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Biomedical subjects

K Becker

Publications and source records attributed to K Becker.

At least 73 records · Page 4Linked to original sources
PubMed1985

[Antibiotic therapy in patients with immunologic deficiency].

Basic aspects in the treatment of immunocompromised patients are discussed with respect to medical and paediatric oncology, surgical intensive care and clinical pathology. Defining the type of immunological deficiency seems of primary importance, since it can be caused by haematological diseases, their treatment, by repeated surgery or by a polytrauma. The degree of immune deficiency should be quantitated by laboratory procedures, whenever possible. The treatment of these patients may include substitution therapy, decontamination and antimicrobial chemotherapy. Since the immune deficiency can only rarely be specifically substituted, hygiene plans should be made up for every patient, including the selective decontamination. An intensive microbiological surveillance can give early information about the prevalence of certain microorganisms, thereby facilitating a subsequent treatment. The antimicrobial chemotherapy of an overt infection in medical and pediatric oncology can follow fixed schedules, taking into account the various causative agents that can be expected. This procedure has proven to be efficient in the treatment of infections occurring during the therapy of acute lymphoblastoid leukemia in childhood. In surgical intensive care units, however, treatment of infections should be based on microbiological findings in conjunction with the local profile of bacterial resistance. Furthermore, it is important to be aware that "non-pathogenic" microorganisms can be the cause of life-threatening infections in immunocompromised patients. Our experience shows that interdisciplinary cooperation and a mutual exchange of information is important for an efficient treatment of infections in patients with immunological deficiencies.

Animals↗
PubMed1985

Establishment and characterization of the pluripotent mouse teratocarcinoma cell line TCE.

Embryonal carcinoma cells, the stem cells of teratocarcinomas, are a convenient model system for the study of embryonic development and cell differentiation. We established the pluripotent teratocarcinoma cell line TCE from embryoid bodies of teratocarcinoma strain OTT6050. The feeder independent cell line was characterized with regard to karyotype, differentiation capacities, developmentally regulated gene products, such as alkaline and acid phosphatase, cell surface markers, and by intermediate filament proteins. These parameters are discussed with respect to the developmental potency of the cell line TCE.

Acid Phosphatase↗
PubMed1984

[Serum levels and urine excretion of L-carnitine in patients with normal and impaired kidney function].

The influence of age, sex, and renal function on serum levels and urinary excretion of free carnitine was studied in 187 subjects. Sixty-one subjects with normal renal function (creatinine clearance greater than 100 ml/min) showed a serum carnitine level of 72.2 +/- 23.2 mumol/l. The carnitine values of males (76.8 +/- 23.3 mumol/l, n = 39) were higher (p less than 0.05) than those of females (64.0 +/- 21.0 mumol/l, n = 22). Carnitine levels did not correlate with age. Values in patients with normal renal function did not differ from serum carnitine levels in healthy controls (74.7 +/- 17.5 mumol/l, n = 49). The mean urinary carnitine excretion per day was 163.5 mumol (range 63.7-419.6 mumol) in patients with intact renal function. Extreme impairment of glomerular filtration rate (creatinine clearance less than 20 ml/min) resulted in higher carnitine concentrations in serum (108.9 +/- 39.4 mumol/l, n = 18, p less than 0.05), lower carnitine elimination per day (78.5 mumol, range 14.5 - 424.3 mumol, n = 18, p less than 0.05) and a decreased carnitine clearance (0.8 ml/min, range 0.2 - 3.8 ml/min). These data together with earlier results obtained in dialysis patients suggest that carnitine metabolism in renal failure is altered by reduction of both endogenous carnitine biosynthesis and renal carnitine clearance.

Adolescent↗
PubMed1984

The basic structural lesion of persistent neonatal hypoglycaemia with hyperinsulinism: deficiency of pancreatic D cells or hyperactivity of B cells?

