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Kiran Bharthapudi has more than seven years of experience in print, broadcast and new media journalism. He has contributed to several major news agencies, including United Nations radio, BBC online and "Consumer Reports" magazine. His articles specialize in the areas of business, technology and new media. He has a Ph.D. in mass communications.

Thu, 19 Nov 2015 17:34:00 -0600 en-US text/html https://smallbusiness.chron.com/converting-character-date-sas-37424.html
Killexams : Obesity and the Metabolic Syndrome in Children and Adolescents

Anthropometric and Metabolic Phenotype

Table 1. Table 1. Baseline Anthropometric and Metabolic Characteristics of the Study Cohort.

Anthropometric and metabolic data are shown in Table 1. Values for glucose, insulin, insulin resistance, triglycerides, C-reactive protein, interleukin-6, and systolic blood pressure, as well as the prevalence of impaired glucose tolerance, increased significantly with increasing obesity, whereas HDL cholesterol and adiponectin levels decreased with increasing obesity (Table 1). Moderately and severely obese black subjects had lower triglyceride and higher HDL cholesterol levels than similar white and Hispanic subjects. The percentage of subjects with impaired glucose tolerance increased directly with the severity of obesity in subjects in all racial and ethnic groups, a trend that persisted after adjustment for sex, pubertal status, and race or ethnic group. The severity of obesity and the prevalence of the metabolic syndrome were strongly associated after adjustment for race and ethnic group (P=0.009) and for race and ethnic group and sex (P=0.03).

The overall prevalence of the metabolic syndrome was 38.7 percent in moderately obese subjects and 49.7 percent in severely obese subjects; no overweight or nonobese subject met the criteria for the metabolic syndrome. The prevalence of the metabolic syndrome in severely obese black subjects was 39 percent. When we analyzed our data according to the commonly accepted criteria of the National Cholesterol Education Program26 (which are not specific to any race or ethnic group), the prevalence of the metabolic syndrome among severely obese black subjects was only 27 percent.

Factor Analysis

Table 2. Table 2. Pearson Correlation Coefficients of Variables in the Analysis. Table 3. Table 3. Principal-Factor Analysis and Oblique Analysis of the Whole Cohort of Obese and Overweight Children and Adolescents, According to Risk Factors for the Metabolic Syndrome.

As shown in Table 2 and Table 3, three factors were sufficient to explain correlations between variables — obesity and glucose metabolism, the degree of dyslipidemia, and blood pressure. The three factors explained 58 percent of the total variance in the data (27 percent of the variance was explained by the first factor, an additional 17 percent by the second factor, and another 14 percent by the third factor). The first factor was obesity and glucose metabolism, reflecting strong correlation with the z score for the body-mass index, insulin resistance, and fasting and two-hour plasma glucose levels. The second factor was dyslipidemia, reflecting a positive correlation of insulin resistance with the triglyceride level and a negative correlation of insulin resistance with the HDL cholesterol level. The third factor was blood pressure, reflecting a positive correlation with systolic and diastolic blood pressure. When the C-reactive protein level was incorporated into the analysis (for 293 subjects), it loaded significantly only with the obesity and glucose metabolism factor.

Insulin Resistance

Figure 1. Figure 1. Effect of Insulin Resistance on the Prevalence of the Metabolic Syndrome in White Subjects (Panel A), Hispanic Subjects (Panel B), and Black Subjects (Panel C), According to the Degree of Obesity.

Subjects were grouped into three categories of insulin resistance, with cutoffs at the 33rd and 66th percentiles.

To test the effect of insulin resistance on the prevalence of the metabolic syndrome, we categorized the subjects according to three insulin-resistance categories, using the 33rd and 66th percentiles as cutoffs, and race or ethnic group, with adjustment for the degree of obesity (Figure 1). The prevalence of the metabolic syndrome increased significantly with increasing insulin resistance (P for trend, <0.001) after adjustment for race or ethnic background and obesity group. The prevalence was lower in black subjects than in white subjects (P<0.001) but not than in Hispanic subjects (P=0.20), and it was higher in severely obese subjects than in moderately obese subjects (P=0.03).

