tbuckley/cabot-search huggingface dataset:
Randomised, double blind placebo controlled trial of pentoxifylline in the treatment of venous leg ulcers
Authors: J J Dale, C V Ruckley, D R Harper, B Gibson, E A Nelson, R J Prescott
Journal: BMJ (1999)

<h3>Abstract</h3> <b>Objective:</b> To determine whether pentoxifylline 400 mg (Trental 400) taken orally three times daily, in addition to ambulatory compression bandages and dressings, improves the healing rate of pure venous ulcers. <b>Design:</b> Randomised, double blind placebo controlled trial, parallel group study of factorial design, permitting the simultaneous evaluation of alternative pharmaceutical, bandaging, and dressings materials. <b>Setting:</b> Leg ulcer clinics of a teaching and a district general hospital in southern Scotland. <b>Participants:</b> 200 patients with confirmed venous ulcers and in whom other major causal factors were excluded. <b>Interventions:</b> Pentoxifylline 400 mg three times daily or placebo. <b>Main outcome measure:</b> Complete healing (full epithelialisation) of all ulcers on the trial leg. <b>Results:</b> Complete healing occurred in 65 of the 101 (64%) patients receiving pentoxifylline and 52 of the 99 (53%) patients receiving placebo. <b>Conclusions:</b> The difference in the healing rates between patients taking pentoxifylline and those taking placebo did not reach statistical significance. <h3>Key messages</h3> Leg ulcers cost the NHS around £400 million per annum 50%-75% of venous leg ulcers can be succesfully treated with dressings and compression bandages but take many months to heal A drug that reduced the healing time of venous ulcers would be useful, although no agent has been proved to be effective to date Trials with pentoxifylline, a vasoactive drug used in the treatment of peripheral vascular diseases, as an adjunct to the treatment of venous ulcers have been inconclusive At the 5% level, pentoxifylline had a non-significant effect on healing rates of pure venous ulcers
Massive bladder haemorrhage
Authors: J. McIvor, G. Williams, M Y Ezzibdeh
Journal: BMJ (1986)

succession of withdrawals of non-steroidal antiinflammatory drugs, including several of the most recently introduced and best tested products.The supporting evidence for withdrawal has not been published, but the decisions seem to have been based on yellow cards or journal anecdotes.Such reports are useful for generating hypotheses about possible risks but are of practical value only when the events reported are very rare or unusual.NHS data cannot be used to provide estimates for the number of patients who might be at risk from adverse reactions.For example, 12 000 pre- scriptions could provide a month's supply for 12 000 patients or a year's supply for 1000.Some of the non-steroidal anti-inflammatory drugs, such as indomethacin, have been used by many patients for up to 20 years, while others, such as piroxicam, have been available for five years or less.The authors cannot distinguish short term from long term use among their patients or distinguish between individuals whose ulcers were caused by non-steroidal anti-inflammatory drugs and those whose ulcers would have occurred spontaneously.They have no estimate of the
More consultant "generalists" are needed to deliver seven day hospital care, report says
Authors: Z. Kmietowicz
Journal: BMJ (2013)

Reviewing hospital patients on Saturdays and Sundays would lead to earlier discharges, more availability of beds, and safer and more effective care, says a report from more than 20 royal colleges and faculties.

But this will require more consultants to be “generalists” with the skills to manage patients across different specialty areas, says the report by the Academy of Medical Royal Colleges.1

Currently, 11% of people occupying hospital beds do not need to be in hospital and their discharge is delayed by non-medical factors, says the academy.

Although keeping hospitals fully functioning at weekends is likely to require investment in both hospital and community services in the first instance, over time costs could fall, it adds.

In a foreword to the report Norman Williams, steering group chairman and president of the Royal College of Surgeons, and Terence Stephenson, chairman of the Academy of Medical Royal Colleges, say …
Utilization of biomarker data for clinical and environmental intervention.
Authors: D C Christiani
Journal: Environmental Health Perspectives (1996)

