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Biomedical subjects

K Meyer

Publications and source records attributed to K Meyer.

At least 217 records · Page 12Linked to original sources
PubMed1989

Estimation of additive maternal and cytoplasmic genetic variances in animal models.

Two pathways for maternal genetic effects to act on production traits are additive maternal and cytoplasmic. Estimation of these variances have generally assumed that the correct maternal pathway is known. A method is described that allows simultaneous estimation of additive maternal and cytoplasmic genetic variances as well as additive direct genetic variances and error variances using an animal model. Data were simulated assuming an additive maternal model, cytoplasmic model, or both. The method was tested by analyzing the data under the true or incorrect maternal model using REML with an animal model that accounted for additive genetic relationships. Additive direct, additive maternal, cytoplasmic, and error variances were correctly partitioned when estimated under the true model. However, when additive maternal or cytoplasmic genetic effects were ignored in the model used for analysis, estimates of additive direct variance were significantly inflated. Also, under an additive maternal genetic model, a small cytoplasmic variance was estimated although none was present in the data.

Analysis of Variance↗
PubMed1988

Translocation t(11;19)(q21;p13.1) as the sole chromosome abnormality in a cystadenolymphoma (Warthin's tumor) of the parotid gland.

Cytogenetic findings on a cystadenolymphoma (Warthin's tumor) of the parotid gland are reported. In the primary culture, a reciprocal balanced translocation t(11;19)(q21;p13.1) as the sole clonal abnormality was found in the majority of metaphases. At this time, the proliferation of epithelial cells was observed in the cultures. Later passages showed overgrowing fibroblasts, and the abnormal metaphases disappeared. This result should stimulate further efforts for cytogenetic investigations of the epithelial part and permit a better understanding of the histogenesis of this particular tumor.

Adenolymphoma↗
PubMed1988

A causal relationship between chromosomal rearrangements and the genesis of salivary gland pleomorphic adenomas.

The results of chromosome analyses performed on 50 pleomorphic salivary gland adenomas in Germany are summarized herein and compared with those obtained on 100 adenomas studied in Sweden. In both series, characteristic or even specific structural chromosomal rearrangements involving either chromosome 8 or 12 were found that allowed the cytogeneticist to distinguish between subgroups. However, the significantly higher percentage of tumors with chromosome abnormalities in the adenomas examined in Germany is particularly noteworthy. In the near future, cytogenetic investigations together with molecular methods will allow investigators to describe basic mechanisms for the development of pleomorphic adenomas in terms of oncogenetics.

Adenoma, Pleomorphic↗
PubMed1988

[Coronary risk factors and their relation to psychosocial factors in females with myocardial infarct].

UNLABELLED: 237 female patients aged 31-76 years with documented first myocardial infarction were examined on an average of 3 month after the acute event. Risk factors of coronary heart disease, sociobiological and psychosocial variables were assessed via standardized questionnaire. Risk factors were correlated with social characteristics, somatic and psychosocial variables. RESULTS: 1. Hyperlipoproteinemia is correlated with risk factors of nutrition (hypercholesterinemia resp. hypertriglyceridemia, obesity). 2. The analysis of smoking habits reveals a positive correlation with social characteristics (e.g. professional status) and also with the amount of experienced stress. 3. The use of oral contraceptives corresponded with young age of fertile women and also with professional status. Furthermore a correlation with a positive working attitude and smoking behavior was found.

Adult↗
PubMed1988

Joint sire and cow evaluation for conformation traits using an individual animal model.

A joint sire and cow evaluation for selected type traits has been carried out for the Canadian Holstein population using an individual animal model accounting for all known relationships. Only first lactation, first classification linear records were utilized. Linear scores for final class/final score (combined), feet and legs, mammary system, and stature were analyzed. The model of analysis included animals' additive genetic merit as random and herd-round-classifier subclasses as fixed effects. Calving age and stage of lactation at classification were fitted as linear and quadratic covariables. There were 282,030 cows with records, 198,871 dams without records, and 8481 sires (i.e., 489,382 animals in total). Combined with 33,968 herd-round-classifier effects in 9654 herds and four regression coefficients, a system of 523,354 equations required simultaneous solution. Solutions were obtained iteratively for one trait at a time. The computing strategy utilized is described, and a detailed worked example is given. Correlations between sire proofs and the current Holstein sire proofs were .89 to .96 for sires with at least 20 daughters in five or more herds. Correlations between cow indexes and phenotypic scores ranged from .53 to .76. The coefficient of determination in a multiple regression of daughter's index on dam's index and sire's and maternal grandsire's proof was 78 to 92% but only 59 to 83% when dam's index was replaced by dam's phenotypic record.

