tbuckley/cabot-search huggingface dataset:
Cetirizine inhibits bradykinin‐induced cutaneous wheal and flare in atopic and healthy subjects
Authors: R. Fadel, I. Ramboer, N. Chatterjee, J.‐P. Rihoux, M.‐P. Derde
Journal: Allergy (2000)

Kinins are vasoactive mediators involved in allergic reactions. When applied on the skin or in the nose, bradykinin (BK) elicits inflammation that is poorly affected by previous H1-blockade. The aim of this study was to compare the possible effect of cetirizine (an H1-antagonist) on wheal and flare responses to BK, histamine, and compound 48/80 in atopic and healthy subjects.In a randomized, double-blind, crossover study, eight atopic and eight healthy subjects received cetirizine (10 mg/day) or placebo for 3 days before cutaneous tests. Intradermal tests (IDT) and prick tests (PT) were performed with BK (20 nmol/ml for IDT and 20 micromol/ml for PT), histamine (100 microg/ml IDT and 100 mg/ml PT), and compound 48/80 (100 microg/ml IDT and 100 mg/ml PT) as positive controls and saline as negative control. The skin responses were monitored by measurement of wheal and flare areas.BK, histamine, and 48/80 induced wheal and flare reactions in all placebo-treated subjects. Histamine elicited larger wheal and flare reactions than BK and 48/80. IDT with BK induced four- to sixfold larger wheal and flare reaction than PT. No differences in BK-induced wheal and flare were observed between atopic and healthy subjects. In atopic subjects, cetirizine induced a significant reduction of flare reactions after the BK test (80% for IDT, and 94% for PT [P < 0.01]). Moreover, cetirizine reduced significantly BK-induced wheals by 70% for IDT (P < 0.01) and 65% for PT (P < 0.01). A similar inhibiting effect of cetirizine was also observed in healthy subjects.These findings showed that the wheal and flare reactions induced by BK challenge were markedly inhibited by previous intake of cetirizine. The mechanism by which this effect is mediated cannot be established at present.
The TODAY Study: An NIH Perspective on Its Implications for Research
Authors: Barbara L. Linder, Judith E. Fradkin, Griffin P. Rodgers
Journal: Diabetes Care (2013)

Once referred to as adult-onset diabetes, type 2 diabetes (T2D) has emerged in youth as a consequence of the worldwide increase in obesity. The development of T2D among young individuals has significant public health consequences as these youth are likely to manifest the complications of diabetes, including retinopathy, nephropathy, neuropathy, and cardiovascular disease, at a time that should be the most active and productive of their lives.

In response to the emergence of T2D among youth in the mid-1990s, the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health sought to foster research to understand and address this public health threat. Since most of our knowledge about the epidemiology of T2D in the pediatric population was based on small clinic-based reports, NIDDK partnered with the Centers for Disease Control and Prevention (CDC) to establish the SEARCH for Diabetes in Youth Study to provide population-based statistics for diabetes in U.S. youth (1). SEARCH data from 2002–2003 indicated that approximately 3,700 youth were being diagnosed annually with T2D (2). T2D is rarely seen in children younger than 10 years. In non-Hispanic white youth 10–19 years of age, T2D represents 15% of the new cases of diabetes. However, T2D predominates in 10- to 19-year-old minority youth, representing 86% of the new cases among American Indians, 70% among Asian/Pacific Islanders, 58% in blacks, and 46% in Hispanics. SEARCH is continuing to ascertain diabetes incidence and is poised to provide critical information on trends in the incidence for both type 1 diabetes and T2D among U.S. youth. SEARCH has also described in great detail the characteristics of U.S. youth with T2D. Perhaps of greatest concern is that 27% of the youth with T2D enrolled in …
Evaluation of Safety Balls and Faceguards for Prevention of Injuries in Youth Baseball
Authors: Stephen W. Marshall, Frederick O. Mueller, Daniel P. Kirby, Jingzhen Yang
Journal: JAMA (2003)

