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Biomedical subjects

L M Brown

Publications and source records attributed to L M Brown.

At least 73 records · Page 4Linked to original sources
PubMed1995

Pentobarbital differentially inhibits N-methyl-D-aspartate and kainate-stimulated [3H]noradrenaline overflow in rat cortical slices.

1. This study examined the ability of pentobarbital to inhibit NMDA and kainate-stimulated [3H]noradrenaline ([3H]NA) overflow in rat brain cortical slices. 2. Pentobarbital inhibited NMDA-evoked [3H]NA overflow at 100 microM and greater and inhibited kainate-evoked [3H]NA overflow at 10 microM and greater. 3. The ability of pentobarbital to inhibit concentration-response curves for NMDA and kainate-evoked overflow of [3H]NA were also examined. Pentobarbital (300 microM) caused a 20% reduction in NMDA and a 50% reduction in kainate-induced maximal responses.

Adrenergic alpha-Agonists↗
PubMed1995

Coping strategies of caregivers of family members with dementia.

Data derived from a national sample of 89 caregivers of non-institutionalized family members with dementia were examined in order to identify the specific coping strategies caregivers utilized and whether the identified strategies were associated with negative or positive outcomes. Results from this study indicated that caregivers predominantly used problem-focused strategies. Further analysis demonstrated that employing more positive coping strategies did not necessarily result in a reduced sense of burden.

Adaptation, Psychological↗
PubMed1994

Cigarette smoking and pancreas cancer: a case-control study based on direct interviews.

BACKGROUND: Cigarette smoking is the most consistently reported risk factor for pancreas cancer, yet the dose-response relationship in many pancreas cancer studies is weak. Because of the poor prognosis for pancreas cancer, many case-control studies have been based largely on interviews with proxy respondents, who are known to report less reliable information on detailed smoking habits than original subjects. PURPOSE: Our purpose was to evaluate cigarette smoking as a risk factor for pancreas cancer based on data obtained only from direct interviews and to estimate the effects of quitting smoking and of switching from nonfiltered to filtered cigarettes on risk. Our objective also was to estimate the contribution of cigarette smoking toward explaining the higher pancreas cancer incidence experienced by black Americans compared with white Americans. METHODS: A population-based, case-control study of pancreas cancer was conducted during 1986-1989 in Atlanta, Ga., Detroit, Mich., and 10 counties in New Jersey. Direct interviews were successfully completed with 526 case patients and 2153 control subjects aged 30-79 years, making this the largest population-based, case-control study of pancreas cancer to date based only on direct interviews. RESULTS: Cigarette smokers had a significant, 70% increased risk of pancreas cancer compared with the risk in nonsmokers. A significant, positive trend in risk with increasing duration smoked was apparent (P < .0001), with long-term (> or = 40 years) smokers experiencing a modest 2.1-fold risk. We also observed a negative trend in risk with increasing years quit smoking. Smokers who quit for more than 10 years experienced about a 30% reduction in risk relative to current smokers; quitters of 10 years or less experienced no risk reduction. Switching from nonfiltered to filtered cigarettes did not appear to decrease risk. Compared with nonsmokers, subjects who smoked only filtered cigarettes had a 50% elevated risk and those who smoked only nonfiltered cigarettes had a 40% elevated risk. The proportion of pancreas cancer attributable to cigarette smoking was 29% in blacks and 26% in whites. CONCLUSIONS: The relationship between cigarette smoking and pancreas cancer risk is likely to be causal, despite the weakness of the dose-response data. Long-term smoking cessation clearly reduces risk, whereas switching from nonfiltered to filtered cigarettes may not be beneficial. Cigarette smoking appears to explain little of the excess pancreas cancer risk experienced by blacks. IMPLICATIONS: Elimination of cigarette smoking would eventually prevent approximately 27% of pancreas cancer, saving 6750 lives in the United States annually.

Adult↗
PubMed1994

Are racial differences in squamous cell esophageal cancer explained by alcohol and tobacco use?