Animals↗
PubMed1988

[Cardiac exercise tolerance of infarct patients in exercise therapy].

UNLABELLED: 92 female patients with myocardial infarction were divided into three exercise groups of 25 W, 50 W and 75 W according to their symptom-limited working capacity and examined during bicycle ergometer training. Exercise tolerance, training heart rate and arterial lactic acid were analyzed. RESULTS: 1. Increase in maximal working capacity corresponds to a decrease in limiting cardiac symptoms, or an increase of limiting symptoms, e.g., in tired leg muscles. 2. Intensity of training (as a percentage of maximal symptom-limited work capacity) is 55 +/- 21%, 73 +/- 15%, and 90 +/- 8% for groups of 25, 50 and 75 W (p less than 0.05) respectively. 3. Training heart rate and lactic acid increase significantly proportional to the increase of work capacity. 4. In all three exercise groups, training heart rate corresponds to about 84% maximal heart rate measured at maximal working capacity. 5. Mean maximal lactic acid level is at 3.18 +/- 0.97 mmol/l for the whole exercise group on 75 W. Within this group, only a small subgroup of seven women, who were limited in maximal working capacity by tired leg muscles, reached the so-called anaerobic threshold of 4 mmol/l lactic acid. 6. Female patients greater than or equal to 60 years have partially significant higher mean lactic acid levels for the same exercise load as women less than or equal to 59 years. CONCLUSION: Gender specific differences in performance in women and the cardiac situation in female patients were considered on the basis of symptom-limited performance and body-weight-related physical training, regulated by individual training heart rate.

Angina Pectoris↗
PubMed1987

Inhibition of fibrin polymerization by serum amyloid P component and heparin.

The effects of serum amyloid P component (SAP) and heparin on the thrombin-catalyzed formation of polymeric fibrin from purified fibrinogen were examined using a turbidometric method to quantify fibrin polymerization. SAP and heparin acted synergistically to inhibit the lateral aggregation of fibrin fibrils, resulting in the formation of fibrils with a smaller mass to length ratio. Heparin did not enhance the incorporation of SAP into fibrin clots, and the effect of heparin and SAP did not seem to be related to inhibition of thrombin or of fibrinopeptide release. The evidence suggests that a soluble complex of SAP and heparin inhibits fibrin polymerization.

Calcium↗
PubMed1987

Amino acid sequence of a peptide from keratan sulfate II-core protein linkage regions.

Keratan sulfate II was prepared from the proteolytic digest of pig nucleus pulposus proteoglycan. The polysaccharide chains containing the fragment peptides of the core protein at their reducing terminal were subjected to anhydrous HF-solvolysis reaction and one of the glycopeptides from the keratan sulfate II-core protein linkage regions was isolated. The amino acid sequence of the peptide was deduced to be Ala-Pro-Ser-Pro-Gly, which is different from those reported for the attachment sites of chondroitin sulfate on core proteins from various sources. The results provided the first solid amino acid sequence for the keratan sulfate II-core protein linkage regions and suggested that the amino acid sequence of the core protein might determine the distribution of chondroitin sulfates and keratan sulfates along the core protein of the proteoglycan molecule.

Amino Acid Sequence↗
PubMed1986

Effects of arm ergometry training in an adolescent with myelodysplasia. A case report.

