Search PubMed⌕ Search

Biomedical subjects

B Kahan

Publications and source records attributed to B Kahan.

36 records · Page 2Linked to original sources
PubMed1985

A teratocarcinoma-derived endoderm stem cell line (1H5) that can differentiate into extra-embryonic endoderm cell types.

We investigated the ability of the teratocarcinoma-derived, epithelial-type cell line 1H5 to differentiate into either of the two pathways to primary endoderm, and tested the hypothesis that 1H5 represents a state similar to primitive endoderm in the late 4th-day blastocyst. Like other endodermal cell types, 1H5 cells mixed with embryonal-carcinoma cells sort out into "embryoid bodies" or structures that resemble 4th-day mouse embryos. The epithelial line conforms morphologically and biochemically to the few known characteristics typical of primitive endoderm. The present study demonstrates that the formation in vitro of overt visceral endoderm is readily achieved. The spontaneous arrangement of the cells into a cystic form is followed by the appearance of several markers of visceral endoderm, most notably alphafetoprotein, which is detected when 1H5 cells are cultured either in the presence of retinoic acid or when the cells interact with embryonal-carcinoma cells in a specific spatial arrangement after sorting out. However, some less specific properties of visceral endoderm are not expressed. Although 1H5 differentiates histologically into parietal-like endoderm in the tumor form, parietal cells cannot yet be identified with certainty in vitro because of the paucity of parietal-specific markers. The 1H5 cell line could provide a useful system for studying the characteristics and mechanisms underlying visceral-endoderm differentiation in vitro, since it has the distinct advantage that homogeneous cultures are produced, in contrast to other teratocarcinoma cell lines such as F9 which differentiate into a mixture of cell types.

Animals↗
PubMed1984

Azathioprine-associated interstitial pneumonitis.

Seven renal allograft recipients taking azathioprine (Imuran) for immunosuppression developed bilateral pulmonary infiltrates and a falling pO2 that did not respond to antibiotic therapy. Open lung biopsies revealed changes ranging from diffuse alveolar damage (DAD) to usual interstitial pneumonia (UIP) culminating in pulmonary fibrosis. There was no evidence of immune deposits, eosinophilia, vasculitis, granulomas, or microorganisms by cultures and appropriate stains. Following discontinuance of Imuran, the two cases with DAD revealed a significant clearing of the lung infiltrates, whereas four of five patients with UIP died while suffering from respirator-dependent ARDS. Biopsies showing hyaline membranes, intraalveolar edema and cuboidalization of alveolar epithelium were associated with total doses from 2,850 to 4,355 mg, whereas atypical epithelial hyperplasia, reorganization of distal air spaces, and fibrosis were noted in cases receiving from 5,600 to 28,625 mg of azathioprine. Ultrastructural changes were indistinguishable from those induced by other drugs causing pulmonary toxicity. In three cases atypical epithelial cells were detected cytologically in brushing specimens and appeared identical to those noted in the lung biopsies. Our findings are consistent with the view that azathioprine should be added to the list of agents capable of causing direct, dose-dependent pulmonary toxicity. Accordingly, drug-associated diffuse interstitial pulmonary disease should enter the differential diagnosis of a lung infiltrate that develops in renal transplant patients receiving Imuran.

Adult↗
PubMed1982

Histocompatibility and isoenzyme differences in commercially supplied "BALB/c" mice.

BALB/c mice obtained commercially were found to differ significantly from the standard phenotype of BALB/c strain mice. Isoenzyme tests and H-2 haplotype analyses indicated that the majority of mice from two of the three sources tested appeared mixed, frequently heterozygous, and did not consistently express either the expected H-2 or glucose phosphate isomerase type.

Animals↗
PubMed1980

Autonomous gene expression on the human inactive X chromosome.

Local derepression of the hpt locus on the human inactive X chromosome obtained in human female fibroblast x mouse L cell somatic cell hybrids was not correlated with the presence or absence of any specific human chromosome in the hybrids. Loss of the human active X, in particular, did not result in observable derepression of genes on the inactive X. Introduction of an active X, via a second hybridization of human cells having an active X with hybrid cells containing a locally derepressed X chromosome, did not restore repression of the derepressed hpt allele. The rate of hpt locus derepression in hybrid cells was estimated to be 10(-6) per inactive X chromosome per cell generation.