BACKGROUND: In the United States, incidence rates of squamous cell esophageal cancer are more than five times higher among black men than among white men. Reasons that might explain this large racial disparity are being sought. PURPOSE: We evaluated whether differential use of alcohol and tobacco can fully account for the excess of squamous cell esophageal cancer among U.S. blacks. METHODS: We conducted a population-based, case-control study with in-person interviews with 373 squamous cell esophageal cancer case patients (124 white males and 249 black males) and 1364 control subjects (750 white males and 614 black males) from three U.S. geographic areas. Histologically confirmed cases of squamous cell esophageal cancer newly diagnosed from August 1, 1986, through April 30, 1989, among white and black men aged 30-79 years were included. RESULTS: Alcohol use of more than one drink per day and/or current cigarette use of at least one pack per day accounted for 92.7% (95% confidence interval [CI] = 86.8%-98.5%) of the squamous cell esophageal cancers in blacks, versus 86.3% (95% CI = 75.5%-97.1%) in whites, and for 94% of the difference between the black and white annual incidence rates. The interaction between race and the continuous drinking/smoking variable in a logistic regression analysis was statistically significant (two-sided, P = .02). Exposure rates among controls at all levels of combined alcohol and tobacco use examined were slightly higher among blacks and accounted for a small portion of the racial differences in incidence rates. CONCLUSION: Although the vast majority of esophageal cancers in both blacks and whites in our data can be explained by use of alcohol and tobacco, it is not clear why heavy consumption of alcohol and/or tobacco is responsible for 14.9 per 100,000 per year more cases of squamous cell esophageal cancer among blacks than among whites. The differences in the odds ratios appear to account for more of the racial differences in incidence rates than do the prevalences of exposure to alcohol and tobacco alone. The reasons for this apparent racial difference in carcinogenic risk from the same level of alcohol and tobacco use are unknown, but they may include qualitative differences in alcohol consumption, differences in other environmental exposures that interact with alcohol and/or tobacco to modify risks, or differences in susceptibility to these factors.

Adult↗
PubMed1994

Antiepileptics inhibit cortical N-methyl-D-aspartate-evoked [3H]norepinephrine efflux.

The antiepileptic drugs phenytoin, valproic acid and phenobarbital were examined for their ability to inhibit N-methyl-D-aspartate (NMDA)-stimulated [3H]norepinephrine efflux from rat brain cortical slices. All three drugs inhibited efflux at varying concentrations. Valproic acid was the most potent and inhibited efflux at 0.01 mg/ml. Phenytoin and phenobarbital inhibited efflux at 0.1 mg/ml. These results indicate that some antiepileptic drugs are capable of inhibiting NMDA receptor function in the therapeutic range.

Animals↗
PubMed1994

Racial variation in serum-soluble interleukin-2 receptor levels: a population-based study of healthy smokers and nonsmokers.

To investigate the influence of race and cigarette smoking on serum levels of soluble interleukin-2 receptors (sIL-2R), we studied a population-based cohort of 282 white and 173 black adults, ages 20-69 years. Serum sIL-2R concentrations in this healthy population ranged from 146 to 2623 U/ml. Whites had significantly higher sIL-2R levels than blacks (455 versus 365 U/ml; P < 0.001), and cigarette smokers had significantly higher levels than nonsmokers (508 versus 420 U/ml; P = 0.01). White smokers had the highest levels (550 U/ml); white nonsmokers and black smokers had intermediate levels (455 and 450 U/ml, respectively); and black nonsmokers had the lowest levels (365 U/ml). Smoking cessation appeared to normalize sIL-2R levels; exsmokers who had not smoked for at least 2 years had sIL-2R levels similar to those of never smokers. These data demonstrate the wide range of serum sIL-2R concentrations found in normal healthy adults and the significant influence of race and cigarette smoking. Further investigation of this natural heterogeneity may provide insights into the mechanisms underlying genetic and environmental influences on this important immunologic parameter.

Adult↗
PubMed1994

Factors influencing serum neopterin and beta 2-microglobulin levels in a healthy diverse population.

Sera and questionnaire data from a population-based random sample of healthy adults was used to evaluate factors influencing neopterin and beta 2-microglobulin (beta 2m) values. Both neopterin and beta 2m levels increased with age and were higher among white than blacks (mean values for whites and blacks: neopterin, 5.06 vs 4.49 nmol/L; beta 2m, 1.36 vs 1.28 mg/L). Gender differences were noted for beta 2m but not neopterin values (beta 2m males vs females: 1.37 vs 1.29 mg/L). Neopterin values were lower among current smokers than among nonsmokers (4.32 vs 5.16 nmol/L) and were higher among users of antihistamines (5.46 among users vs 4.65 nmol/L among nonusers). Neopterin and beta 2m were correlated in this healthy adult population (adjusted r = 0.53, P = 0.001), yet no other interrelationships with numerous biologic markers except between beta 2m and serum-soluble interleukin-2 receptor levels (adjusted r = .41, P = 0.05) were observed. These findings provide important baseline information to consider before planning or evaluating studies utilizing neopterin or beta 2m levels.

