tbuckley/cabot-search huggingface dataset:
Spectrum of cutaneous manifestations of type 1 diabetes mellitus in 500 south Asian patients
Authors: G.U. Sawatkar, A.J. Kanwar, S. Dogra, S.K. Bhadada, D. Dayal
Journal: British Journal of Dermatology (2014)

Data on cutaneous manifestations of type 1 diabetes mellitus (DM) is scarce.To study the spectrum of dermatoses in patients with type 1 DM and the effects of disease duration and long-term glucose control on these cutaneous manifestations.After prior consent, clinical examination and relevant investigations were done in 500 subjects with type 1 DM enrolled between July 2011 and June 2012. Statistical tests were performed using SPSS 16. The presence of various dermatoses was correlated with the duration of diabetes.Of five hundred subjects, 339 (67·8%) had one or more dermatoses. The mean age of the patients was 16·9 ± 6·9 years (range 1-25 years) and mean total duration of diabetes was 4·43 ± 4·4 years. Cutaneous adverse effects related to insulin injections (CAII), comprising lipohypertrophy (41%), post-inflammatory hyperpigmentation (3%), lipoatrophy (0·6%) and acanthosis nigricans (0·4%), were the most common findings, followed by limited joint mobility (LJM) (16·8%), xerosis (15·8%) and scleroderma-like skin changes (10%). Patients having long-duration DM (> 4·4 years) were significantly more likely to have lipohypertrophy (P = 0·000), LJM (P = 0·000), scleroderma-like skin changes (P = 0·000), diabetic dermopathy (P = 0·000), acanthosis nigricans (P = 0·005) and skin tags (P = 0·002). Lipohypertrophy, LJM and scleroderma-like skin changes also showed significant correlation with blood glucose level.Our study suggests that cutaneous changes are common in young Asian patients with type 1 DM. Information, education and counselling of patients and care givers, and awareness among physicians is essential for the prevention and early management of these dermatoses.
Review: In relapsing–remitting multiple sclerosis, disease-modifying agents reduce annual relapse rates
Authors: Brian G. Weinshenker
Journal: Annals of Internal Medicine (2014)

ACP Journal Club18 March 2014Review: In relapsing–remitting multiple sclerosis, disease-modifying agents reduce annual relapse ratesBrian G. Weinshenker, MD, FRCP(C)Brian G. Weinshenker, MD, FRCP(C)Mayo Clinic, Rochester, Minnesota, USA (B.G.W.)Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-160-6-201403180-02005 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Source CitationCADTH Therapeutic Reviews. Management of relapsing–remitting multiple sclerosis [Internet]. Ottawa, ON: Canadian Agency for Drugs and Technologies in Health;Oct 2013. https://pubmed.ncbi.nlm.nih.gov/24279002Clinical Impact RatingsGIM/FP/GP: Neurology: References1 Complete response letter for Lemtrada: Genzyme receives complete response letter from FDA on Lemtrada (alemtuzumab) application. www.drugs.com/nda/lemtrada_131230.html (accessed 8 Jan 2014). Google Scholar2 Jones JL, Phuah CL, Cox AL, et al. IL-21 drives secondary autoimmunity in patients with multiple sclerosis, following therapeutic lymphocyte depletion with alemtuzumab (Campath-1H). J Clin Invest. 2009;119:2052-61. [PMID: 19546505] Google Scholar Author, Article, and Disclosure InformationAuthors: Brian G. Weinshenker, MD, FRCP(C)Affiliations: Mayo Clinic, Rochester, Minnesota, USA (B.G.W.)This article was published at Annals.org on 4 March 2014. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byMarkers of oxidative stress in plasma and saliva in patients with multiple sclerosis 18 March 2014Volume 160, Issue 6Page: JC5KeywordsDrugsInterferonsInternetLesionsMultiple sclerosisNetwork analysisNeurologyOral administrationSafetySerious adverse events ePublished: 18 March 2014 Issue Published: 18 March 2014 Copyright & PermissionsCopyright © 2014 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
A firm foundation for senior house officers
Authors: Derek Gallen, Ed Peile
Journal: BMJ (2004)

