tbuckley/cabot-search huggingface dataset:
Trends in Community Knowledge of the Warning Signs and Risk Factors for Stroke
Authors: Alexander T. Schneider, Arthur M. Pancioli, Jane C. Khoury, Eric Rademacher, Alfred Tuchfarber, Rosemary Miller, Daniel Woo, Brett Kissela, Joseph P. Broderick
Journal: JAMA (2003)

<h3>Context</h3> Poor public knowledge of stroke warning signs and risk factors limits effective stroke intervention and prevention. <h3>Objective</h3> To examine temporal trends in public knowledge of stroke warning signs and risk factors. <h3>Design and Setting</h3> Population-based random-digit telephone survey conducted in July-November 2000 among individuals in the greater Cincinnati, Ohio, region. <h3>Participants</h3> A total of 2173 survey respondents (69% response rate) were randomly identified based on their demographic similarities to the ischemic stroke population with regard to age, race, and sex. <h3>Main Outcome Measures</h3> Spontaneous recall of at least 1 important stroke warning sign and 1 established stroke risk factor in comparison with findings from the same survey in 1995. <h3>Results</h3> In 2000, 70% of respondents correctly named at least 1 established stroke warning sign vs 57% in 1995 (<i>P</i>&lt;.001), and 72% correctly named at least 1 established stroke risk factor vs 68% in 1995. Groups of individuals with the highest risk and incidence of stroke, such as persons at least 75 years old, blacks, and men, were the least knowledgeable about warning signs and risk factors. Television was the most frequently cited source of knowledge, 32% in 2000 vs 24% in 1995 (<i>P</i>&lt;.001). <h3>Conclusions</h3> Public knowledge of stroke warning signs within the greater Cincinnati region has significantly improved from 1995 to 2000, although knowledge of stroke risk factors did not improve significantly during the same time period. Public education efforts must continue and should focus on groups at the highest risk of stroke.
Tear gas--harassing agent or toxic chemical weapon?
Authors: H. Hu
Journal: JAMA (1989)

Tear gas has gained widespread acceptance as a means of controlling civilian crowds and subduing barricaded criminals. The most widely used forms of tear gas have been o-chlorobenzylidenemalononitrile and omega-chloroacetophenone. Proponents of their use claim that, if used correctly, the noxious effects of exposure are transient and of no long-term consequences. The use of tear gas in recent situations of civil unrest, however, demonstrates that exposure to the weapon is difficult to control and indiscriminate, and the weapon is often not used correctly. Severe traumatic injury from exploding tear gas bombs as well as lethal toxic injury have been documented. Moreover, available toxicological data are deficient as to the potential of tear gas agents to cause long-term pulmonary, carcinogenic, and reproductive effects. Published and recent unpublished in vitro tests have shown o-chlorobenzylidenemalononitrile to be both clastogenic and mutagenic. Sadly, the nature of its use renders analytic epidemiologic investigation of exposed persons difficult. In 1969, eighty countries voted to include tear gas agents among chemical weapons banned under the Geneva Protocol. There is an ongoing need for investigation into the full toxicological potential of tear gas chemicals and renewed debate on whether their use can be condoned under any circumstances.
Association of Cyclooxygenase-1-Dependent and -Independent Platelet Function Assays With Adverse Clinical Outcomes in Aspirin-Treated Patients Presenting for Cardiac Catheterization
Authors: Andrew L. Frelinger, YouFu Li, Matthew D. Linden, Marc R. Barnard, Marsha L. Fox, Douglas J. Christie, Mark I. Furman, Alan D. Michelson
Journal: Circulation (2009)