Animals↗
PubMed1979

Ovarian localization by embryonal teratocarcinoma cells derived from female germ gells.

Embryonal carcinoma cells derived from several different spontaneous ovarian teratocarcinomas of strain LT mice form tumors that are located exclusively, in many cases, in the ovaries of female mice. Embryonal cells previously unselected for site specificity localize in the ovaries regardless of route of entry of the cells, and produce very few tumors in males following intraperitoneal injections. The ovary tumors have been verified as originating from the injected cells by chromosomal and drug resistance markers, as well as by general in vitro growth characteristics. Cell-cell adhesion studies suggest specificity at the level of tumor cell-ovary organ cell interaction.

Animals↗
PubMed1978

Radioimmunoassay for urinary albumin.

We describe a rapid, sensitive, and precise radioimmunoassay for urinary albumin (Ualb). Aliquots of diluted urine were incubated at room temperature for 1 h with 125I-labeled albumin and a rabbit antiserum monospecific for human albumin. Phase separation was effected by the double-antibody technique. The dose-response curve as linear in the range of 15.6-10000 ng, equivalent to 4 to 3000 mg/liter of urine. The limit of sensitivity was 16 ng of albumin. The coefficient of assay variation was 4.8%, both at 44 mg/liter and at 1304 mg/liter. A displacement curve obtained with a serially diluted urine sample of high albumin concentration was completely superimposable with the curve for which human albumin was used as a standard. In 26 normal individuals the range for Ualb was 2.2--12.6 mg/24h, and for albumin clearance (Calb, 1.8 x 10(-5)-19.6 x 10(-5) ml/min. After renal homografts in 25 patients, Ualb ranged from 16.9 to 9928 mg/24 h, and Calb from 2.7 x 10(-4) to 1.7 x 10(-1) ml/min. Both increased Ualb and Calb correlated well with the severity of renal homograft rejection.

Albuminuria↗
PubMed1975

Adenine phosphoribosyltransferase and hypoxanthine-guanine phosphoribosyltransferase immunoprecipitation reactions in human-mouse and human-hamster cell hybrids.

Male New Zealand White rabbits were immunized with human adenine phosphoribosyltransferase (APRT) and hypoxanthine-guanine phosphoribosyltransferase (HGPRT), which were purified about 2000-fold and 800-fold, respectively, from erythrocytes by DEAE-cellulose chromatography, ammonium sulfate precipitation and preparative polyacrylamide gel electrophoresis. Specific immunoprecipitations of APRT and HGPRT were achieved with the antisera that were obtained and by using polyethylene glycol as a substitute for goat anti-(rabbit) gamma globulin. The activities of the human forms of these enzymes, whether from red blood cells or from cultured cells, were almost completely eliminated under the conditions of immunoprecipitation used. Little or no reduction of APRT and HGPRT activities from mouse and Chinese hamster cells was observed. This discriminatory capacity of the antisera was successfully used for the identification of human APRT and HGPRT in human-mouse and human-hamster cell hybrids using the immunoprecipitation reaction.

Adenine Phosphoribosyltransferase↗
PubMed1975

Localized Derepression on the Human Inactive X Chromosone in Mouse-Human Cell Hybrids.

Evidence for derepression of the gene for hypoxanthine phosphoribosyltransferase (HPRT; IMP: pyrophosphate phosphoribosyltransferase, EC 2.4.2.8) on the human inactive X chromosome was obtained in hybrids of mouse and human cells. The mouse cells lacked HPRT and were also deficient in adenine phosphoribosyltransferase (APRT; AMP: pyrophosphate phosphoribosyltransferase; EC2.4.2.7). The human female fibroblasts were HPRT-deficient as a consequence of a mutation on the active X but contained a normal HPRT gene on the inactive X. The two human X chromosomes were further distinguished by differences in morphology: the inactive X was morphologically normal while the active X included most of the long arm of autosome no. 1 translocated to the distal end of the X long arm. Forty-one hybrid clones were first isolated by selection for the presence of APRT; when these clones were selected for HPRT, six of them yielded derivatives having human HPRT with incidences of about 1 in 10-6 APRT-selected hybrid cells. The HPRT-positive derivatives contained a normal-appearing X chromosome indistinguishable from the inactive X of the parental human fibroblasts. The active X with the translocation was not found in any of the HPRT-positive hybrid cells. Human phosphoglycerokinase (ATP:3-phospho-D-glycerate 1-phosphotransferase. EC 2.7.2.3) and glucose-6-phosphate dehydrogenase (D-glucose 6-phosphate: NADP 1-oxidoreductase, EC 1.1.1.49), which are specified by X-chromosomal loci, were not detected in the hybrids expressing HPRT even though they contained an apparently intact X chromosome. The observations are most simply explained by the infrequent, stable derepression of inactive X chromosome segments that include the HPRT locus but not the phosphoglycerokinase and glucose-6-phosphate dehydrogenase loci.