Of the 189 air toxics listed in the Clean Air Act, a substantial number are important in potentially causing adverse health effects in several organ systems. Although the major health effects are manifested as respiratory diseases, especially airways disease, these agents may cause cancer and premature mortality, probably from cardiopulmonary disease. Validated biologic markers may be useful in identifying early effects to improve our understanding of exposure-response relationships and clarify susceptibility. However, the knowledge obtained from epidemiologic studies utilizing these new molecular tools will reduce morbidity and mortality from air toxics only when they can be applied effectively in the prevention and control of disease. Intervention strategies using these markers can be used to identify etiologic factors and assess the effectiveness of exposure reduction, and, in some instances, chemoprevention. This paper illustrates examples of these intervention strategies and reviews the current strengths and limitations of environmental molecular epidemiology in controlling disease caused by air toxics.
Increased duodenal iron uptake and transfer in a rat model of chronic hypoxia is accompanied by reduced hepcidin expression
Authors: P S Leung
Journal: Gut (2005)

<b>Background:</b> Despite the requirement for increased iron delivery for erythropoiesis during hypoxia, there is very little information on how duodenal iron uptake and its transfer to the blood adapts to this condition. <b>Aims:</b> To assess the effects of 30 days of chronic hypoxia in rats on luminal iron uptake and transfer of the metal to blood, together with gene expression of hepcidin, a proposed negative regulator of iron transport. <b>Methods:</b> 59-Fe uptake by isolated duodenum and its transfer to blood by in vivo duodenal segments was measured after exposure of rats to room air or 10% oxygen for four weeks. Liver hepcidin expression was measured by real time reverse transcription-polymerase chain reaction. The effects of hypoxia on hepcidin gene expression by HepG2 cells was also determined. <b>Results:</b> Hypoxia did not affect villus length but enhanced (+192.6%) luminal iron uptake by increasing the rate of uptake by all enterocytes, particularly those on the upper villus. Hypoxia promoted iron transfer to the blood but reduced mucosal iron accumulation in vivo by 66.7%. Hypoxia reduced expression of hepcidin mRNA in both rat liver and HepG2 cells. <b>Conclusions:</b> Prolonged hypoxia enhances iron transport from duodenal lumen to blood but the process is unable to fully meet the iron requirement for increased erythropoiesis. Reduced secretion of hepcidin may be pivotal to the changes in iron absorption. The processes responsible for suppression of hepcidin expression are unknown but are likely to involve a direct effect of hypoxia on hepatocytes.
Treating anorexia nervosa
Authors: J. Russell
Journal: BMJ (1995)

“None of these cases, however exhausted, are really hopeless as long as life exists,” commented William Gull about anorexia nervosa in 1873.1 Doctors have up to now been exhorted never to give up in the attempt to induce anorectic patients to eat and restore weight even if, as Gull also said, this might entail the need to “fight for every mouthful.” Two personal views in this week's journal2 3 and a recent paper on treating anorexia nervosa as a terminal disease4 raise disturbing questions for those who battle with this common and tragic illness.

Treatment of patients with anorexia nervosa must be constantly reviewed to ascertain that it accords with the five ethical principles of beneficence, autonomy, non-maleficence, justice, and utility. All …
Abstract 3983: Evaluation of data compression strategies for genetic variation calling using next generation sequencing data in normal and tumor samples
Authors: Chunlin Xiao, Eugene Yaschenko, Mikhail Kimelman, Kurt Rodarmer, Stephen Sherry
Journal: Cancer Research (2012)

Abstract The per-base cost of whole genome sequencing has dropped dramatically due to recent advancement of next generation sequencing (NGS) technologies, and a number of large-scale re-sequencing projects, e.g. 1000 Genomes, ICGC, TCGA, GO-ESP, and CGCI etc., have been initiated to extend our knowledge of single nucleotide polymorphisms (SNPs), short insertions/deletions (INDELs) and structural variations (SVs), and relate these variants to human diseases. To date, various compression technologies, including NCBI's cSRA and EBI's CRAM etc., have been developed to significantly reduce the storage footprints and costs. However, whether or not such compression treatments have any impact on genetic variant callings has not been systematically assessed and validated with large scale NGS datasets as different calling algorithms for different variant classes (SNPs, INDELs, or SVs) may have different underlying data requirements. We have developed an integrated analysis framework (VarPipe) to profile genetic mutations using NGS data generated from various sequencing platforms in a uniform manner. This pipeline is also applied to the official data from 1000Genomes (normal samples) and Cancer Genome Characterization Initiative (tumor samples) projects to evaluate the compressions effects on variation callers. With defined quality metrics, the variant callsets from compression-treated and untreated data are carefully evaluated as well as compared to the official variation releases of the corresponding projects so that optimal compression strategy can be developed and recommended for variation detection using NGS data. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3983. doi:1538-7445.AM2012-3983
227 NON-CIRRHOTIC PORTAL HYPERTENSION IN HIV-INFECTED PATIENTS
Authors: I. Maida, E. Vispo, M. Nelson, M. Rios, V. Asensi, G. Sotgiu, P. Barreiro, G. Panos, M. Rodriguez, A. Schofield, V. Soriano
Journal: Journal of Hepatology (2009)
The adipocyte fatty acid-binding protein aP2 is required in allergic airway inflammation
Authors: Bennett Ov Shum, Charles Reay Mackay, Cem Z Gorgun, Melinda J Frost, Rakesh K Kumar, Gokham S Hotamisligil, Michael S Rolph
Journal: Journal of Clinical Investigation (2006)