Poor clinical outcome in aspirin-treated patients has been termed aspirin resistance and may result from inadequate inhibition of platelet cyclooxygenase-1 (COX-1) by aspirin. The objectives of this study were to determine prospectively whether COX-1-dependent and other platelet function assays correlate with clinical outcomes in aspirin-treated patients.Blood was collected before percutaneous coronary intervention from 700 consecutive aspirin-treated (81 or 325 mg for > or =3 days) patients. Platelet function was tested by (1) serum thromboxane B(2); (2) arachidonic acid-stimulated platelet surface P-selectin and activated glycoprotein IIb/IIIa and leukocyte-platelet aggregates; and (3) platelet function analyzer (PFA)-100 collagen-epinephrine and collagen-ADP closure time (CT). Adverse clinical outcomes of all-cause death, cardiovascular death, and major adverse cardiovascular events (cardiovascular death, myocardial infarction, hospitalization for revascularization, or acute coronary syndrome) were assessed by telephone interview and/or medical record review. Clinical outcomes information was obtained at 24.8+/-0.3 months after platelet function testing. By univariate analysis, COX-1-dependent assays, including serum thromboxane B(2) level, were not associated with adverse clinical outcomes, whereas the COX-1-independent assay, PFA-100 collagen-ADP CT <65 seconds, was associated with major adverse cardiovascular events (P=0.0149). After adjustment for covariables (including sex, aspirin dose, Thrombolysis in Myocardial Infarction risk score, clopidogrel use), both serum thromboxane B(2) >3.1 ng/mL and PFA-100 collagen-ADP CT <65 seconds were associated with major adverse cardiovascular events. In contrast, indirect measures of platelet COX-1 (arachidonic acid-stimulated platelet markers, shortened PFA-100 collagen-epinephrine CT) were not significantly associated with adverse clinical outcomes even after adjustment for covariables.In this prospective study of 700 aspirin-treated patients presenting for angiographic evaluation of coronary artery disease, residual platelet COX-1 function measured by serum thromboxane B(2) and COX-1-independent platelet function measured by PFA-100 collagen-ADP CT, but not indirect COX-1-dependent assays (arachidonic acid-stimulated platelet markers, shortened PFA-100 collagen-epinephrine CT), correlate with subsequent major adverse cardiovascular events. This study suggests that multiple mechanisms, including but not confined to inadequate inhibition of COX-1, are responsible for poor clinical outcomes in aspirin-treated patients, and therefore the term aspirin resistance is inappropriate.
Effects of Chlorothiazide on Systemic Hemodynamics in Essential Hypertension
Authors: HERMAN VILLARREAL, JOSÉ EMILIO EXAIRE, ANDRÉS REVOLLO, JORGE SONÍ
Journal: Circulation (1962)

Nineteen observations were made in 12 patients with early essential hypertension. The comparative effects upon mean arterial blood pressure, cardiac index, and total peripheral resistance of the acute and long-term administration of chlorothiazide were studied. With acute administration of the drug, a 10 per cent drop in mean arterial blood pressure, a decrease of 18 per cent in cardiac index, and an increase of 7 per cent in peripheral resistance were observed. With long-term administration, a decrease of 21 per cent in mean arterial blood pressure, an increase of 4 per cent in cardiac index, and a drop of 26 per cent in peripheral resistance were found. The conclusion is drawn that reduction of mean arterial blood pressure with acute administration of chlorothiazide is due to decrease in cardiac output, whereas with long-term use it is due to reduction in total peripheral resistance.
Manipulating Hemodynamics and Oxygen Transport in Critically Ill Patients
Authors: Charles Hinds, David Watson
Journal: New England Journal of Medicine (1995)

Survival after trauma, surgery, or sepsis is associated with the attainment of high levels of oxygen delivery and oxygen consumption.1 This observation has fueled the expectation that the outcome of critical illness may be improved by attempts to replicate the hemodynamic values and patterns of oxygen transport found in survivors of serious illness or injury. Such treatment has been thought to prevent or reverse tissue hypoxia by compensating for the increased demand for oxygen imposed by critical illness, as well as the maldistribution of blood flow that often occurs both regionally and in the microcirculation; in addition, this treatment has . . .
Cultivation of aorta-gonad-mesonephros–derived hematopoietic stem cells in the fetal liver microenvironment amplifies long-term repopulating activity and enhances engraftment to the bone marrow
Authors: Masaki Takeuchi, Takashi Sekiguchi, Takahiko Hara, Taisei Kinoshita, Atsushi Miyajima
Journal: Blood (2002)
Impact of Respiratory Maneuvers on Cardiac Volume Within Left-Breast Radiation Portals
Authors: Ming Hui Chen, Michael L. Chuang, Bruce A. Bornstein, Rebecca Gelman, Jay R. Harris, Warren J. Manning
Journal: Circulation (1997)