<h3>Context</h3> Safety balls and faceguards are widely used in youth baseball, but their effectiveness in reducing injury is unknown. <h3>Objective</h3> To evaluate the association of the use of faceguards and safety balls and injuries in youth baseball. <h3>Design, Setting, and Participants</h3> Ecological study using a national database of compensated insurance claims maintained by Little League Baseball Incorporated, combined with data on the number of participants in Little League and data from a census of protective equipment usage for youth aged 5 to 18 years participating in Little League Baseball in the United States during 1997-1999. <h3>Main Outcome Measures</h3> Rate of injury and injury rate ratio comparing users with nonusers of protective equipment. <h3>Results</h3> A total of 6 744 240 player-seasons of follow-up and 4233 compensated injury claims were available for analysis. The absolute incidence of compensated injury per 100 000 player-seasons was 28.02 (95% confidence interval [CI], 26.76-29.29) for ball-related injury and 2.71 (95% CI, 2.32-3.11) for facial injury. Overall, use of safety balls was associated with a reduced risk of ball-related injury (adjusted rate ratio, 0.77; 95% CI, 0.64-0.93). This reduction was essentially due to 1 type of safety ball, known as the reduced-impact ball (adjusted rate ratio, 0.72; 95% CI, 0.57-0.91). Use of faceguards reduced the risk of facial injury (adjusted rate ratio, 0.65; 95% CI, 0.43-0.98). Metal and plastic guards appeared to be equally effective. Safety balls appeared to be more effective in the minor division (ages 7-12 years) than in the regular division (ages 9-12 years). <h3>Conclusions</h3> Reduced-impact balls and faceguards were associated with a reduced risk of injury in youth baseball. These findings support increased usage of these items; however, it should be noted that the absolute incidence of injury in youth baseball is low and that these equipment items do not prevent all injuries.
Public scare has not deterred Finnish teenagers from using oral contraceptives
Authors: E. Kosunen, H. Huhtala, A. Rimpela, M. Rimpela, A. Liinamo
Journal: BMJ (1997)

Introducing the postoperative care team Effective postoperative care remains surgeons' roleEditor-I am concerned that the suggestions made by David R Goldhill might be taken too seriously rather than remain a point for discussion. 1 Goldhill is right in his assertion that patients can fare badly in their postoperative course because of lack of attention by their attendants and lack of understanding of common postoperative complications.I believe, however, that he has missed the opportunity to lay the blame at the correct door.Surely it is the surgeons' role to carry out preoperative assessment, surgery, and effective postoperative care.If they choose to emphasise their importance in the operating theatre, delegating their other responsibilities to their trainees, the nurse practitioners, and the anaesthetists, why should we encourage this path?Undoubtedly, anaesthetists are fast becoming the new generalists, with an increasing role outside the operating theatre.These new skills and responsibilities include pain control, intensive care, and transoesophageal echocardiography, to name but a few.Some of my professional colleagues may relish even more diversification and abhor my comments.Goldhill implies that anaesthetists and postoperative care nurses will lead the postoperative care team; indeed, this is already happening in North America, where they have been sent to run preoperative assessment clinics by surgeons based in the operating room.If the surgical ward round in your hospital has become a quick look through the laboratory results and a glance at the chest radiograph before a rush to the changing rooms then I suggest that waiting for the confidential inquiry into perioperative deaths to point out the obvious is not the solution.
Effect of Heart Irregularity on Left Ventricular and Arterial Peak Systolic Pressures in Aortic Stenosis
Authors: W. S. BREALL, A. B. SHAFFER
Journal: Circulation (1959)

In aortic stenosis, systemic arterial peak systolic pressure may remain relatively steady in the face of marked, arrhythmia-induced, variations in left ventricular peak systolic pressure. A possible basis for this phenomenon is presented. It is suggested that beat-to-beat variations in the systolic pressure gradient across the aortic valve region may not always reflect variations in stroke volume.
Formation of an Intermediate in Prostaglandin Biosynthesis and Its Association with the Platelet Release Reaction
Authors: J. B. Smith, Carol Ingerman, J. J. Kocsis, M. J. Silver
Journal: Journal of Clinical Investigation (1974)

