tbuckley/cabot-search huggingface dataset:
Impact of hepatitis B and C virus on kidney transplantation outcome
Authors: Philippe Mathurin, Catherine Mouquet, Thierry Poynard, Cheickna Sylla, Hadjira Benalia, Catherine Fretz, Vincent Thibault, Jean-François Cadranel, Brigitte Bernard, Pierre Opolon, Pierre Coriat, Marc Olivier Bitker
Journal: Hepatology (1999)

The impact of hepatitis B (HBV) and C (HCV) on patient survival after kidney transplantation is controversial. The aims of this study were (1) to assess the independent prognostic values of HBsAg and anti-HCV in a large renal transplant population, (2) to compare infected patients with noninfected patients matched for factors possibly associated with graft and patient survival, and (3) to assess the prognostic value of biopsy-proven cirrhosis. Eight hundred thirty-four transplanted patients were included: 128 with positive HBsAg (group I), 216 with positive anti-HCV (group II), and 490 without serological markers of HBV and HCV (group III). Fifteen percent and 29% of patients were HBsAg-positive and anti-HCV-positive, respectively. Ten-year survivals of group I (55 +/- 6%) and group II (65 +/- 5%) were significantly lower than survival of group III (80 +/- 3%, P <.001). At 10 years, among overall patients with HCV screening (n = 834), four variables had independent prognostic values in patient survival: age at transplantation (P <.0001), year of transplantation (P =.02), biopsy-proven cirrhosis (P =.03), and presence of HCV antibodies (P =.02). In the case control study, comparison of infected patients with their matched control patients showed that age at transplantation (P <.05), HBsAg (P =.005), and anti-HCV (P =.005) were independent prognostic factors. HCV, biopsy-proven cirrhosis, and age are independent prognostic factors of 10-year survival in patients with kidney grafts. The case-control study showed that anti-HCV and HBsAg were independently associated with patient and graft survivals. In infected patients, a routine liver histological analysis would improve selection of patients for renal transplantation.
The CAVENDISH LECTURE on the ETIOLOGY and DIAGNOSIS of CEREBRO-SPINAL FEVER: Read before the West London Medico-Chirurgical Society
Authors: W. Osler
Journal: BMJ (1899)

IN practice we occasionally meet with a meningitis which is not tuberculous, which is not a complication of pneumonia or ulcerative endocarditis, and which is not a sequence of ear disease or of injury, and which is not a terminal infection in some chronic malady.As the meninges of both brain and cord are diffusely inflamed, we label the condition cerebro- spinal meningitis.At intervals, in certain regions, the cases multiply, and we then speak of epidemic cerebro-spinal fever.Until recently my experience, though somewhat varied, had been confined to a few instances in which the absence of the usual factors justified the diagnosis of the sporadic form of this disease.Within the past year a small outbreak in Baltimore has enabled me to study certain points in the etiology and diagnosis of this most interesting affection.
Chondromucoprotein-degrading neutral protease activity in rheumatoid synovial fluid.
Authors: G.C Wood, R.H Pryce-Jones, D.D White, G Nuki
Journal: Annals of the Rheumatic Diseases (1971)

Erosion of articular cartilage, which is characteristic of inflammatory joint diseases, including rheumatoid arthritis (RA), is due in part to enzymic breakdown of the components of the cartilage matrix (Bollet, 1963), particularly collagen and chondromucoprotein (CMP).It has been suggested that lysozomal hydrolases, possibly derived from cells of the syno- vial membrane or from leucocytes present in synovial fluid, are involved in this process (Dingle, 1962;Weissmann, 1966).In this communication we report the existence, in the synovial fluids of patients with rheumatoid arthritis, of protease activity which degrades CMP optimally near neutral pH.It thus differs from the majority of lysozomal enzymes, which are optimally active at pH values lower than those (Goldie and Nachemson, 1969) likely to appertain at the cartilage surface.Conchie, 1966) and hyaluronidase viscometrically, using chondroitin sulphate and hyaluronic acid as substrates. ResultsWhen cell extracts, or dilutions thereof, were added to CMP, a fall in specific viscosity of up to 80 per cent.was observed in 1 hr, the change being similar copyright.
Seroepidemiology of water-borne hepatitis in India and evidence for a third enterically-transmitted hepatitis agent Arankalle VA, Chadha MS, Tsarey SA, Emerson Su, Risbud AR, Baneriee K, Purcell RH. Proc Natl Acad Sci U S A 1994; 91: 3428?3432
Authors: E MAST
Journal: Hepatology (1995)
Comment on Tsuda et al. Poor Glycemic Control Is a Major Factor in the Overestimation of Glomerular Filtration Rate in Diabetic Patients. Diabetes Care 2014;37:596–603
Authors: Pierre Delanaye, André J. Scheen
Journal: Diabetes Care (2014)