social services continues to fall-down 40% since 1993. 7 There has been a great deal of policy commentary on this transfer of financial responsibility from the state to older people in the lower to middle income range, who may be struggling to afford to purchase care and are often deterred by payments. 8 9Asking people to pay for elements of their care assumes that they will exercise choices in ways that maximise their own wellbeing, largely uninfluenced by social and other considerations, but this is often not the case. 10 Such evidence begs the question: do we want a system that offers greater equity of access to help ensure that care needs are met, as the majority commissioners argued?Or do we continue to leave this to the market as the government decided for those with means?There are different distributional effects, for both finance and provision, in the two positions.The minority commissioners and the government argue that they have maintained a level of private finance, to the tune of £1.1bn, from those individuals with means so they can focus a publicly funded safety net on those without.The main counterargument, from the majority commissioners, is that the current settlement seems to be unfair compared with NHS policy-equal needs are clearly not being treated equally 11 -and in our own research we have found that 60% of the public believe this situation to be unfair. 12 So, in the ever more complicated policy jungle boundaries between public and private finance and provision of traditional welfare services are becoming increasingly blurred.Within this blurring, though, important trade offs are being made.The lesson from long term care shows that New Labour tends to favour greater equity of finance to equity of access when it is given the choice
Mechanisms of Toxic Action and Structure-Activity Relationships for Organochlorine and Synthetic Pyrethroid Insecticides
Authors: Joel R. Coats
Journal: Environmental Health Perspectives (1990)

The mechanisms and sites of action of organochlorine (DDT-types and chlorinated alicyclics) and synthetic pyrethroid insecticides are presented with discussion of symptoms, physiological effects, and selectivity. The structural requirements for toxicity are assessed, and structure-activity relationships are considered for each subclass. Lipophilicity is important for all the groups because it facilitates delivery of these neurotoxicants to the site of action in the nerve. Steric factors including molecular volume, shape, and isomeric configuration greatly influence toxicity. Electronic parameters also have been demonstrated to affect biological activity in some of the groups of insecticides, e.g., Hammett's sigma and Taft's sigma * as indicators of electronegativity. New synthetic pyrethroids continue to be developed, with varied structures and different physicochemical and biological properties.
DILATATION OF THE CERVIX IN ECLAMPSIA
Authors: C. Rogerson
Journal: BMJ (1913)

<h3>Summary</h3> A hemagglutinin fraction (HAF) of influenza A (PR8) virus, purified by sucrose density gradient centrifugation and shown to be highly homogenous by analytical ultracentrifugation, electron microscopy and a gel diffusion test, was used as an immunizing antigen in these studies. Sera of guinea pigs immunized intraperitoneally with purified HAF contained antibodies which exhibited hemagglutination-inhibiting, virus neutralizing, and toxin neutralizing properties. Mice immunized with purified HAF prepared from PR8 virus were resistant to challenge infection with the homologous strain of virus but susceptible to infection with a heterologous (FM1) strain of virus. Guinea pigs immunized with whole virus and challenged intranasally with homologous virus exhibited more extensive and intensive histopathologic changes than nonimmunized animals; intranasal challenge of immunized animals with purified HAF duplicated some of the pathologic changes caused by challenge of immunized animals with whole virus.
Merkel cell carcinoma in a black human immunodeficiency virus-infected patient
Authors: E. Matichard, V. Descamps, M. Grossin, R. Genin, E. Bouvet, B. Crickx
Journal: British Journal of Dermatology (2002)

Summary Merkel cell carcinoma (MCC) is a rare malignant tumour that develops in sun-exposed areas in immunocompromised patients (chronic lymphocytic leukaemia, transplant recipients) older than 50 years. We report MCC in a young black woman with human immunodeficiency virus (HIV) infection. A 2-cm binodular violaceous lesion developed on her left ear lobe. Extensive work-up, including computed tomographic scans of the neck, chest, abdomen and pelvis, octreotide scan and sentinel node biopsy, did not demonstrate any metastasis. A wide excision was performed and the patient remained free of disease after 9 months. This case is the fourth observation of MCC in an HIV-infected patient.
Maturation of ureter-bladder connection in mice is controlled by LAR family receptor protein tyrosine phosphatases
Authors: Noriko Uetani, Kristen Bertozzi, Melanie J. Chagnon, Wiljan Hendriks, Michel L. Tremblay, Maxime Bouchard
Journal: Journal of Clinical Investigation (2009)