A compound that could be converted to prostaglandin F(2alpha) by mild chemical reduction was formed by human platelets in response to arachidonic acid, collagen, or L-epinephrine. It was present in maximal amounts at about 1 min after addition of arachidonic acid or collagen to platelet-rich plasma. Its initial formation appeared to precede platelet aggregation by these agents and was closely correlated with the release of adenine nucleotides and radioactive 5-hydroxytryptamine from platelets. Moreover, the compound was itself found outside the platelets. This compound is probably an endoperoxide intermediate in prostaglandin biosynthesis and may be a trigger for the platelet release reaction.
Effects of Dextran 40 on Red Cell Aggregation in Rabbits
Authors: J. Engeset, A. L. Stalker, N. A. Matheson
Journal: Cardiovascular Research (1967)

The effect of dextran 40 (Rheomacrodex) on intravascular red cell aggregation was studied at high magnification using a rabbit ear-chamber. A dramatic improvement in blood flow together with dispersion of aggregated red cells is demonstrated. The dispersing effect is shown to result from haemodynamic changes rather than from specific properties of dextran 40 against red cell aggregation in the rabbit.
Differential pp60c-src activity in well and poorly differentiated human colon carcinomas and cell lines.
Authors: T K Weber, G Steele, I C Summerhayes
Journal: Journal of Clinical Investigation (1992)

The results presented in this report demonstrate increased pp60c-src kinase activity associated with moderate to well differentiated colon tumors, corroborating previous observations by other groups. Extension of this analysis to include a small number of poorly differentiated colon carcinomas revealed src kinase activity comparable to that observed in normal colonic mucosa, considerably less than that observed in moderate/well differentiated lesions. Correlations of src kinase activity with differentiation was confirmed within a panel of colon cell lines where increased activity, associated with moderate/well differentiated lines, was accompanied by increased expression of pp60c-src protein. Use of an antiphosphotyrosine antibody in immunoprecipitation revealed the presence of novel phosphotyrosyl cellular substrates in human colon cell lines displaying elevated pp60c-src kinase activity. These observations suggest a role for the src protooncogene in colonic differentiation pathways.
Abstract 1303: The Wilms’ tumor gene, WT1, regulates E-cadherin expression and migration of prostate cancer cells.
Authors: Adina Brett, Gail Fraizer
Journal: Cancer Research (2012)

Abstract Carcinoma of the prostate is one of the most common malignancies and second leading cause of death among American men. Even though patients with localized disease have high survival rates, patients with detectable metastasis have a median survival of only 12-15 months. One key step in the metastatic process is the loss of E-cadherin expression associated with tumor invasion. However the regulation of E-cadherin gene expression in prostate cancer (PrCa) cells is not well understood. Recently, the zinc finger transcription factor, WT1 was shown to regulate E-cadherin in NIH 3T3 cells and epicardial cells. We have previously reported the presence of WT1 protein in high grade prostate tumor sections, with little or no WT1 staining in non-neoplastic or benign prostatic hyperplasia (BPH) tissues. However, the significance of WT1 expression in prostate cancer has not been established. The objective of this study was to determine whether WT1 might contribute to increase migration of PrCa cells by repressing E-cadherin expression. Using quantitative real-time PCR (QRTPCR), WT1 and E-cadherin mRNA levels were measured and found to be inversely related in PrCa cells. Similarly, QRTPCR results showed a decrease in E-cadherin mRNA in GFP/WT1 transfected PrCa cells, while E-cadherin levels were increased in PrCa cells with suppressed WT1 expression. Titration of WT1 levels also affected the migration of PrCa cells in wound healing and transwell migration assays. Silencing of WT1 by siWT1 RNA decreased the migratory potential of PC3 cells and the overexpression of GFP/WT1 increased the migration of LNCaP cells. A bioinformatics approach was used to identify potential WT1 binding sites in E-cadherin promoter, then direct in vivo binding of WT1 to the E-cadherin promoter in the chromatin of PrCa cells was confirmed by Chromatin Immunoprecipitation. Transcriptional control was quantified by co-transfection of a GFP/WT1 expression construct with E-cadherin promoter constructs. Results showed that WT1 decreased the activity of the proximal E-cadherin promoter in PC3 cells and DU145 cells. Using site directed mutagenesis, a newly identified WT1 binding site located 146 bp from the transcription start site was shown to be required for the repression of the E-cadherin proximal promoter by WT1. Overall these results demonstrate that WT1 transcriptionally down-regulates E-cadherin expression and thereby increases migration of PrCa cells. This finding suggests that the biological significance of WT1 expression in high grade prostate cancer lies in its contribution to cell migration and potentially to the promotion of metastasis. Supported by NIHR15CA11360 and the Ohio Board of Regents. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1303. doi:1538-7445.AM2012-1303
Massive pulmonary embolism in healthy people.
Authors: H. A. Fleming, S. M. Bailey
Journal: BMJ (1966)