Background Late cardiac morbidity and mortality have been reported among left-breast cancer survivors treated with radiation therapy. Radiation-induced cardiotoxicity is affected by the volume of myocardium included in the radiation portals. We hypothesize that simple respiratory maneuvers may alter the position of the heart relative to the portals without altering the radiation dose delivered to the breast. Methods and Results Fourteen healthy female adult volunteers underwent cardiac MRI to determine the cardiac volume included in the typical left-breast radiation field during respiratory maneuvers. Cardiac volume within the radiation portals was assessed from a transverse stack of 14 1-cm-thick contiguous slices covering the entire heart, obtained during breath holding at end-tidal volume (baseline), deep inspiration, and forced expiration. Thirteen subjects (92%) had inclusion of a portion of the heart within the radiation portals at end-tidal volume (median, 20.9 cm 3 ; range, 1.3 to 88.4 cm 3 ). In these subjects, inspiration decreased the cardiac volume included within the radiation portals (median change: −10.7 cm 3 [−40.2%], P &lt;.001 versus end-tidal volume), whereas expiration increased the cardiac volume included (median change: 4.0 cm 3 [21.5%]; P &lt;.001 versus end-tidal volume). Conclusions Inclusion of a portion of the heart in the left-breast radiation field is common. The use of simple inspiratory maneuvers significantly decreases cardiac volume within the radiation portals. Such an approach during delivery of radiation therapy may allow for preservation of radiation dosage to the breast while reducing cardiac involvement and subsequent mortality.
Secondhand Smoke: Displaced Enthusiasm?
Authors: John Manuel
Journal: Environmental Health Perspectives (2007)

Rallying Around the Environmental FlagSocial scientists have long studied competition for natural resources as a source of conflict around the world, but they have paid little attention to the environment in postconflict societies.Must the environment invariably suffer in the wake of conflict?Can former combatants rally around the environment to help sustain peace?These were the types of questions asked at a November
A tax on indoor tanning would reduce demand in Europe
Authors: S. N. Williams
Journal: BMJ (2012)

The use of indoor tanning beds has been established to be a serious risk to human health.1 In the European Union, Northern Ireland is the latest country to pass legislation that prohibits under 18s from using indoor tanning equipment. Although this will protect children from this risk, more needs to be done if we are to respond to the International Agency for Research on Cancer’s suggestion that we need also to “discourage young adults from using indoor tanning equipment.”1

Globally, the incidence of cutaneous melanoma has increased faster than any other common cancer, with an approximate doubling of rates every 10-20 years in countries with predominantly white populations.2 For instance, in 2008 there were about 70 000 incidences of, and more than 14 000 deaths from, melanoma in the European Union.3 Although attempts at public education by health agencies and charities have increased, these are being obscured by spurious claims by the indoor tanning industry of the benefits of indoor tanning.4

Recent lessons from tobacco control in the EU teach us that tax increases are the single most effective intervention to reduce demand for harmful products.5 The EU needs to follow the example of the United States by introducing a so called tan tax; an excise on indoor tanning services. A new EU directive for the taxation of indoor tanning services would complement existing directives focused on product safety.6 Importantly, these excise duties would provide additional revenue for governments and reduce numbers of melanomas and other skin cancers—something that would also subsequently reduce governments’ healthcare costs. All or a portion of this revenue could be earmarked for public health education initiatives warning of the dangers of ultraviolet radiation exposure.

As …
Genes inducing iPS phenotype play a role in hepatocyte survival and proliferation <i>in vitro</i> and liver regeneration <i>in vivo</i>
Authors: Vishakha S. Bhave, Shirish Paranjpe, William C. Bowen, Shashikiran Donthamsetty, Aaron W. Bell, Jaspal S. Khillan, George K. Michalopoulos
Journal: Hepatology (2011)

Reprogramming factors have been used to induce pluripotent stem cells as an alternative to somatic cell nuclear transfer technology in studies targeting disease models and regenerative medicine. The neuronal repressor RE-1 silencing transcription factor (REST) maintains self-renewal and pluripotency in mouse embryonic stem cells by maintaining the expression of Oct3/4, Nanog, and cMyc. We report that primary hepatocytes express REST and most of the reprogramming factors in culture. Their expression is up-regulated by hepatocyte growth factor (HGF) and epidermal growth factor (EGF). REST inhibition results in down-regulation of reprogramming factor expression, increased apoptosis, decreased proliferation, and cell death. The reprogramming factors are also up-regulated after 70% partial hepatectomy in vivo . Conclusion: These findings show that genes inducing the iPS phenotype, even though expressed at lower levels than embryonic stem cells, nonetheless are associated with control of apoptosis and cell proliferation in hepatocytes in culture and may play a role in such processes during liver regeneration. (Hepatology 2011)
Referral Patterns and Perceived Barriers to Adult Congenital Heart Disease Care
Authors: Susan M. Fernandes, Paul Khairy, Laurie Fishman, Patrice Melvin, Joanne O'Sullivan-Oliveira, Gregory S. Sawicki, Sonja Ziniel, Petar Breitinger, Roberta Williams, Masato Takahashi, Michael J. Landzberg
Journal: Journal of the American College of Cardiology (2012)
Effects of potassium channel modulation during global ischaemia in isolated rat heart with and without cardioplegia
Authors: M. Galinanes, M. J Shattock, D. J Hearse
Journal: Cardiovascular Research (1992)