The adipocyte fatty acid-binding protein aP2 regulates systemic glucose and lipid metabolism. We report that aP2, in addition to being abundantly expressed by adipocytes, is also expressed by human airway epithelial cells and shows a striking upregulation following stimulation of epithelial cells with the Th2 cytokines IL-4 and IL-13. Regulation of aP2 mRNA expression by Th2 cytokines was highly dependent on STAT6, a transcription factor with a major regulatory role in allergic inflammation. We examined aP2-deficient mice in a model of allergic airway inflammation and found that infiltration of leukocytes, especially eosinophils, into the airways was highly dependent on aP2 function. T cell priming was unaffected by aP2 deficiency, suggesting that aP2 was acting locally within the lung, and analysis of bone marrow chimeras implicated non-hematopoietic cells, most likely bronchial epithelial cells, as the site of action of aP2 in allergic airway inflammation. Thus, aP2 regulates allergic airway inflammation and may provide a link between fatty acid metabolism and asthma.
Facilitating prevention in primary care.
Authors: G. Fowler, E. Fullard, M. Gray
Journal: BMJ (1992)

We believe that many general practitioners would practice preventive medicine if they had the opportunity to organise their practice to do this. We therefore provided a "facilitator," who understands the work of a general practice, to help practices that were interested in prevention to set up programmes. She, for example, helped the primary care team to set up objectives, trained practice nurses to measure blood pressure, and set up a system to measure the progress of the programme.
Angiotensin II directly stimulates sodium transport in rabbit proximal convoluted tubules.
Authors: V L Schuster, J P Kokko, H R Jacobson
Journal: Journal of Clinical Investigation (1984)

Numerous previous studies have proposed a role for angiotensin II (AII) in the renal regulation of salt balance. At least one nephron site, the proximal convoluted segment, has been implicated in this role. We used in vitro microperfusion of rabbit proximal convoluted tubules to further examine this question. To insure use of appropriate in vivo concentrations as well as potency of the hormone in vitro, we measured plasma AII levels by radioimmunoassay in normal, sodium-depleted, and adrenalectomized rabbits, and measured AII activity by bioassay after incubation in various microperfusion baths. Plasma levels ranged from approximately 2 X 10(-11) to 5 X 10(-11) M. AII activity was stable in Ringer's solution plus albumin, but not in rabbit serum or Ringer's solution plus fetal calf serum. In Ringer's solution plus albumin, physiologic concentrations of AII stimulated volume reabsorption (Jv). 10(-11) M AII increased Jv by 16% (P less than 0.01). 10(-10) M AII produced a lesser increase, 7.5% (P less than 0.05). At a frequently studied, but probably pharmacologic dose, 10(-7) M AII inhibited Jv by 24% (P less than 0.001). AII at 10(-11) M did not stimulate Jv in the presence of 10(-7) M saralasin. Though previous studies have suggested agonistic effects of saralasin alone in epithelia, we found no significant effect of 10(-7) M saralasin on Jv. None of the AII doses measurably changed transepithelial voltage. We conclude that AII in physiologic doses directly stimulates Jv in proximal convoluted tubules and this effect is probably receptor mediated and, within the limits of detection, electroneutral.
Use-dependent prolongation of ventricular tachycardia cycle length by type I antiarrhythmic drugs in humans.
Authors: G A Kidwell, A J Greenspon, R M Greenberg, K J Volosin
Journal: Circulation (1993)