Accurate assessment of kidney function is of major clinical importance for the management of patients with diabetes. We read with interest the article by Tsuda et al. (1). The authors proposed a new equation to estimate glomerular filtration rate (GFR), including glycemic control as a new variable. They concluded that poor glycemic control is a major factor in the overestimation of GFR in diabetic patients. There are several important limitations in this study. First, the sample ( n = 80, all Japanese subjects) must be considered as too limited to propose a new equation. For …
Health Care Ethics Consultation Competences and Standards: A Roadmap Still Needing a Compass
Authors: Keith M. Swetz, C. Christopher Hook, Joan M. Henriksen Hellyer, Paul S. Mueller
Journal: The American Journal of Bioethics (2013)

Tarzian and the American Society of Bioethics and Humanities (ASBH) Core Competencies Update Task Force have published a revision to the 1998 (first edition) of the Core Competencies and Emerging S...
Comparative Effects of Basic Fibroblast Growth Factor and Vascular Endothelial Growth Factor on Coronary Collateral Development and the Arterial Response to Injury
Authors: Daisy F. Lazarous, Matie Shou, Mickey Scheinowitz, Everett Hodge, Venugopal Thirumurti, Anastasia N. Kitsiou, Jonathan A. Stiber, Arlene D. Lobo, Sally Hunsberger, Esther Guetta, Stephen E. Epstein, Ellis F. Unger
Journal: Circulation (1996)

We have shown that the angiogenic peptides basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) enhance canine coronary collateral development when administered for > or = 4 weeks. bFGF, a pluripotent mitogen of mesodermally derived cells, could theoretically exacerbate neointimal smooth muscle cell hyperplasia, a fundamental component of atherosclerosis. VEGF, an endothelial cell-specific mitogen and vascular permeability factor, could have deleterious effects related to vascular hyperpermeability. The present investigation had two aims: (1) to ascertain whether brief (7-day) systemic arterial treatment with bFGF or VEGF would improve myocardial collateral perfusion and (2) to determine whether these peptides induce neointimal accumulation in vivo.Dogs were subjected to ameroid-induced occlusion of the left circumflex coronary artery and randomized to bFGF 1.74 mg (n = 9), VEGF 0.72 mg (n = 9), or saline (n = 10) as a daily left atrial bolus (days 10 to 16). Additional dogs were randomized to VEGF 0.72 mg (n = 6) or saline (n = 5); however, treatment was delayed by 1 week. Coincident with the institution of treatment, all dogs underwent balloon denudation injury of the iliofemoral artery. bFGF markedly increased maximal collateral flow but did not exacerbate neointimal accumulation. VEGF had no discernible effect on maximal collateral flow, but it exacerbated neointimal thickening after vascular injury.Short-term treatment with bFGF enhanced collateral development without increasing neointimal accumulation at sites of vascular injury. Although VEGF did not increase collateral development as administered in this study, it significantly exacerbated neointimal accumulation. These data provide support for the clinical investigation of bFGF in selected patients with ischemic heart disease.
Pulmonary Function and the Chronic Fatigue Syndrome
Authors: Charles B. Payne
Journal: Annals of Internal Medicine (1989)

