tbuckley/cabot-search huggingface dataset:
Attitudes to flexible training
Authors: G. Norcliffe, C. Finlan
Journal: BMJ (1999)

Over recent years, the Junior Doctors Committee (JDC) has made considerable efforts to improve the opportunities for flexible training in hospitals and the conditions applying to those in such training. Among the improvements the JDC has been seeking are flexible training being available for all those who want it; competency based assessment, rather than a time served approach; and standard rates of pay being payable to those undertaking flexible training for the first 40 contracted hours they work.

To provide detailed evidence of the current position, the committee has worked with the BMA's health policy and economic research unit to undertake a detailed survey of flexible trainees in the United Kingdom. Flexible trainees were sent the questionnaire in the latter half of November last year and asked to return them by the middle of December. Postgraduate deans' offices, which held the most up to date lists of flexible trainees in their region or province, helped by mailing out the survey. No reminders were sent. The results of the survey will be announced at the junior doctors' forum on the future of flexible training on 25 February, organised by the Junior Doctors Committee.

One of the most striking features of the results was the response rate. Generally, surveys of junior doctors do not get a good response, but in this case 70% (797) of flexible trainees responded. This level of interest has been echoed in the number of applications to attend the junior doctors' forum (170 for the 100 …
Clindamycin-Associated Colitis
Authors: RALPH F. WELLS
Journal: Annals of Internal Medicine (1974)

Editorials1 October 1974Clindamycin-Associated ColitisRALPH F. WELLS, M.D.RALPH F. WELLS, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-81-4-547 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptThe subject of antibiotic-related, nonstaphylococcal pseudomembranous colitis has appeared sporadically in the medical literature for more than 20 years (1). Most of the broad-spectrum antibiotics have been implicated at one time or another. A new concern with the problem is reflected in reports of cases in which lincomycin or its 7-deoxy, 7-chloro derivative, clindamycin, seems to be the causative agent. Clindamycin continues in wide use because of its efficacy against some Gram-negative anaerobes, notablyBacteroidesspecies, and its value as an alternative antiobiotic agent for the penicillin-sensitive person with certain Gram-positive infections. Because pseudomembranous colitis may occur with other antibiotics...References1. REINERSCHLESINGERMILLER LMG: Pseudomembranous colitis following Aureomycin and Chloramphenicol. Arch Pathol 54:39-67, 1952 MedlineGoogle Scholar2. GOULSTONMCGOVERN SV: Pseudo-membranous colitis. Gut 6:207-212, 1965 CrossrefMedlineGoogle Scholar3. TEDESCOBARTONALPERS FRD: Clindamycin-associated colitis. A prospective study. Ann Intern Med 81:429-433, 1974 LinkGoogle Scholar4. COHENMCNEILLWELLS LCR: Clindamycin-associated colitis. JAMA 223:1380-1381, 1973 CrossrefGoogle Scholar5. STROEHLEINSEDLACKHOFFMAN JRH: Clindamycin-associated colitis. Mayo Clin Proc 49:240-243, 1974 MedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: MC Gastroenterology Service Brooke Army Medical Center Fort Sam Houston, Texas PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByKolon und RektumDie chronisch entzündlichen DarmkrankheitenDrug Effects in Geriatric PatientsClindamycin Associated DiarrheaClindamycin-associated Colitis in ChildrenPseudomembranous colitis associated with antibioticsPrinciples of the Antimicrobial Therapy of Head and Neck InfectionsColitis associated with oral clindamycin therapyClindamycin-associated colitisDangers of Indiscriminate Antibiotic TherapyClindamycin-Associated ColitisKIRON M. DAS, M.D., PH.D., WILLIAM F. ERBER, M.D. 1 October 1974Volume 81, Issue 4Page: 547-548KeywordsAntibioticsBacteroidesC difficile colitisClindamycinColitis Issue Published: 1 October 1974 PDF DownloadLoading ...
Serological Overlap Between Lupus Erythematosus, Rheumatoid Arthritis, and Thyroid Auto-immune Disease
Authors: W. Hijmans, D. Doniach, I. M. Roitt, E. J. Holborow
Journal: BMJ (1961)