Objective: The opening of potassium (K+) channels during regional ischaemia may, by inducing rapid contractile arrest, be an intrinsic energy sparing mechanism. Thus K+ channel openers (for example, lemakalim) exert significant anti-ischaemic effects, whereas glibenclamide exacerbates ischaemic contracture and limits postischaemic functional recovery. The aim of the study was to investigate the ability of these compounds to influence ischaemic injury when used either alone or in combination with rapid arrest induced by a high K+cardioplegic solution. Methods: Contractile function of isolated Langendorff perfused rat hearts was assessed using an intraventricular balloon. Hearts were subjected to normothermic global ischaemia (20 min) or cardioplegic arrest (35 min) with and without glibenclamide or lemakalim. Lemakalim (10 μmol·litre−1) or glibenclamide (10 μmol·litre−1) was given, in the presence or absence of cardioplegia, for 2 min immediately prior to the onset of ischaemia. The rate of ischaemia induced contractile failure, the severity of ischaemic contracture, and the degree of postischaemic functional recovery were all measured. Results: In the absence of cardioplegia, the time to contractile arrest in control hearts was 133 (SEM 4) s. This was increased by glibenclamide, to 145(6) s, and decreased by lemakalim, to 112(6) s. The time to onset of ischaemic contracture [8(1) min] was accelerated by glibenclamide [4(1) min] and delayed by lemakalim [14(1) min]. Lemakalim significantly improved the recovery of left ventricular developed pressure from 49(7)% in control hearts to 65(3)%, and left ventricular end diastolic pressure from 41(3) to 21(4) mm Hg. Hearts pretreated with glibenclamide showed similar recoveries to control hearts. During reperfusion, lemakalim exerted a transient vasodilator effect whereas glibenclamide caused a transient vasoconstriction. When either glibenclamide or lemakalim was added to a high K+ cardioplegic solution and hearts rendered ischaemic for 35 min, the ability of both compounds to influence ischaemic contracture and postischaemic functional recovery was lost. In additional studies the effect of lemakalim on the relative times to ischaemia induced mechanical failure and electrical arrest was assessed. In control hearts the time to contractile failure was 128(5) s and the time to electrical arrest was 241(30) s, while in the lemakalim treated hearts the values were 103(2) s and 509 (161) s, respectively. In the lemakalim group all the hearts showed sustained ventricular arrhythmias; in the control group there were no arrhythmias. Conclusions: Lemakalim can exert a significant anti-ischaemic effect when given alone. This effect is lost when it is used in combination with high K+ cardioplegia. The anti-ischaemic properties of lemakalim may thus be limited to its ability to accelerate contractile arrest. Cardiovascular Research 1992;26:1063-1068
Weight loss in people with Alzheimer's disease: a prospective population based analysis
Authors: D. Cronin-Stubbs, L. A Beckett, P. A Scherr, T. S Field, M. J Chown, D. M Pilgrim, D. A Bennett, D. A Evans
Journal: BMJ (1997)

