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Biomedical subjects

J Weissmann

Publications and source records attributed to J Weissmann.

At least 19 recordsLinked to original sources
PubMed1999

Vulvar carcinoma: a retrospective analysis of 80 patients.

We evaluated the files of 80 women who were treated for vulvar carcinoma. In 13 women radiotherapy was used as primary treatment, in 45 cases postoperatively and in 22 women because of local recurrence. Patients older than 60 years had a significantly worse 5-year survival rate (39%) than younger women (57%) (p = 0.02). The 5-year survival rate for patients with negative nodes was 72% versus 46% for the N1- and 47% for the N2-status, respectively (p = 0.027). The 5-year actuarial survival rate for patients with tumor manifestation in the clitoris was 77.9% versus 26.1% for patients with tumors in the labia majora (p = 0.0044). There was no difference in survival in patients who had been treated with radical vulvectomy and bilateral groin dissection plus local radiotherapy when compared with patients who had been irradiated (whole pelvis) after tumor resection alone. The 5-year survival rates and the median survival time were identical in both groups (61%/62 months).

Adenocarcinoma↗
PubMed1991

Crack cocaine burns of the larynx.

Burn injuries of the larynx are a previously unrecognized complication of cocaine abuse. The clinical presentations and magnetic resonance imaging findings of two patients are presented. Recognition of this entity is important to avoid errors in diagnosis and in management.

Adult↗
PubMed1988

Endocrine myopathies.

The atrophy produced by endocrine disorders is primarily due to alterations in protein and carbohydrate metabolism. Type II muscle fibers are more severely affected than are Type I fibers. Steroid myopathy and the myopathy associated with excess ACTH have a typical pattern of proximal weakness affecting the legs more than the arms. Steroid myopathy is usually not apparent until other signs of glucocorticoid excess are present. Treatments of steroid myopathy are as follows: Lower the dose of steroid, use a nonfluorinated glucocorticoid, and exercise or physical therapy. Adrenal insufficiency produces generalized weakness, muscle cramping, and fatigue in 50 per cent of patients. Some patients also develop hyperkalemic paralysis. The treatment is hormone replacement. Thyrotoxicosis produces myopathy caused by net protein catabolism, accelerated basal metabolic rate and impaired carbohydrate metabolism. Shortening of contraction time may result from accelerated myosin ATPase activity and enhanced calcium uptake by the sarcoplasmic reticulum. Depolarization of the muscle fiber and impaired Na-K activity in muscle may predispose to thyrotoxic periodic paralysis. Neuromuscular presynaptic impairment may account for the worsening of myasthenia gravis by thyrotoxicosis. In hypothyroidism, impaired energy metabolism may limit force generation. Slow contraction and relaxation reflect reduction in myosin ATPase activity and impaired calcium uptake by the sarcoplasmic reticulum. Treatment for thyroid-associated muscle disorders is restoration of a euthyroid state. Muscle weakness associated with hypopituitarism is due to loss of thyroid and adrenal cortical hormones. Children require growth hormone for muscle development. T3 and growth hormone synergize to maintain normal protein synthesis. Primary and secondary hyperparathyroidism and osteomalacia are often associated with proximal weakness and fatigability. The myopathy improves with restoration of normal PTH levels and vitamin D replacement. Hypoparathyroidism and pseudohypothyroidism are associated with tetany. Tetany is worsened by alkalosis and is treated by calcium and magnesium replacement.

Endocrine System Diseases↗
PubMed1987

Acute inhalation toxicity of aliphatic (C1-C5) nitrites in rats.