Adenine Phosphoribosyltransferase↗
PubMed1974

The locus for human adenine phosphoribosyltransferase on chromosome no. 16.

Evidence for assigning the locus determining the structure of adenine phosphoribosyltransferase (APRT) to human chromosome No. 16 is presented. Hybrids of APRT-deficient mouse cells and of human fibroblasts having normal APRT were isolated by fusing the parental cells with Sendai virus, blocking de novo purine nucleotide synthesis with azaserine and selecting for hybrids that could use exogenous adenine. The hybrid clones that were studied had only APRT activity that was indistinguishable from human APRT with regard to electrophoretic migration and reaction with antibodies against the partially purified human enzyme. No. 16 was the only human chromosome consistently present in all of the clones, and in one clone, it was the only human chromosome detected. Selection against hybrid cells with 2,6-diaminopurine (DAP) yielded DAP-resistant survivors that lacked chromosome No. 16. One hybrid that originally had an intact No. 16 yielded adenine-utilizing subclones that lacked No. 16 but had a new submetacentric chromosome. The distribution of centromere-associated heterochromatin and the fluorescence pattern indicated that this chromosome consisted of a mouse telocentric chromosome and the long arm of No. 16. Cells having the submetacentric chromosome had human APRT. Both the enzyme and the chromosome were absent in DAP-resistant derivatives. These results suggest that the structure of APRT is defined by a locus on the long arm of human chromosome No. 16.

Adenine↗
PubMedDate not supplied

Forces, moments, and accelerations acting on an unrestrained dummy during simulations of three wheelchair accidents.

To determine the magnitude and distribution of the forces, moments, and accelerations acting on an individual sitting in a wheelchair during three possible accidents occurring while negotiating a sidewalk curb, experimental trials were performed in a bioengineering laboratory using a 50th percentile Hybrid III dummy seated in a standard wheelchair. A ramp was designed with an adjustable incline to allow the wheelchair to reach the edge of a sidewalk height platform at the desired forward speed of 2.5 miles per hour (comfortable walking speed). The wheelchair velocity was monitored via an optical pickup. Three types of accidents were simulated: (1) a wheelchair hitting straight into a curb; (2) a wheelchair falling forward straight off a curb; (3) a wheelchair falling diagonally off a curb. Each experiment was repeated three times. Each run was photographed using high-speed cameras and videotaped from three perspectives: frontal, lateral, and overhead. The results were averaged and compared with published injury Assessment Values (IAV) and Head Injury Criteria (HIC). Of significance were the following results. In the straight into a curb experiments, the wheelchair remained upright and the dummy seated. Low magnitude forces (23-73 N), moments (1-12 Nm), and accelerations (0.2-1 G) were recorded at the neck and head. The HIC was low at 0.3. These results were of no clinical significance. In the straight off a curb experiments, properly attached footrests prevented the wheelchair from toppling over but did not prevent the dummy from falling off the wheelchair. Forces (187-4,176 N), moments (3-178 Nm), and accelerations (131-206 G) of great magnitude were recorded at the head and neck when the dummy fell off the wheelchair. These values were above IAV. The HIC was 960. In the diagonally off a curb experiments, both the wheelchair and the dummy fell sideways. High-magnitude forces (274-2,313 N), moments (4-110 Nm), and acceleration (140-236 G) were recorded in the head and neck regions. The HIC was 975. These values were close to IAV and may signify potential serious injuries.

Acceleration↗