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Biomedical subjects

J W Allen

Publications and source records attributed to J W Allen.

At least 127 records · Page 7Linked to original sources
PubMed1991

The microbial flora of the respiratory tract in feedlot calves: associations between nasopharyngeal and bronchoalveolar lavage cultures.

The upper and lower respiratory tracts of 59 feedlot calves with clinical signs of naturally occurring respiratory disease (cases) and 60 comparison (control) animals were cultured before treatment, using nasopharyngeal swabs (NPS) and bronchoalveolar lavage (BAL). The most prevalent organisms were Pasteurella multocida and Mycoplasma bovis. Isolations of P. multocida from NPS and BAL fluid were found to be significantly associated with morbidity (p less than or equal to 0.05), but the frequency with which other organisms were isolated from the nasopharynx and lungs was similar in cases and controls. There was evidence of moderate agreement between NPS and BAL isolates at the individual calf level using the kappa statistic, (range of kappa values = 0.47-0.61) but the variability of the kappa statistics was large. Therefore, in an individual calf NPS cultures did not accurately predict BAL cultures. The NPS and BAL culture results were quite similar at the group level, however.

Animals↗
PubMed1991

Characterization of eugonic fermenters group EF-4 by polyacrylamide gel electrophoresis and protein immunoblot analysis.

Whole-cell lysates and proteinase K-extracted lipopolysaccharide (LPS) of 19 strains of the group eugonic fermenter-4 (EF-4) were analyzed by electrophoresis and protein immunoblotting. These strains were isolated from dog- and cat-bite abscesses in human beings, ferret and human gastric lesions, and cat-lung infections. These strains represent 2 biovar groupings; EF-4a biovars ferment glucose and possess arginine dihydrolase activity, whereas EF-4b biovars do not. Electrophoresis of whole-cell lysates could distinguish between these biovars groups. Electrophoresis of LPS extracts revealed that all strains of EF-4 possess smooth chemotypes. Two strains of EF-4a reacted weekly in protein immunoblots and revealed distinct LPS profiles. These studies suggests that subgroups of EF-4 biovars may exist.

Animals↗
PubMed1991

Stage-specific damage to synaptonemal complexes and metaphase chromosomes induced by X rays in male mouse germ cells.

Synaptonemal complexes reveal mutagen-induced effects in germ cell meiotic chromosomes. This study was aimed at characterizing relationships between damage to synaptonemal complexes and metaphase I chromosomes following radiation exposure at various stages of spermatogenesis. Male mice were irradiated with doses of 0, 2, or 4 Gy, and spermatocytes were harvested at times consistent with earlier exposures as spermatogonial stem cells, preleptotene cells (premeiotic DNA synthesis), or meiotic prophase cells. After stem-cell exposure, twice as many rearrangements were observed in synaptonemal complexes as in metaphase I chromosomes. Irradiation during premeiotic DNA synthesis resulted in dose-related increases in synaptonemal complex breakage and rearrangements (including novel forms) and in metaphase chromosomal aberrations. Following prophase exposure, various types and levels of damage to synaptonemal complexes and metaphase chromosomes were observed. Irradiation of zygotene cells led to high frequencies of chromosome multivalents in metaphase I without a correspondingly high level of damage in preceding prophase synaptonemal complexes. Thus irradiation of premeiotic and meiotic cells results in variable relationships between damage to synaptonemal complexes and metaphase chromosomes. Interpretations of these relationships are based upon what is known about both radiation clastogenesis and the structural/temporal relationships between synaptonemal complexes at prophase and chromosomes at metaphase I of meiosis.

Animals↗
PubMed1990

Percutaneous double balloon valvotomy for severe rheumatic mitral stenosis.

Percutaneous double balloon valvotomy for severe rheumatic mitral stenosis was successfully performed in 281 of 285 consecutive patients. The changes evoked were a decrease of the mean transvalvular gradient from 16 +/- 7 to 5 +/- 3 mm Hg, an increase in cardiac output from 3.8 +/- 1.0 liters/min to 5.4 +/- 1.5 liters/min and an increase in mitral valve area from 0.86 +/- 0.24 cm2 to 2.41 +/- 0.54 cm2. The mean pulmonary artery pressure decreased from 37 +/- 13 mm Hg to 27 +/- 12 mm Hg and the pulmonary vascular resistance decreased from 307 +/- 181 to 238 +/- 122 dynes/s/cm-5. Symptomatic improvement occurred in 272 of the 285 (95%) patients. There were 3 procedure-related deaths (1%). Postdilatation mitral regurgitation was not significant in most patients. Therefore, this procedure can be performed at a low risk with effective results and a fast recovery.

Adult↗
PubMed1990

Further evidence that dichloromethane does not induce chromosome damage.