Letters and Corrections15 November 1989Pulmonary Function and the Chronic Fatigue SyndromeCharles B. Payne Jr., MD, Helen E. Sloan, MDCharles B. Payne Jr., MDSearch for more papers by this author, Helen E. Sloan, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-111-10-860_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor:The chronic fatigue syndrome has received considerable attention since its appearance approximately 4 years ago. Reports have focused on the immunologic evidence of Epstein-Barr virus infection in the pathogenesis of the syndrome. A working case definition was recently published (1). We have studied a 35-year-old woman who had the persistent symptoms of exertional dyspnea, malaise, and the inability to work because of a febrile "viral" illness that had presented about 6 months previously and was initially associated with muscle weakness and cough. Her symptoms met the working definition of the syndrome. On 27 February 1989, her quantitative...References1. Holmes G, Kaplan J, and Gantz N. Chronic fatigue syndrome: a working case definition. Ann Intern Med. 1988;108:387-9. LinkGoogle Scholar2. Fridy W, Ingram R, and Hierholzer J. Airways function during mild viral respiratory illnesses. Ann Intern Med. 1974;80:150-5. LinkGoogle Scholar3. Picken J, Niewoehner D, and Chester E. Prolonged effects of viral infections of the upper respiratory tract upon small airways. Am J Med. 1972;52:738-46. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Charles B. PayneJr., MD; Helen E. Sloan, MDAffiliations: Wright State University School of Medicine Dayton, OH 45401-0927 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byChronic fatigue syndrome: an allergic entity?Chronic fatigue syndrome: cause, controversy and carePsychological Aspects of Chronic Fatigue SyndromeChronic Fatigue Syndrome: A Conundrum 15 November 1989Volume 111, Issue 10Page: 860-860KeywordsChronic fatigue syndromeDyspneaEpstein-Barr virusMusclesPathogenesisPulmonary function ePublished: 1 December 2008 Issue Published: 15 November 1989 PDF downloadLoading ...
Abstract LB-62: Inhibitor of differentiation 4 (ID4) maintains mammary stem cell homeostasis and identifies a poor-prognosis subset of basal-like breast cancers with a putative stem cell of origin
Authors: Simon Junankar, Laura Baker, Kyuson Yun, Alexander Swarbrick
Journal: Cancer Research (2014)

Abstract Basal-like breast cancers (BLBC) are heterogenous, poorly differentiated and present with limited therapeutic opportunities and a poor prognosis. We have investigated the role of the HLH transcription factor ID4 in breast stem cells and basal breast cancer aetiology. Using an Id4GFP knock-in mouse and single cell gene expression studies we show that ID4 defines a subset of Cd24+Cd29hi basal mammary epithelial cells enriched for stem cell gene expression and mammary repopulating capacity. Homozygous deletion of Id4 followed by mammary transplantation reveals a cell-autonomous requirement for Id4 in mammary ductal morphogenesis in vivo. shRNA-mediated depletion of Id4 in the Comma-D mammary stem cell line in vitro shows that Id4 is required for epithelial cell proliferation. Conversely, over-expression of Id4 maintains the stem cell pool by restricting luminal differentiation of Comma-D cells. This effect of Id4 is mediated via suppression of BrCa1 expression and the Notch-Elf5 axis. In clinical breast cancer specimens, ID4 expression is absent in luminal tumours but very high in approximately half of all BLBCs, a proportion of which possess ID4 gene amplification. These tumours are characterized by unique transcriptomes with many features of mammary stem cells. Furthermore, ID4-positive BLBCs have a very poor prognosis across multiple independent tissue cohorts. This study identifies ID4 as a master regulator of mammary stem cell homeostasis and suggests that a subset of aggressive BLBCs derive from a primitive mammary stem or progenitor cell with basal characteristics. Citation Format: Simon Junankar, Laura Baker, Kyuson Yun, Alexander Swarbrick. Inhibitor of differentiation 4 (ID4) maintains mammary stem cell homeostasis and identifies a poor-prognosis subset of basal-like breast cancers with a putative stem cell of origin. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr LB-62. doi:10.1158/1538-7445.AM2014-LB-62
PLIGHT OF AMERICAN INSTRUMENT MAKERS
Authors: W. W. Keen
Journal: JAMA (1924)

<h3>To the Editor:</h3> —I want to call attention to a serious condition which the profession throughout the country can remedy to a large extent. I learn that a number of our own American instrument makers are going out of business because surgeons and hospitals are purchasing approximately 95 per cent, of their steel instruments of German manufacture. This is surely not patriotic. They should encourage our own instrument makers instead of those of any other nation, and especially those of Germany. If we are ever to be a self-contained nation, we ought, for patriotic reasons, if for no other, to encourage our own manufacturers. I know of no better way in which this can be brought home to the profession than through the columns ofThe Journal.
Increased Fas ligand expression by T cells and tumour cells in the progression of actinic keratosis to squamous cell carcinoma
Authors: A.C. Satchell, R.StC. Barnetson, G.M. Halliday
Journal: British Journal of Dermatology (2004)

