tbuckley/cabot-search huggingface dataset:
Incidence and Progression of Diabetic Retinopathy in Hispanics and Non-Hispanic Whites With Type 2 Diabetes. San Luis Valley Diabetes Study, Colorado
Authors: Stephanie M Tudor, Richard F Hamman, Anna Baron, David W Johnson, Susan M Shetterly
Journal: Diabetes Care (1998)

OBJECTIVE To learn if Hispanic people with type 2 diabetes have excess incidence and/or progression of diabetic retinopathy and to explore the association of risk factors with diabetic retinopathy. RESEARCH DESIGN AND METHODS There were 244 subjects with type 2 diabetes (65.3% Hispanic) with at least one follow-up visit between 1984 and 1992 examined for the development of retinopathy over a median of 4.8 years (range 2.0−6.6 years). Stereo fundus photos were graded by the University of Wisconsin Reading Center. RESULTS Of the 169 subjects without retinopathy at baseline, 47 developed some retinopathy, an incidence rate of 63.7 per 1,000 person-years (PY), or a 4-year cumulative incidence of 22.5%. The Hispanic incidence rate was 58.3/1,000 PY (95% CI: 39.4−83.3), which was lower than among non-Hispanic whites, 76.1/1,000 PY (44.3−121.9). Progression occurred in 24 of the 75 subjects with retinopathy at baseline, a 4-year cumulative rate of 24.1%. Logistic regression showed that insulin treatment was associated with higher risk of any retinopathy (odds ratio [OR] = 8.45, 2.65−26.97), and both systolic blood pressure (odds ratio [OR] = 1.58, 0.99−2.52) and total GHb (OR = 1.46, 0.99−2.17) nearly attained statistical significance. After adjustment for multiple potential risk factors, the Hispanic/non-Hispanic white OR was 0.66 (0.28−1.57). CONCLUSIONS No excess risk for incident retinopathy was found among Hispanic compared with non-Hispanic white subjects in this population. These results are consistent with our previously reported prevalence data from the same population but differ from reports of excess prevalence among Texas Hispanics. No other Hispanic incidence data are available to assist in reconciling this difference.
Overexpression of p53: A rare event in a large series of white patients with hepatocellular carcinoma
Authors: Pierre Laurent-Puig, Jean-François Flejou, Monique Fabre, Pierre Bedossa, Jacques Belghiti, François Gayral, Dominique Franco
Journal: Hepatology (1992)

Mutant p53 has been found in a wide variety of human malignancies including carcinomas of the lung, breast and colon. Because of the controversial mutational rate of the p53 gene in hepatocellular carcinoma, a large series of liver tumors from white patients with different risk factors was examined immunohistochemically for expression of the p53 mutant to assess its prevalence and the relationships between p53 overexpression and clinicopathological data. Nine of 58 specimens were found to have detectable evidence of p53 gene mutation by virtue of the immunohistochemical detection of mutant p53 protein. The p53 mutation was more frequent in patients with serological hepatitis B and C markers than in patients without these markers (p = 0.046). The prevalence of p53-positive tumors was also significantly higher in the group of tumors with invaded portal branches than in the group without (p = 0.02). Our results showed that p53-positive hepatocellular carcinoma is a rare finding in patients exposed to a low dietary aflatoxin intake and that p53 mutation seems to occur at a late stage of the tumoral process and could contribute to an aggressive tumoral phenotype.
Low concentration zinc sulphate solution in the management of recurrent herpes simplex infection
Authors: R.M. Graham, M.P. James, S. Bennett
Journal: British Journal of Dermatology (1985)

Journal Article Low concentration zinc sulphate solution in the management of recurrent herpes simplex infection Get access R.M. Graham, R.M. Graham The Department of Dermatology, The Royal Berkshire Hospital, Reading, U.K. Search for other works by this author on: Oxford Academic Google Scholar M.P. James, M.P. James The Department of Dermatology, The Royal Berkshire Hospital, Reading, U.K. Search for other works by this author on: Oxford Academic Google Scholar S. Bennett S. Bennett The Department of Applied Statistics, Reading University, Reading, U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 112, Issue 1, 1 January 1985, Pages 123–124, https://doi.org/10.1111/j.1365-2133.1985.tb02303.x Published: 01 January 1985
Furosemide and Increases in Liver Enzymes
Authors: Irene Lang
Journal: Annals of Internal Medicine (1988)

