tbuckley/cabot-search huggingface dataset:
Ethnic Disparities in Health: The Public's Role in Working for Equality
Authors: David Satcher
Journal: PLoS Medicine (2006)

As Assistant Secretary for Health (1998–2001) and Surgeon General (1998–2002) of the United States, I had the opportunity to lead in the development of Healthy People 2010. Healthy People 2010 is the current phase of the Healthy People Initiative, which began in 1979 with the vision of making America's communities healthier and happier places (http://www.healthypeople.gov). Healthy People 2010 is a comprehensive set of health objectives to be achieved over the first decade of the century. The overarching goals are to increase the quality of life and years of healthy life for all Americans and to eliminate racial and ethnic health disparities [1]. This has been an ambitious undertaking, but we are making progress.

Americans have gained 30 years in life expectancy in the last century overall, from 47 years in 1900 to 77.6 years in 2003. But African American men, with a life expectancy of 69.2 years compared to 76.1 years for African American women and 75.4 years for white men, continue to lag behind. Nevertheless, all groups have made significant progress in years of life lived. However, 50 percent of persons over 80 are incapacitated physically, mentally, or both—illustrating the importance of both quality of life and years of healthy life.

The significant gender and racial gaps for African American men are likely to persist because of death rates associated with the prevalence of cardiovascular disease, diabetes, hypertension, cancer, HIV/AIDS, and homicide among this group. African American men are more likely to die from these diseases, or their associated problems, and from homicide than their white counterparts.

The significant gender and racial gaps for African American men are likely to persist.

However, we have made significant progress in addressing racial and ethnic disparities in the number of children immunized and in screenings for breast cancer. But ethnic and racial disparities persist in areas such as diabetes, HIV/ AIDS, cardiovascular disease, and others for both African American men and women.
Effect of Haemophilus influenzae endotoxin on the synthesis of IL-6, IL-8, TNF-alpha and expression of ICAM-1 in cultured human bronchial epithelial cells
Authors: OA Khair, JL Devalia, MM Abdelaziz, RJ Sapsford, H Tarraf, RJ Davies
Journal: European Respiratory Journal (1994)

Although studies of infective lung diseases have demonstrated that Haemophilus influenzae is a major pathogen, the mechanisms underlying pathogenesis by this organism are not clear. We have cultured human bronchial epithelial cells (HBEC) to confluency and have investigated the effect of H. influenzae endotoxin (HIE) on: 1) epithelial permeability, by movement of 14C-bovine serum albumin (14C-BSA) across HBEC and measurement of electrical resistance of HBEC; 2) release of interleukin-6 (IL-6), interleukin-8 (IL-8) and tumour necrosis factor-alpha (TNF-alpha) into the supernatant, by enzyme-linked immunosorbent assay (ELISA); and 3) expression of intercellular adhesion molecule-1 (ICAM-1), by immunofluorescence staining. HIE did not significantly increase the movement of 14C-BSA across HBEC. In contrast, HIE progressively increased the electrical resistance of HBEC, such that this was significant after 24 h. Compared with untreated cells, 10-100 micrograms.ml-1 HIE-treated cells released significantly greater amounts of IL-6, IL-8 and TNF-alpha, after 24 h, which was blocked by 10(-5) M hydrocortisone. Similarly, incubation of HBEC with 10-100 micrograms.ml-1 HIE, significantly increased the total number of ICAM-1 positive cells, which were significantly decreased on incubation of the cells in the presence 10(-5) M hydrocortisone. Conditioned medium from HIE-exposed HBEC lead to significant increase in neutrophil chemotaxis and adhesion to endothelial cells in vitro. These results suggest that HIE may affect epithelial cell function and influence inflammation of the airway mucosa via induction of proinflammatory mediators.
The Safety of Rosuvastatin as Used in Common Clinical Practice
Authors: Alawi A. Alsheikh-Ali, Marietta S. Ambrose, Jeffrey T. Kuvin, Richard H. Karas
Journal: Circulation (2005)

