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Biomedical subjects

G C Davis

Publications and source records attributed to G C Davis.

At least 19 recordsLinked to original sources
PubMed2001

Patient satisfaction in ambulatory surgery.

The purpose of this study was to explore the relationships between patient satisfaction and selected variables that were identified as important in ambulatory surgery. The study addressed whether the selected variables are associated with the satisfaction of patients admitted to the hospital for ambulatory surgery. A descriptive correlational study was conducted in two hospital settings with 130 ambulatory surgical patients. Nurses (n = 16) in the ambulatory surgery departments completed a nurse demographic data form. The patient sample differed between settings in age, diagnosis, and use of computers. The nurse sample differed in the number of nurses with computers in their homes and their satisfaction with nursing. Results showed that patients' higher ratings of postoperative pain correlated with higher patient satisfaction. Patients with high postoperative pain rated satisfaction with pain management lower. A point biserial correlation (rpb = .22) indicated a significant correlation between patient satisfaction and nurses' use of computers to collect and record patient information (P = .01). The patient sample in the setting where computers were used showed a higher mean patient satisfaction.

Adult↗
PubMed2000

A second look at comorbidity in victims of trauma: the posttraumatic stress disorder-major depression connection.

BACKGROUND: We examine whether traumatic events increase the risk for major depression independent of their effects on posttraumatic stress disorder (PTSD). METHODS: Data come from the Epidemiologic Study of Young Adults in southeast Michigan (N = 1007). Retrospective and prospective data were used to estimate the risk of major depression in persons with PTSD and persons exposed to trauma with no PTSD, compared with persons who did not experience a trauma. National Comorbidity Survey data were used to evaluate the influence of trauma type. RESULTS: In the retrospective lifetime data, hazard ratios were, for first-onset major depression in exposed persons with PTSD, 2.8 and, in exposed persons with no PTSD, 1.3 (not significant), as compared with persons who were not exposed. Corresponding estimates from the prospective data were 11.7 and 1.4 (not significant). The difference in the risk for depression associated with PTSD versus exposure without PTSD is unlikely to be due to differences in trauma type. CONCLUSIONS: The findings of a markedly increased risk for major depression in persons with PTSD, but not in exposed persons without PTSD, do not support the hypothesis that PTSD and major depression in trauma victims are influenced by separate vulnerabilities.

Adult↗
PubMed2000

Ethanol downregulates transcription of the PAI-1 gene in cultured human endothelial cells.

Human endothelial cells are a major site of synthesis for plasminogen activator inhibitor type-1. Elevated plasminogen activator inhibitor type-1 levels in young survivors of myocardial infarction [1] suggest that plasminogen activator inhibitor type-1 may have an important pathologic role in the development of coronary artery disease. Epidemiological studies indicate that moderate alcohol consumption (1-2 drinks/day) reduces the risk for cardiovascular mortality. This cardioprotective benefit has been attributed in part to an increase in fibrinolysis, which decreases fibrin-based thrombosis. The studies described herein were performed to determine whether moderate levels of ethanol affect plasminogen activator inhibitor type-1 gene expression. Cultured human endothelial cells were exposed to 0.1% v/v ethanol for 1 hour. Following incubation in the absence of ethanol plasminogen activator inhibitor type-1, mRNA levels were decreased in a time- and dose-dependent manner, reaching a maximum decrease of 3- to 4-fold at 2 to 4 hours following ethanol challenge. This decline in mRNA occurs at the transcription level; therefore, nuclear transcription run-on assays were performed. A 2.5- to 5-fold decrease in the rate of plasminogen activator inhibitor type-1 gene transcription was measured at 2 and 4 hours following ethanol challenge. Next, a 3.4- and a 1.1-kb fragment from the plasminogen activator inhibitor type-1 promoter region were linked to a luciferase reporter gene, and these constructs were transfected into human endothelial cells. Treatment of these transiently transfected human endothelial cells with ethanol showed a 2- to 3.5-fold decrease in promoter activity, respectively. These results indicate that low doses of ethanol downregulate transcription of the plasminogen activator inhibitor type-1 gene in cultured human endothelial cells. However, the mechanism(s) for this transcriptional decrease is currently unknown.