BACKGROUND Type I antiarrhythmic drugs block the cardiac sodium channel in a use-dependent fashion. This use-dependent behavior causes increased drug binding and consequently increased sodium channel blockade at faster stimulation rates. Importantly, the kinetics of drug association and dissociation from the sodium channel differ for each type I antiarrhythmic drug. METHODS AND RESULTS Thirty-five patients receiving type I antiarrhythmic drugs for the treatment of sustained monomorphic ventricular tachycardia (VT) were studied before and after drug therapy. A total of 41 drug studies were performed (lidocaine, n = 10; procainamide, n = 16; flecainide, n = 15). Sustained monomorphic VT of an identical electrocardiographic morphology was induced during the control and follow-up drug studies. During the control study, there was no significant change in the VT cycle length over time. Compared with control, significant prolongation of the onset VT cycle length was observed after treatment with procainamide and flecainide (increase of 52 +/- 24 and 80 +/- 49 msec, respectively) but not after treatment with lidocaine (increase of 8 +/- 37 msec). Additional drug-induced prolongation of the VT cycle length occurred during a 40-second observation period. This secondary "use-dependent" cycle length prolongation contributed significantly to the steady-state VT cycle length during treatment with flecainide (increase of 82 +/- 34 msec; p &lt; 0.0001). Although a use-dependent increase in VT cycle length was observed with procainamide and lidocaine, the increase was not statistically significant (increase of 12 +/- 15 and 8 +/- 8 msec, respectively). The estimated time constants for the onset of use-dependent VT cycle length prolongation were distinctly different for the three drugs. Flecainide's prolongation of the VT cycle length occurred slowly, with an estimated time constant of 12.5 +/- 5.0 seconds. In contrast, the time course of VT cycle length prolongation was rapid during treatment with lidocaine and intermediate during treatment with procainamide (time constants of 0.52 +/- 0.51 and 4.0 +/- 1.3 seconds, respectively). CONCLUSIONS Use-dependent prolongation of VT cycle length during treatment with type I antiarrhythmic drugs was observed in humans. This effect was clinically significant during treatment with flecainide (i.e., the use-dependent slowing of the heart rate improved the hemodynamic tolerance of the arrhythmia). Finally, the estimated time constants for the use-dependent prolongation of VT cycle length by the three test drugs are similar to their reported in vitro time constants for use-dependent sodium channel blockade.
Occupational Lung Disease and Compensation
Authors: JAMES P. KEOGH
Journal: Annals of Internal Medicine (1983)

Letters and Corrections1 April 1983Occupational Lung Disease and CompensationJAMES P. KEOGH, M.D.JAMES P. KEOGH, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-98-4-553 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: As an internist with an active interest in work-related diseases, I was dismayed by the article by Richman (1) and Morgan's accompanying editorial (2).My patients encounter great delays in obtaining compensation; any co-existent disease serves to deny or reduce the award; and the amounts awarded through the system are not great. When patients are unable to continue working due to acute poisoning, insurance carriers may cut off benefits arbitrarily and the worker must await a hearing to regain them. Patients have been evicted, harassed by collection agencies, and end up receiving public assistance while waiting. An...References1. RICHMAN S. Why change? A look at the current system of disability determination and workers compensation for occupational lung disease. Ann Intern Med. 1982;97:908-14. LinkGoogle Scholar2. MORGAN W. The adversary system: cui bono? Ann Intern Med. 1982;97:919-21. LinkGoogle Scholar1. RICHMAN S. Why change? A look at the present system of disability determination and workers' compensation for occupational lung disease. Ann Intern Med. 1982;97:908-14. LinkGoogle Scholar2. . An Interim Report to Congress on Occupational Diseases. Washington D.C.: U. S. Government Printing Office; 1980:2. Google Scholar3. MORGAN W. The adversary system: cui bono? Ann Intern Med. 1982;97:919-21. LinkGoogle Scholar4. BARTHHUNT PW. Workers' Compensation and Work Related Illnesses and Diseases. Cambridge, Massachusetts: The MIT Press; 1980:16. Google Scholar5. EDES N. Compensation for occupational diseases. Labor Law J. 1980;31:596-601. Google Scholar1. RICHMAN S. Why change? A look at the current system of disability determination and workers' compensation for occupational lung disease. Ann Intern Med. 1982;97:908-14. LinkGoogle Scholar2. . An Interim Report to the Congress on Occupational Diseases. Washington, D.C.: U. S. Government Printing Office; 1980:2. Google Scholar3. MORGAN W. The adversary system: cui bono? Ann Intern Med. 1982;97:919-21. LinkGoogle Scholar4. Wall Street Journal. 1982; August 27. Google Scholar5. BARTHHUNT PW. Workers' Compensation and Work-Related Illnesses and Diseases. Cambridge, Massachusetts: The MIT Press; 1980:180. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byOccupational Lung DiseaseW. K. C. MORGAN, M.D. 1 April 1983Volume 98, Issue 4Page: 553-554KeywordsHearingLungs Issue Published: 1 April 1983 PDF downloadLoading ...
Hemolytic uremic syndrome developing during remission of acute myelomonocytic leukemia
Authors: Hirokazu Okumura, Shinobu Nakamura, Shigeki Ohtake, Takashi Yoshida, Kazumi Kobayashi, Yohko Okabe, Sadaya Matano, Katsunori Kyohda, Tamotsu Matsuda
Journal: American Journal of Hematology (1993)