Statins are currently the mainstay of dyslipidemia management for the primary and secondary prevention of cardiovascular disease. Controversial concerns about the safety of the newly marketed statin rosuvastatin have been raised on the basis of premarketing studies and a few postmarketing reports.We reviewed rosuvastatin-associated adverse events reported to the US Food and Drug Administration over its first year of marketing. On the basis of prescription data obtained from IMS Health, rates of adverse event reports (AERs) per million prescriptions were calculated. Rates of rosuvastatin-associated AERs over its first year of marketing were compared with those seen with atorvastatin, simvastatin, and pravastatin over the concurrent timeframe and during their respective first years of marketing. Comparison was also made to the first year of marketing of cerivastatin. The primary analysis examined the composite end point of AERs of rhabdomyolysis, proteinuria, nephropathy, or renal failure. With either timeframe comparison, rosuvastatin was significantly more likely to be associated with the composite end point of rhabdomyolysis, proteinuria, nephropathy, or renal failure AERs. Reported cases of rhabdomyolysis, proteinuria, or renal failure tended to occur early after the initiation of therapy and at relatively modest doses of rosuvastatin. The increased rate of rosuvastatin-associated AERs relative to other widely used statins was also observed in secondary analyses when other categories of AERs were examined, including adverse events with serious outcomes, liver toxicity, and muscle toxicity without rhabdomyolysis.The present analysis supports concerns about the relative safety of rosuvastatin at the range of doses used in common clinical practice in the general population.
To stain HUH7 cells with hepcidin using immunohistochemistry
Authors: A. Sangwaiya, A. Dhar, F. Siddiqui, M. Busbridge, J. Arnold, M. Thursz
Journal: Gut (2011)

<h3>Introduction</h3> Hepcidin is a central iron regulator, formed predominantly in the liver. Hepcidin-25 causes hypoferremia by binding to ferroportin channels present on enterocytes, macrophages and hepatocytes. This study was to examine the presence of hepcidin in HuH7 cell line with use of immunohistochemical staining. <h3>Methods</h3> Immunohistochemistry was then carried out on HuH7 cells. The cells were cultured. Slides were then incubated with blocking solution, (3% FBS, 1% BSA, 0.05% Tween in Tris-buffered saline (TBS)) for 30 min, followed by a 4°C overnight incubation with purified rabbit antihepcidin purified primary antibody (1 in 800 dilution). Sections were then incubated for 1 h with secondary antirabbit antibody conjugated with horseradish peroxidase (HRP; Sigma Aldrich). The reaction was visualised by the addition of 3,39diaminobenzidine (DAB) substrate (Sigma Aldrich) for 5 min, and the reaction was stopped by washing with laboratory-grade water. Sections were counterstained with haematoxylin (Sigma Aldrich, UK) for 1 min. Slides were then dehydrated in a 70%, 95% and 100% ethanol (2 min each), cleared in xylene for 5 min and then mounted in DPX (Sigma Aldrich). <h3>Results</h3> Using rabbit polyclonal antibody against human hepcidin, the authors were able to stain the HuH 7 cells with hepcidin and demonstrate a cytoplasmic staining pattern (see figure 1). <h3>Conclusion</h3> The findings are in keeping with the current knowledge of cytoplasmic presence of hepcidin. With demonstration of hepcidin in HuH7 cells should pave way for further studies in the pathways of hepcidin regulation.
Emerging role of cannabinoids in gastrointestinal and liver diseases: basic and clinical aspects
Authors: A A Izzo, M Camilleri
Journal: Gut (2008)

A multitude of physiological effects and putative pathophysiological roles have been proposed for the endogenous cannabinoid system in the gastrointestinal tract, liver and pancreas. These range from effects on epithelial growth and regeneration, immune function, motor function, appetite control, fibrogenesis and secretion. Cannabinoids have the potential for therapeutic application in gut and liver diseases. Two exciting therapeutic applications in the area of reversing hepatic fibrosis as well as antineoplastic effects may have a significant impact in these diseases. This review critically appraises the experimental and clinical evidence supporting the clinical application of cannabinoid receptor-based drugs in gastrointestinal, liver and pancreatic diseases. Application of modern pharmacological principles will most probably expand the selective modulation of the cannabinoid system peripherally in humans. We anticipate that, in addition to the approval in several countries of the CB<sub>1</sub> antagonist, rimonabant, for the treatment of obesity and associated metabolic dysfunctions, other cannabinoid modulators are likely to have an impact on human disease in the future, including hepatic fibrosis and neoplasia.
Acute Myoglobinuria and Heroin Snorting
Authors: Richard S. D'Agostino
Journal: JAMA (1979)

