Search PubMed⌕ Search

Biomedical subjects

K Becker

Publications and source records attributed to K Becker.

At least 397 records · Page 22Linked to original sources
PubMed1983

[2-dimensional transesophageal echocardiography: comparison of echocardiographic and anatomic section pictures].

Conventional two-dimensional echocardiography has become a well established tool for evaluation of cardiovascular diseases. Recent introduction of two-dimensional transesophageal echocardiography has widened the ultrasonic examination possibilities for the heart and the great vessels. This paper describes 6 standard transesophageal transducer positions which have proven to be representative and of diagnostic value. In order to facilitate structure identification and interpretation of the anatomic relation transesophageal recordings were compared with corresponding anatomic sections.

Echocardiography↗
PubMed1983

Quantitative assessment of carnitine loss during hemodialysis and hemofiltration.

Carnitine deficiency has been claimed to be responsible for the myo- and cardio-myopathy observed in dialysis patients and has been attributed to the loss of carnitine during dialysis. To quantitate carnitine loss, we determined the carnitine concentrations in 29 patients on chronic hemodialysis, 10 patients on chronic hemofiltration, and 8 patients on CAPD. Mean plasma carnitine levels in hemodialysis and hemofiltration patients (39.8 +/- 2.7 mumoles/liter; N = 39) were significantly lower (P less than 0.01) than in controls (49.8 +/- 2.0 mumoles/liter; N = 43). Hemodialysis or hemofiltration led to a further reduction (33.2 +/- 3.5 mumoles/liter; P less than 0.001). There was no significant difference in the mean plasma carnitine level between CAPD patients (40.0 +/- 5.7 mumoles/liter) and controls. Hemofiltration treatment resulted in a weekly loss of 795 +/- 84 mumoles of carnitine. This was significantly lower (P less than 0.0001) than the urinary carnitine excretion in healthy controls (1534 +/- 134 mumoles per week; N = 27) and the carnitine elimination in the dialysate of CAPD patients (1905 +/- 236.6 mumoles per week; N = 8). It is concluded that carnitine deficiency in dialysis patients cannot be explained by loss into dialysate or filtrate. Because intestinal reabsorption of carnitine does not seem to be impaired, decreased endogenous carnitine synthesis is considered as the most plausible explanation for the moderate degree of carnitine deficiency observed in dialysis patients.

Adult↗
PubMed1983

Quantitative assessment of carnitine loss during haemodialysis and haemofiltration.

Carnitine concentrations were measured in plasma, haemofiltrate, dialysate and urine of patients on regular dialysis treatment and in normal controls. Patients on haemofiltration and on haemodialysis exhibited moderately decreased plasma values, whereas in eight patients on CAPD mean values did not differ from controls. Carnitine loss into the haemofiltrate was significantly lower than urinary carnitine excretion in normal subjects. Major disturbances of intestinal carnitine absorption in patients on regular dialysis treatment were not observed. It is concluded that patients on regular dialysis are in a state of moderate carnitine deficiency and that therapeutically induced carnitine losses or grossly impaired intestinal absorption are not major factors in the development of carnitine deficiency in these patients.

Blood↗
PubMed1982

Expression of genetic damage induced by alkylating agents in germ cells of female mice.

The purpose of the present experiments was to analyse the frequencies of meiotic non-disjunction and structural aberrations by comparative cytogenetic investigations in unfertilized mII oocytes and first-cleavage metaphases after pre-ovulatory treatment of female mice with alkylating agents. We also present data on the expression of both types of aberration during embryogenesis in terms of dominant lethal effects. Trenimon (TR, 1 mg/kg) induced meiotic non-disjunction, but no structural aberrations were detected at metaphase II. On the contrary, at first-cleavage metaphase, TR revealed a strong clastogenic effect. A dose of 0.25 mg TR/kg increased the frequency of cells with structural aberrations to 51.79%. Mainly chromatid and a few isochromatid aberrations were found. These results support the observations previously made (see Brewen and Preston, 1979; Obe and Beek, 1979) that an intervening round of DNA replication is necessary for a TR-induced DNA lesion to be transformed into a structural aberration. The frequency of aberrant eggs in toto analysed at first cleavage (63.39%) can be quantitatively correlated to the rate of embryonic mortality (55.17%) as measured in the dominant lethal assay at the first day after treatment. We also present data on the effects of cyclophosphamide (CYC) on the first meiotic division. CYC (150 mg/kg) enhanced the incidence of meiotic non-disjunction only slightly, but induced a high frequency of dominant lethal effects (58.94%) at the first day after application.

Alkylating Agents↗
PubMed1982

[Utilization of urea infused into the abomasum in growing lambs].

