tbuckley/cabot-search huggingface dataset:
Negro Enrollment in Medical Schools
Authors: Anne E. Crowley
Journal: JAMA (1969)

For the past decade more and more attention has been directed to disadvantaged groups in the American population. Many educational institutions are showing an increasing awareness of the need to give special consideration to persons from impoverished backgrounds, specifically the American Negroes. Because Negroes are underrepresented in the medical profession, educators in that field are also becoming interested in this problem. Even though more than 11% of the nation's population is Negro, less than 2% of American physicians are black. Or to put it another way, among white citizens, one American in 560 becomes a doctor; among Negroes, it is one in 3,800 (<i>Statistical Abstracts of the United States, 1968</i>, Bureau of Census, p 23).
Plasma Protein and Lipoprotein Distribution of Clozapine
Authors: Ric M. Procyshyn, Nathan B. Kennedy, Samantha Marriage, Kishor M. Wasan
Journal: American Journal of Psychiatry (2001)

The authors' goal was to determine what effect dyslipidemia has on clozapine's plasma distribution.[(3)H]Clozapine plus cold clozapine (335 ng/ml) were incubated in plasma samples with varying total cholesterol, lipoprotein cholesterol, and triglyceride concentrations. Following incubation, the plasma was separated into its lipoprotein and lipoprotein-deficient fractions by density gradient ultracentrifugation and clozapine distribution was determined.Compared with the plasma standard, significantly more clozapine was recovered in the very-low-density lipoprotein fraction, which contained elevated total cholesterol and triglycerides. Correlation analysis revealed a positive correlation between total plasma triglyceride concentration and clozapine recovery in this fraction.In plasma samples with elevated triglycerides, clozapine shifts from the lipoprotein-deficient fraction to the very-low-density lipoprotein fraction. This redistribution of clozapine may affect the pharmacological activity of clozapine.
SEX, OBESITY AND TYPE 2 DIABETES AFFECT THE INTRAMYOCELLULAR FATE OF GLUCOSE IN HUMANS
Authors: Linda Ruth Peterson, Pilar Herrero, C. Huie Lin, Matthew Lyons, Carmen Dence, Zulfia Kisrieva-Ware, Alan D. Waggoner, Victor G. Davila-Roman, Deborah Delano, Robert J. Gropler
Journal: Journal of the American College of Cardiology (2011)
Abstract P1-03-12: The First Reproducible Model of Primary Human Ductal Carcinoma In Situ (DCIS) Using the Mouse Intraductal (MIND) Method
Authors: K Valdez, W Smith, F Fan, D Medina, F. Behbod
Journal: Cancer Research (2010)

Abstract Past studies of the molecular mechanisms regulating human DCIS progression to invasion have been limited by a lack of suitable human models. The current models have not utilized primary human DCIS placed in their natural microenvironment, i.e., inside the mammary ducts, and do not mimic the heterogeneity of human DCIS. Previously, we reported the development of a mouse xenograft model using established breast DCIS cell lines, SUM-225 and DCIS.COM by the mouse intraductal (MIND) method. MIND involves injection of human DCIS cells into the primary ducts of immunodeficient mouse mammary glands via the nipple. In this study we demonstrate the reproducible growth of human primary DCIS cells derived from patient biopsy samples using the MIND model. Core biopsies from consenting patients are processed to isolate the epithelial cell component and injected. To date, 69 patients have consented to provide core biopsy tissue and we have received tissue from 38. Of these, 14 samples have been confirmed as positive for DCIS, and 2 as atypical hyperplasia, based on the pathology report of adjacent biopsies. The biopsy samples were heterogeneous with respect to ER, PR, Ki67, Her-2 and histology. A total of 24 mammary glands from immunodeficient mice have been injected with these cells and analyzed for growth by immunofluorescent (IF) with antibodies directed at human-specific cytokeratin-5 and/or 19 and smooth muscle actin. Table 1. Summary of grewlh of human primary biopsies in (tie MIND xenograft The average number of cells recovered per mg of tissue are shown in Table 1. Biopsies diagnosed as normal yielded only 91±34 cells/mg compared with most DCIS cases that showed an average cell number of 971 per mg tissue. Our results indicate that human DCIS and hyperplasia cells from biopsy samples are capable of growing within the NOD-SCID IL2Rgammanull (NSG) mouse mammary ducts. NSG mice mammary ducts are more suitable hosts for the growth of human primary DCIS cells, compared to SCID-Beige. Furthermore, the higher number of cells recovered following digestion predicted the positive DCIS growth rate. DCIS cells formed single and multi-layered epithelium inside the ducts and were heterogeneous with respect to the expression of human specific cytokeratins. The MIND xenografts recapitulated the patient's original DCIS as evidenced by IF staining for the biomarkers ER and Her-2 in the primary human biopsies and MIND xenografts. These results provide the first reproducible model of primary human DCIS for studying the temporal processes of early breast cancer progression. Future experiments will characterize the cellular basis for the subtypes of DCIS and delineate the distinct molecular and cellular mechanisms of early breast cancer invasion, and cancer stem cell growth and self-renewal. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr P1-03-12.
Inhaled nitric oxide in congenital heart disease.
Authors: J D Roberts, P Lang, L M Bigatello, G J Vlahakes, W M Zapol
Journal: Circulation (1993)