ACUTE rhabdomyolysis with myoglobinuria has been associated with hereditary enzyme deficiencies, severe exertion, metabolic derangements, trauma, and toxins, most notably alcohol. In recent years, intravenous heroin injection has been reported increasingly as a cause of acute rhabdomyolysis. This report details a case of myoglobinuria associated with inhalation of a heroin mixture as snuff. <h3>Report of a Case</h3> A 20-year-old man was hospitalized because of muscle pain of four days' duration. He was in good health until five days previously, when he noted tea-colored urine. The following day he experienced cramping pain in both thighs that was aggravated by movement. Attempts to relieve the pain by exercising increased the discomfort. Over the next several days, the pain worsened and spread to involve the calves and upper arms. He denied recent trauma or strenuous exercise. He admitted occasional use of alcohol and marijuana but denied the use of any other drugs. He
The Art of Pimping
Authors: Allan S. Detsky
Journal: JAMA (2009)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Nebuliser performance, pharmacokinetics, airways and systemic effects of salbutamol given via a novel nebuliser delivery system ("Ventstream").
Authors: D M Newnham, B J Lipworth
Journal: Thorax (1994)

BACKGROUND--Currently available nebulisers are inefficient and show variable aerosol deposition in the lung owing to the differences in the particle size generated. The aim of this study was to compare systemic absorption and bronchodilator effects of salbutamol given via a novel ("Ventstream") and a conventional ("Hudson Updraft II") nebuliser system, having initially evaluated the performance of both nebulisers in vitro. The "Ventstream" nebuliser uses a one way valve system to provide an additional inspiratory side flow to match aerosol delivery with tidal volume. METHODS--Nebuliser output and particle distribution from 10 Ventstream and 10 Hudson nebulisers were compared in vitro. Eight asthmatic patients, FEV1 55(2)% predicted, were then randomised to receive salbutamol via Ventstream or Hudson nebulisers on separate days. On each day cumulative doses of inhaled salbutamol were given: 1.25 mg, 2.5 mg (1.25 + 1.25 mg), and 5.0 mg (2.5 + 2.5 mg). Airways responses, systemic responses, and plasma salbutamol concentrations were measured at each dose and for up to 240 minutes after the final dose. RESULTS--The in vitro comparison showed a greater respirable fraction with a higher percentage volume of particles &lt; 5 microns in diameter using Ventstream than Hudson nebulisers (mean (95% CI) for difference): 25.4% (95% CI 22.4% to 28.3%), and a higher aerosol rate of output: 0.08 g/min (95% CI 0.05 to 0.11 g/min). At the 5.0 mg dose the Ventstream produced a twofold greater concentration of plasma salbutamol than the Hudson nebuliser (AUC0-240): 392.1 ng/ml.min (95% CI 240.6 to 543.6 ng/ml.min). There was a higher AUC0-240 for PEFR with the Ventstream than with the Hudson nebuliser: 74.161 x 10(2) (95% CI 39.50 to 108.821 x 10(2). For FEV1 and FEV25-75 there was a difference in the peak response between the 5.0 mg and 2.5 mg doses with the Ventstream only. Extrapulmonary beta 2 responses were greater with the Ventstream than with the Hudson at 2.5 mg and 5.0 mg doses, although the differences did not appear to be clinically relevant. CONCLUSIONS--The Ventstream produced a twofold increase in the delivery of salbutamol to the lung compared with the Hudson nebuliser, and there was an associated increase in systemic beta 2 responses with an improvement in some parameters of bronchodilator efficacy. As a consequence of improved delivery with the Ventstream, it may be possible to halve the drug dose to produce similar bronchodilator efficacy at reduced cost. Further studies are required to evaluate the value of the Ventstream for delivery of nebulised antibiotics and corticosteroids.
Economic evaluation in health: a thumb nail sketch
Authors: D P Kernick
Journal: BMJ (1998)