In the counterattack model of tumorigenesis, it has been proposed that tumours develop resistance to attack from Fas ligand (FasL)-expressing cytotoxic T cells by downregulating Fas (immune escape), while at the same time upregulating FasL expression to induce apoptosis in Fas-expressing T cells (counterattack).The aim of this study was to examine Fas and FasL expression on tumour cells and infiltrating T cells during the progression of actinic keratoses (AK), the benign precursor lesion, to squamous cell carcinoma (SCC).Samples of AK (n = 20) and SCC (n = 20) were collected from immunocompetent patients attending dermatology clinics. Double-label immunohistochemistry was performed on frozen sections using mouse monoclonal antibodies to Fas or FasL, simultaneously with a rabbit polyclonal antibody to either CD3 or cytokeratin, markers of T cells and keratinocytes, respectively. Cell densities and the optical density of tumour Fas expression were measured using image analysis.FasL-expressing T cells were observed in nine of 19 SCCs, compared with three of 20 AKs (P < 0.05). FasL-expressing tumour cells were found in nine of 18 SCCs, compared with only one of 20 AK specimens (P < 0.005). There was no difference in the number of Fas-expressing T cells infiltrating AK and SCC. Fas expression by keratinocytes, measured by optical density, was lower in SCC (range 0.1-40, median 17) compared with AK (range 4-62, median 25) (P < 0.05).These results suggest that the greater numbers of FasL-expressing T cells infiltrating into SCC compared with AK are targeting Fas-expressing tumour cells. As AK cells progress to SCC, they subvert this T-cell-mediated killing of tumour cells by downregulating their Fas expression (immune escape). Furthermore, tumour cells upregulate their expression of FasL, possibly as a counterattack measure to induce apoptosis in the increased number of tumour-infiltrating T cells. Thus changes in Fas/FasL-mediated interactions between T cells and tumour cells occur during the progression of AK into SCC.
Reply to “…and secreted tumour suppressors”
Authors: Roy A. Jensen, Marilyn E. Thompson, Thomas L. Jetton, Riet van der Meer, Bassam Helou, Carlos L. Arteaga, David L. Page, Jeffrey T. Holt, Steven R. Tronick, Allen M. Gown, Marilyn Skelly, Beth Ostermeyer, David Schieltz, Csilla I. Szabo, Mary-Claire King
Journal: Nature Genetics (1996)
Medications as a source of human exposure to phthalates.
Authors: Russ Hauser, Susan Duty, Linda Godfrey-Bailey, Antonia M Calafat
Journal: Environmental Health Perspectives (2004)

Phthalates are a group of multifunctional chemicals used in consumer and personal care products, plastics, and medical devices. Laboratory studies show that some phthalates are reproductive and developmental toxicants. Recently, human studies have shown measurable levels of several phthalates in most of the U.S. general population. Despite their widespread use and the consistent toxicologic data on phthalates, information is limited on sources and pathways of human exposure to phthalates. One potential source of exposure is medications. The need for site-specific dosage medications has led to the use of enteric coatings that allow the release of the active ingredients into the small intestine or in the colon. The enteric coatings generally consist of various polymers that contain plasticizers, including triethyl citrate, dibutyl sebacate, and phthalates such as diethyl phthalate (DEP) and dibutyl phthalate (DBP). In this article we report on medications as a potential source of exposure to DBP in a man who took Asacol [active ingredient mesalamine (mesalazine)] for the treatment of ulcerative colitis. In a spot urine sample from this man collected 3 months after he started taking Asacol, the concentration of monobutyl phthalate, a DBP metabolite, was 16,868 ng/mL (6,180 micro g/g creatinine). This concentration was more than two orders of magnitude higher than the 95th percentile for males reported in the 1999-2000 National Health and Nutrition Examination Survey (NHANES). The patient's urinary concentrations of monoethyl phthalate (443.7 ng/mL, 162.6 micro g/g creatinine), mono-2-ethylhexyl phthalate (3.0 ng/mL, 1.1 micro g/g creatinine), and monobenzyl phthalate (9.3 ng/mL, 3.4 micro g/g creatinine) were unremarkable compared with the NHANES 1999-2000 values. Before this report, the highest estimated human exposure to DBP was more than two orders of magnitude lower than the no observable adverse effect level from animal studies. Further research is necessary to determine the proportional contribution of medications, as well as personal care and consumer products, to a person's total phthalate burden.
Metabolic Acidosis Reversed by the Combination of Magnesium Hydroxide and a Cation-Exchange Resin
Authors: Pedro C. Fernandez, Paul J. Kovnat
Journal: New England Journal of Medicine (1972)