Congenital heart lesions may be complicated by pulmonary arterial smooth muscle hyperplasia, hypertrophy, and hypertension. We assessed whether inhaling low levels of nitric oxide (NO), an endothelium-derived relaxing factor, would produce selective pulmonary vasodilation in pediatric patients with congenital heart disease and pulmonary hypertension. We also compared the pulmonary vasodilator potencies of inhaled NO and oxygen in these patients.In 10 sequentially presenting, spontaneously breathing patients, we determined whether inhaling 20-80 ppm by volume of NO at inspired oxygen concentrations (FIO2) of 0.21-0.3 and 0.9 would reduce the pulmonary vascular resistance index (Rp). We then compared breathing oxygen with inhaling NO. Inhaling 80 ppm NO at FIO2 0.21-0.3 reduced mean pulmonary artery pressure from 48 +/- 19 to 40 +/- 14 mm Hg and Rp from 658 +/- 421 to 491 +/- 417 dyne.sec.cm-5.m-2 (mean +/- SD, both p < 0.05). Increasing the FIO2 to 0.9 without adding NO did not reduce mean pulmonary artery pressure but reduced Rp and increased the ratio of pulmonary to systemic blood flow (Qp/Qs), primarily by increasing Qp (p < 0.05). Breathing 80 ppm NO at FIO2 0.9 reduced mean pulmonary artery pressure and Rp to the lowest levels and increased Qp and Qp/Qs (all p < 0.05). While breathing at FIO2 0.9, inhalation of 40 ppm NO reduced Rp (p < 0.05); the maximum reduction of Rp occurred while breathing 80 ppm NO. Inhaling 80 ppm NO at FIO2 0.21-0.9 did not alter mean aortic pressure or systemic vascular resistance. Methemoglobin levels were unchanged by breathing up to 80 ppm NO for 30 minutes.Inhaled NO is a potent and selective pulmonary vasodilator in pediatric patients with congenital heart disease complicated by pulmonary artery hypertension. Inhaling low levels of NO may provide an important and safe means for evaluating the pulmonary vasodilatory capacity of patients with congenital heart disease without producing systemic vasodilation.
The nontrivial doctrine of cognitive neuroscience
Authors: Valerie Gray Hardcastle
Journal: Behavioral and Brain Sciences (1999)

Gold &amp; Stoljar's “trivial” neuron doctrine is neither a truism in cognitive science nor trivial; it has serious consequences for the future direction of the mind/brain sciences. Not everyone would agree that these consequences are desirable. The authors' “radical” doctrine is not so radical; their division between cognitive neuroscience and neurobiology is largely artificial. Indeed, there is no sharp distinction between cognitive neuroscience and other areas of the brain sciences.
Out of the Shadows: Registration of Unreported Trials
Authors: Frank Davidoff
Journal: Annals of Internal Medicine (1997)