Health economics uses traditional economic theory to consider problems in health care. Although health economics can be applied at a number of levels, including analysis of the demand for health care, planning and budgeting, monitoring and evaluation, it is economic evaluation of treatments that will be of most interest to doctors. Against a background of increasing demands on limited health resources, economic evaluation helps decision making by considering the "outputs" of competing interventions in relation to the resources that they consume (figure). To address these issues, relevant outputs must be defined, costs measured, and studies relating outputs to their costs undertaken.1 Economic evaluation relates outputs of competing interventions to the resources consumed Doctors will be presented with increasing numbers of economic studies relevant to all aspects of health care. All studies will have the same basic constructs. Here, simple analysis of the title page and summary of a published paper on ramipril in heart failure (reprinted in the box) is used to highlight issues to be borne in mind when assessing ductory texts economic evaluations in health. Points at issue are italicised and numbered in relation to subsequent annotations. #### Summary points Economic evaluations utilise economic theory to facilitate choice between competing health interventions when resources are scarce Guidelines for the conduct of these studies exist, but disagreement over methodology and inherent problems in many areas, such as valuation of human life and wellbeing, remain A working knowledge of the subject is essential if those delivering health care are … RETURN TO TEXT
Abstract 4345: Proteasome inhibitor, bortezomib, inhibits cell proliferation and induces apoptosis of medulloblastoma cells
Authors: Fan Yang, Veronica Jove, Shirley Chang, Michael Hedvat, Xiangli Liu, Yun Yen, Richard Jove
Journal: Cancer Research (2010)

Abstract Medulloblastoma is the most common brain tumor in children. Proteasome inhibitors have been reported to inhibit cell proliferation and survival in a variety of tumor cells. Bortezomib (Velcade), an inhibitor of the 26S proteasome, has been approved by FDA to treat multiple myeloma. Here, we investigated effects of bortezomib on human medulloblastoma cells. Bortezomib inhibited cell proliferation and induced apoptosis of Daoy medulloblastoma cells in a time- and dose-dependent manner. Significantly, a relatively low dose of 10 nM bortezomib effectively inhibited the viability of Daoy cells within 48 h. Bortezomib increased the release of cytochrome C to cytosol, resulting in activation of caspase-9 and caspase-3, and cleavage of poly(ADP-ribose) polymerase (PARP). Caspase inhibitor (Z-VAD-FMK) could rescue tumor cells from the cytotoxicity of bortezomib on both cell proliferation and survival. Bortezomib increased expression of the pro-apoptotic protein, Bak, and cleavage of the anti-apoptotic protein, Mcl-1. In addition, bortezomib increased the expression of p21Cip1, a negative regulator of cell cycle progression. Bortezomib also induced the accumulation of phosphorylated I[[Unable to Display Character: &amp;#312;]]Bα in Daoy cells, resulting in inhibition of NF[[Unable to Display Character: &amp;#312;]]B signaling. MG-132, another proteasome inhibitor, had similar effects on Daoy cells. Moreover, bortezomib inhibited the growth of human medulloblastoma cells in a mouse xenograft model. Our data suggest that proteasome inhibitors are promising drugs for the treatment of pediatric medulloblastomas. Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4345.
Partitioning of Respiratory System Resistance in Children with Respiratory Insufficiency
Authors: ATHANASIOS G. KADITIS, SHEKHAR T. VENKATARAMAN, WALTER A. ZIN, ETSURO K. MOTOYAMA
Journal: American Journal of Respiratory and Critical Care Medicine (1999)

Using end-inspiratory airway occlusion, respiratory system resistance (Rrs) can be partitioned into a flow-resistive component (Rint), and an additional component ( Δ R), reflecting viscoelasticity and time constant inequalities. We studied flow and volume dependence of Rrs and its subdivisions (Rint and Δ R) in 13 children, seven mechanically ventilated for pulmonary insufficiency (Group 1; six with parenchymal lung disease; one with lower airway obstruction) and six without primary lung disorder (Group 2). In comparison with healthy children, Rint was increased in the patient with lower airway obstruction and five of six patients without primary lung disorder but in only one of six with parenchymal lung disease. Δ R was increased in all seven patients in Group 1 and in four of six patients in Group 2. The directions of changes in Rint and Rrs with increasing flow (isovolume conditions) and with increasing volume (isoflow conditions) were variable. Δ R decreased exponentially (p < 0.05) with increasing flow in 11 of 13 subjects and increased with increasing tidal volume (Vt) in 12 of 13. Thus, Δ R was increased in most children on mechanical ventilation with or without primary lung disease; its volume and flow dependence were opposite to that of airway resistance.
Cancer's killing fields
Authors: K. Abbasi
Journal: BMJ (1998)