WE recently observed the reversal of metabolic acidosis in a patient with chronic renal failure after the use of a cation-exchange resin, sodium polystyrene sulfonate (Kayexalate), and magnesium hydroxide (milk of magnesia) used as a cathartic to reinforce the action of the resin.Case ReportA 43-year-old man with chronic membranoproliferative glomerulonephritis and nephrotic syndrome was admitted to the Philadelphia Veterans Administration Hospital because of uncontrolled hypertension and chronic renal failure. Positive physical findings included a blood pressure of 230/160, marked retinal arteriolar narrowing, with waxy exudates, bilateral papilledema with a pericentral scotoma on the right, appreciable cardiomegaly with a . . .
Fatigue among general practice attenders.
Authors: P J Whorwell
Journal: BMJ (1991)

the colour and a tell tale extension of pigment at one edge.As the checklist acknowledges, change in behaviour is the most important fact to emphasise in a public education campaign.But some patients are oblivious to change,' I and their melanoma is diagnosed incidentally by someone else.It is thus important that doctors, paramedics, and the public are exposed to as much visual material depicting melanomas as possible, either on television or in poster form.Those doctors who see patients with malignant melanoma should show the lesions to as many colleagues as possible.
Management of Refractory Neurocardiogenic Syncope
Authors: Kenneth A. Ellenbogen
Journal: Annals of Internal Medicine (1998)

Letters1 January 1998Management of Refractory Neurocardiogenic SyncopeKenneth A. Ellenbogen, MD, Mark A. Wood, MD, and Hermes A. Kontos, MD, PhDKenneth A. Ellenbogen, MDMedical College of Virginia; Richmond, VA 23298Search for more papers by this author, Mark A. Wood, MDMedical College of Virginia; Richmond, VA 23298Search for more papers by this author, and Hermes A. Kontos, MD, PhDMedical College of Virginia; Richmond, VA 23298Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-128-1-199801010-00021 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Therapy for neurally mediated syncope and related syndromes has recently received considerable attention. Few randomized trials of any specific therapeutic agents have been performed. β-blockers, mineralocorticoids, theophylline, serotonin receptor blockers, disopyramide, and peripheral vasoconstrictors (α-agonists) have all been used with some success [1]. There still remains, however, a group of patients whose condition is refractory to medical and pacing therapy. We describe four patients with refractory, disabling neurocardiogenic syncope whose symptoms improved markedly after therapy with diphenylhydantoin and carbamazepine after drug or pacemaker therapy had failed.The clinical characteristics and drug levels associated with suppression of recurrent ...References1. Morillo CA, Brignole M, Wood MA, Ellenbogen KA. Management of head-up tilt induced neurocardiogenic (vasovagal) syncope. Pacing Clin Electrophysiol. [In press]. Google Scholar2. Ellenbogen KA, Morillo CA, Smith ML, Wood MA, Gilligan DM, Eckberg DL, et al. Neural monitoring of vasovagal syncope. Pacing Clin Electrophysiol. 1997; 20:788-94. Google Scholar3. Taylor PH, Gray K, Bicknell PG, Rees JR. Glossopharyngeal neuralgia with syncope. J Laryngol Otol. 1977; 91:859-68. Google Scholar Author, Article, and Disclosure InformationAffiliations: Medical College of Virginia; Richmond, VA 23298 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 January 1998Volume 128, Issue 1Page: 73KeywordsBrainstemDrug therapyDrugsNervesPacemakersRandomized trialsReflexesSerotonin receptorSurgerySyncope Issue Published: 1 January 1998 CopyrightCopyright © 1998 by American College of Physicians. All Rights Reserved.PDF DownloadLoading ...
Interleukin-33 attenuates sepsis by enhancing neutrophil influx to the site of infection
Authors: Jose C Alves-Filho, Fabiane Sônego, Fabricio O Souto, Andressa Freitas, Waldiceu A Verri, Maria Auxiliadora-Martins, Anibal Basile-Filho, Andrew N McKenzie, Damo Xu, Fernando Q Cunha, Foo Y Liew
Journal: Nature Medicine (2010)