Editorials1 October 1997Out of the Shadows: Registration of Unreported TrialsFrank Davidoff, MD, EditorFrank Davidoff, MD, EditorOn Behalf of the Medical Editors Trial AmnestySearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-127-7-199710010-00009 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Reports of properly conducted randomized, controlled trials are the foundation of safe and effective health care. However, a substantial proportion of all such trials never contribute to our knowledge base because they are not submitted for publication [1, 2]. This fact has several important implications for patient care. First, underreporting of trials reduces the power of systematic reviews to detect moderate but clinically important treatment effects. As a result, patients may be denied effective forms of health care. Second, because trials that show more promising treatment effects are more likely to be submitted for publication, research syntheses based on published ...References1. Dickersin K, Min YI. NIH clinical trials and publication bias. J Curr Clin Trials [serial on-line]. 28 April 1993; Doc. No. 50. Google Scholar2. Easterbrook PJ, Berlin JA, Gopalan R, Matthews DR. Publication bias in clinical research. Lancet. 1991; 337:867-72. Google Scholar3. Egger M, Davey Smith G. Misleading meta-analysis. BMJ. 1995; 310:752-4. Google Scholar4. Savulescu J, Chalmers I, Blunt J. Are research ethics committees behaving unethically? Some suggestions for improving performance and accountability. BMJ. 1996; 313:1390-3. Google Scholar Author, Article, and Disclosure InformationAuthors: Frank Davidoff, MD, EditorAffiliations: On Behalf of the Medical Editors Trial Amnesty PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byOutcomes in TransfusionDecreasing publication bias 1 October 1997Volume 127, Issue 7Page: 567-568KeywordsHealth careInformation technologyInternetMammographyPatientsRacial and ethnic issuesResearch designResearch reporting guidelinesSteroidsSystematic reviews ePublished: 15 August 2000 Issue Published: 1 October 1997 Copyright & PermissionsCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Reforming clinical research and development in England
Authors: N. McNally
Journal: BMJ (2003)

The United Kingdom is trying to bring more non-governmental funding into NHS research through partnerships with the commercial and voluntary sectors. But it is still unclear exactly how the reforms in England will work and how trusts will resolve the tensions between patients' needs, financial viability, and the commercial exploitation of research findings 

Essential research into health services is often unattractive to commercial sector funders and requires government support.1 Although appreciable NHS funding has been earmarked for this purpose, critics have argued that much of the budget has disappeared into the general funds for service delivery.2 In 2000, the Department of Health announced a major overhaul of health related research within the NHS aimed at providing a clearer strategic direction.3 The reforms signal an increased role for the commercial sector in the identification of strategic objectives, setting priorities, and in the delivery and exploitation of clinical research. This paper provides an overview of the new funding and organisational arrangements for NHS research in England.

Funding of health research in the United Kingdom is complex. Although most health related research is funded from the commercial sector, the Department of Health is a major contributor (table). In 2002-03 the Department of Health contributed £540m to research on health.4 The current pattern of funding (fig 1) reflects the work of the Culyer review, which was carried out because of concerns over the financial viability of large teaching hospitals after the introduction of the internal market in the NHS. In 1994, the Culyer taskforce recommended that Department of Health funding of health related research should be allocated to support research and development activity in NHS trusts and be clearly identifiable and distinct from funding for clinical services.5 Some 77% (£418m in 2002/03) of research funding is currently allocated to …
New fish-killing alga in coastal Delaware produces neurotoxins.
Authors: Andrea J Bourdelais, Carmelo R Tomas, Jerome Naar, Julia Kubanek, Daniel G Baden
Journal: Environmental Health Perspectives (2002)