Kamran Abbasi looks at how Channel 4's Cancer Wars (8 pm on January 18 and 25 and February 1 and 8) explores the political dimensions of cancer 

Nazi scientists working sinisterly in dark laboratories; a whole town suffering the harsh discipline of the Third Reich; the triumphant Allies showering gifts on liberated townsfolk. It might sound like the storyline from a second world war yarn, but in fact these are images from Channel 4's Cancer Wars . Billed as a “major four part series telling the story of cancer through the eyes of those who have suffered, those who have tried to combat it and those who have stood in the way,” Cancer Wars begins with Hitler's Germany.

While the Jews were being terrorised, it seems Hitler was on a mission to improve the health of the Aryan race. German scientists investigated smoking and cancer and found a link. In the German town of Jena …
Studies of Venereal Disease
Authors: King K. Holmes
Journal: JAMA (1967)

Previous studies of the treatment of nongonococcal urethritis (NGU) have generally not been closely controlled, and have often produced conflicting results. In the present study, 96 men with NGU were treated with placebo or tetracycline hydrochloride while "confined" aboard an aircraft carrier at sea. A seven-day tetracycline regimen was more effective than a four-day tetracycline regimen or placebo in the short-term cure of NGU.
607 DEFICIENT THYMOPOIESIS CONTRIBUTES TO PERIPHERAL T CELL COMPARTMENT DEPLETION IN CIRRHOSIS
Authors: M. Lario, L. Muñoz, J. Monserrat, M. Ubeda, M.J. Borrero, L.E. Chara, M.A. Sánchez, D. Díaz, M. Alvarez-Mon, A. Albillos
Journal: Journal of Hepatology (2011)
Cyclic Strain–Induced Monocyte Chemotactic Protein-1 Gene Expression in Endothelial Cells Involves Reactive Oxygen Species Activation of Activator Protein 1
Authors: B. S. Wung, J. J. Cheng, H. J. Hsieh, Y. J. Shyy, D. L. Wang
Journal: Circulation Research (1997)

Abstract Endothelial cells (ECs) are constantly exposed to blood pressure–induced mechanical strain. We have previously demonstrated that cyclic strain can induce gene expression of monocyte chemotactic protein-1 (MCP-1). The molecular mechanisms of gene induction by strain, however, remain unclear. Recent evidence indicates that intracellular reactive oxygen species (ROS) can act as a second messenger for signal transduction and thus affect gene expression. The potential role of ROS in strain-induced MCP-1 expression was investigated. ECs under cyclic strain induced a sustained elevated production of intracellular superoxide. ECs under strain or pretreated with either H 2 O 2 or xanthine oxidase/hypoxanthine induced MCP-1 expression. Strain- or oxidant-induced MCP-1 mRNA levels could be inhibited by treating ECs with catalase or antioxidant N -acetyl-cysteine (NAC). Functional analysis of MCP-1 promoter and site-specific mutations indicates that the proximal tissue plasminogen activator–responsive element (TRE) in the −60-bp promoter region is sufficient for strain or H 2 O 2 inducibility. Electrophoretic mobility shift assays demonstrated an increase of nuclear proteins binding to TRE sequences from ECs subsequent to strain or H 2 O 2 treatment. NAC or catalase pretreatment of ECs inhibited the strain- or H 2 O 2 -induced AP-1 binding. These results clearly indicate that cyclic strain inducibility of MCP-1 in ECs uses the interaction of AP-1 proteins with TRE sites via the elevation of intracellular ROS levels in strained ECs. These findings emphasize the importance of intracellular ROS in the modulation of hemodynamic force–induced gene expression in vascular ECs.
Interleukin 12 and myeloperoxidase (MPO) in Vietnamese children with acute respiratory distress syndrome due to Avian influenza (H5N1) infection☆
Authors: Thuy T.B. Phung, San T. Luong, Shoji Kawachi, Hiroyuki Nunoi, Liem T. Nguyen, Toshinori Nakayama, Kazuo Suzuki
Journal: Journal of Infection (2010)