Congenital anomalies affecting the ureter-bladder junction are frequent in newborns and are often associated with other developmental defects. However, the molecular and morphological processes underlying these malformations are still poorly defined. In this study, we identified the leukocyte antigen-related (LAR) family protein tyrosine phosphatase, receptor type, S and F (Ptprs and Ptprf [also known as Lar], respectively), as crucially important for distal ureter maturation and craniofacial morphogenesis in the mouse. Embryos lacking both Ptprs and Ptprf displayed severe urogenital malformations, characterized by hydroureter and ureterocele, and craniofacial defects such as cleft palate, micrognathia, and exencephaly. The detailed analysis of distal ureter maturation, the process by which the ureter is displaced toward its final position in the bladder wall, leads us to propose a revised model of ureter maturation in normal embryos. This process was deficient in embryos lacking Ptprs and Ptprf as a result of a marked reduction in intrinsic programmed cell death, thereby causing urogenital system malformations. In cell culture, Ptprs bound and negatively regulated the phosphorylation and signaling of the Ret receptor tyrosine kinase, whereas Ptprs-induced apoptosis was inhibited by Ret expression. Together, these results suggest that ureter positioning is controlled by the opposing actions of Ret and LAR family phosphatases regulating apoptosis-mediated tissue morphogenesis.
Prospective, Randomized, Multicentric, Open, Comparative Study on the Efficacy of a Prophylactic Single Dose of 500mg Levofloxacin versus 1920mg Trimethoprim/Sulfamethoxazole versus a Control Group in Patients Undergoing TUR of the Prostate
Authors: F.M.E. Wagenlehner, C. Wagenlehner, S. Schinzel, K.G. Naber
Journal: European Urology (2005)
Disorders of the Respiratory Tract in Children
Authors: Richard W. Newcomb
Journal: JAMA (1978)

I was startled to find that this new edition was here before I had finished reading the old one. In the last four years, there were plenty of occasions to look things up and be thankful that Kendig's book was handy, but there was never enough time to settle down and really read both volumes. Now we have the new and improved Kendig, back to its proper size of one volume, and with a distinguished associate editor. It really is up to date, with references extending even into 1977. It really is improved, both by revisions of all sections and by the addition of seven new chapters. And there really are sections that are both readable and of enough general interest to warrant being read by everyone caring for children. The entire first section is a good introduction to the pathophysiology of pediatric chest disease. If you include also the
Agminated Pyogenic Granuloma–Like Growth Arising in a Congenital Hemangioma
Authors: Benjamin Barrick, Julia Lehman, Megha Tollefson
Journal: JAMA Dermatology (2014)

several months.Our patient was without hydroxyurea for 2 months and showed no improvement.Only after the hydroxyurea therapy was discontinued permanently was her ulcer finally able to resolve with medical and surgical intervention.Another complicating factor in our patient's wound healing was the immunosuppressive effects of the prednisone and azathioprine, which likely led to intermittent superinfection and prevented the ulcer from healing on its own.Why does hydroxyurea cause cutaneous ulceration?Almost all patients taking hydroxyurea develop megaloblastic erythrocytes within 24 hours, causing decreased susceptibility to deformation that impairs capillary blood flow to the skin. 4,5 The result is cutaneous anoxia followed by ulceration.This mechanism may explain why the malleolus, a frequent site of trauma, is a common location for these ulcers.In our patient, the ulcer developed after cryotherapy, which led to skin breakdown and ultimately ulceration.MTHFR polymorphisms, such as the homozygous C→T substitution at nucleotide 677 found in our patient and in 10% to 13% of the white population, can lead to arterial occlusive disease and ulceration.This results from decreased enzyme activity, which causes an increased total homocysteine level in the presence of suboptimal folate intake. 6 The concurrent existence of an MTHFR polymorphism or other thrombophilic genetic mutation in a patient taking hydroxyurea could be the complicating insult that leads to cutaneous ulceration.Therefore, we recommend screening for an array of coagulation abnormalities that predispose to thrombophilia (including MTHFR polymorphisms) in patients with ulcers unresponsive to standard therapy as well as the use of B vitamin supplementation in patients with a MTHFR polymorphism.
Erratum: Corrigendum: A catalytically silent FAAH-1 variant drives anandamide transport in neurons
Authors: Jin Fu, Giovanni Bottegoni, Oscar Sasso, Rosalia Bertorelli, Walter Rocchia, Matteo Masetti, Ana Guijarro, Alessio Lodola, Andrea Armirotti, Gianpiero Garau, Tiziano Bandiera, Angelo Reggiani, Marco Mor, Andrea Cavalli, Daniele Piomelli
Journal: Nature Neuroscience (2013)
Influence of Competitive Pulmonary Blood Flow on the Bidirectional Superior Cavopulmonary Shunt
Authors: Steven A. Webber, Pavel Horvath, Jacques G. LeBlanc, Zdenek Slavik, Robert K. Lamb, James L. Monro, Oleg Reich, Jaroslav Hruda, George G.S. Sandor, Barry R. Keeton, Anthony P. Salmon
Journal: Circulation (1995)

