat hippocampus. The use of specific inhibitors allowed the differentiation between aryl-, carboxyl- and acetylesterases. The thiolacetic acid reaction at pH = 5.2 and 7.0 proved to be a favourable method for the conditions of the hippocampus. Liver tissue served for control purposes. In the pyramidal cells carboxylesterase could be demonstrated on membranes and cisternes of the endoplasmic reticulum on polysomes and in the nuclear envelope. Arylesterase was localized in numerous synaptic vesicles and in the myeline sheath of axons. In lysosomes and in mitochondria an esterase activity was demonstrable, which behaved like an acetylesterase. In the hippocampus carboxylesterase could be shown only at pH = 7.0, whereas in liver this enzyme also give a clear reaction at pH = 5.2. Aryl- and acetylesterase reacted at both pH-ranges in the hippocampus. Biochemical investigations showed that the tissue pretreatment, which is necessary for the ultrahistochemical demonstration of nonspecific esterases considerable decreased the enzyme activity. Formaldehyde and glutaraldehyde have thereby a different action on the several esterase types.

Animals↗
PubMed1982

Neurosecretory nerve cells of rat and fish brain are rich in thiol-protein disulphide oxidoreductase (TPO) immunoreactivity.

Thio-protein disulphide oxidoreductase (TPO) was demonstrated in rat and fish brain by use of the indirect peroxidase-antiperoxidase technique. TPO immunoreactivity was found to be widely distributed throughout rat CNS. Whereas most nerve cells possessed only weak immunoreactivity to the enzyme, the neurosecretory cells of Nuc. supraopticus and Nuc. paraventricularis were heavily laden with immune products. In fishes (rudd) the neurosecret-producing neurons of the Nuc. preopticus were the only locus being positive for TPO. From our findings we conclude that thiol-protein disulphide oxidoreductase might be involved into the process of neurophysin synthesis.

Animals↗
PubMed1982

Pneumococcal polysaccharide immunization of children with sickle cell disease. I. Clinical reactions to immunization and relationship to preimmunization antibody.

Vaccine reaction data were obtained from 154 patients with sickle cell disease immunized with tetradecavalent pneumococcal polysaccharide vaccine. There was a high rate (70%) of mild reactions, primarily at the site of injection. Fever over 100 degrees F was uncommon and precipitation of symptoms similar to sickling crisis was rare. Development of local reactions was associated with the level of preimmunization pneumococcal antibody titer.

Anemia, Sickle Cell↗
PubMed1982

Pneumococcal polysaccharide immunization of children with sickle cell disease. II. Serologic response and pneumococcal disease following immunization.

One-hundred seventy-four children with sickle cell disease (SCD) were immunized with a single dose of tetradecavalent pneumococcal vaccine. Preimmunization and postimmunization antibody against 13 of the 14 pneumococcal capsular antigens was measured by indirect hemagglutination (IHA). The ability of each antigen to stimulate antibody following immunization was characterized by one of three types of responses: (1) poor antibody response regardless of the age at immunization (capsular types 6A, 14, and 19F); (2) improving antibody response with advancing age at immunization (capsular types 1, 4, 9N, 12F, 18C, and 23F); and (3) good antibody response regardless of age at immunization (capsular types 2, 3, 7F, and 8). An increase in antibody following immunization was significantly correlated (P less than 0.0005) with an increasing level of preimmunization antibody titer for all 13 antigens. Through the first 24 months of study, two episodes of pneumococcal sepsis caused by group 23 pneumococci were documented in two children immunized prior to 24 months of age (incidence rate, 4.40/100 patient-years in children less than 5 years of age), and one additional episode caused by a group 23 pneumococcus occurred in a 5 7/12-year-old child (incidence rate, 0.66/100 patient-years in children greater than 5 years of age). These observations suggest that anamnestic immune response significantly contributed to the enhanced antibody response observed in older children and adults. Only modest vaccine efficacy may be expected among children with SCD who receive a single dose of pneumococcal vaccine.

Adolescent↗