Cells, Cultured↗
PubMed1999

Previous exposure to trauma and PTSD effects of subsequent trauma: results from the Detroit Area Survey of Trauma.

OBJECTIVE: With the exception of a few reports of higher rates of childhood trauma in Vietnam veterans with posttraumatic stress disorder (PTSD), little is known about the influence of previous exposure to trauma on the PTSD effects of subsequent trauma. The authors examine interrelated questions about the effects of previous exposure to trauma. METHOD: A representative sample of 2,181 individuals in southeast Michigan were interviewed by telephone to record lifetime history of traumatic events specified in DSM-IV as potentially leading to PTSD. PTSD was assessed with respect to a randomly selected index trauma from the list of events reported by each respondent. RESULTS: History of any previous exposure to traumatic events was associated with a greater risk of PTSD from the index trauma. Multiple previous events had a stronger effect than a single previous event. The effect of previous assaultive violence persisted over time with little change. When they examined several features of the previous exposure to trauma, the authors found that subjects who experienced multiple events involving assaultive violence in childhood were more likely to experience PTSD from trauma in adulthood. Furthermore, previous events involving assaultive violence--single or multiple, in childhood or later on--were associated with a higher risk of PTSD in adulthood. CONCLUSIONS: Previous exposure to trauma signals a greater risk of PTSD from subsequent trauma. Although these results are consistent with a sensitization hypothesis, like the results from previous research on PTSD, they do not address the mechanism of increased responsivity to trauma. Long-term observational studies can further elucidate these observations.

Adolescent↗
PubMed1999

Aerobic exercise attenuates blood pressure reactivity to cold pressor test in normotensive, young adult African-American women.

Exaggerated blood pressure reactivity to behavioral stress has been observed in the African-American population, and such a pressor response is believed to play a role in hypertension. Regular aerobic exercise has been shown to exert an anti-hypertensive effect, and this may alter the blood pressure hyperreactivity observed in African Americans. To test the hypothesis that aerobic exercise attenuates pressor reactivity in African Americans, we studied eight healthy aerobically-trained normotensive African-American females and five similar sedentary females. The stress stimuli consisted of the cold pressor test with the foot immersed in ice water for two minutes. The aerobic exercise training protocol consisted of six weeks of jogging at 60-70% of peak oxygen uptake (VO2peak), three days/week for 35 min/exercise session. Systolic blood pressure, diastolic blood pressure, mean arterial blood pressure, heart rate, cardiac output, total peripheral resistance, and forearm blood flow were measured. Manifestation of a training effect was illustrated by a 24.1 +/- 0.2% increase in VO2peak (26.9 +/- 1.2 mL x kg(-1) min(-1) vs 35.4 +/- 1.6 mL x kg(-1) min(-1)) (P<.05). Within the exercise-trained group there was a 6.3 +/- .15% decrease in systolic pressure (129 +/- 4.6 mm Hg vs. 121 +/- 5.4 mm Hg) (P<.05), and a 5.0 +/- .05% decrement in mean arterial blood pressure (99 +/- 3.3 mm Hg vs 94 +/- 3.6 mm Hg) (P<.05) during the cold pressor test. Pressor reactivity to cold stress did not change in the untrained group. Measures of heart rate, cardiac output, total peripheral resistance, and forearm blood flow were unaltered during conditions of the cold pressor test. We conclude that aerobic exercise attenuates the blood pressure reactivity to behavioral stress in young, adult normotensive African-American females. A lifestyle change such as exercising may play a role in reducing the risk of hypertension in African-American women.

Adult↗
PubMed1998

Trauma and posttraumatic stress disorder in the community: the 1996 Detroit Area Survey of Trauma.