Background It is common practice to interrupt all alternative sources of pulmonary blood flow (“competitive flow”) at the time of a bidirectional superior cavopulmonary anastomosis (BCPA), although the merits of this have not been systematically studied. Methods and Results We reviewed the early and medium-term clinical and hemodynamic findings in 108 consecutive patients 3 weeks to 25 years old (median, 1.9 years) undergoing BCPA at one of three institutions. Preoperatively, pulmonary blood flow was dependent on antegrade ventricular flow (n=50), systemic-to-pulmonary shunts (n=33), or mixed sources (n=25). Postoperatively, competitive sources of pulmonary blood flow were left patent in 43 of 108 patients (40%). There were four early (3.7%) and four late deaths, none related to persistence of competitive flow. After BCPA, patients with competitive flow had significantly higher systemic oxygen saturations at 1 hour (85% versus 79%), 24 hours (84% versus 78%), and at hospital discharge (84% versus 78%) and required a shorter period of artificial ventilation (median, 9 versus 24 hours) and intensive care (median, 2 versus 4 days). Oxygen saturations at late follow-up (median, 2.8 years; range, 1 to 7) did not differ (83% versus 82%). No patient developed pulmonary arteriovenous malformations. Conclusions Competitive flow is well tolerated in the short and medium term after BCPA, and early postoperative systemic oxygen saturations are improved. The long-term influence of competitive flow on pulmonary arterial growth, arteriovenous malformation development, and ventricular function warrants investigation.
Different mutations in the COL4A5 collagen gene in two patients with different features of Alport syndrome
Authors: Hubert J.M. Smeets, Jos J. Melenhorst, Henny H. Lemmink, Cock H. Schröder, Marcel R. Nelen, Jing Zhou, Sirkka L. Hostikka, Karl Tryggvason, Hans-Hilger Ropers, Maaike C.E. Jansweijer, Leo A.H. Monnens, Han G. Brunner, Bernard A. van Oost
Journal: Kidney International (1992)
Thiabendazole—A New Anthelmintic Drug
Authors: B. H. KEAN
Journal: Annals of Internal Medicine (1967)

Editorial Notes1 August 1967Thiabendazole—A New Anthelmintic DrugB. H. KEAN, M.D., F.A.C.P.B. H. KEAN, M.D., F.A.C.P.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-67-2-461 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptFor the past several decades, the field of clinical helminthology has had two major goals: finding a single drug that, when administered orally in one dose, would force the five major types of roundworms from the intestinal tract; and developing a drug that would kill circulating larvae or parasites localized in the tissues. There have been major limitations to achieving these goals. First, parasitologists have been slow to use some of the more precise methods of studying living organisms. They have too often been content to test new drugs in a rather haphazard fashion—with inadequate designs for therapeutic assessment and...References CUCKLERMEZEY ACKC: The therapeutic efficacy of thiabendazole for helminthic infections in man. A literature review. Arzneimittelforschung 16: 411, 1966. MedlineGoogle Scholar FRANZSCHNEIDERPOHLMAN KHWJMH: Clinical trials with thiabendazole against intestinal nematodes infecting humans. Amer. J. Trop. Med. 14: 383, 1965. CrossrefMedlineGoogle Scholar TOCCOROSENBLUMMARTINROBINSON DJCCMHJ: Absorption, metabolism and excretion of thiabendazole in man and laboratory animals. Toxic. Appl. Pharmacol. 9: 31, 1966. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Cornell University Medical College New York, N. Y. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited ByTherapy in trichinosisTrichinosis in cork 1 August 1967Volume 67, Issue 2Page: 461-462KeywordsDrugs Issue Published: 1 August 1967 PDF DownloadLoading ...
The pursuit of imperfection
Authors: Des Spence
Journal: BMJ (2013)

Tall, young, slim, bright, sporty, polite, athletic, controlled, musical, socially polished, good looking, sensible, and obedient, with straight white teeth: these traits of perfection are the aspirations of many parents and adults alike. And medicine is a candle to the perfect and perfectionism—a perfect degree, status, job, and career. But time is life’s great leveller, slowly turning, shaking, and unravelling all our misguided youthful aspirations, laying waste to perfection. 