Letters and Corrections15 November 1988Furosemide and Increases in Liver EnzymesIrene Lang, MD, Kurt Huber, MD, Julia Capek, MD, Dietmar H. Glogar, MD, Peter Probst, MD, Fritz Kaindl, MDIrene Lang, MDSearch for more papers by this author, Kurt Huber, MDSearch for more papers by this author, Julia Capek, MDSearch for more papers by this author, Dietmar H. Glogar, MDSearch for more papers by this author, Peter Probst, MDSearch for more papers by this author, Fritz Kaindl, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-109-10-845 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the Editor:Acute increases (hepatitis-like) in liver enzymes, without clinical evidence of viral hepatitis, have been reported only occasionally and have been termed ischmic hepatitis (1-6). From September 1985 to September 1987, hepatitis-like increases in liver enzymes have occurred in 12 patients at our cardiac care unit 6 to 72 hours after a documented drop in systemic systolic blood pressure below 70 mm Hg (duration range, 4 to 48 hours). Peak values of plasma aspartate aminotrans- ferase (1302 ± 450 U/mL), alanine aminotransferase (1514 ± 1026 U/mL), and lactic dehydrogenase (2387 ± 1324 U/mL) could be measured after 48...References1. CohenKaplan JM. Left-side heart failure presenting as hepatitis. Gastroenterology. 1978;74:583-7. CrossrefMedlineGoogle Scholar2. BynumBoitnottMaddrey TJW. Ischemic hepatitis. Dig Dis Sci. 1979;24:124-35. CrossrefGoogle Scholar3. NovelHeninoBennuauDegottRueffBenhamou OJJCBJ. Fulminant hepatic failure due to transient circulatory failure in patients with chronic heart disease. Dig Dis Sci. 1980;25:49-52. CrossrefMedlineGoogle Scholar4. GibsonDudley PF. Ischaemic hepatitis: clinical features, diagnosis and prognosis. Aust NZ J Med. 1984;14:822-5. CrossrefMedlineGoogle Scholar5. Ischaemic hepatitis [Editorial]. Lancet. 1985;1:1019-20. MedlineGoogle Scholar6. HigginsLane RD. Ischaemic hepatitis. Lancet. 1985;1:1449. CrossrefMedlineGoogle Scholar7. BulkleyOshimaBailey GAR. Pathophysiology of hepatic ischemia in cardiogenic shock. Am J Surg. 1986;151:87-97. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: University of Vienna Vienna Austria PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byHypoxic hepatitis and furosemide 15 November 1988Volume 109, Issue 10Page: 845-845KeywordsAlanine aminotransferaseBlood plasmaBlood pressureCardiac care unitDehydrogenasesEnzymesHepatitisLiverSystolic pressure Issue Published: 15 November 1988 PDF downloadLoading ...
Probes for Identifying Listeria
Authors: Atin R. Datta
Journal: JAMA (1989)

To the Editor.—  I read with great interest the review article by Drs Gellin and Broome. 1 The article is well written and provides an in-depth study of the problem of listeriosis. However, there is one element in the article that needs further clarification. The authors state that both monoclonal antibody— and DNA probe—based tests identify Listeria at the genus level. While this is true for the antibody-based assay, it is not true for the probe, which has been developed by my colleagues and myself at the Food and Drug Administration. The natural DNA probe that the authors quote 2 in their article has been developed from a putative β-hemolysin gene fragment of Listeria monocytogenes cloned by Robert K. Flamm, PhD. 3 To date, our results have shown that this probe hybridizes only with L monocytogenes strains and does not react with any other Listeria and non- Listeria strains in
[640] BASELINE FACTORS ASSOCIATED WITH ANEMIA DURING PEGYLATED INTERFERON PLUS RIBAVIRIN COMBINATION THERAPY FOR CHRONIC HEPATITIS C
Authors: J.P. Sampaio, P.N. El Batah, L.L. Schiavon, R.J. Carvalho Filho, J.L. Narciso, M.L.G. Ferraz, A.E.B. Silva
Journal: Journal of Hepatology (2007)
Idiopathic facial palsy.
Authors: E. D. Campbell
Journal: BMJ (1968)

gations: chest x-ray normal; Hb 55%; W.B.C. 7,100 with normal diffierential; iron deficiency on the blood film; E.S.R. 138 mm. in one hour; Paul-Bunnell test negative.Blood culture revealed Haemophilus influenzae type B sensitive to all the usual antibiotics except sulphonamide.This child was treated with ampicillin and made a good recovery.My point in recording this case history is to emphasize that septicaemia due to Haemo- philus influenzae may not be as rare as we had thought and one can easily envisage such a child as I have mentioned developing osteomyelitis due to this organism.-Iam, etc.,
The course of lung function in treated tropical pulmonary eosinophilia
Authors: S. C. Poh
Journal: Thorax (1974)