Dichloromethane (DCM) is a widely used industrial solvent that has been determined to be a carcinogen in rats and mice. In vitro and in vivo analyses of chromosome damage induced by this agent have provided conflicting results. In order to further investigate the clastogenic potential of DCM in vivo, we analyzed sister chromatid exchanges (SCEs) and chromosome aberrations (CAs) in mouse bone marrow cells following intraperitoneal exposures of 100-2000 mg kg-1 DCM. Dichloromethane failed to increase the frequencies of either SCEs or CAs.

Animals↗
PubMed1990

Genotoxicity of inhibitors of DNA topoisomerases I (camptothecin) and II (m-AMSA) in vivo and in vitro.

The present study was designed to determine and compare the clastogenicity of m-AMSA and camptothecin (CAMP) in vivo in mouse bone marrow and peripheral blood lymphocytes (PBLs), and in vitro in mouse lymphoma L5178Y cells. m-AMSA interferes with topoisomerase II to induce double-strand DNA breaks. CAMP interferes with topoisomerase I to induce single-strand DNA breaks. Thus, we expected the two drugs to induce different types of chromosomal aberrations (CAs). However, both drugs produced quantitatively and qualitatively similar numbers and types of aberrations under similar experimental conditions. In mouse bone marrow exposed over and 18-h period, both drugs (3 mg/kg) induced approximately 30 damaged cells, with an average of 0.4 chromatid breaks per cell (in 100 cells analyzed/mouse). In addition, both drugs induced only chromatid-type aberrations in mouse bone marrow in vivo when exposure occurred during G2. Cell cycle specificity was indicated by the absence of CAs when exposure to the drugs occurred in vivo in mouse PBLs during G0. In L5178Y cells, m-AMSA was considerably more potent for the induction of mutations and somewhat more potent for the induction of CAs than CAMP was. In contrast to the in vivo bone marrow results, the drugs induced high levels of both chromatid- and chromosome-type aberrations in vitro. The ultimate types of chromosomal damage induced by m-AMSA and CAMP result from a complex interaction of (i) cell cycle specific variations in topoisomerase enzyme levels, (ii) the abilities of these drugs to interfere with the orderly DNA breakage/reunion associated with topoisomerase activity, and (iii) the processing of the damage resulting from these interactions.

Amsacrine↗
PubMed1990

Bleomycin effects on mouse meiotic chromosomes.

The effects of a radiomimetic chemical, bleomycin (BLM), on meiotic chromosomes was evaluated in mice treated by intraperitoneal (i.p.) or intratesticular (i.t.) injection. Chromosome aberrations were analyzed at meiotic metaphase I, and damage to the synaptonemal complex (SC) was analyzed in meiotic prophase cells. In the metaphase aberration studies, an i.p. injection of 80 mg/kg BLM, timed to precede or coincide with pre-meiotic S phase, led to a significant increase in structural damage (P less than 0.01) in cells reaching metaphase I 12 days after treatment. However, no increases in clastogenic effects were observed at metaphase I after treatment of cells during various stages of prophase. SC analyses in pachytene cells following an i.p. or i.t. injection at S phase revealed various forms of synaptic errors and structural anomalies, including qualitative changes similar to those observed following irradiation. I.p. doses ranging from 25 to 100 mg/kg, and i.t. doses as low as 0.5 mg/kg, caused roughly 6-fold increases over control levels in the number of damaged cells. SC analyses in pachytene cells following BLM treatments 2 days earlier (at leptotene-zygotene) or 16 h earlier (at early-mid pachytene), also revealed induced structural and synaptic anomalies. Following the treatment at early-mid pachytene, there was some suggestion of interference with chiasma formation as evidenced by univalent-like configurations detected at diakinesis-metaphase. It was concluded that BLM is clastogenic for meiotic chromosomes; however, it does not reveal the strong S-independent clastogenic activity at meiosis that is characteristic of its activity at meiosis. SC analysis indicated that some damage is induced at meiotic prophase, although structurally aberrant cells are not recoverable at meiotic metaphase I. The results call forth various possible explanations for germ-line specific responses to BLM clastogenic activity.

Animals↗
PubMed1990

Micronuclei in epithelial cells from sputum of uranium workers.

The cytogenetic effects of exposure to radon progeny and cigarette smoke were assessed with the exfoliated-cell micronucleus assay among 99 uranium workers. Cells with micronuclei were determined in one sputum specimen from each worker. Exposure to radon progeny and smoking habits were classified from interview data collected at the same time as the sputum specimens. Underground miners were considered exposed to radon progeny, and the other workers were considered unexposed. Neither radon progeny exposure nor cigarette smoking had any appreciable effect on the prevalence of cells with micronuclei; the crude prevalence ratios for the two groups were 1.0 (95% confidence interval 0.7-1.4) and 0.9 (95% confidence interval 0.6-1.3), respectively. The effects of radon and smoking were not confounded by each other or by age, nor were they synergistic. These findings cast doubt on the use of sputum-based micronucleus assay in epidemiologic studies of other populations exposed to occupational or environmental lung carcinogens.