The purpose of this article is to report the effects of arm ergometry training on upper extremity strength, body composition, and oxygen uptake in a 13-year-old adolescent with myelodysplasia. The subject trained three times a week for eight weeks at 75% of maximum heart rate. The following measurements were determined before and after the training period: maximal and submaximal heart rate and oxygen uptake, percent body fat, and peak torque of the elbow and shoulder flexor and extensor muscles. The results indicated that maximal oxygen uptake and percent body fat did not change, but maximal physical work capacity increased from 274 kg . m/min to 569 kg X m/min. Heart rate and oxygen uptake decreased at each submaximal work load, and peak torque increased an average of 22.3% for the movements tested. We concluded that arm ergometry training in an adolescent with myelodysplasia can reduce the energy cost of performing submaximal arm ergometry work.

Adipose Tissue↗
PubMed1986

Development of cyclooxygenase and lipoxygenase metabolites of arachidonic acid after transient cerebral ischemia.

Vasoactive arachidonic acid metabolites are postulated to play a role in the pathogenesis of cerebral ischemia. In order to characterize the local generation of cyclooxygenase and lipoxygenase metabolites of arachidonic acid in transient ischemia with reperfusion, Mongolian gerbils were studied for regional cerebral blood flow (CBF), using the hydrogen clearance technique, and for cerebral levels of the thromboxane metabolite TXB2, and prostaglandins 6-keto-PGF1 alpha and PGE2, as well as the leukotriene LTB4. The gerbils were anesthetized with pentobarbital, and half of the animals were pretreated with the cyclooxygenase inhibitor indomethacin. All received 10 or 20 minutes of dense forebrain ischemia followed by reperfusion of 10 minutes, 50 minutes, or 100 minutes. A separate control group received no ischemic lesion. Regional CBF decreased significantly from 23.7 +/- 2.6 to 4.3 +/- 1.7 cc/100 gm/min during ischemia (p less than 0.01). Reperfusion resulted in initially normal flows (22.5 +/- 5.1 cc/100 gm/min) followed by a progressive hypoperfusion (11.3 +/- 2.7 cc/100 gm/min). All metabolites showed parallel significant (p less than 0.05) increases after transient ischemia and reperfusion compared to baseline levels (values (in pg/mg protein) were: TXB2 45.5 +/- 7.1 vs 23.3 +/- 3.6; 6-keto-PGF1 alpha 262.8 +/- 47.9 vs 175.8 +/- 26.8; PGE2 256.5 +/- 35.6 vs 112.5 +/- 11.2; and LTB4 37.8 +/- 4.6 vs 24.6 +/- 6). These levels were all significantly decreased (p less than 0.05) by pretreatment with indomethacin except for the leukotriene LTB4, which was increased. Transient cerebral ischemia results in a reperfusion abnormality and the local generation of cyclooxygenase products, which are reduced by pretreatment with indomethacin; however, cyclooxygenase inhibition may result in increased substrate availability for the lipoxygenase system. Studies of such an interaction may lead to new understandings of the pharmacological modification of detrimental vascular changes after transient cerebral ischemia.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Fibrinolysis and acquired alpha-2 plasmin inhibitor deficiency in amyloidosis.

A patient with plasma cell myeloma and amyloidosis presented with a severe bleeding disorder. There was laboratory evidence of fibrinolysis and severe deficiency of alpha-2 plasmin inhibitor. Treatment with epsilon aminocaproic acid was associated with diminished bleeding and marked increase in the plasmin inhibitor level. This is the first report of acquired alpha-2 plasmin inhibitor deficiency in the fibrinolytic state associated with amyloidosis.

Aged↗
PubMed1985

Gastric ulcer localization by direct in vivo labeling of sucralfate. Work in progress.

We developed and evaluated a new procedure for imaging gastric ulcer disease with technetium 99m-labeled sucralfate. The new method employs direct in vivo labeling of sucralfate instead of in vitro labeling using human serum albumin, as previously reported in the literature. Tests using hydrochloric acid and a rabbit ulcer model showed the efficacy of the direct in vivo labeling technique and the ability of the tagged material to bind to ulcers, respectively. In 26 studies using humans with sucralfate labeled directly in vivo, 15 gave true-negative results and 11 gave true-positive results. Of 14 studies using humans with in vitro labeled sucralfate, three gave true-negative results, three gave true-positive results, and the results of eight were either false-negative or could not be interpreted because of high levels of activity remaining in the stomach. We suggest that the direct in vivo labeling method significantly improves the sucralfate gastric ulcer imaging technique.

Aluminum↗