<b>Poh, S. C. (1974).</b><i>Thorax</i>, <b>29</b>, 710-712. <b>The course of lung function in treated tropical pulmonary eosinophilia.</b> A follow-up study over a period of two years in the lung function of 15 patients with tropical pulmonary eosinophilia successfully treated with diethylcarbamazine is reported. A return to normal of the lung function with the exception of the transfer factor and forced expiratory volume is observed by the end of six months and these abnormalities persist up to the end of the study. The possible pathological causes of this defect are discussed.
Drug maker’s PR firm is force behind blood clot awareness campaign
Authors: Ray Moynihan
Journal: BMJ (2008)

The international public relations firm Fleishman-Hillard, working with funds from the drug maker Sanofi-Aventis, is helping run a high profile campaign to raise public awareness about blood clots.

The campaign, currently running in Australia under the banner of a coalition of health professionals, has generated headlines claiming that blood clots are more deadly than AIDS and articles suggesting that injections for patients at risk of developing clots may become mandatory.

A national expert on drugs, Alasdair Millar, said that any suggestion that all medical in-patients should receive injections to prevent clots are “extreme and scandalous” and “could cause more harm than good.”

Evidence suggests that many hospital patients, whether surgical or medical, could benefit from a greater use of drugs to prevent serious clots, including low molecular weight heparins. But Professor Millar is concerned that these drugs will be given to patients who do not need them, thus exposing them unnecessarily to the risk of bleeding.

Since the launch …
Heat-shock response and limitation of tissue necrosis during occlusion/reperfusion in rabbit hearts.
Authors: R W Currie, R M Tanguay, J G Kingma
Journal: Circulation (1993)

Induction of stress proteins, such as heat-shock protein 71 (HSP71), is associated with cardioprotection in isolated ischemic myocardium. We tested this hypothesis in rabbits pretreated with whole-body hyperthermia and then subjected to 30 or 45 minutes of regional coronary occlusion (CO) followed by 3 hours reperfusion (Rep).Control rabbits did not undergo whole-body hyperthermia; heat-shocked (HS) rabbits were subjected to whole-body hyperthermia at 42 degrees C for 15 minutes. Rabbits were allowed to recover from whole-body hyperthermia for 24 or 40 hours and were then subjected to CO/Rep. Heart rate and arterial blood pressure were recorded during the experiments. Area of necrosis (tetrazolium staining) was normalized to anatomic risk zone size (microsphere autoradiography). In rabbits treated with whole-body hyperthermia and 24 hours of recovery, infarct size was significantly reduced in HS rabbits compared with control rabbits (41.2 +/- 7.8% versus 23.2 +/- 6.6%; p < or = 0.05; mean +/- SD) after 30 minutes of CO and 3 hours of Rep. Risk zone size was similar for the two experimental groups. In rabbits treated with whole-body hyperthermia and 40 hours of recovery, infarct size was similar for control and HS animals with either 30 or 45 minutes of CO (p = NS) and 3 hours of Rep. Risk zone size and area of necrosis were similar for these experimental groups. Biopsies from ischemic and nonischemic myocardium were obtained from rabbits at 24 and 40 hours after heat shock and control rabbits to verify expression of HSP71; expression was determined by Western blot analysis.Our findings demonstrate a considerable increase in expression of HSP71 in myocardium from hyperthermia-treated rabbits. Infarct size was significantly reduced after 30 minutes of CO and 3 hours of Rep in hearts at 24 but not 40 hours after heat shock compared with control hearts. We conclude that heat shock-induced cardioprotection is transient and delays the onset of irreversible myocardial injury caused by ischemia.
AN AMINO-ACID DEFICIENCY AS THE PRIMARY ETIOLOGIC FACTOR IN PELLAGRA
Authors: JOSEPH GOLDBERGER
Journal: JAMA (1922)

