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Biomedical subjects

A Becker

Publications and source records attributed to A Becker.

At least 433 records · Page 24Linked to original sources
PubMed1987

Evaluation of three dosage-prediction methods for initial in-hospital stabilization of warfarin therapy.

Three dosage-prediction methods for initial in-hospital stabilization of warfarin therapy were evaluated. Adult inpatients who had received warfarin sodium 10 mg daily for less than three days were eligible for the study. After receiving their third warfarin dose, patients were randomly assigned to have their warfarin dosages adjusted using one of three dosage-prediction methods: by analog computer (n = 31), linear regression (n = 22), or empiric dosing by the physician (n = 34). A prothrombin time (PT) ratio (patient PT divided by control PT) between 1.3 and 2.5 was considered to be in the therapeutic range. For patients who achieved a stable PT ratio (defined as a PT ratio between 1.3 and 2.5 that varied by less than 0.05 on two consecutive days or by less than 0.1 on three consecutive days without a dosage change) before discharge, the number of days (time to stabilization) from administration of the first warfarin dose to achievement of the warfarin dosage that produced a stable PT ratio (stabilization dosage) was compared. A total of 54 patients met the study criteria for a stable PT ratio before hospital discharge (analog computer, n = 20; linear regression, n = 15; empiric dosing, n = 19). The mean times to stabilization were 6.8 days in the analog-computer group, 7.3 days in the linear-regression group, and 8.4 days in the empiric-dosing group; these times were not significantly different. All 20 stabilized patients in the analog-computer group achieved a stable PT ratio by the fourth dosage prediction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1986

Inhibin and beta type transforming growth factor (TGF beta) have opposite modulating effects on the follicle stimulating hormone (FSH)-induced aromatase activity of cultured rat granulosa cells.

We have recently observed that attomolar concentration of exogenously added TGF beta, a molecule structurally related to inhibin, can stimulate the basal secretion of FSH in a pituitary cell culture. Inhibin purified from porcine follicular fluid antagonizes this activity of TGF beta. To understand further the homeostatic regulatory properties of inhibin and TGF beta we have investigated whether the aromatase activity of ovarian granulosa cells is also subject to intra-ovarian modulation by these peptides. Granulosa cells from immature hypophysectomized diethylstilbestrol-treated rats were cultured for 2 days with androstenedione (10(-7) M) as a substrate, oFSH (2 ng), and different amounts of TGF beta or inhibin. Basal estrogen secretion was negligible and remained unaffected by treatment with purified TGF beta or inhibin (10 ng/ml), whereas treatment with oFSH (2 ng/ml) produced a 100-fold increase in estrogen accumulation. The concurrent application of increasing concentrations (10 pg-10 ng/ml) of TGF beta produced dose-dependent increments in the FSH-stimulated accumulation of estrogen with a ED50 of 0.3 +/- 0.02 ng/ml. On the other hand, concurrent incubation of FSH with inhibin ranging from 10 pg to 10 ng/ml decreases the FSH-mediated estrogen secretion. TGF beta antagonizes the inhibition of inhibin on aromatase activity. These findings suggest that inhibin and TGF beta, two closely related molecules, play novel and opposite roles in modulating the follicular functions.

Androstenedione↗
PubMed1986

Type beta transforming growth factor (TGF-beta) is a potent stimulator of the basal secretion of follicle stimulating hormone (FSH) in a pituitary monolayer system.

In view of striking similarities between TGF-beta and inhibin, we investigated the possibility that TGF-beta might modulate pituitary hormone release in vitro. Long term incubations of beta transforming growth factor (TGF-beta) with rat anterior pituitary cells for 48 hr stimulates the basal secretion of FSH in a dose-dependent manner. The secretion of LH, TSH, GH, ACTH and PRL is not modified by TGF-beta. The minimal effective concentration of TGF-beta is 10 pg/ml (less than 500 attomolar) and is dose dependent over a range from 1 pg to 10 ng/ml. Treatment of cells with TGF-beta for short incubation times (4 hr) in assays similar to that used for hypophysial releasing factors is not effective, indicating that TGF-beta acts through a cellular mechanism distinct from that of LRF. Inhibin-A, recently characterized on the basis of its capacity to specifically inhibit the secretion of FSH in the 48 hr bioassay system inhibits the stimulatory effect of TGF-beta on FSH-release. Analyses of the dose response curves indicate that the interaction occurs in a typical non-competitive manner. The results suggest that a TGF-beta-like molecule, present in follicular fluid, may be responsible for the FSH-releasing activity ("anti-inhibin" activity) observed by us and others during the process of isolating inhibin from follicular fluids. They also suggest an important role for inhibin and the TGF-beta related molecules in modulating pituitary gonadotropin release.