Circulating auto-antibodies are being reported in an increasing number of diseases, but their role in the pathogenesis of these disorders is far from clear.The clinical interrelationships and the serological overlap between the " auto-immune" diseases is of particular relevance to the understanding of the fundamental disturbances underlying these phenomena.The occasional finding of L.E. cells in patients with thyroid disorders (Wilkinson and Sacker, 1957;
Distinct H3F3A and H3F3B driver mutations define chondroblastoma and giant cell tumor of bone
Authors: Sam Behjati, Patrick S Tarpey, Nadège Presneau, Susanne Scheipl, Nischalan Pillay, Peter Van Loo, David C Wedge, Susanna L Cooke, Gunes Gundem, Helen Davies, Serena Nik-Zainal, Sancha Martin, Stuart McLaren, Victoria Goody, Ben Robinson, Adam Butler, Jon W Teague, Dina Halai, Bhavisha Khatri, Ola Myklebost, Daniel Baumhoer, Gernot Jundt, Rifat Hamoudi, Roberto Tirabosco, M Fernanda Amary, P Andrew Futreal, Michael R Stratton, Peter J Campbell, Adrienne M Flanagan
Journal: Nature Genetics (2013)
Dietary Antioxidant Vitamins and Death from Coronary Heart Disease in Postmenopausal Women
Authors: Lawrence H. Kushi, Aaron R. Folsom, Ronald J. Prineas, Pamela J. Mink, Ying Wu, Roberd M. Bostick
Journal: New England Journal of Medicine (1996)

The role of dietary antioxidant vitamins in preventing coronary heart disease has aroused considerable interest because of the knowledge that oxidative modification of low-density lipoprotein may promote atherosclerosis.We studied 34,486 postmenopausal women with no cardiovascular disease who in early 1986 completed a questionnaire that assessed, among other factors, their intake of vitamins A, E, and C from food sources and supplements. During approximately seven years of follow-up (ending December 31, 1992), 242 of the women died of coronary heart disease.In analyses adjusted for age and dietary energy intake, vitamin E consumption appeared to be inversely associated with the risk of death from coronary heart disease. This association was particularly striking in the subgroup of 21,809 women who did not consume vitamin supplements (relative risks from lowest to highest quintile of vitamin E intake, 1.0, 0.68, 0.71, 0.42, and 0.42; P for trend 0.008). After adjustment for possible confounding variables, this inverse association remained (relative risks from lowest to highest quintile, 1.0, 0.70, 0.76, 0.32, and 0.38; P for trend, 0.004). There was little evidence that the intake of vitamin E from supplements was associated with a decreased risk of death from coronary heart disease, but the effects of high-dose supplementation and the duration of supplement use could not be definitely addressed. Intake of vitamins A and C did not appear to be associated with the risk of death form coronary heart disease.These results suggest that in postmenopausal women the intake of vitamin E from food is inversely associated with the risk of death from coronary heart disease and that such women can lower their risk without using vitamin supplements. By contrast, the intake of vitamins A and C was not associated with lower risks of dying from coronary disease.
Plerixafor (AMD3100) and granulocyte colony-stimulating factor (G-CSF) mobilize different CD34+ cell populations based on global gene and microRNA expression signatures
Authors: Robert E. Donahue, Ping Jin, Aylin C. Bonifacino, Mark E. Metzger, Jiaqiang Ren, Ena Wang, David F. Stroncek
Journal: Blood (2009)
Cell of origin strongly influences genetic selection in a mouse model of T-ALL
Authors: Katherine E. Berquam-Vrieze, Kishore Nannapaneni, Benjamin T. Brett, Linda Holmfeldt, Jing Ma, Oksana Zagorodna, Nancy A. Jenkins, Neal G. Copeland, David K. Meyerholz, C. Michael Knudson, Charles G. Mullighan, Todd E. Scheetz, Adam J. Dupuy
Journal: Blood (2011)
Which is the best medical school?
Authors: D. Spence
Journal: BMJ (2013)

The scramble for university places in the United Kingdom has begun. So which is the best medical school? In terms of attainment, Oxbridge cleans up again.1 2 Interestingly, in one year only 45 children who receive free school meals were admitted to Oxbridge,3 fewer than were accepted from Winchester, a single private school. As someone who qualified for free school meals, I was lucky to get into medicine at all. We comprehensive types may tend to end up …
Primate theory of mind is a Turing test
Authors: Robert W. Mitchell, James R. Anderson
Journal: Behavioral and Brain Sciences (1998)

Heyes's literature review of deception, imitation, and self-recognition is inadequate, misleading, and erroneous. The anaesthetic artifact hypothesis of self-recognition is unsupported by the data she herself examines. Her proposed experiment is tantalizing, indicating that theory of mind is simply a Turing test.
Do Primary Physicians Actually Manage Their Patients' Fee-for-Service Care?
Authors: A J Dietrich, E C Nelson, J W Kirk, M Zubkoff, G T O'Connor
Journal: JAMA (1988)