DNA Damage↗
PubMed1989

Effects of atenolol on left ventricular hypertrophy and early left ventricular function in essential hypertension.

Echocardiographic studies of left ventricular (LV) hypertrophy indicate clinical benefits of antihypertensive therapy. Therefore, M-mode and Doppler techniques were used to assess changes in LV hypertrophy after 10, 30 and 50 weeks of atenolol therapy (50 or 100 mg once daily) in 19 patients with essential hypertension. After 50 weeks of atenolol treatment, the most notable changes were: for M-mode parameters, increases (p less than 0.05) in diastolic LV internal dimension, radius to thickness ratio and stroke volume, and decreases (p less than 0.01) in total wall thickness and heart rate; for Doppler parameters, increases (p less than 0.01) in slope and peripheral resistance, and decreases (p less than 0.01) in heart rate, stroke volume and cardiac output. The decreased total wall thickness and increased radius to thickness ratio suggest a trend toward regression of LV hypertrophy. These findings, along with improvements in blood pressure, pulse and exercise stress tests, indicate potential benefits of atenolol in managing patients with essential hypertension and LV hypertrophy.

Adult↗
PubMed1989

Micronuclei in binucleated lymphocytes of mice following exposure to gamma radiation.

Experiments were designed to investigate the induction of micronuclei (MN) in mouse peripheral blood lymphocytes (PBLs) after in vitro or in vivo exposure to 60Co gamma radiation. For the in vitro experiments, 4 ml of blood from male C57BL/6J mice were either irradiated in 6 ml Falcon culture tubes as whole blood or isolated to obtain mononuclear leukocytes (MNLs) that were pelleted by centrifugation and then irradiated in RPMI 1640. For the in vivo analysis, mice received whole body irradiation, blood was obtained by cardiac puncture, and the MNLs were isolated for each mouse. Exposures were at a rate of 0.82 to 0.90 Gy/min to yield doses of 0.5, 1, 2, 3, or 4 Gy. MNLs were cultured using cytochalasin B for MN analysis in binucleated PBLs. There was a significant dose-dependent increase in MN observed at all doses. Dose-response curves for the in vivo and in vitro whole blood experiment were not significantly different. However, for isolated pelleted MNLs irradiated in vitro, the MN frequency at 4 Gy was less than one-half that seen in the in vivo experiment. The large difference in MN response is thought to be due to the radioprotective effect of hypoxia.

Animals↗
PubMed1989

The effects of acrylamide on mouse germ-line and somatic cell chromosomes.

The industrial chemical acrylamide is suspected to induce potentially heritable genetic damage. While several studies in rodents have indicated that this substance can damage spermiogenic cells, resulting in dominant lethals and heritable translocations, cytogenetic assessments of premeiotic and meiotic cells after exposure have produced equivocal results. In the present study, various cytogenetic endpoints in both somatic and germ-line cells from acrylamide-treated mice were evaluated. Sister chromatid exchanges and micronuclei, but not chromosome aberrations, were induced in spleen cells; synaptonemal complex irregularities (asynapsis), but not chromosome aberrations, were induced in germ cells.

Acrylamide↗
PubMed1989

Evidence for chromosomal replicons as units of sister chromatid exchanges.

Chromosomal replicons have been described as the cytological counterpart of DNA replicon clusters and have previously been studied in vitro using premature chromosome condensation-sister chromatid differentiation (PCC-SCD) techniques. Chromosomal replicons are visualized as small SCD segments in S-phase cells, and measurement of these segments can provide estimates of relative chromosomal replicon size corresponding to DNA replicon clusters functioning coordinately in S-phase. Current hypotheses of sister chromatid exchange (SCE) formation postulate that sites of SCE induction are associated with active replicons or replicon clusters. We have applied the PCC-SCD technique to in vivo studies of mouse bone marrow cells that have been treated with cyclophosphamide (CP) for two cell cycles. We have been able to visualize chromosomal replicons, as well as SCEs which have been induced in vivo by CP treatment, simultaneously in the same cells. Chromosomal replicons visualized as small SCD segments were measured in PCC cells classified at early or late S-phase based on SCD segment size prevalence. Early S-phase (E/S) PCC cells contained 90% of the SCD segments measured clustered in a segment size range of 0.1 to 0.8 micron with a peak value around 0.3 to 0.6 micron regardless of CP treatment. As the cells progressed through S-phase, late S-phase (L/S) PCC cells were characterized by the appearance of larger SCD segments and even whole SCD chromosomes in addition to small SCD segments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Mutagenic screening of marker grenade dyes by the Salmonella reversion assay, L5178Y/TK+/- mouse lymphoma assay, and in vivo sister chromatid exchange analysis in mice.