Animals↗
PubMed1986

Antibiotic stability in an implantable pump.

We measured the stability of vancomycin, amikacin, netilmicin, tobramycin, gentamicin, clindamycin, and aztreonam in an implantable drug pump. Two pumps were filled with the antibiotic being tested and were incubated at 37 degrees for 3 weeks. Samples were taken daily. At 3 weeks the pumps were disassembled and examined microscopically for signs of deterioration. If the pumps were intact, bioassays were used to quantitate the biologic activity of each daily antibiotic sample. Vancomycin degraded the pump. Amikacin, netilmicin, tobramycin, gentamicin, clindamycin, and aztreonam had no effect on the pump and maintained their biologic activity over the 3-week period.

Amikacin↗
PubMed1986

The expression of the evolutionarily conserved GATA/GACA repeats in mouse tissues.

Simple repeated GATA and GACA sequences were initially identified in sex-specific snake satellite DNA. The organization of these sequences in the mouse genome is described in Schäfer et al. 1986. The expression of these simple repeats was studied here in several mouse tissues using a variety of different probes: oligonucleotides and "single-stranded" as well as nick-translated DNA. The transcription of discrete RNA species was found to be differentially regulated in several organs but sex differences in transcription were not observed. GATA- and GACA-containing cDNA clones were isolated and sequenced and a genomic clone was characterized with respect to the transcription of GATA flanking sequences. Functional aspects of GATCA simple DNA repeats are discussed in terms of internally repetitive, hydrophobic translation products.

Animals↗
PubMed1986

Change in antigen specificity of cytotoxic T lymphocytes is associated with the rearrangement and expression of a T-cell receptor beta-chain gene.

Cloned H-Y-specific murine cytotoxic T lymphocytes, which alter antigen specificity in vitro ("aging"), simultaneously exhibit changes in the T-cell antigen receptor beta-chain rearrangements and respective mRNAs expressed. beta-chain cDNA clones were isolated from a library prepared from mRNA of aged killer T cells. The sequence of the beta-chain variable region element (VAK) was found to be identical with germ-line DNA. Four bases at the beta-chain diversity-joining region (D beta--J beta) junction cannot be explained by known germ-line D beta and J beta elements. These results illustrate that in T-cell clones altered antigen specificity correlates with a switch in productive beta-chain rearrangements of the T-cell receptor. When tested for its expression under physiological conditions, significant levels of VAK mRNA were found in normal lymphocyte populations.

Amino Acid Sequence↗
PubMed1986

Cell surface glycoproteins of hepatocytes and hepatoma cells identified by monoclonal antibodies.

Eight hybridoma cell lines secreting monoclonal antibodies (MABs) directed to cell surface components of rat hepatocytes were isolated. The antigens of seven MABs were identified as glycosylated plasma membrane proteins. The presence of these glycoproteins on normal hepatocytes and hepatocellular carcinoma cells was analyzed. A semi-quantitative enzyme-linked immunosorbent assay revealed that only two MABs (Be 8.7, Ne 11.3) recognized proteins which were expressed not only in normal liver but also in chemically induced transplantable Morris hepatomas and hepatoma-derived cell lines. The expression of six antigens was found to be sensitive to transformation. The domain specificity of the MABs was determined by indirect immunofluorescence on sections of liver tissue containing neoplastic nodules. Three MABs (Be 8.4, Ne 11.1, Ne 11.3) specifically bound to the sinusoidal domain and two MABs (Be 9.2, De 13.4) to the bile canalicular domain. These five antigens were transformation-sensitive except for the glycoprotein recognized by the MAB Ne 11.3. Three MABs (Be 8.7, Be 9.1, De 13.2) also showed intracellular immunofluorescence. Two of the antigens (Be 9.1, De 13.2) were not present in hepatomas. The relative molar masses (Mr) of the glycoproteins were determined after protein immunoblotting and immunoprecipitation. Four MABs (Be 8.7, Be 9.1, Be 9.2, De 13.4) recognized antigens with a Mr of 110 000 but did not mutually cross-react. The antigen recognized by MAB De 13.4 was identified as the ectoenzyme dipeptidyl peptidase IV (EC 3.4.14.-).