In what proportion of a patient's total health care is the primary physician involved? By means of calendar diaries and telephone interviews, 211 primary care patients from community practices of the Dartmouth Primary Care Cooperative Information Project were followed prospectively for one year. We found that a substantial proportion of care was managed (that is, either actually provided or coordinated in advance) by the patient's primary physician. Specifically, criteria for a primary physician's role in management were met by 75% of 1379 ambulatory visits to physicians, 33% of 786 visits to nonphysician health care providers, 81% of 26 nonemergency hospitalizations, and 78% of 2769 prescriptions. Primary physicians in these settings appear to function as case managers even when they are not participating in formal managed-care systems. (<i>JAMA</i>1988;259:3145-3149)
Dust mite exposure modifies the effect of functional IL10 polymorphisms on allergy and asthma exacerbations
Authors: Gary M. Hunninghake, Manuel E. Soto-Quirós, Jessica Lasky-Su, Lydiana Avila, Ngoc P. Ly, Catherine Liang, Barbara J. Klanderman, Benjamin A. Raby, Diane R. Gold, Scott T. Weiss, Juan C. Celedón
Journal: Journal of Allergy and Clinical Immunology (2008)
188. Internalization of Novel Delivery Vector TAT-Streptavidin into Human Cells
Authors: Johanna Rinne, Brian Albarran, Juulia Jylhävä, Teemu O. Ihalainen, Pasi Kankaanpää, Vesa P. Hytönen, Patrick S. Stayton, Markku S. Kulomaa, Maija Vihinen-Ranta
Journal: Molecular Therapy (2006)

The cell penetrating peptide derived from the Human immunodeficiency virus-1 Tat protein possesses the capacity to promote the effective uptake of various cargo molecules across the cellular plasma membrane in vitro and in vivo. The objective of this study was to characterize the uptake and delivery mechanisms of a novel TAT-streptavidin (TAT-SA) construct in human cells. By confocal and immunoelectron microscopy the majority of internalized TAT-SA was shown to accumulate in perinuclear vesicles. The uptake studies in living cells with various fluorescent endocytic markers or inhibitors of cellular entry pathways suggested that TAT-SA internalized cells efficiently using both clathrin-mediated endocytosis and lipid-raft mediated macropinocytosis. When endosomal release of TAT-SA was enhanced through the incorporation of a biotinylated, pH-responsive polymer poly(propylacrylic acid) (PPAA), nuclear localization of TAT-SA was markedly improved. Additionally, no cytotoxicity of TAT-SA construct was detected. In conclusion, the non-viral vector TAT-SA may be utilized in protein therapeutics to deliver a wide range of biotinylated molecules into mammalian cells.
Inhibition of soluble antigen-induced T cell proliferation by warm-reactive antibodies to activated T cells in systemic lupus erythematosus.
Authors: A Yamada, J B Winfield
Journal: Journal of Clinical Investigation (1984)

One of the fundamental immunologic characteristics of systemic lupus erythematosus (SLE) is a depressed T cell proliferative response to various specific and nonspecific stimuli. Both intrinsic cellular defect(s) and inhibitory influences of humoral factors, e.g., antilymphocyte autoantibodies or immune complexes, have been postulated to underly this functional abnormality. Because patient serum can induce SLE-like T cell dysfunction in normal cells, an extrinsic mechanism is probably responsible, but the nature and site of action of this humoral activity has not been defined. This laboratory recently described a novel antibody specific for activated T cells in SLE, which raised the possibility that suppression of T cell proliferation by SLE serum involved antibodies directed to surface determinants expressed during the process of activation. In experiments to examine this concept further, relatively warm-reactive antibodies to T cell blasts were found to inhibit strongly the well-characterized T cell response to tetanus toxoid. These antibodies were distinct from conventional cold-reactive IgM antibodies to resting T cells, which exhibited little inhibitory activity. Inhibition involved noncytotoxic effects on early activation events at the level of the responding T cell, which markedly reduced the expression of receptors for interleukin 2. Inhibitory effects on antigen-pulsed macrophages or on T cells already committed to proliferate were not demonstrable. Anti-T blast antibodies were characteristic of active SLE and were detected only occasionally in patients with inactive disease or non-SLE rheumatic disorders. Although the exact antigenic specificity was not identified, considerable evidence was obtained against the presence of antibodies to Ia and certain other surface determinants of functional relevance. Our observations concerning the suppressive effects of anti-T blast antibodies in SLE serum on the T cell response to tetanus toxoid should provide new insight into mechanisms of in vivo T cell dysfunction in this and other immunologic disorders.
GCIP Is a Tumor Suppressor in Breast Cancer.
Authors: T. Chang, M. Chang
Journal: Cancer Research (2009)