The 4-hr inhalation LC50 was determined for methyl-, ethyl-, n-propyl-, n-butyl-, isobutyl-, and isopentyl nitrite in Sprague-Dawley rats. LC50 values were 176, 160, 300, 420, 777, and 716 ppm, respectively. The dose-mortality curves were characterized by extremely steep slopes. Toxic signs observed during exposure included cyanosis, prostration, and rarely, convulsions. There were no effects of exposure on body weight gain during a 14-day postexposure observation period. Signs of pulmonary hemorrhage were apparent in rats which died during exposure but were much less prominent in rats sacrificed at study termination. No animals died after cessation of exposure, and rapid recovery was apparent after exposure. Concentration X Time (CT) relationships suggested that the actual concentration was more important than the "dose" in determining the lethal effects of inhalation exposure to nitrites. Because of the extremely steep dose-mortality curves, the aliphatic nitrites are more hazardous than the LC50 values would indicate.

Animals↗
PubMed1983

[Comparative studies on properdin factor B (Bf) polymorphism in random samples from Brazil, Germany and Guinea-Bissau].

Three different population samples have been tested for properdin factor B markers: 395 individuals from Schleswig-Holstein (Germany), 343 individuals (Europids) from Southern Brazil, and 309 individuals (Negroids) from Guinea-Bissau (Western Africa). These samples are showing marked differences in the distribution of Bf gene frequencies. As for the sample from Southern Brazil the Bf data are confirming the assumption that the Caucasoid population in Southern Brazil is somewhat mixed with Negroids.

Alleles↗
PubMed1982

[Serum markers in Portugal: C3, Gc, Hp and Tf].

The phenotypes C3, Gc, Hp and Tf were determined in 426, 1000, 1000 and 426, respectively, unrelated individuals living in Portugal. The calculated gene frequencies are: C3S = 0.7981, C3F = 0.2019; Gc1 = 0.715, Gc2 = 0.285; Hp1 = 0.430, Hp2 = 0.570; TfC = 1,000.

Alpha-Globulins↗
PubMed1982

[High association between properdin factors BfF1 and HLA-B 18 in a Portuguese family (author's transl)].

The HLA and the Bf systems were studied as part of a family investigation carried out in Portugal. In four generations the rare phenotype BfF1 could be determined four times and the BfF1S phenotype six times, HLA-B18 being simultaneously positive in all cases. Since the frequencies of the individual factors F1 and B18 do not differ essentially from those obtained in Central Europe and no inbreeding situation was present, the high-grade linkage disequilibrium between F1 and B18 may also be presumed for the Portuguese population. Neither among the F1/B18 homozygous nor among the heterozygous subjects could one discern any morbid state (e.g., insulin-dependent diabetes mellitus) from which an association with the F1/B18 haplotype could be deduced. Finally, the rarity of Bf factors, such as F1 and S0.7, is discussed from the standpoint of selection vs. mutation.

Complement Factor B↗
PubMed1981

[Interchange of babies in Portugal by exclusions in the ADA, GPT, ESD and HLA systems (author's transl)].

The suspicion of an interchange of babies in two Portuguese families could not be dissipated in the first course of testing the following systems being considered: AB0, MNSs, Rhesus, Kell, Cellano, Duffy. Including further markers in an additional opinion, multiple father- and mother-exclusions could be made in the systems of ADA, GPT, EsD, and HLA. The suspicion thus showed to be justified and the children were given back to their natural parents.

Blood Group Antigens↗
PubMed1981

Properdin factor B polymorphism in Portugal.

The distribution of properdin factor B (Bf) phenotypes and the corresponding gene frequencies in a population sample from Portugal was investigated by agarose-gel electrophoresis and immunofixation. The following gene frequencies were found in Portugal: BfS = 0.6535, BfF = 0.2775, BfS0.7 = 0.0263, and BfF1 = 0.0427.

Alleles↗
PubMed1980

[Frequencies of red cell enzyme polymorphisms acP, ADA, AK, EsD, 6-PGD, and PGM1 determined by parallel investigations of Turks and Germans living in the Lübeck area (author's transl)].

Gene frequencies for enzyme polymorphisms in the acP, ADA, AK, EsD, 6-PGD, and PGM1 systems were determined by a random sample (n = 281-556-575) Turks living in Lübeck. The results were compared with those of a parallel inquiry on Germans from Lübeck. The following gene frequencies were detected: (table: see text).

Acid Phosphatase↗