Multiple Logistic-Regression Analysis

For the multiple logistic-regression analysis of risk factors associated with the metabolic syndrome in overweight and obese children and adolescents, we incorporated age, sex, z score for BMI, race or ethnic group, and insulin-resistance level into the model. The overall significance of the model was P<0.001. Increasing insulin-resistance levels according to the homeostatic-model assessment were significantly related to the risk of the metabolic syndrome (odds ratio for each increase of one unit, 1.12; 95 percent confidence interval, 1.07 to 1.18). Each half-unit increase in the z score for the body-mass index (one half of 1 SD) was associated with a significant increase in the risk of the metabolic syndrome (odds ratio, 1.55; 95 percent confidence interval, 1.16 to 2.08). White subjects had a higher risk of the metabolic syndrome than black subjects (odds ratio, 2.20; 95 percent confidence interval, 1.35 to 3.59); there was no significant difference in risk between Hispanic subjects and black subjects. Girls were at lower risk for the metabolic syndrome than boys (odds ratio, 0.59; 95 percent confidence interval, 0.39 to 0.89). When the z score for the body-mass index was excluded, the odds ratios associated with each unit of increase in insulin resistance, female sex, and white race as compared with black race did not change significantly.

Proinflammatory and Antiinflammatory Markers and Insulin Resistance

Figure 2. Figure 2. C-Reactive Protein and Adiponectin Levels According to the Degree of Obesity and the Insulin-Resistance Category.

Panel A shows C-reactive protein levels. P<0.001 for the association with the obesity group, and P=0.12 for the association with insulin-resistance category. P=0.64 for the interaction between the obesity group and the insulin-resistance category. Panel B shows adiponectin levels. P=0.04 for the association with the obesity group, and P=0.005 for the association with the insulin-resistance category. P=0.07 for the interaction between the obesity group and the insulin-resistance category. After stratification according to the obesity group, the effect of the insulin-resistance category was evident in moderately obese subjects; those in the highest category of insulin resistance had significantly lower adiponectin levels than those in the middle and low categories (P=0.04 and P=0.002, respectively, with Holm's adjustment).

C-reactive protein levels (Figure 2A ) were significantly related to the degree of obesity (P<0.001) but not to the level of insulin resistance (P=0.12). The levels tended to rise with the number of components of the metabolic syndrome in this cohort, but the trend did not reach statistical significance.

Adiponectin levels decreased with increasing obesity (Table 1). When the subjects were stratified according to obesity group and insulin-resistance category (Figure 2B), the adiponectin levels were significantly associated with the obesity category (P=0.04) and insulin-resistance category (P=0.005); the adiponectin levels were lowest in subjects with the highest level of insulin resistance. There was an interaction between obesity and insulin resistance, but it was not statistically significant (P=0.07). After stratification according to obesity group, the effect of insulin-resistance category was evident in the moderately obese group; subjects in the highest category of insulin resistance had significantly lower adiponectin levels than those in the middle and low categories (P=0.04 and P=0.002, respectively, with Holm's adjustment). In contrast, adiponectin levels in the severely obese group did not vary significantly according to the insulin-resistance category. Adiponectin levels were negatively correlated with C-reactive protein levels (R=–0.18, P=0.005).

Interleukin-6 levels rose significantly with the degree of obesity (Table 1) and were correlated with C-reactive protein levels (R=0.37, P<0.001) but not with the degree of insulin resistance. The relation between interleukin-6 and C-reactive protein levels persisted after adjustment for the z score for the body-mass index (R=0.29, P<0.001).

The Metabolic Syndrome Phenotype after Two Years of Follow-up

Seventy-seven subjects underwent a second comprehensive assessment after a mean (±SD) interval of 21.5±10.5 months. Twenty-four of the 34 subjects in this group who had met the criteria for the metabolic syndrome initially met these criteria at the time of the second evaluation as well. The 10 who did not meet the criteria on follow-up were among the subjects who had a lower BMI initially (z score, 2.42±0.07 vs. 2.62±0.06; P=0.06), had gained less weight (3.74±2.6 kg vs. 11.93±2.9 kg, P=0.05), and tended to have decreased insulin resistance (a reduction from 9.68±1.14 to 7.54±0.82, P=0.07). The syndrome developed over time in 16 of 43 children who did not have the metabolic syndrome at the time of the first evaluation. The baseline z score for the body-mass index in these 16 subjects was similar to that in the 10 subjects who had improvement during follow-up (2.39±0.11 and 2.42±0.07, respectively; P=0.86), yet they gained significantly more weight (16.91±4.4 kg vs. 3.74±2.6 kg, P=0.02). In eight subjects, all of whom had impaired glucose tolerance at the first evaluation, type 2 diabetes developed during follow-up.