Abstract Background: GCIP protein is a HLH-leucine zipper (HLH-LZ) proteins without basic DNA-binding region, which was identified to be a cyclin D1-binding protein and also was recognized as a human homologue of MAID protein (HHM). Recently, GCIP was found to function as a tumor suppressor in liver and colon tumorigenesis. In this study, we examined in vitro the functional role of GCIP in various breast cancer cell lines.Material and Methods: GCIP-directed siRNA construct was prepared and stable downregulation of GCIP in epithelial-like and nonaggressive/differentiated breast cancer cell line, MCF-7, were selected. In addition, two aggressive/ invasive breast cancer cells (MDA-MB231 and MDA-MB435s) that exhibit low levels of endogenous GCIP expression were transfected with p3x-GCIP-flag, respectively and stable GCIP-re-expressing transfectants were selected. The phalloidin staining cell morphology and functional assays with these stable GCIP downregulating or GCIP re-expressing were performed to characterize the biological effects of GCIP.Results: Stable MCF-7 cells with down-regulated GCIP expression acquired a mesenchymal-like shape and exhibited increased colony formation, migration and invasion capabilities. Furthermore, this was found to be associated with the loss of membrane E-cadherin and increased expression of the mescenchymal marker vimentin. In addition, both the stable MDA-MB231 and MDA-MB435s with GCIP-re-expression acquired an epithelial-like shape and exhibited decreased colony formation, migration and invasion capabilities.Conclusion: our previous study found that decreased expression of GCIP in breast carcinomas compared with normal ductal epithelium (P &amp;lt; 0.001). In this study, we present evidence that GCIP inactivation contributes to the enhanced migratory and invasive capacity of MCF-7 and that GCIP re-expression inhibits a wild range of cellular functions related to the malignant properties of MDA-MB231 and MDA-MB435s, confirming that GCIP is a tumor suppressor in breast cancer. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 3158.
Glossing over too much
Authors: Gin McCollum
Journal: Behavioral and Brain Sciences (1997)

Although Phillips &amp; Singer's proposal of commonalities seems sound, information theory and artificial neural network modeling omit important detail. An example is given of a distributed neural transformation that has been characterized mathematically and found to have both overall commonalities and differences of detail in different regions. P&amp;S's contextual field is compared to inclusive regions in a formalism relevant for modeling bodily-kinaesthetic intelligence.
Brain and Heart— The Autonomic Connection
Authors: Samuel Vaisrub
Journal: JAMA (1975)

When we indicate the brain in accounting for a cardiac disorder, we usually do so in the context of psychosomatic medicine. We recognize that, triggered by emotion, impulses from the brain may derange the rate or the rhythm of the heart through the mediation of the autonomic nervous system. What is not so well appreciated is that organic brain damage, as in intracranial hemorrhage, can also affect the heart. And what is even less well recognized is that it may do so frequently and with serious consequences.  Nearly thirty years ago, Byer et al 1 reported tall, upright T waves and prolonged QT intervals in a patient with subarachnoid hemorrhage. In 1954, Burch and associates 2 described a similar pattern, but with frequently inverted T waves and large U waves in patients with cerebrovascular accidents. Since then, a number of other reports have related various ischemic and arrhythmic electrocardiographic findings
Invasive Intraductal Papillary Mucinous Tumor of the Pancreas with Simultaneous Invasion of the Stomach and Duodenum
Authors: I. S. Jung, C. S. Shim, Y. K. Cheon, S. Bhandari, S. W. Cha, J. H. Moon, Y. D. Cho, J. H. Kim, Y. S. Kim, M. S. Lee, B. S. Kim
Journal: Endoscopy (2004)

An 81-year-old woman was admitted with epigastric pain and weight loss. She had been diagnosed with an intraductal papillary mucosal tumor (IPMT) 7 years previously, but had refused surgery for religious reasons. Esophagogastroduodenoscopy revealed a nodular, elevated lesion that was discharging mucin into the duodenal bulb and posterior wall of the upper body of the stomach. Endoscopic ultrasonography, abdominal computed tomography, and endoscopic retrograde cholangiography were carried out, and a highly invasive IPMT with simultaneous invasion of the stomach and duodenum was diagnosed.
A familial FTD associated with C9orf72 repeat expansion and dysplastic gangliocytoma
Authors: Mia Kero, Raffaele Ferrari, Kin Mok, Anders Paetau, Pentti J Tienari, Olli Tynninen, John Hardy, Parastoo Momeni, Auli Verkkoniemi-Ahola, Liisa Myllykangas
Journal: Molecular Neurodegeneration (2013)