Animals↗
PubMed1986

Identification of a transformation-sensitive 110-kDa plasma membrane glycoprotein of rat hepatocytes.

Monoclonal antibodies were used to define cell surface antigens which are present on rat hepatocytes but are absent from hepatoma cells. One monoclonal antibody, referred to as Be 9.2, recognizes a major component of purified rat liver plasma membranes with a Mr of 110 000. This antigen (gp110) was not found in the transplantable Morris hepatoma 9121 and 7777 nor on two cultured hepatoma cell lines. Isoelectric focussing showed that gp110 is a very acidic membrane component with an isoelectric point of 3.6 to 3.8. Treatment with neuraminidase reduced the Mr to 95 000. Gp110 while bound to the membrane was resistant to trypsin, but sensitive to papain. The tissue distribution of gp110 was examined by indirect immunofluorescence in frozen sections. The antigen was found on the bile canalicular domain of hepatocytes, the microvillous zone of enterocytes of the small intestinal villi, the luminal plasma membrane of acinar cells in the submaxillary and extraorbital gland and of epithelial cells of the vesicular gland. Gp110 could not be detected in the stomach, pancreas, large intestine, kidney, thymus, spleen, heart, lung, muscle cells and fibers and in the brain. Identical results were obtained by the use of an antiserum raised against purified gp110. They confirm the transformation-sensitive character of this glycoprotein. A possible identity with dipeptidyl peptidase IV and aminopeptidase M, which have similar molecular weights and are also present in rat liver on the bile canalicular domains, could be excluded. The results suggest that the loss of gp110 might be regarded as a marker for transformation or dedifferentiation of hepatocytes.

Animals↗
PubMed1985

Diachronic variation in cranial thickness of Near Eastern populations.

Cephalometric radiographs were taken of 111 skulls of skeletal remains of populations living in Israel and Jordan during the last 12,000 years. From these radiographs, skull length and height, and cranial thickness were measured. For each sex and period, high correlations were found between cranial thickness at vertex, bregma, and lambda. Cranial thickness at nasion was correlated with sinus width but not sinus height. All measurements were correlated with skull length but not skull breadth. Using multivariate analysis, no significant differences in cranial thickness were found between the sexes. Significant diachronic trends were found in lambda and sinus width, and they were independent of variation in skull length.

Adolescent↗
PubMed1985

Coronary atherosclerosis revisited. A pathologist's view.

For many years the paradigm of coronary atherosclerosis, set by pathologists, was the far-advanced lesion containing extensive atheromatosis with calcifications. From the point of view of understanding atherogenesis, however, it is much more rewarding to study the coronary artery in patients without clinical evidence of obstructive coronary artery disease. In fact, the normal coronary artery is most revealing in showing discrete intimal changes, which consist of a splitting of the internal elastic lamina accompanied by a proliferation of vascular smooth muscle cells. This process eventually results in the formation of the musculo-elastic layer. In time the cellular and muscular appearance of this layer gradually transforms into a more densely packed fibrous texture. It is of interest, from a point of view of atherogenesis, that the early atherosclerotic lesions often display the histologic features of the musculo-elastic layer at the base of the plaque. Hence, these observations support the concept that the basic lesion in coronary atherosclerosis is a proliferation of vascular smooth muscle cells, most likely as a response to injury. To this extent a dysfunction of the endothelial cell barrier may by crucial. The observations also indicate that the mechanisms involved in atherogenesis also may alter vascular tone and hence, may contribute to a "spastic state" of the coronary arteries. A classification of angina pectoris, on the basis of pathogenesis into organic and spastic may thus prove to be simplistic.

Coronary Disease↗