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Biomedical subjects

L Zech

Publications and source records attributed to L Zech.

At least 55 records · Page 3Linked to original sources
PubMed1980

Chromosome aberrations and sister chromatid exchanges in Swedish paint industry workers.

Workers in the Swedish paint industry exposed to a mixture of organic solvents, mainly containing xylene or toluene, were investigated for genotoxic effects. No difference in the frequency of sister chromatid exchanges (SCE), 0.192 and 0.193 per chromosome, respectively, was noted in the peripheral lymphocytes of the exposed group of 17 workers and their matched reference group. No correlation was found between xylene or toluene exposure and SCE frequency nor between total solvent exposure and SCE frequency. The frequency of chromosome aberrations was also investigated for the five most exposed workers and their matched referents, and no difference was found. There was no correlation between SCE and chromosome breaks.

Adult↗
PubMed1980

Nonrandom chromosomal aberrations in chronic lymphocytic leukemia revealed by polyclonal B-cell-mitogen stimulation.

Peripheral blood lymphocytes from 11 patients with chronic lymphocytic leukemia were stimulated by Epstein-Barr virus (EBV), lipopolysaccharide from Escherichia (LPS), and phytohemagglutinin (PHA). Chromosome analysis with the Q-banding technique after 5 days incubation revealed an extra chromosome 12 in 5 of the patients and a translocation between chromosome 11 and chromosome 14 in 1. Two patients had a deletion of chromosome 6, and only 3 patients had a normal karyotype. In most patients, the abnormalities were found in the majority of metaphases after stimulation with EBV, LPS, or both mitogens, while PHA revealed a normal karyotype, with the exception of a total of 4 metaphases in 3 patients. An extra chromosome 12 appears to be specifically associated with chronic lymphocytic leukemia. The frequency of chromosomal abnormalities in this disease appears to be much higher than has previously been thought.

B-Lymphocytes↗
PubMed1980

Studied of very low density lipoprotein triglyceride metabolism in an obese population with low plasma lipids: lack of influence of body weight or plasma insulin.

Pima Indians have a high prevalence of hyperinsulinemia, obesity, and diabetes, but they have low plasma cholesterol levels, reduced low density lipoprotein synthesis, and little arteriosclerotic heart disease. To investigate lipoprotein metabolism further in this group, very low density lipoprotein (VLDL) metabolism was studied, using [3H]glycerol as an endogenous precursor of triglyceride (TG) synthesis, in 15 obese Pima nondiabetic males and compared to that of 10 obese and 13 normal weight, normolipidemic, nondiabetic Caucasian males. The resultant kinetic data were analyzed using a multicompartmental model which includes two pathways for VLDL-TG synthesis and a process of stepwise delipidation for VLDL catabolism. As compared to obese Caucasians, the obese Pimas had a lower rate of VLDL-TG synthesis, and a lower proportion of slow pathway for synthesis. The fractional catabolic rate in the Pimas was higher than in either Caucasian group, a larger proportion of VLDL-TG was delipidized at each step, and particle residence time was shorter. When the relation between VLDL-TG metabolism and plasma insulin was examined, plasma insulin levels in the Pima were not correlated with VLDL-TG synthetic rates, catabolic rates, or plasma pools. On the other hand VLDL-TG synthetic rates were correlated with plasma free fatty acid levels. Thus, in this population with low plasma lipids and reduced arteriosclerotic heart disease, VLDL-TG synthesis is low, VLDL-TG catabolism is accelerated, and VLDL pools appear to be insensitive to the influence of body weight and hyperinsulinemia.

Adolescent↗
PubMed1979

Simultaneous staining of sister chromatid exchanges and Q-bands in human chromosomes after treatment with methyl methane sulphonate, quinacrine mustard, and quinacrine.

Human peripheral lymphocyte chromosomes were stained simultaneously for sister chromatid exchanges (SCEs) and Q-banding. No effect of treatment with MMS, QM, and Q on the distribution of SCEs in chromosomes was found compared with controls. The SCEs were distributed between chromosomes roughly according to metaphase length, with the shorter chromosomes underrepresented. The majority of SCEs were located to pale bands, while a few occurred in bright bands and at interfaces between pale and bright bands. A greater frequency than expected of SCEs had occurred at identical sites in homologous chromosomes. This frequency was significantly increased after treatment with MMS.

Chromosome Banding↗
PubMed1979

Growth of diploid, Epstein-Barr virus-carrying human lymphoblastoid cell lines heterotransplanted into nude mice under immunologically privileged conditions.