The evidence now available abundantly demonstrates that pellagra is a manifestation of dietary deficiency. Exactly what dietary factor or factors are concerned, however, is not so clear, although the indications have for some time increasingly pointed to the protein,<sup>1</sup>that is, to some amino-acid deficiency, as the essential primary factor concerned in the causation of the disease. In support of this interpretation, we reported<sup>2</sup>last spring the recurrence of pellagra in five patients in spite of a daily consumption, during periods of not less than two and one-half months before the appearance of the distinctive eruption, of a diet presumably adequately supplied with both minerals and known vitamins, thus tending to exclude these and pointing to amino-acid deficiency as the essential factor. Since that report was written, we have been able to make some additional observations that point even more strongly to amino-acid deficiency as the primary etiologic
Stop digging: CAM modalities have been tested and found wanting
Authors: P. Morgan
Journal: BMJ (2012)

For far too long the pseudoscience behind so called complementary and alternative medicine (CAM) has been lent false authority by the teaching of such nonsense in academic institutions.1 The failure to find evidence of benefit for CAM modalities such as acupuncture, homeopathy, and chiropractic, despite many years of research and the attention …
Abstract 10: DNA repair and nutritional risk models of triple-negative breast cancer
Authors: Jennifer Hu, Eunkyung Lee, Glenn Allen
Journal: Cancer Research (2014)

Abstract Purpose: Triple negative breast cancer (TNBC), which lacks treatment targets for estrogen receptor (ER), progesterone receptor (PR) and human epidermal growth factor receptor 2 (HER2), has been associated with African-American race, BRCA1/2 mutations, TP53 mutations, and poor prognosis. However, the etiology of TNBC remained unknown, which represents a critical barrier in reducing breast cancer mortality. Therefore, we designed a case-only study to test combined genetic and nutritional risk models of TNBC. Methods: In 354 breast cancer patients diagnosed between 1998 and 2004, we evaluated 18 DNA-repair non-synonymous single nucleotide polymorphisms (nsSNPs) using the Sequenom MassARRAY system. The 110-item Block 1998 food frequency questionnaire was used to evaluate dietary/nutritional intakes. The Multivariate Adaptive Regression Splines (MARS)-logit models were used to define nutritional intakes cut-offs for their associations with TNBC. Results: TNBC was associated with 6 DNA-repair nsSNPs, ERCC4 R415Q (rs1800067), MSH3 R940Q (rs184967), MSH6 G39E (rs1042821), POLD1 R119H (rs1726801), XRCC1 R194W (rs1799782), and XPC A499V (rs2228000) and/or 3 micronutrients (zinc, folate, and β-carotene). Combined DNA-repair risk genotypes and lower micronutrient intakes had a significant dosage-dependent association with TNBC (p&amp;lt;0.001): ORs=2.77 (95%CI=1.01-7.64), 9.57 (95%CI=2.87-31.84), and 20.78 (95%CI=2.46-175.71) for 2, 3, and at least 4 risk factors combined, respectively. Conclusion: To the best of our knowledge, this is the first study to demonstrate multiple DNA repair nsSNPs and nutritional factors are associated with TNBC. Our results suggest that dietary modulation and micronutrient supplementation may have implication in preventing or reversing TNBC, particularly in genetically susceptible women. Citation Format: Jennifer Hu, Eunkyung Lee, Glenn Allen. DNA repair and nutritional risk models of triple-negative breast cancer. [abstract]. In: Proceedings of the AACR Special Conference: Cancer Susceptibility and Cancer Susceptibility Syndromes; Jan 29-Feb 1, 2014; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(23 Suppl):Abstract nr 10. doi:10.1158/1538-7445.CANSUSC14-10
Tetanus Immune Globulin (Human)
Authors: Richard P. Giliberty
Journal: JAMA (1965)