Ten fish mortality events, involving primarily Atlantic menhaden, occurred from early July through September 2000 in several bays and creeks in Delaware, USA. Two events involved large mortalities estimated at 1-2.5 million fish in Bald Eagle Creek, Rehoboth Bay. Samples from Indian Inlet (Bethany Beach), open to the Atlantic, as well as from an enclosed area of massive fish kills at nearby Bald Eagle Creek and Torque Canal were collected and sent to our laboratory for analysis. Microscopic examination of samples from the fish kill site revealed the presence of a single-cell Raphidophyte alga Chattonella cf. verruculosa at a maximum density of 1.04 x 10(7) cells/L. Naturally occurring brevetoxins were also detected in the bloom samples. Besides the Chattonella species, no other known brevetoxin-producing phytoplankton were present. Chromatographic, immunochemical, and spectroscopic analyses confirmed the presence of brevetoxin PbTx-2, and PbTx-3 and -9 were confirmed by chromatographic and immunochemical analyses. This is the first confirmed report in the United States of brevetoxins associated with an indigenous bloom in temperate Atlantic estuarine waters and of C. cf. verruculosa as a resident toxic organism implicated in fish kills in this area. The bloom of Chattonella continued throughout September and eventually declined in October. By the end of October C. cf. verruculosa was no longer seen, nor was toxin measurable in the surface waters. The results affirm that to avoid deleterious impacts on human and ecosystem health, increased monitoring is needed for brevetoxins and organism(s) producing them, even in areas previously thought to be unaffected.
Adoptive transfer studies demonstrating the antiviral effect of natural killer cells in vivo.
Authors: J F Bukowski, J F Warner, G Dennert, R M Welsh
Journal: The Journal of Experimental Medicine (1985)

We carried out adoptive transfer studies to determine the role of natural killer (NK) cells in resistance to murine cytomegalovirus (MCMV) and lymphocytic choriomeningitis virus (LCMV). We transferred leukocytes from adult mice into suckling mice 1 d before injecting them with virus. Resistance was measured by enhancement of survival and reduction of virus multiplication in the spleens of recipient mice. The phenotype of the cell population capable of mediating resistance to MCMV was that of a nylon wool-nonadherent, asialo GM1+, NK 1.2+, Ly-5+, Thy-1-, Ia-, low density lymphocyte; this is the phenotype of an NK cell. Cloned NK cells, but not cloned T cells, provided resistance to MCMV in suckling mice. Cloned NK cells also provided resistance to MCMV in irradiated adult mice, and antibody to asialo GM1, which depletes NK cell activity in vivo, enhanced the synthesis of MCMV in athymic nude mice. Neither adult leukocytes nor cloned NK cells influenced LCMV synthesis in suckling mice. We conclude that a general property of NK cells may be to provide natural resistance to virus infections, and that NK cells can protect mice from MCMV but not from LCMV.
Primary medical care outside normal working hours: review of published work
Authors: L Hallam
Journal: BMJ (1994)

Systemic lupus erythematosus(SLE) is a chronic autoimmune disease,characterised by alterations in both the innate and adaptive immune system ultimately leading to the loss of immunologic tolerance and occurrence of autoantibodies against nuclear material. Lupus nephritis is one of the most severe features of SLE determining an increase in morbidity e mortality rates.Renal biopsy still represent a fundamental diagnostic and prognostic tool for LN.Therefore, non-invasive surrogate biomarkers of active LN are urgently needed.Circulating, heterogeneous subcellular microparticles(MPs) are released from cells and platelets constitutively and upon cellular activation or apoptosis.Such MPs may reflect the state of their parental cells and tissues, and could serve as markers of pathology. Particularly in SLE, MPs are potential biomarkers and triggers of autoimmunity.Recent studies have demonstrated increased of plasmatic EMPs in patients with SLE active disease and their reduction after treatment. The aim of this study was to investigate levels of EMPs in a cohort of SLE patients with and without renal involvement compared to healthy controls. MPs were isolated from plasma and urine and characterised by flow cytometry using AnnessinV (a probe that binds to the exposed phosphatidilserine – PS)and antibodies against surface markers endothelial cells(CD31 +CD41-). Sixty SLE patients and 29HC were studied. Twenty-eight patients had renal involvement. The total number of plasmatic MPs was lower in SLE patients than HC(p=0.001). In contrast there was no significant difference EMPs between the two groups. When the patients were divided according to renal involvement, the patients with active-LN(A-LN) showed lower plasmatic EMPs in comparison to inactive LN(I-LN) (p=0.01), while the patients with I-LN had higher EMPs than HC(p=0.002).There was no significant difference of total urinaryMPs between SLE patients and HC. UrinaryEMPs were higher in SLE and in LN patients than HC. The results of the present study show increased EMPs in patients with LN in remission. Circulating-EMPs have been considered as a potential biomarker of endothelial activation and damage in several autoimmune disorders, and higher EMP have been detected in patients with vasculitis and associated with disease activation. According to our results, plasmatic EMPs are higher in inactive-LN patients than in HC. These results may suggest a potential role of EMP as a biomarker of LN.
Lymphocyte arrest requires instantaneous induction of an extended LFA-1 conformation mediated by endothelium-bound chemokines
Authors: Revital Shamri, Valentin Grabovsky, Jean-Marc Gauguet, Sara Feigelson, Eugenia Manevich, Waldemar Kolanus, Martyn K Robinson, Donald E Staunton, Ulrich H von Andrian, Ronen Alon
Journal: Nature Immunology (2005)
Effects of prematurity and intrauterine growth on respiratory health and lung function in childhood.
Authors: R J Rona, M C Gulliford, S Chinn
Journal: BMJ (1993)