Eight lambs were fed 100 g sucrose per day plus pelleted NaOH-straw ad lib. Additionally 50 g casein were infused daily into the abomasum. As a supplement two lambs respectively received 22 g urea per day with their diet (A), half with their diet and half with the infusion (B) or all infused (C). Irrespective of the site of supply the urea supplement caused an increase in intake of straw and a remarkable improvement of-N-retention.

Abomasum↗
PubMed1982

A computerized study of knee-ligament injuries: repair versus removal of the torn anterior cruciate ligament.

A retrospective review of 202 patients with acute injury to knee ligaments was carried out by chart review, scored questionnaire and scored physical examination. Of 62 patients with complete midsubstance injury to the anterior cruciate ligament, repair was attempted in 46, while 16 had complete excision of the ligament without replacement or augmentation. Computer analysis revealed that these groups were similar with respect to mean age of the patients, sex distribution, incidence of meniscectomy and distribution of associated injuries. At 4-year follow-up, there was no advantage of primary repair over excision for these injuries. In fact, repair seemed to be subjectively and objectively worse than excision, being associated with increased pain and decreased range of motion. The high rate of signs and symptoms of deterioration in both groups suggests a need for better alternatives in the acute phase of anterior cruciate ligament injury.

Adolescent↗
PubMed1982

[Diffuse oncocytosis of the parotid gland. Definition and differential diagnosis].

Diffuse oncocytosis represents an extremely rare, nontumourous alteration of the parotid gland which could be observed in only 2 cases in a group of over 7000 salivary gland cases. Viewed under the light microscope, the glandular lobuli show complete oncocytic metaplasia of the acinar cells and the duct epithelia. The oncocytic cells are characterized by a swollen granular acidophilic cytoplasm. In semi-thin sections, transformed oncocytic clear basal cells are found in the vicinity of typical oncocytes. The electron microscope shows that the oncocytes contain multiple mitochondria in the cytoplasm. The mitochondria are almost always swollen, display cristolysis very often and contain osmiophilic granules. The ductular oncocytes are characterized by isolated tonofilaments, whereas the myoepithelial oncocytes are notable for peripherally arranged myofilaments. The endothelial cells of the vessels show hydropic swelling. Ultrastructural changes are observed in the terminal axons of the vegetative nervous system of the parotid gland. Diffuse oncocytosis is an intracellular metabolic disturbance associated with mitochondriopathy. Its occurrence in elderly persons is suggestive of an age-dependent metabolic defect. In differential diagnosis, diffuse oncocytosis must be differentiated from sialadenosis which is a primarily vegetative neuropathy with secretory disturbance of the acinic cells, and from oncocytic neoplasias, especially from oncocytomas and cystadenolymphomas. Oncocytic adenomatous hyperplasia is a different disease. It represents a multifocal oncocytic proliferation of the duct system. Typical oncocytomas may perhaps develop from such oncocytic proliferation by a tendency to confluent growth.

Adenoma↗
PubMed1982

[Current determination of ovulation time. 2. Optimization of timing for oocyte recovery].

Knowledge of probable ovulation date is essential to the recovery of pre-ovulatory oocytes for in vitro fertilisation. The authors used a commercially available LH-RIA kit for blood and urine samples together with the HI-Gonavis test for urine assay for high-accuracy determination of luteinising hormone (LH) in the peri-ovulatory cycle phase. Follicle status and oocyte quality were laparoscopically described of seven patients, between the eleventh and 16th days p.m. Optimum timing for oocyte recovery has not even become known by knowledge of LH rise. Different recommendations by other authors are discussed, and reference is made to unanswered problems.

Body Temperature↗
PubMed1981

[Phaenotypic aspects of hereditary aminoacidopathies (author's transl)].

Despite considerable diagnostic progress from mass screening tests in all newborns or from sophisticated analytical efforts some patients with inborn errors of amino acid metabolism are detected only after some more or less specific clinical signs have appeared. Those may include a peculiar odor of the sweat or urine, disturbances or normal growth, and skeletal, eye, hair and skin alterations. While some of these features appear early in the course of disease and may be of diagnostic and therapeutic significance (e.g. defects in the oxidation of the branched-chain amino acids) others are noticed only in a later stage with further progress of the disease (e.g. cystathionine synthetase deficient homocystinuria tryosinemia type II, or ornithine aminotransferase deficient hyperornithinemia), when the disease may have more advanced. Therefore the physician who is engaged in the care of the newborn or takes part in any investigation program for the developing child should be aware of these signs in order to initiate further diagnostic, therapeutic, or preventive measure for the patient and his family.

Amino Acid Metabolism, Inborn Errors↗