Two dyes (C.I. Solvent Yellow No. 33 and a mixture of C.I. Solvent Yellow No. 33 and C.I. Solvent Green No. 3) were tested for mutagenicity in the Salmonella reversion assay and the L5178Y/TK+/- mouse lymphoma assay, and also for sister chromatid exchange (SCE) induction in vivo in C57B1/6J mice. In addition, a greater than 99.9% pure sample of the yellow dye [2-(2'-quinolyl)-1,3-indandione] was tested with and without exogenous activation in the Salmonella reversion assay and the L5178Y/TK+/- mouse lymphoma assay. Neither C.I. Solvent Yellow No. 33 nor the C.I. Solvent Yellow No. 33 and Solvent Green No. 3 mixture was positive for inducing SCEs in vivo. All three dyes were tested in the standard plate incorporation test in seven Salmonella strains TA98, TA100, TA102, TA104, TA1535, TA1537, and TA1538. The dyes were negative with and without exogenous activation in TA98, TA1535, and TA1538. One test with TA1537 was positive with the greater than 99.9% purified yellow dye. All three dyes gave weakly positive results (less than a twofold increase) with S-9 in TA100 and were clearly positive in TA102 and TA104 both with and without S-9. They also induced mutation at the thymidine kinase locus in mouse lymphoma cells, produced both large- and small-colony trifluorothymidine-resistant mutants, and were clastogenic. The purified yellow dye was further tested for SCE induction in mouse lymphoma cells and was determined to give a slightly positive response in the presence of S-9.

Animals↗
PubMed1988

Synaptonemal complex damage as a measure of genotoxicity at meiosis.

Synaptonemal complex aberrations can provide a sensitive measure of chemical-specific alterations to meiotic chromosomes. Mitomycin C, cyclophosphamide, amsacrine, ellipticine, colchicine, vinblastine sulfate, and cis-platin exposures in mice have been shown to cause various patterns of synaptonemal complex structural damage and synaptic irregularity. These effects are suggestive of abnormal homologue pairing/synapsis/recombination effects which, theoretically, could be implicated in mechanisms leading to aneuploidy and other potentially heritable chromosomal disorders.

Alkaloids↗
PubMed1988

Synaptonemal complex damage induced by clastogenic and anti-mitotic chemicals: implications for non-disjunction and aneuploidy.

Mice were treated with mitomycin C, cyclophosphamide, amsacrine, colchicine, or vinblastine sulfate, and meiotic prophase cells analyzed for synaptonemal complex (SC) damage. All test agents caused synaptonemal complex breakage and synapsis irregularities, although propensities for inducing specific types of damage at S-phase or prophase stages varied among the chemicals. The data indicate that SC analysis can reveal chemical-specific alterations to meiotic homologue pairing/synapsis which have not generally been recognized, and which theoretically may be implicated in non-disjunction.

Aneuploidy↗
PubMed1988

Synaptonemal complex damage in relation to meiotic chromosome aberrations after exposure of male mice to cyclophosphamide.

The genetic implications of induced synaptonemal complex (SC) damage are not known. However, on theoretical grounds, such aberrations could be involved in mechanisms leading to potentially heritable defects. Cyclophosphamide (CP), a chemical reported to cause structural and numerical chromosomal aberrations in the mouse, was used to determine if SC damage observed in meiotic prophase is related to subsequent metaphase chromosomal aberrations. Male mice were injected i.p. with CP. In some instances, mice were also injected simultaneously with tritiated thymidine to label DNA so that cells could be tracked autoradiographically through spermatogenesis. Prophase, primary metaphase (M1), and secondary metaphase (M2) samples were sequentially harvested at appropriate times from the same individual, and nuclei were examined for aberrations. Correlation coefficients between SC and metaphase chromosome aberrations were calculated. The inclusion of tritium labeling increased the number and significance of positive correlations. Positive correlations were found between (1) dose-dependent total SC damage and damage to M1, and to a lesser extent, M2 chromosomes; (2) SC breaks/fragments and M1 chains/rings as well as isochromatid breaks/fragments; (3) SC asynapsis and M1 chromatid breaks/fragments; (4) SC multi-axial configurations and M1 chains/rings as well as isochromatid and chromatid breaks/fragments; and (5) SC multi-axial configurations and M2 hyperploidy. These correlations do not define mechanistic or causal relationships between SC and chromosomal damage. However, taken together with the observation that induced SC damage is many times greater than ensuing metaphase chromosome damage, they substantiate SC analysis as a highly sensitive indicator of potentially heritable effects of this (and presumably other) genotoxic agents.

Aneuploidy↗