Objectives: To study the ictal phenomenology, aetiology, and outcome of convulsions occurring within seconds of impact in violent collision sport.Design: Retrospective identification of convulsions associated with concussive brain injury from case records from medical officers of football clubs over a 15 year period.Subjects: Elite Australian rules and rugby league footballers.Main outcome measures: Neuroimaging studies, electroencephalography, neuropsychological test data, and statistics on performance in matches to determine presence of structural or functional brain injury.Clinical follow up and electroencephalography for evidence of epilepsy.Results: Twenty two cases of concussive convulsions were identified with four events documented on television videotape.Convulsions began within 2 seconds of impact and comprised an initial period of tonic stiffening followed by myoclonic jerks of all limbs lasting up to 150 seconds.Some asymmetry in the convulsive manifestations was common, and recovery of consciousness was rapid.No structural or permanent brain injury was present on clinical assessment, neuropsychological testing, or neuroimaging studies.All players returned to elite competition within two weeks of the incident.Epilepsy did not develop in any player over a mean (range) follow up of 3.5 (1-13) years.Conclusions: These concussive or impact convulsions are probably a non-epileptic phenomenon, somewhat akin to convulsive syncope.The mechanism may be a transient traumatic functional decerebration.In concussive convulsions the outcome is universally good, antiepileptic treatment is not indicated, and prolonged absence from sport is unwarranted.
The cyclooxygenase system participates in functional mdr1b overexpression in primary rat hepatocyte cultures
Authors: Christina Ziemann, Dirk Schäfer, Gudrun Rüdell, Georg F. Kahl, Karen I. Hirsch-Ernst
Journal: Hepatology (2002)

Overexpression of mdr1-type P-glycoproteins (P-gps) is thought to contribute to primary chemotherapy resistance of untreated hepatocellular carcinoma. However, mechanisms of endogenous multidrug resistance 1 (mdr1) gene activation still remain unclear. Because recent studies have demonstrated overexpression of cyclooxygenase-2 (COX-2) in hepatocytes during early stages of hepatocarcinogenesis, we investigated whether the COX system, which catalyzes the rate-limiting step in prostaglandin synthesis, participates in mdr1 gene regulation. In the present study, primary rat hepatocyte cultures, exhibiting time-dependent mdr1b overexpression, demonstrated basal COX-2 and COX-1 mRNA expression and liberation of prostaglandin E2 (PGE2), indicative of an active COX-dependent arachidonic acid metabolism. PGE2 accumulation in culture supernatants was further enhanced by arachidonic acid (1μmol/L) and epidermal growth factor (EGF) (16 nmol/L). PGE2 and prostaglandin F2α (PGF2α) (3-6μg/mL), added directly to the culture medium, significantly up-regulated intrinsic mdr1b mRNA overexpression and mdr1-dependent transport activity. Up-regulation was maximal after 3 days of culture. Like prostaglandins, the COX substrate, arachidonic acid, also induced mdr1b gene expression. Apart from this, structurally different COX inhibitors (indomethacin, meloxicam, NS-398) mediated significant inhibition of time-dependent and EGF-induced mdr1b mRNA overexpression, resulting in enhanced intracellular accumulation of the mdr1 substrate, rhodamine 123 (Rho123). Thus, the present data support the conclusion that the release of prostaglandins through activation of the COX system participates in endogenous mdr1b gene regulation. COX-2 inhibition might constitute a new strategy to counteract primary mdr1-dependent chemotherapy resistance.
Immunity, Emotions and Stress
Authors: George F. Solomon, Alfred A. Amkraut, Phyllis Kasper
Journal: Psychotherapy and Psychosomatics (1974)

Evidence from a variety of sources supports the notion that stress and emotional distress may relate to dysfunction and hypofunction of the immunologic system. We have experimental evidence that some forms of stress reduce primary and secondary antibody response to low dose antigen stimulation in rats and that adult immunologic responsivity may be altered by early infantile experience. Mixed-sex group housing at high male-female ratios increases severity of adjuvant-induced arthritis in the male rat. Graft-versus-host reactions are diminished by food-limitation stress to recipient animals. Sex segregated group-housed mice show larger murine virus-induced sarcomas when inoculated at 6 and 9 months of age than males housed individually with two or more females. Electric shock stress for 3 days prior to inoculation with virus reduces incidence and size of MSV tumors, while shock administered 3 days following inoculation increases tumor size. Female mice that develop spontaneous fighting behavior show significantly greater resistance to MSV tumors. Acutely ill schizophrenic patients with relatively high levels of IgA and IgG have a poorer short-term prognosis. Electrolytic lesions of the ventromedial and posterior nuclei of the hypothalamus of recipient and possibly also of donor animals impair the GVH reaction. Our experimental findings suggest that stress and central nervous system lesions affect thymus-derived lymphocytes (T-cells) and play a role in cell-cell interaction or the release of mediators from reacting lymphocytes. Ultimately, we may find that stress affects the macrophage, a hormone-sensitive cell that plays a role in afferent, central and efferent limbs of the immune system.