Mon, 06 Jun 2022 05:42:00 -0500 en text/html https://www.nejm.org/doi/full/10.1056/NEJMoa031049
Killexams : Celecoxib for the Prevention of Colorectal Adenomatous Polyps

The following persons participated in the PreSAP trial: Steering Committee — N. Arber, W. Atkin, C.J. Eagle, A. Dannenberg, R. DuBois, B. Levin, R. Stockbrugger, B.C.Y. Wong, A.G. Zauber; Statistical Team — A.G. Zauber, R. Rosenstein, J. Tang, P. Bhadra, J. Wittes, R. Fowler; Medical Monitors — M.J. Lechuga, P. Gerletti; Central Pathology Review — Diagnostic Cytology Laboratories (Indianapolis); Third-Party Pathology Reviewer — K. Geisinger; Project Director — C.J. Eagle; Data and Safety Monitoring Board — S. Winawer (chair), J. Brinker, G. Elfring (independent statistician), J.P. Faivre, J. Lee, A.I. Neugut; Co-Lead Principal Investigators: N. Arber (Tel Aviv Sourasky Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel), B. Levin (the University of Texas M.D. Anderson Cancer Center, Houston); Principal Investigators — Australia: J. Croese (Mater Misericordiae Hospital, Pimlico, Queensland), V.D. Watters (Geelong Hospital Ryrie, Geelong); Belgium: M. De Vos (Ghent University Hospital, Ghent), J. Deviere (Erasme University Hospital, Brussels), D. Urbain (Vrije Universiteit Brussel, Brussels), H. Piessevaux (Université Catholique de Louvain, Brussels); Brazil: F. Oliveira Ferreira (Hospital do Câncer–A.C. Camargo, São Paulo), I. Maguilnik (Hospital de Clinicas de Pôrto Alegre, Pôrto Alegre); Canada: F. Bursey (Health Sciences Center, Saint John's, Newf.), R. Enns (St. Paul's Hospital, Vancouver, B.C.), R.N. Fedorak (University of Alberta, Edmonton, Alta.), J. Howard (London Health Sciences Centre, London, Ont.), H. Pluta (Gastroenterology and Hepatology Clinic, Abbotsford, B.C.), J. Simon (Hotel-dieu Hospital, Kingston, Ont.), A. Weiss (Vancouver Hospital and Health Sciences Center, Vancouver, B.C.); Chile: F. Lopez (Pontificia Universidad Catolica de Chile, Santiago), J. Valenzuela (Clinica Las Condes, Santiago); China: L. Cheng (General Hospital of the Chinese People's Liberation Army, Beijing); J. Qian (Peking Union Medical College Hospital, Beijing); Czech Republic: P. Dite (Faculty Hospital Brno Bohunice, Brno), J. Dosedel (Hospital of Merciful Sisters St. Charles Borromeo, Prague), J. Hajer (Faculty Hospital Královské Vinohrady, Prague), P. Hulek (Faculty Hospital Hradec Králové, Hradec Králové), J. Janku (Hospital Liberec, Liberec), J. Spicak (Institute for Clinical and Experimental Medicine, Prague), M. Zavoral (Central Military Hospital, Prague); Denmark: S. Lauerberg (Aarhus Amtssygehus, Aarhus); Finland: S. Niemelä (Oulu University Hospital, Oulu); France: R. Benamouzig (Hôpital Avicenne, Bobigny), G. Lledo (Cabinet Médical Lledo, Lyon), S. Chaussade (Groupe Hospitalier Cochin, Paris), J. Sahel (Hôpital Ste. Marguerite, Marseille); Germany: B. Birkner (Munich), D. Mueller, S. Boehm (Philipps-Universität Marburg/Lahn, Marburg), H.G. Dammann (Klinische Forschung Hamburg, Hamburg), A. Dettmer (Munich), R.R. Fink (Freising), H.D. Janisch (Erlangen), C. Klein (Kuenzing), J.F. Riemann (Klinikum der Stadt Ludwigshafen, Ludwigshafen), A. Roempp, C. Weber (Universitätsklinikum Ulm, Ulm), B. Wiedenmann (Universitätsklinikum Charité, Berlin); Hong Kong: F. Chan (Chinese University of Hong Kong, Shatin), B.C.Y. Wong (University of Hong Kong, Hong Kong); Hungary: I. Rácz (Petz Aladár County Hospital, Gyõr), L. Simon (Tolna County Hospital, Szekszárd); Ireland: P. Macmathuna (Mater Misericordiae Hospital, Dublin), F.E. Murray (Beaumont