OBJECTIVE--To determine whether birth weight and gestational age are associated with respiratory illness and lung function in children aged 5-11 years. DESIGN--Cross sectional analysis of parent reported birth weight, gestational age, and respiratory symptoms; parental smoking and social conditions; forced vital capacity (FVC), forced expiratory volume in one second (FEV1), forced expiratory rates between 25% and 75% and 75% and 85% (FEF25-75 and FEF75-85), and height. SETTING--Primary schools in England and Scotland in 1990. SUBJECTS--5573 children aged 5-11 (63.3% of eligible children) had respiratory symptoms analysed and 2036 children (67.1% of eligible children) had lung function measured. MAIN OUTCOME MEASURES--Symptoms of asthma, bronchitis, occasional and frequent wheeze, cough first thing in the morning, and cough at any other time and lung function. RESULTS--Birth weight adjusted for gestational age was significantly associated with all lung function measurements, except FEF25-75. The association remained for FVC (b = 0.475, 95% confidence interval 0.181 to 0.769) and FEV1 (b = 0.502, 0.204 to 0.800) after adjustment for gestational age, parental smoking, and social factors. FEF75-85 was the only lung function related to gestational age. Respiratory symptoms, especially wheeze most days (adjusted odds ratio 0.9, 0.84 to 0.97) were significantly associated with prematurity. Every extra week of gestation reduced the risk of severe wheeze by about 10%. CONCLUSIONS--Lung function is affected mainly by intrauterine environment while respiratory illness, especially wheezing, in childhood is related to prematurity.
ABC of colorectal diseases. Pilonidal sinus.
Authors: D. J. Jones
Journal: BMJ (1992)

Pilonidal disease is a common affliction of young adults that causes considerable suffering, inconvenience, and time lost from work.Treatment varies greatly and is often less than satisfactory.The rate of recurrence after surgery is purported to be as high as 50%.Pilonidal sinus with hairy natal cleft and .secondarylateral openings.What is a pilonidal sinus?*;> ; ; 0:; Y; A pilonidal sinus consists of a characteristic midline opening or series of penings in the natal cleft about 5cm from the anus.The skin enters the '.i''-,.''sinus, giving the opening a smooth edge.This primary track leads into a subcutaneous cavity which contains granulation tissue and usually a nest of ..:* .'f..i r:.i..'ĩ i,f. .hairs, which may be seen projecting through the skin opening.Many patients have secondary lateral openings 2-5 cm above the midline pit.The skin opening and superficial portion of the track are lined with squamous 0e$ R 100 cell epithelium, but the deep cavity and its extensions are not.Non-infected pilonidal sinus. Pathogenesis.W ~~~~~~~~~af X _y ^h_A 8a 3A ~~~~~~~~~~~Pilonidal sinuses are now widely accepted to be acquired abnormalities, although theories ofai congenital origin, from postcoccygeal cells or vestigial scent glands, were once popular.Sinuses to the neural canal and dura are ~~r ~~rare; they usually present in childhood and are in the lumbar rather than ~~~~~* ~~~~~~sacral region.Pilonidal disease starts at the onset of puberty, when sex hormones start .~actingon ilosebaceous glands in the na'tal cleft.A hair follicle becomes distended with keratinand subsequently infected, leading to a folliculitis Mechanism ~~~~~~~~hv trck whicheesi pas cadlyan hspilonidal sinusestn.