Pancreatic tissue obtained at subtotal pancreatectomy from 15 infants with persistent hypoglycaemia with hyperinsulinism, and autopsy specimens from 23 age-matched normoglycaemic controls, were studied with morphometric methods after immunocytochemical staining of the four main islet cell types (A, B, D and pancreatic polypeptide cells). In three cases, a focal lesion was detected by gross examination. Macroscopic or microscopic examination did not distinguish the 12 other cases from controls. As found previously, nesidioblastosis was not a specific feature of the pancreas in infantile hypoglycaemia, being observed in age-matched controls as well. In cases with hypoglycaemia the volume density of B cells was not significantly increased; that of the A cells was within normal range. The volume density of pancreatic polypeptide cells was markedly augmented and that of somatostatin cells was significantly decreased. The mean nuclear volume of the B cells was increased by 40% in cases with diffuse changes, but in cases with a focal lesion this increase was restricted to the abnormal area. This finding is of decisive importance for diagnosis and has therapeutic implications. The increase in B-cell nuclear size is thought to reflect an enhanced functional activity of these cells. On the other hand, the figures obtained for the volume density of B and D cells must be viewed with some reservation because degranulation may interfere with accurate detection of these cells.

Cell Count↗
PubMed1984

Injection of murine embryonal carcinoma cells and embryo-derived pluripotential cells into mouse blastocysts.

Two pluripotential mouse cell lines, the OTT 6050-derived cell line TCE and the embryo-derived stem cell line BLC-1, were injected into blastocysts to analyze their developmental potential. The contribution of TCE cells to the embryo was found to be limited and sporadic. There was no indication of a preferential colonization of extraembryonal membranes or developmentally related tissues in adult chimeras. BLC-1 cells failed to colonize the embryo. This indicates that a normal karyotype, pluripotency, and cell surface markers which are shared by cells of early embryos are not necessarily sufficient markers for their ability to participate in embryogenesis.

Animals↗
PubMed1984

[Nitrogen and mineral metabolism of growing lambs fed straw treated in different ways].

Lambs were fed diets containing 500 g straw, 50 g sucrose and 30 g minerals per day. The straw was untreated (A), wafered after addition of NaOH (B) or gassed with ammonia. Diets A and B, in addition contained urea, so that equal amounts of dietary N were offered. Digestibility of OM was increased by 12 units after addition of NaOH and by 8 units after gassing with NH3. As significantly more faecal N was excreted in animals fed diet C, it is concluded that N of NH3-treated straw is less available than of added urea. When NaOH-treated straw was fed, renal excretion of phosphorus was increased.

Ammonia↗
PubMed1983

[Plasma cell granuloma of the lung (inflammatory pseudotumor)].

Plasma cell granuloma of the lung is a rare, benign focal lesion of nonspecific inflammatory genesis with few symptoms and often discovered by chance during mass-radiography. Radiologically it is characterized by a usually well-circumscribed solitary round focus (70% of cases), as an infiltrate or as atelectasis if it grows endobronchially. The histological picture is polymorph with mature plasma cells, lymphocytes, vacuolized histiocytes, fibroblasts and other elements of the reticulo-endothelial system. It has been given many names, pseudotumour appearing in the older literature. In the differential diagnosis a peripheral lesion can be mistaken for benign tumour, specific granuloma or metastasis, the more central form for bronchial carcinoma. The condition was observed in six personal cases, operated on between 1967 and 1982.

Adolescent↗
PubMed1983

[Rapid method for indirect determination of total microbial count in perishable foods].

A method is presented for the determination in one hour of aerobic microorganisms (Total Plate Count) in food in the range between 10(4) and 10(7) bacteria per ml resp. g. This method was developed mainly for rapid microbial analysis of perishable foodstuffs. The method operates by polarographic measurement of oxygen consumption in a tight cell, filled with the liquid product to be evaluated. The correlations between microbial counts and oxygen consumption rates are shown for samples of pasteurized milk and semi-liquid egg.

Animals↗
PubMed1983

Investigations on the mutagenic activity of STS 557.

The progestin STS 557 was tested for mutagenic activity in the rec-type repair test with Proteus mirabilis, the Ames-test and the host-mediated assay with Salmonella typhimurium, the cytogenetic assays with ascites tumour and bone-marrow cells of mice and the dominant lethal test with male and female mice. All results obtained indicate the absence of a genotoxic activity of STS 557.

Animals↗
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↗
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↗