Adult↗
PubMed1994

Adenocarcinoma of the esophagus and esophagogastric junction in white men in the United States: alcohol, tobacco, and socioeconomic factors.

In the United States, the incidence of adenocarcinoma of the esophagus, including the esophagogastric (EG) junction, has been increasing rapidly over the past two decades. Except for an association with Barrett's esophagus, little is known about the etiology of these cancers. A population-based case-control interview study of 174 White men with adenocarcinoma of the esophagus and 750 controls living in three areas of the United States offered the opportunity to investigate the relationship of these cancers with smoking, alcohol drinking, socioeconomic factors, and history of ulcer. There were significantly elevated risks for men who smoked cigarettes (odds ratio [OR] = 2.1) or drank liquor (OR = 1.6). For both cigarette smoking and liquor drinking, there were significant dose gradients with amount consumed. No reduction in risk was observed following smoking cessation. Subjects who switched from nonfilter to filter cigarettes experienced half the risk of those who only smoked nonfilter cigarettes. Inverse risk gradients were seen with increasing recent annual income, with the highest risk (OR = 3.4) for the lowest category. The risk for a history of ulcer (OR = 1.7), especially of the duodenum (OR = 2.2), was also significantly elevated. These data suggest that tobacco and alcohol may be etiologic factors for adenocarcinoma of the esophagus and EG junction, but these factors do not appear to explain the rapid rise in incidence of these tumors. The associations with low social class and history of ulcer need to be explored in greater detail along with other factors that may account for the temporal trends in esophageal adenocarcinomas.

Adenocarcinoma↗
PubMed1994

Tobacco use and prostate cancer in blacks and whites in the United States.

Prostate cancer occurs more frequently in Blacks than Whites in the United States. A population-based case-control study which investigated the association between tobacco use and prostate cancer risk was carried out among 981 pathologically confirmed cases (479 Blacks, 502 Whites) of prostate cancer, diagnosed between 1 August 1986 and 30 April 1989, and 1,315 controls (594 Blacks, 721 Whites). Study subjects, aged 40 to 79 years, resided in Atlanta (GA), Detroit (MI), and 10 counties in New Jersey, geographic areas covered by three, population-based, cancer registries. No excesses in risk for prostate cancer were seen for former cigarette smokers, in Blacks (odds ratio [OR] = 1.1, 95 percent confidence interval [CI] = 0.7-1.5) and in Whites (OR = 1.2, CI = 0.9-1.6), or for current cigarette smokers, in Blacks (OR = 1.0, CI = 0.7-1.4) and in Whites (OR = 1.2, CI = 0.8-1.7). Increases in risk were noted for smokers of 40 or more cigarettes per day, among former (OR = 1.4, CI = 1.0-1.5) and current (OR = 1.5, CI = 1.0-2.4) smokers. Duration of cigarette use and cumulative amount of cigarette use (pack-years) were not associated with prostate cancer risk for Blacks or Whites. By age, only the youngest subjects, aged 40 to 59 years, showed excess risk associated with current (OR = 1.5, CI = 1.0-2.3) and former (OR = 1.7, CI = 1.1-2.6) use of cigarettes, but there were no consistent patterns in this group according to amount or duration of smoking.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Multiple myeloma among blacks and whites in the United States: the role of chronic antigenic stimulation.

Multiple myeloma (MM) is twice as common among Blacks than Whites in the United States. The reasons for this racial disparity are unknown, and the etiology of this cancer, in general, is poorly understood. Repeated or chronic antigenic stimulation (CAS) of the immune system has been suggested as a risk factor. Previous case-control studies have reported inconsistent CAS associations based on evaluations of individual and biologic categories of medical conditions. Interview data from 573 cases and 2,131 population-based controls were used to investigate further the CAS hypothesis using an immunologically based approach, and to determine whether CAS accounts for the excess of myeloma among Blacks. Over 50 medical conditions were grouped into biologically and immunologically related categories, and B-cell- and T-cell-mediated response groups. Except for urinary tract infections among Black men (odds ratio [OR] = 2.0), no significantly increased risks of MM were observed. However, there was a suggestion of increased risk among Blacks with an increased exposure to anaphylactic conditions. Analysis by immunoglobulin type revealed significantly elevated risks of IgG myeloma with eczema (OR = 2.1), the biologic category 'allergic conditions' (OR = 1.6), and the immunologic category 'anaphylaxis response' (OR = 1.6) among Whites, with Blacks having slightly lower risks. Our findings do not support a causal relationship between CAS and MM, nor do they explain the higher incidence among Blacks.