Human Epstein-Barr virus-carrying lymphoid cell lines which have been classified on the basis of studies on clonality and morphological, chromosomal and functional parameters as lymphoblastoid cell lines (LCL) of presumed non-neoplastic origin were inoculated intracerebrally into nude mice. All eighteen of them grew, killing the host mice within 7 to 25 days, except for 2 which grew more slowly. At autopsy, the brain of the nudes was found to be invaded by infiltrating lymphomas. Sixteen of these lymphomas, when recultured in vitro, gave rise to cell lines with growth properties and morphology indistinguishable from those of the inoculated LCL. Chromosomal examinations showed that 3/7 cell lines injected, which grew as lymphomas in the brain, were still normal diploid on reexplantation whereas the remaining four had become aneuploid. Four lines derived from intracerebral lymphomas (2 diploid, 1 aneuploid and 1 untested) were inoculated subcutaneously into adult nude mice. None of them grew. When the corresponding four original LCL lines were inoculated subcutaneously into newborn nude mice, they grew rapidly, but failed to do so in newborn normal mice or intracerebrally in adult normal mice. One such line, U-1450, was treated with anti-lymphocyte serum (ALS). Small nodules developed at the site of inoculation. From one nodule a cell line was cultured, 1450 ALSAD. It was morphologically indistinguishable from the line of origin. The lines obtained from nude mice inoculated with polyclonal LCL seem to have a restricted clonal representation, but were not monoclonal, as evidenced by analyses of their pattern of immunoglobulin synthesis.

Aneuploidy↗
PubMed1979

Isochromosome 17 in a patient with a myeloproliferative disorders terminating in eosinophilic leukemia.

A patient is described, who for more than two years had a myeloproliferative disorder which terminated in eosinophilic leukemia. Chromosome analysis revealed an isochromosome 17 in all metaphases of bone marrow cells. This abnormality has now been found in two out of six patients with eosinophilic leukemia investigated by banding techniques, and may therefore have etiologic importance. Chromosome analysis in the hypereosinophilic syndrome has practical value for differentiating malignant and non-malignant disease.

Aged↗
PubMed1979

Transport of very low density lipoprotein triglycerides in varying degrees of obesity and hypertriglyceridemia.

Measurements of transport of triglycerides (TG) in very low density lipoproteins (VLDL) were carried out in 59 patients by injection of radioactive glycerol, determinations of specific activities of VLDL-TG for 48 h thereafter, and treatment of the data by multicompartmental analysis. The patients were divided into three groups: normal weight (89-120% ideal weight), mildly obese (120-135% ideal weight), and markedly obese (135% ideal weight). They had varying levels of VLDL-TG ranging from normal to markedly elevated. In many subjects, there was a positive correlation between concentrations and transport of VLDL indicating that overproduction of VLDL-TG contributed to hypertriglyceridemia. In others, and particularly in several markedly obese subjects, transport rates were greatly increased without significant hypertriglyceridemia, suggesting that they had enhanced capacity to clear TG. In all groups, however, there were patients whose degree of hypertriglyceridemia seemed out of proportion to their transport rates. This finding and the fact that many patients have increased secretion of VLDL-TG without elevated plasma TG suggests that both overproduction of VLDL-TG and insufficient enhancement of clearance contributed to the development of hypertriglyceridemia.The data showed a poor correlation between transport rates determined by our multicompartment analysis and single-exponential analysis used previously by other investigators (r = 0.46); this comparison was not improved by segregating patients according to their degree of obesity. Although two conversion pathways (fast and slow synthetic paths) were required to fit the data, there was no correlation between transport rates and the ratio of the two pathways. Also, despite the known pathway of conversion of VLDL to low density lipoprotein, no correlation was found between VLDL-TG transport rates and estimated low density lipoprotein-cholesterol concentrations.

Biological Transport↗
PubMed1978

Trisomy 8 in the chronic phase of Philadelphia negative chronic myelocytic leukaemia.

An unusual case of Philadelphia negative chronic myelocytic leukaemia and an extra chromosome 8 in all bone marrow cells is described. The abnormality was present at diagnosis of the disease and throughout the chronic phase which lasted for somewhat less than 2 years. The patient died soon after the blastic transformation with no other chromosomal abnormalities.

Aged↗
PubMed1977

A new translocation involving three chromosomes in chronic myelocytic leukemia, 46,XY,t(9;11;22).

Bone-marrow metaphases in a 63-year-old male with newly discovered chronic myelocytic leukemia (CML) showed a complex translocation involving chromosomes 9, 11, and 22. About half of the short arm of chromosome 11 was translocated to the terminal part of the long arm of chromosome 9, and the missing fragment on chromosome 22 was translocated to the short arm of the abnormal chromosome 9. The clinical features were typical of CML, and the patient is in good physical condition 10 months after diagnosis on a regimen of busulfan.

Chromosome Aberrations↗