Early Chronic Bronchitis MEDICAL JOURNAL nor therapy had any effect on the rate of decline of F.E.V. or on the volume or purulence of sputum specimens.We wish to record our appreciation to Pfizer Limited for their generous supply of oxytetracycline and indistinguishable dummy tablets, and for their willing cooperation in the analysis of numerous blood and urine samples for oxytetracycline, both before and during the trial ; and to Messrs. Parke Davis and Co. for their supply of chloramphenicol, sulphamethoxypyridazine, and penicillin capsules.Numerous members of the staff of the Pneumoconiosis Research Unit assisted with the packing and dispatch of over a million tablets, but the main burden of this work fell on Mrs. J. P. Duimovich, who also kept the statistical records of the trial.We would like to thank the officers of the Ministry of Pensions and National Insurance who provided us with records of the sickness absence of the patients in the trial, and the staff and health visitors of the different clinics for their continual help, especially for the extra evening sessions that were necessary, since the patients were nearly all at wvork during the day.The participating clinics and hospitals were
Review: Routine venous thromboembolism prophylaxis in hospitalized frail older patients has uncertain benefit
Authors: Elie A. Akl, Gordon Guyatt
Journal: Annals of Internal Medicine (2013)

Source Citation Greig MF, Rochow SB, Crilly MA, Mangoni AA. Routine pharmacological venous thromboembolism prophylaxis in frail older hospitalised patients: where is the evidence? Age Ageing. 2013 Apr 4 [Epub ahead of print]. 23557678
Malignancy in coeliac disease--effect of a gluten free diet.
Authors: G K Holmes, P Prior, M R Lane, D Pope, R N Allan
Journal: Gut (1989)

Two hundred and ten patients with coeliac disease previously reported from this unit were reviewed at the end of 1985 after a further 11 years of follow up. The initial review at the end of 1974 could not demonstrate that a gluten free diet (GFD) prevented these complications, probably because the time on diet was relatively short. The same series has therefore been kept under surveillance with the particular aim of assessing the effects of diet on malignancy after a further prolonged follow up period. Twelve new cancers have occurred: of which one was a carcinoma of the oesophagus and two lymphomas. Thirty nine cancers developed in 38 patients and of 69 deaths, 33 were the result of malignancy. A two-fold relative risk (RR) of cancer was found and was because of an increased risk of cancer of the mouth and pharynx (RR = 9.7, p less than 0.01, 95% confidence interval (CI) = 2.0-28.3), oesophagus (RR = 12.3, p less than 0.01, CI = 2.5-36.5), and of non-Hodgkin9s lymphoma (RR = 42.7, p less than 0.001, CI = 19.6-81.4). The results indicate that for coeliac patients who have taken a GFD for five years or more the risk of developing cancer over all sites is not increased when compared with the general population. The risk is increased, however, in those taking a reduced gluten, or a normal diet, with an excess of cancers of the mouth, pharynx and oesophagus (RR = 22.7, p &lt; 0.001), and also of lymphoma (RR = 77.8, p &lt; 0.001). A significant decreasing trend in the excess morbidity rate over increasing use of a GFD was found. The results are suggestive of a protective role for a GFD against malignancy in coeliac disease and give further support for advising all patients to adhere to a strict GFD for life.
Correction: Authors of Letters
Authors: Richard N. Greenberg
Journal: Annals of Internal Medicine (1989)