Background A hexanucleotide repeat expansion, in the chromosome 9 open reading frame 72 gene (C9orf72), has been identified the most common genetic cause of FTD/ALS. Here we describe the clinical, pathologic and genetic features of a Finnish C9orf72 expansion carrier, who developed a dysplastic gangliocytoma, a rare hamartoma of cerebellar granule cells, associated with PTEN mutations. In addition to the dysplastic gangliocytoma, the patient showed TDP43-pathology in the cortex and in the substantia nigra, and p62-positive/TDP43-negative inclusions in the cerebellar granule cells. His sister carried the same gene defect and showed similar type of TDP43/p62-pathology in her brain. Our findings confirm the clinical and pathological picture of C9orf72 mutation carriers is more heterogeneous than originally thought and warrant further studies on the possible involvement of PTEN pathway in the specific cerebellar granule cell pathology associated with C9orf72 expansion.
Cellular and biochemical actions of adrenal glucocorticoid hormones on rat thymic lymphocytes.
Authors: D A Young, B P Voris, M L Nicholson
Journal: Environmental Health Perspectives (1981)

The molecular, biochemical, and cellular effects of adrenal glucocorticoid hormones on thymic lymphocytes are reviewed, with emphasis on their relationship to the growth suppressive and lethal actions that occur in lymphoid tissues when glucocorticoids are administered to the whole animal. The data support the hypothesis that the hormonal inhibition of growth and development is a consequence of its ability to suppress cellular energy production, causing the cells to behave as though they were in a more stringent environment. Slight changes in ratios of adenine and guanine nucleotides appear to account for the reordering of metabolic priorities that occurs, with processes related to growth and development curtailed in favor of those more essential to immediate cell survival. The lethal glucocorticoid actions appear to be the result of the operation of separate mechanisms (unrelated to energy metabolism) that lead to lethal attack at the level of the nuclear membrane. Resistance to the lethal effects appears to occur via the selection (in the case of cancer cells where the animal or patient is undergoing chemotherapy with glucocorticoids) or the normal development (in the case of immunologically noncommitted thymocytes progressing to immunologically committed ones) of cells with hardier membranes. This progression is associated with a change in a few cellular proteins. One such protein appears identical in both kinds of cells, offering itself as a candidate for an intracellular mechanism conferring resistance. Evidence is also presented for the appearance of hormone-induced proteins that could be metabolic regulators that mediate the individual cellular and biochemical actions of glucocorticoids. It is proposed that toxins could alter cellular metabolism through mechanisms similar to those utilized by steroid hormones, or possibly alter the sensitivity of cells to steroids, or vice versa.
Combined C3b and Factor B Autoantibodies and MPGN Type II
Authors: Qian Chen, Dominik Müller, Birgit Rudolph, Andrea Hartmann, Eberhard Kuwertz-Bröking, Kaiyin Wu, Michael Kirschfink, Christine Skerka, Peter F. Zipfel
Journal: New England Journal of Medicine (2011)

To the Editor: The decision by the Food and Drug Administration (FDA) not to approve the use of 5αreductase inhibitors as a means of prevent ing prostate cancer, as discussed by Theoret et al. (July 14 issue), 1 illustrates the challenges that thwart efforts to develop agents for this purpose.To support its position, the FDA reanalyzed two major trials. 2,3It cited the fact that the incidence of tumors with modified Gleason scores between 7 and 10 was not reduced and that the absolute incidence of tumors with modified Gleason scores between 8 and 10 was increased by 0.7% with finasteride and by 0.5% with dutasteride. 1 However, there is no evidence of increased mor tality attributable to the use of 5αreductase in hibitors.When the FDA said that reducing the incidence of lowgrade cancer was "unlikely to be clinically significant," 1 it did not consider the fact that such a diagnosis leads most men to elect some intervention, often with lifealtering complica tions. 4We believe that the FDA's emphasis on the theoretical risk of accelerated progression rather than on the benefits of reduced detection of low grade prostate cancer will risk converting suc cess into failure, stymie the development of pre vention strategies, and interfere with the progress being made in the clinical management of this complex but prevalent disease.