BACKGROUND: The study estimates the relative importance of specific types of traumas experienced in the community in terms of their prevalence and risk of leading to posttraumatic stress disorder (PTSD). METHODS: A representative sample of 2181 persons in the Detroit area aged 18 to 45 years were interviewed by telephone to assess the lifetime history of traumatic events and PTSD, according to DSM-IV. Posttraumatic stress disorder was assessed with respect to a randomly selected trauma from the list of traumas reported by each respondent, using a modified version of the Diagnostic Interview Schedule, Version IV, and the World Health Organization Composite International Diagnostic Interview. RESULTS: The conditional risk of PTSD following exposure to trauma was 9.2%. The highest risk of PTSD was associated with assaultive violence (20.9%). The trauma most often reported as the precipitating event among persons with PTSD (31% of all PTSD cases) was sudden unexpected death of a loved one, an event experienced by 60% of the sample, and with a moderate risk of PTSD (14.3%). Women were at higher risk of PTSD than men, controlling for type of trauma. CONCLUSIONS: The risk of PTSD associated with a representative sample of traumas is less than previously estimated. Previous studies have overestimated the conditional risk of PTSD by focusing on the worst events the respondents had ever experienced. Although recent research has focused on combat, rape, and other assaultive violence as causes of PTSD, sudden unexpected death of a loved one is a far more important cause of PTSD in the community, accounting for nearly one third of PTSD cases.

Adolescent↗
PubMed1998

Genotype-specific transcriptional regulation of PAI-1 gene by insulin, hypertriglyceridemic VLDL, and Lp(a) in transfected, cultured human endothelial cells.

Plasminogen activator inhibitor-1 (PAI-1) has been shown to be an independent risk factor for coronary artery disease. Variations in plasma PAI-1 levels have been attributed to variations in the PAI-1 gene, and associations between PAI-1 levels and PAI-1 genotypes suggest that PAI-1 expression may be regulated in a genotype-specific manner by insulin, hypertriglyceridemic (HTG) very low density lipoprotein (VLDL), or lipoprotein(a) [Lp(a)]. Polymerase chain reaction-amplified 1106-bp fragments of the promoter of the 1/1 and 2/2 PAI-1 genotypes were sequenced and showed 5 regions of small nucleotide differences in the 1/1 versus 2/2 PAI-1 promoters that consistently occurred with high frequency. These fragments were ligated into the luciferase reporter gene, and 1/1 and 2/2 PAI-1 genotype human umbilical vein endothelial cell (HUVEC) cultures were transiently transfected with their respective p1PAI110/luc and p2PAI110/luc constructs and vice versa. Insulin induced an approximately 12- to 16-fold increase in luciferase activity in both the 1/1 and 2/2 PAI-1 genotype HUVEC cultures transfected with the p1PAI110/luc construct. HTG-VLDL and Lp(a) induced luciferase activity by approximately 14- to 16- and approximately 8- to 11-fold, respectively, in both the 1/1 and 2/2 PAI-1 genotype HUVEC cultures transfected with the p2PAI110/luc construct. The positive control interleukin-1 showed an approximately 7- to 12-fold response in the 1/1 and 2/2 PAI-1 genotype HUVEC cultures transfected with either of the constructs. These cross-over results demonstrate that regulation of either the 1/1 or 2/2 PAI-1 genotype by its respective inducer is due to the promoter itself and not to some factor(s) expressed differently in the 1/1 or 2/2 PAI-1 genotype HUVEC cultures.

Cells, Cultured↗
PubMed1998

Alcohol-induced upregulation of plasminogen activators and fibrinolytic activity in cultured human endothelial cells.

Clinical studies suggest that moderate alcohol consumption may decrease the risk for coronary artery disease and myocardial infarction. This effect may be attributed, in part, to the alcohol-mediated increase in endothelial cell (EC)-mediated fibrinolytic activity mediated by the increase in synthesis and/or activity of tissue-type plasminogen activators (t-PAs) and/or urokinase-type PA (u-PAs). To determine whether low alcohol levels (0.01 to 0.1%, v/v) induced the expression of these proteins, cultured human saphenous vein ECs (HSVECs) were preincubated in the absence/presence of ethanol for 5 to 120 min at 37 degrees C, washed, refed, and further incubated for 8 and 24 hr without alcohol. PA mRNA (reverse transcriptase-polymerase chain reaction) and secreted antigen (ELISA) levels were analyzed after incubation for 8 and 24 hr and the net expression of (sustained) endogenous PA-mediated surface-localized HSVEC fibrinolytic activity (plasmin generation) quantitated by activation of 125I-Glu-plasminogen after incubation for 24 hr. A brief 5 to 30 min preincubation (induction) of both t-PA and u-PA antigen increased approximately 3-fold (t-PA control, 14.2 +/- 1.7, plus alcohol, 25.4 +/- 5 ng/ml; u-PA control, 15 +/- 0.8, plus alcohol, 46.4 +/- 1.3 ng/ml) and mRNA levels approximately 2-fold, as compared with controls. Increased PA expression was associated with a significant concomitant approximately 2-fold increase in surface-localized fibrinolytic activity (control, 96 +/- 2.8, plus alcohol, 255 +/- 42 fmol/ well). These combined results indicate that a brief exposure (<30 min) to low levels of alcohol can induce synthesis of EC-produced t-PA and u-PA resulting in an increased expression of HSVEC surface-localized fibrinolytic activity and may account, in part, for the apparent cardioprotective benefit associated with moderate alcohol consumption.