Hospital, Dublin), E. Quigley (Cork University Hospital, Wilton); Israel: N. Arber (Tel Aviv Sourasky Medical Center and Sackler School of Medicine, Tel Aviv University, Tel Aviv), S. Bar-Meir (Sheba Medical Center, Tel-Hashomer), A. Eliakim (Rambam Medical Center, Haifa), A. Fich (Soroka University Medical Center, Beersheba), Z. Fireman (Hillel Yaffe Medical Center, Hadera), E. Goldin (Hadassah Medical Center, Jerusalem), Y. Niv (Rabin Medical Center, Petah-Tikva), H. Shirin (Wolfson Medical Center, Holon); Italy: A. Andriulli (Casa Sollievo della Sofferenza, San Giovanni Rotondo, Foggia), V. Casale, M. Crespi (Polo Oncologico Regina Elena, Rome), R. Cestari (Ospedali Civili, Brescia), C. Crosta (Istituto Europeo di Oncologia, Milan), G. Frosini (Policlinico Le Scotte, Siena), S. Morini (Ospedale Nuovo Regina Margherita, Rome); the Netherlands: R.W. Stockbrugger (Academisch Ziekenhuis Maastricht, Maastricht); Norway: G. Huppertz-Hauss, J. Sauar (Medical Department Sykehuset Telemark, Skien); Peru: O. Frisancho (Hospital Nacional Edgardo Rebagliati Martins, Lima), J. Watanabe (Policlinico Peruano Japones, Lima); Poland: E. Butruk (Medical Centre for Postgraduate Education, Institute of Oncology, Warsaw); Portugal: C. Nobre Leitão (Instituto Português de Oncologia, Lisbon); Russian Federation: G.P. Arutyunov (Hospital #4, Moscow), O.N. Minushkin (Hospital #51, Moscow), O. Naumov (City Clinical Hospital #24, Moscow), B.K. Poddubny (Blokhina Cancer Research Center, Moscow), S.G. Shapovaliants (Hospital #31, Moscow), V.V. Veselov (State Scientific Center for Coloproctology, Moscow); Singapore: K.G. Yeoh (National University Hospital, Singapore), K.M. Fock (Changi General Hospital, Singapore); Slovak Republic: I. Ďuriš (University Hospital, Bratislava), A. Vavrecka (St. Cyril's and Method's Hospital, Bratislava); South Africa: R. Jobson (Sandton Clinic, Johannesburg), B. Shmeizer (Sunninghill Hospital, Johannesburg), H.R. Schneider (Milpark Hospital, Johannesburg), J.P. Wright (Kingsbury Hospital, Cape Town); Spain: J.I. Arenas (Hospital Nuestra Señora de Aránzazu, San Sebastián), A. Castells (Hospital Clínic de Barcelona, Barcelona), J. Herrerias (Hospital Universitario Virgen Macarena, Seville), A. Obrador (Hospital Son Dureta, Palma de Mallorca), L. Rodrigo (Hospital Central de Asturias, Oviedo); Sweden: B. Kollberg (Mag-Tarm-centrum, Stockholm), L. Pahlman (Akademiska Sjukhuset, Uppsala); Switzerland: A. Hadengue (Hôpitaux Universitaires de Genève, Geneva); Taiwan: T.-M. King (Veterans General Hospital, Kaohsiung); United Kingdom: W. Atkin (Coordinator) (Imperial College, London), K. Vellacott (Royal Gwent Hospital, Gwent), B. Saunders (St. Mark's Hospital, Harrow, Middlesex), N. Mortensen (John Radcliffe Hospital, Oxford); United States: M.T. Bennett (Medical Associates Research Group, San Diego, Calif.), S.A. Cohen (Thomas Jefferson University Hospital, Philadelphia), D.Y. Graham (Veterans Affairs Medical Center, Houston), D.M. Kruss (Veterans Affairs Medical Center, North Chicago, Ill.), S.J. Meltzer (University of Maryland School of Medicine–Baltimore, Baltimore), N.N. Ravendhran (Digestive Disease Associates, Baltimore), M.L. Schubert (McGuire Veterans Affairs Medical Center, Richmond, Va.), D.S. Weinberg (Fox Chase Cancer Center, Philadelphia), K.L. Woods (Medical Center Endoscopy, Houston); Uruguay: H. Cohen (Clinicas Hospital, Montevideo).

Thu, 11 Mar 2021 17:48:00 -0600 en text/html https://www.nejm.org/doi/full/10.1056/NEJMoa061652
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