Abstract A 47‐year‐old woman was diagnosed with acute myelomonocytic leukemia (AMMoL) and was treated with combination chemotherapy. After one cycle of remission induction therapy, she entered into complete remission and then received three cycles of consolidation therapy. A month after the last consolidation therapy, she was diagnosed with having the complication of chemotherapy‐related HUS (C‐HUS). The C‐HUS improved after initiation of plasma exchange and antiplatelet therapy. In the present case, it seems that the antileukemic agents might play an important role in the development of C‐HUS. © 1993 Wiley‐Liss, Inc.
Polymorphisms in DNA Double-Strand Break Repair Genes and Skin Cancer Risk
Authors: Jiali Han, Graham A. Colditz, Leona D. Samson, David J. Hunter
Journal: Cancer Research (2004)

Abstract UV can cause a wide range of DNA lesions. UVA-induced oxidative DNA damage and blocked DNA replication by UVB-induced photoproducts can lead to double-strand breaks (DSBs). We selected 11 haplotype-tagging single nucleotide polymorphisms in three DSB repair genes XRCC2, XRCC3, and LigaseIV and evaluated their associations with skin cancer risk in a nested case-control study within the Nurses’ Health Study [219 melanoma, 286 squamous cell carcinoma (SCC), 300 basal cell carcinoma (BCC), and 873 controls]. We observed that the XRCC3 18085T (241Met) allele and its associated haplotype were significantly inversely associated with the risks of SCC and BCC, whereas the XRCC3 4552C allele along with its associated haplotype and the XRCC2 30833A allele were significantly associated with increased BCC risk. The LigaseIV 4044T and 4062T alleles were associated with decreased BCC risk; two of four haplotypes were significantly associated with altered BCC risk. A trend toward decreased risk of nonmelanoma skin cancer was found in those harboring a greater number of putative low risk alleles (P for trend, 0.05 for SCC, &amp;lt;0.0001 for BCC). The main effects of these genotypes were essentially null for melanoma risk. This study provides evidence to suggest the role of the DSB repair pathway in skin cancer development, especially for BCC.
Early Immunization Against Whooping-cough
Authors: A. J. Cashman
Journal: BMJ (1955)

HYPERTONIC DEHYDRATIONdose of water and then repeat the serum electrolyte examinations.If the water is not required in the pre-opera- tive state it will rapidly be excreted, but if required it will be retained and the dilution effect described will take place. SummaryIf water is lost in excess of extracellular electrolyte a state of hypertonic dehydration may be induced.In this condition the concentration of extracellular electrolytes may be normal or even above normal when the total quantity of electrolyte is decreased.In the post-operative phase oedema may result if water is given in excess.
Sudanese health minister's advocacy of condoms sparks protest
Authors: Peter Moszynski
Journal: BMJ (2006)

Sudan's new health minister, Dr Tabitha Sokaya, has provoked a political storm by publicly advocating condom use to stem the country's HIV crisis.

Although the extent of the problem was largely unrecognised until monitoring began in southern Sudan last year, latest UNAIDS figures show that Sudan has the highest prevalence in north Africa and the Middle East, with 1.6% of adults and 3-8% of youth infected. An estimated 23 000 people have died of AIDS related illness.

Dr Sokaya, who holds a PhD in nursing from Birmingham University, in the United Kingdom, …