Cells, Cultured↗
PubMed1998

Ethanol transcriptionally upregulates t-PA and u-PA gene expression in cultured human endothelial cells.

Epidemiological studies have suggested that moderate alcohol consumption reduces the risk of cardiovascular mortality. This cardioprotective benefit may be mediated, in part, by promoting fibrinolysis through changes in fibrinolytic components and/or activity, resulting in the decreased risk for thrombosis, coronary artery disease, and eventual myocardial infarction. Endothelial cells (ECs) play a pivotal role in maintaining normal hemostasis by regulating fibrinolysis through the synthesis of plasminogen activators (PAs), tissue-type plasminogen activator (t-PA), and urokinase-type plasminogen activator (u-PA). The studies described herein were conducted to determine whether a single brief preincubation (1 hr, 37 degrees C) of cultured human umbilical vein ECs (HUVECs) with low ethanol (0.1%, v/v), will upregulate t-PA and/or u-PA gene expression at the transcriptional level, using a combination of nuclear transcription run-on assays and transient transfections of cultured HUVECs with the pPA/luc promoter constructs. Nuclear run-on assays showed approximately 2- to 3-fold and approximately 6- to 7-fold increase in the transcription of new t-PA and u-PA mRNAs, respectively. In addition, transient transfections of cultured HUVECs with the pt-PA363/luc and pu-PA236/luc promoter constructs, using lipofectamine, demonstrated approximately 4- to 6-fold and approximately 6- to 9-fold increase in luciferase activity for t-PA and u-PA, respectively. These combined results demonstrate that low ethanol transcriptionally upregulates both t-PA and u-PA gene expression in cultured HUVECs and provides a molecular basis for the ethanol-induced increase in EC-mediated fibrinolytic activity that may underlie and contribute, in part, to the cardioprotective benefit associated with moderate alcohol consumption.

Cells, Cultured↗
PubMed1997

Psychiatric sequelae of posttraumatic stress disorder in women.

BACKGROUND: The risk for first-onset major depression, anxiety, and substance use disorders associated with prior posttraumatic stress disorder (PTSD) was estimated in a sample of women. METHODS: The National Institute of Mental Health Diagnostic Interview Schedule, revised according to DSM-III-R, was used to measure lifetime psychiatric disorders in a stratified random sample of 801 mothers of children, who participated in a study of cognitive and psychiatric outcomes by level of birth weight. Cox proportional hazards models with time-dependent covariates were used to calculate the hazards ratios of first onset of other disorders following PTSD. RESULTS: The lifetime prevalence of traumatic events was 40% and of PTSD, 13.8%. Posttraumatic stress disorder signaled increased risks for first-onset major depression (hazards ratio, 2.1) and alcohol use disorder (hazards ratio, 3.0). The risk for major depression following PTSD was of the same magnitude as the risk for major depression following other anxiety disorders. Women with preexisting anxiety and PTSD had significantly increased risk for first-onset major depression. Additional analysis showed that preexisting major depression increased women's vulnerability to the PTSD-inducing effects of traumatic events and risk for exposure to traumatic events. CONCLUSIONS: Posttraumatic stress disorder influences the risk for first-onset major depression and alcohol use disorder. The causal explanation of these temporally secondary disorders is unclear and might involve the effect of PTSD or underlying vulnerabilities exposed by the traumatic experience.

Adult↗
PubMed1997

Sex differences in posttraumatic stress disorder.