Letters and Corrections1 February 1989Correction: Authors of LettersRichard N. Greenberg, MDRichard N. Greenberg, MDSearch for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-110-3-249_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor:I would like to include Horace M. Perry, MD, as a coauthor of the letter onStreptococcus pyogenesand bone resorption (1)....Reference1. Greenberg R. Streptococcus pyogenes and bone resorption [Letter]. Ann Intern Med. 1988;109:843. LinkGoogle Scholar1. Lindley D and Schleupner C. Aerosolized pentamidine and conjunctivitis [Letter]. Ann Intern Med. 1988;109:988. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: Richard N. Greenberg, MD PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byResearch and development of high-performance polymeric materials including polyimides and fluoro-polyimides and their industrialized products 1 February 1989Volume 110, Issue 3 Page: 249-249 Keywords Bone resorption Streptococcus pyogenes ePublished: 1 December 2008 Issue Published: 1 February 1989 PDF downloadLoading ...
Sarcopenia, intramuscular fat deposition, and visceral adiposity independently predict the outcomes of hepatocellular carcinoma
Authors: Naoto Fujiwara, Hayato Nakagawa, Yotaro Kudo, Ryosuke Tateishi, Masataka Taguri, Takeyuki Watadani, Ryo Nakagomi, Mayuko Kondo, Takuma Nakatsuka, Tatsuya Minami, Masaya Sato, Koji Uchino, Kenichiro Enooku, Yuji Kondo, Yoshinari Asaoka, Yasuo Tanaka, Kuni Ohtomo, Shuichiro Shiina, Kazuhiko Koike
Journal: Journal of Hepatology (2015)

Obesity defined by body mass index (BMI) significantly increases the risk of hepatocellular carcinoma (HCC). In contrast, not only obesity but also underweight is associated with poor prognosis in patients with HCC. Differences in body composition rather than BMI were suggested to be true determinants of prognosis. However, this hypothesis has not been demonstrated conclusively.We measured skeletal muscle index (SMI), mean muscle attenuation (MA), visceral adipose tissue index, subcutaneous adipose tissue index, and visceral to subcutaneous adipose tissue area ratios (VSR) via computed tomography in a large-scale retrospective cohort of 1257 patients with different stages of HCC, and comprehensively analyzed the impact of body composition on the prognoses.Among five body composition components, low SMI (called sarcopenia), low MA (called intramuscular fat [IMF] deposition), and high VSR (called visceral adiposity) were significantly associated with mortality, independently of cancer stage or Child-Pugh class. A multivariate analysis revealed that sarcopenia (hazard ratio [HR], 1.52; 95% confidence interval [CI], 1.18-1.96; p=0.001), IMF deposition (HR, 1.34; 95% CI, 1.05-1.71; p=0.020), and visceral adiposity (HR, 1.35; 95% CI, 1.09-1.66; p=0.005) but not BMI were significant predictors of survival. The prevalence of poor prognostic body composition components was significantly higher in underweight and obese patients than in normal weight patients.Sarcopenia, IMF deposition, and visceral adiposity independently predict mortality in patients with HCC. Body composition rather than BMI is a major determinant of prognosis in patients with HCC.
Epidermal growth factor receptor inhibits colitis-associated cancer in mice
Authors: Philip E. Dubé, Fang Yan, Shivesh Punit, Nandini Girish, Steven J. McElroy, M. Kay Washington, D. Brent Polk
Journal: Journal of Clinical Investigation (2012)

Inflammatory bowel disease (IBD) is a chronic illness caused by complex interactions between genetic and environmental factors that propagate inflammation and damage to the gastrointestinal epithelium. This state of chronic inflammation increases the risk for development of colitis-associated cancer in IBD patients. Thus, the development of targeted therapeutics that can disrupt the cycle of inflammation and epithelial injury is highly attractive. However, such biological therapies, including those targeting epidermal growth factor receptor pathways, pose a risk of increasing cancer rates. Using two mouse models of colitis-associated cancer, we found that epidermal growth factor receptor inactivation accelerated the incidence and progression of colorectal tumors. By modulating inflammation and epithelial regeneration, epidermal growth factor receptor optimized the response to chronic inflammation and limited subsequent tumorigenesis. These findings provide important insights into the pathogenesis of colitis-associated cancer and suggest that epidermal growth factor-based therapies for IBD may reduce long-term cancer risk.