Adult↗
PubMed1994

Sexually aggressive men's perceptions of women's communications: testing three explanations.

The authors tested three explanations of findings that sexually aggressive men perceive women's communications differently than less aggressive men. The first suggests that aggressors are incompetent in decoding women's negative emotions. The second posits that they fail to make subtle distinctions between women's friendliness and seductiveness and between assertiveness and hostility. The third explanation contends that sexual aggressors use a suspicious schema and therefore discount the veridicality of women's communications. These explanations were tested using videotaped scenarios in which a woman's responses to a man's advances were systematically varied. The data were most supportive of the suspicious schema explanation. These findings are integrated with other research on the characteristics of sexual aggressors and on the perceptions of aggressive children and of maritally violent men. Implications for interventions are also discussed.

Aggression↗
PubMed1994

Periodic expression of nuclear and mitochondrial DNA replication genes during the trypanosomatid cell cycle.

In trypanosomatids, DNA replication in the nucleus and in the single mitochondrion (or kinetoplast) initiates nearly simultaneously, suggesting that the DNA synthesis (S) phases of the nucleus and the mitochondrion are coordinately regulated. To investigate the basis for the temporal link between nuclear and mitochondrial DNA synthesis phases the expression of the genes encoding DNA ligase I, the 51 and 28 kDa subunits of replication protein A, dihydrofolate reductase and the mitochondrial type II topoisomerase were analyzed during the cell cycle progression of synchronous cultures of Crithidia fasciculata. These DNA replication genes were all expressed periodically, with peak mRNA levels occurring just prior to or at the peak of DNA synthesis in the synchronized cultures. A plasmid clone (pdN-1) in which TOP2, the gene encoding the mitochondrial topoisomerase, was disrupted by the insertion of a NEO drug-resistance cassette was found to express both a truncated TOP2 mRNA and a truncated topoisomerase polypeptide. The truncated mRNA was also expressed periodically coordinate with the expression of the endogenous TOP2 mRNA indicating that cis elements necessary for periodic expression are contained within cloned sequences. The expression of both TOP2 and nuclear DNA replication genes at the G1/S boundary suggests that regulated expression of these genes may play a role in coordinating nuclear and mitochondrial S phases in trypanosomatids.

Animals↗
PubMed1994

Transesophageal echocardiography: implications for the critical care nurse.

TEE is an exciting and useful diagnostic tool that is rapidly gaining widespread acceptance in both teaching centers and community hospitals. Because of the semi-invasive nature of the procedure, nursing expertise is essential to ensure patient safety and comfort during the TEE examination.

Critical Care↗
PubMed1993

Developmental alterations in N-methyl-D-aspartate stimulated [3H]norepinephrine release in rat brain cortex and hippocampus.

Developmental alterations in N-methyl-D-aspartate (NMDA)-stimulated[3H]norepinephrine release from rat brain cortical and hippocampal slices were studied. NMDA (10-1000 microM) resulted in a concentration-dependent increase in [3H]norepinephrine efflux; maximal responses (% released) in the cortex were: (1.53 +/- 0.12, 3.68 +/- 0.20, 2.94 +/- 0.20, 4.60 +/- 0.28 and 5.28 +/- 0.33) and the hippocampal responses were: (1.90 +/- 0.18, 3.84 +/- 0.23, 3.60 +/- 0.28, 5.16 +/- 0.38 and 5.81 +/- 0.45) at varying postnatal ages (1, 7, 14, 21 and 90 days) respectively. Cortical tissue from 7-day-old pups exhibited a transient increase in maximal efflux and a decrease in EC50. These results indicated that developmental alterations in the NMDA receptor appear to be translated into differences in NMDA stimulated [3H]norepinephrine release.

2-Amino-5-phosphonovalerate↗
PubMed1993

Microscopy in solid state science.

The Microstructural Physics group at the Cavendish Laboratory is actively involved in a considerable number of research projects which cover a broad range of materials science. In this paper, we describe briefly several such projects, with particular emphasis given to the application of parallel-detection electron energy loss spectroscopy (PEELS) on a scanning transmission electron microscope (STEM) to the analysis of materials such as stainless steels, catalysts, and high temperature superconductors. In addition, we describe a number of related projects that are currently being carried out in the group, particularly those which utilise and develop novel STEM imaging and analytical techniques.

Aerosols↗