BACKGROUND: Epidemiologic surveys in the general population documented a higher rate of posttraumatic stress disorder (PTSD) in women than in men. To date, the finding has received little scientific attention. This study examines the extent to which sex differences in PTSD might be explained by previously identified risk factors and whether the sex difference in PTSD varied by age at exposure to traumatic events. METHODS: The NIMH-DIS (NIMH Diagnostic Interview Schedule, Version III Revised) was used to measure DSM-IIIR disorders in a random sample of 1007 young adults. Cox proportional hazards models were used to estimate changes in the hazards ratio for PTSD associated with sex when potential risk factors were included. RESULTS: Lifetime prevalence of exposure to traumatic events and number of traumatic events did not vary by sex. The prevalence of PTSD was higher for women than for men exposed to traumatic events (hazards ratio, 2.3; 95% confidence interval, 1.5-3.6). Preexisting anxiety disorders or major depressive disorders played a part in the observed sex difference in PTSD. Family history of anxiety disorder and early separation from parents, although significant risk factors for PTSD in subjects of both sexes, were unrelated to the sex difference in PTSD. The sex difference in PTSD was markedly greater if exposure occurred in childhood than later on. CONCLUSIONS: Posttraumatic stress disorder is more likely to develop in females than in males after exposure to a traumatic event. Susceptibility to PTSD in females might be greater in childhood than after age 15 years. Explanations of the sex difference might involve characteristics of individuals and of the traumatic experiences.

Adult↗
PubMed1997

Ethanol increases surface-localized fibrinolytic activity in cultured endothelial cells.

Epidemiological studies demonstrated a positive association between moderate alcohol consumption and reduced cardiovascular mortality that may be mediated, in part, through increased fibrinolysis. These studies were conducted to determine whether low concentrations of alcohol (0.025 to 0.1%, v/v) directly affected the surface-localized versus secreted/solution phase fibrinolytic activity in live cultured endothelial cell (EC) types. Confluent live cultured ECs [human umbilical vein ECs (HUVECs), human saphenous vein ECs (HSVECs), and porcine aortic ECs (PAECs)] were preincubated (0 to 20 min, 4 degrees C) in the absence or presence of varying concentrations of alcohol (0 to 0.1%, v/v), in the presence of saturating levels of 125I-labeled Glu-plasminogem (2 microM) and 125I-Plasmin M(r) 20-kDA light-chain formation quantitated by phosphorimaging autoradiography analysis. Endogenous plasminogen activator (PA)-mediated fibrinolytic activity was time- and dose-dependent; reached a maximum approximately 5- to 10-fold increase at 0.05% alcohol in HUVECs, HSVECs, and PAECs; was completely inhibited by anti-t-PA IgG in HUVECs; and partially inhibited by both anti-t-PA (approximately 40%) and anti-u-PA IgG (approximately 60%) in HSVECs. Complete inhibition of alcohol-induced (0.05%) fibrinolytic activity in cultured HUVECs by 2 mM tranexamic acid (an antagonist of plasminogen binding) indicated that the increased fibrinolytic activity was receptor-bound and localized to the EC surface, rather than present in or secreted into the medium (solution phase). Finally, the alcohol-induced increased fibrinolytic activity in cultured HUVECs returned to essentially normal control levels in approximately 1 hr. These studies have demonstrated a direct effect of low alcohol on EC fibrinolytic activity that may contribute, in part, to the decreased risk for thrombosis, coronary artery disease, and myocardial infarction associated with moderate alcohol consumption.

Culture Techniques↗
PubMed1997

Characterization and establishment of specifications for biopharmaceuticals.

This paper describes the role of product characterization and product specifications in the context of an overall control strategy. Due to advances in analytical characterization and biotechnology manufacturing methods, product characterization can now be used as an effective means of assessing the impact of manufacturing process changes on product quality, safety and efficacy, hence obviating the need for repeating clinical testing each time a manufacturing process change is made. The ICH specifications guidance document can serve a key role in harmonising test requirements and regulatory practices with regard to produce characterization. Consumers, regulatory agencies, and biopharmaceutical manufacturers all stand to benefit from this harmonization process.

Biopharmaceutics↗