And perfectionist traits are particularly vulnerable to attrition in the melee of medicine. The unrealistic expectations of a medical career make many doctors …
Abstract 3181: The genomic evolution of prostate cancer under the selective pressure of anti-androgen therapy.
Authors: Joël R. Gsponer, Tanja Dietsche, Alexander Rufle, Elisabeth Lenkiewicz, Tobias Zellweger, Alexander Bachmann, Daniel D. Von Hoff, M T. Barrett, Cyrill Rentsch, Christian Ruiz, Lukas Bubendorf
Journal: Cancer Research (2013)

Abstract Background: The implementation of novel technologies such as array comparative genomic hybridization (aCGH) and next-generation sequencing has led to a deeper understanding of the genomic nature of cancer. However, these analyses have classically been done without respecting intra-tumor heterogeneity. Here, we applied a methodology that allows us analyzing the genomic profile of distinct tumor populations from individual tumors and their clonal evolution during the progression to castration-resistant disease. Methods: Matched pre- and post- hormone treated fresh frozen and/or formalin fixed prostate cancer samples were selected from our biobank. Clonal tumor populations were flow-sorted according to their nuclear DNA content. Sorted tumor populations were subjected to whole genome CGH and to full exome sequencing analyses by the use of Agilent SurePrint 2x400k microarrays and the SureSelect All Exon Kit, respectively. Results: The genomic analyses of the tumor samples underscore the presence of significant intra-tumoral heterogeneity. The analysis of matched tumor specimens allowed us to identify two particular patterns of tumor evolution during the progression after treatment: First, a more parallel pattern of tumor evolution, in which the ancestor population is breeding multiple aneuploid tumor clones. In this case, only the 2N ancestor population is able to withstand therapy by the acquisition of few specific genomic aberrations whereas the aneuploid populations are eradicated. Second, a more sequential pattern of tumor evolution with a tumor population that evolves out of a continuous line of clones. This population shows increasing signs of genomic instability over time, with a punctual event of chromothripsis (a massive destruction and rearrangement of chromosomal structures) resulting in castration-resistant clonal tumor populations. Conclusions: Genomic profiling of distinct clonal tumor populations during prostate cancer progression allows for analysis of intra-tumoral heterogeneity and the underlying clonal evolution. Importantly, this approach identifies genomic aberrations that were selected for under the pressure of hormone ablation therapy. Citation Format: Joël R. Gsponer, Tanja Dietsche, Alexander Rufle, Elisabeth Lenkiewicz, Tobias Zellweger, Alexander Bachmann, Daniel D. Von Hoff, M T. Barrett, Cyrill Rentsch, Christian Ruiz, Lukas Bubendorf. The genomic evolution of prostate cancer under the selective pressure of anti-androgen therapy. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3181. doi:10.1158/1538-7445.AM2013-3181
A portable pulsed electromagnetic field (PEMF) device to enhance healing of recalcitrant venous ulcers: a double-blind, placebo-controlled clinical trial
Authors: M.J. STILLER, GRACE H. PAK, J.L. SHUPACK, S. THALER, CLARE KENNY, LORRIE JONDREAU
Journal: British Journal of Dermatology (1992)

Summary A prospective, randomized, double-bind, placebo-controlled multicentre study assessed the clinical efficacy and safety of pulsed electromagnetic limb ulcer therapy (PELUT) in the healing of recalcitrant, predominantly venous leg ulcers. The portable device was used at home for 3 h daily during this 8-week clinical trial as an adjunct to a wound dressing. Wound surface area, ulcer depth and pain intensity were assessed at weeks 0, 4 and 8. At week 8 the active group had a 47.7% decrease in wound surface area vs. a 42.3% increase for placebo (P<0.0002). Investigator's global evaluations indicated that 50% of the ulcers in the active group healed or markedly improved vs. 0% in the placebo group, and 0% of the active group worsened vs. 54% of the placebo group (P<0.001). Significant decreases in wound depth (P<0.04) and pain intensity (P<0.04) favouring the active group were seen. Patients whose ulcers improved significantly after 8 weeks were permitted to continue double-blind therapy for an additional 4 weeks. Elevan active and one placebo patient continued therapy until week 12, with the active treatment group continuing to show improvement. There were no reports of adverse events attributable to this device. We conclude that the PELUT device is a safe and effective adjunct to non-surgical therapy for recalcitrant venous leg ulcers.