<h3>To the Editor:—</h3> Over one year ago, the pharmacology committee at Nassau Hospital investigated the high incidence of serum reactions which resulted from the use of equine and bovine tetanus antitoxin (TAT) for prophylaxis. In spite of careful skin-testing and desensitization, whenever the skin tests were positive, serum reactions frequently occurred. Some were quite severe and required hospitalization, and some occurred when the skin test was negative. Patients who had previous passive immunization with equine TAT and had a history of having had a reaction, were given bovine TAT following a skin test. All patients who had an allergic history were usually tested with both bovine and equine TAT. To avoid the reactions, patients who had positive skin tests with TAT of equine or bovine origin, or patients who gave a history of serum sickness or allergy, were given tetanus immune globulin of human origin. The product used was Hyper-Tet
Medical pay in self governing trust hospitals
Authors: H M Saxton
Journal: BMJ (1990)

department of our hospital attend because of musculoskeletal complaints and injuries.A glance at the journals of the defence organisations reveals that such injuries are often a fruitful source of litigation.We hope that the omission oforthopaedic surgery is an error in the construction of the questionnaire used in the study rather than a reflection on its lack of teaching.
Textbook of Neuroanatomy
Authors: Wendell J. S. Krieg
Journal: JAMA (1964)

This book is a rewriting of Elliott's<i>Textbook of the Nervous System</i>, which first appeared in 1947. It is not too long or too difficult for medical students and is thoroughly up to date in incorporating periodical literature into the text. The text is divided into six parts, of 60 to 70 pages each: neurohistology, spinal cord and cranial nerves, sensory systems (including thalamus), motor systems (including cerebellum), cerebral hemispheres (including pyramidal system), and accessory structures. The cranial nerves are considered in numerical order, and not primarily by nerve components. Written with a pleasing informality, the book is full of information which, however, smells of the study lamp rather than of xylol and balsam. Some of the text figures are photographs of microscopic preparations, nearly all bearing a credit line. The atlas section consists chiefly of unlabelled photographs of slices of fixed brain and Weigert sections of brain stem, with
Abstract 3822: DNA copy number changes in the PI3K signaling pathway genes in triple negative breast cancer
Authors: Marcia C. Oliveira, Silma R. Pereira, Enilze MF Ribeiro, Rubens S. Lima, Cicero A. Urban, Ana Paula M. Sebastião, Catalin Marian, Bassem R. Haddad, Iglenir J. Cavalli, Luciane R. Cavalli
Journal: Cancer Research (2011)

Abstract Background: Triple negative breast cancer (TNBC) is associated with poor prognosis and a high mortality rate when compared to the other breast cancer subtypes. These tumors lack the expression of ER, PR and HER2 receptors, and do not respond well to the currently available adjuvant therapies. The phosphatidylinositol 3-kinase (PIK3) signaling pathway mediates key cellular functions. Alterations of genes in this pathway have been shown to predict responsiveness to cancer targeted therapies. In this study, five genes involved in this signaling pathway, PIK3CA, AKT1, AKT2, PTEN and FGFR, were evaluated for DNA copy number changes in two sets of TNBC specimens. Methods: TNBC samples were obtained from the Hospital Nossa Senhora das Gracas, Curitiba, PR, Brazil. Two sets of TNBC samples were analyzed: the first set was composed of 30 formalin fixed-paraffin embedded tissue specimens and were analyzed for the PIK3CA, AKT1, AKT2, PTEN and FGFR genes by FISH. Locus-specific probes were prepared from BAC contigs for each gene and a centromeric probe for chromosome 3 was used as a control for copy number. The second set was composed of 17 frozen samples and were analyzed by array-CGH using a 44K-Agilent array platform. Real-Time PCR (TaqMan assay), was used to validate the array-CGH data for the above five genes. Results: FISH: PTEN loss and FGFR3 amplification were the most common findings occurring in 56% and 41% of the TNBC samples respectively. PIK3CA, AKT2 and AKT1 were amplified in 31%, 25% and 9.5% of the samples respectively. Array-CGH/Real time PCR: DNA copy number changes were observed by array-CGH in all, but one TNBC sample. The gene with highest frequency of amplification detected by array-CGH was PIK3CA (amplified in 77% of the cases). These findings were confirmed in 70% of the cases. FGFR2, AKT2 and PTEN were amplified in 35%, 24% and 24% of the cases respectively, These findings were confirmed for FGFR2 in 83% of the samples and for PTEN in all the samples. AKT2 amplification was only confirmed in 25% of the samples. Finally AKT1 was observed amplified in by array-CGH in 6% of the cases, which was confirmed by Real-time PCR.Conclusions: Based on our initial results, we conclude that TNBC presents DNA copy number alterations in genes involved in the PIK3 signaling pathway. Upon validation of these alterations in a larger number of cases, with correlation to prognostic parameters, their potential use as therapeutic targets can be considered for further investigation. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 3822. doi:10.1158/1538-7445.AM2011-3822