tbuckley/cabot-search huggingface dataset:
Physician Noncompliance With the 1993 National Cholesterol Education Program (NCEP-ATPII) Guidelines
Authors: Joseph P. Frolkis, Stephen J. Zyzanski, Jonathan M. Schwartz, Pamela S. Suhan
Journal: Circulation (1998)

Background —We sought to determine the frequency with which physicians follow National Cholesterol Education Program (NCEP-ATPII) guidelines in screening for cardiovascular risk factors and treating hyperlipidemia. Methods and Results —We conducted a retrospective chart review on randomly sampled charts of 225 patients admitted to the coronary care unit between January and June 1996. The main outcome measures were rates of physician screening for coronary heart disease risk factors; rates of counseling for cigarette cessation, diet, and exercise; and extent of use of NCEP algorithms for obtaining LDL cholesterol values and treating hypercholesterolemia. Screening rates for interns (who performed best) were: cigarette use (89%), known coronary heart disease (74%), hypertension (68%), hyperlipidemia (59%), family history (56%), diabetes (37%), postmenopausal hormone therapy (11%), and premature menopause (1%). Four percent of smokers were counseled to quit, 14% of patients were referred to dietitians, and 1% were encouraged to exercise. A full lipid panel was obtained in 50% of patients in whom it was indicated on the basis of NCEP criteria. Patients were more likely to receive lipid-lowering treatment if NCEP criteria indicated that they should, but 36% of hospitalized patients and 46% of patients who should have been treated on discharge were not. Conclusions —Physicians are poorly compliant with NCEP guidelines for risk factor assessment and counseling, even in patients at high risk for coronary heart disease. Physicians follow NCEP-ATPII algorithms for obtaining an LDL value, a key step in evaluating the need for treatment, only 50% of the time. NCEP criteria seem to influence the decision to initiate lipid-lowering therapy, but significant numbers of eligible patients remain untreated.
Auditory sensory ("echoic") memory dysfunction in schizophrenia
Authors: R D Strous, N Cowan, W Ritter, D C Javitt
Journal: American Journal of Psychiatry (1995)

Studies of working memory dysfunction in schizophrenia have focused largely on prefrontal components. This study investigated the integrity of auditory sensory ("echoic") memory, a component that shows little dependence on prefrontal functioning.Echoic memory was investigated in 20 schizophrenic subjects and 20 age- and IQ-matched normal comparison subjects with the use of nondelayed and delayed tone matching.Schizophrenic subjects were markedly impaired in their ability to match two tones after an extremely brief delay between them (300 msec) but were unimpaired when there was no delay between tones.Working memory dysfunction in schizophrenia affects brain regions outside the prefrontal cortex as well as within.
Adhesion molecules expression in noncrescentic acute post-streptococcal glomerulonephritis.
Authors: M P Rastaldi, F Ferrario, L Yang, S Tunesi, A Indaco, H Zou, G D'Amico
Journal: Journal of the American Society of Nephrology (1996)

Clinicomorphological features of 11 cases of non-crescentic acute post-streptococcal glomerulonephritis (APSGN) were reviewed. Intraglomerular and interstitial leukocytes and their possible correlation with the adhesion molecules intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial-leukocyte adhesion molecule-1 (ELAM-1/E-selectin) were investigated by an immunohistochemical method. Intraglomerular leukocytes were primarily granulocytes (11.4 +/- 10 cells/glomerular cross-section) and monocytes-macrophages (13.4 +/- 19.4 cells/glomerular cross-section). The granulocytes outnumbered monocytes-macrophages in 7 of 11 specimens. The number of intraglomerular leukocytes correlated with proteinuria at the time of renal biopsy. Intraglomerular ICAM-1 staining was strongly positive in all biopsies, especially when intraglomerular monocytes-macrophages prevailed. Expression of intraglomerular VCAM-1 and E-selectin in diseased kidneys did not differ from that in normal kidneys. Interstitial leukocytes were primarily monocytes-macrophages (158.9 +/- 96.8 cells/mm2) and T lymphocytes (102.2 +/- 63.9 cells/mm2). The number of interstitial leukocytes, especially monocytes-macrophages, correlated with serum creatinine level at the time of biopsy. Interstitial ICAM-1 staining was strongly positive on tubules, peritubular capillaries, and small vessels. The tubular positivity for ICAM-1 correlated with the number of interstitial monocytes-macrophages. Interstitial VCAM-1 and E-selectin were expressed as in normal kidney tissues. The data from this study demonstrate that APSGN is characterized by the presence of both intraglomerular and interstitial leukocyte infiltration, correlating respectively with proteinuria and serum creatinine at the time of renal biopsy. Among the adhesion molecules studied, ICAM-1 seems the most involved in leukocyte recruitment, especially in that of monocytes-macrophages.
Ondansetron plus dexamethasone is superior to ondansetron alone in the prevention of emesis in chemotherapy-naive and previously treated patients
Authors: R.A. Joss, M. Bacchi, K. Buser, V. Kirchner, H. Neuenschwander, B. Orth, M.S. Aapro, B. Thürlimann
Journal: Annals of Oncology (1994)
Corporate Social Responsibility and Access to Policy Élites: An Analysis of Tobacco Industry Documents
Authors: Gary J. Fooks, Anna B. Gilmore, Katherine E. Smith, Jeff Collin, Chris Holden, Kelley Lee
Journal: PLoS Medicine (2011)

Gary Fooks and colleagues undertook a review of tobacco industry documents and show that policies on corporate social responsibility can enable access to and dialogue with policymakers at the highest level.
Modulation of basophil activity: A novel function of the neuropeptide α-melanocyte–stimulating hormone
Authors: Markus Böhm, Mara Apel, Koji Sugawara, Randolf Brehler, Kerstin Jurk, Thomas A. Luger, Helmut Haas, Ralf Paus, Britta Eiz-Vesper, Andrew F. Walls, Evgeni Ponimaskin, Manuela Gehring, Alexander Kapp, Ulrike Raap
Journal: Journal of Allergy and Clinical Immunology (2011)
Mortality Risk Associated with Short-Term Exposure to Traffic Particles and Sulfates
Authors: Dan Maynard, Brent A. Coull, Alexandros Gryparis, Joel Schwartz
Journal: Environmental Health Perspectives (2007)

BackgroundMany studies have shown that airborne particles are associated with increased risk of death, but attention has more recently focused on the differential toxicity of particles from different sources. Geographic information system (GIS) approaches have recently been used to improve exposure assessment, particularly for traffic particles, but only for long-term exposure.ObjectivesWe analyzed approximately 100,000 deaths from all, cardiovascular, and respiratory causes for the years 1995–2002 using a case–crossover analysis.MethodsEstimates of exposure to traffic particles were geocoded to the address of each decedent on the day before death and control days, with these estimates derived from a GIS-based exposure model incorporating deterministic covariates, such as traffic density and meteorologic factors, and a smooth function of latitude and longitude.ResultsWe estimate that an IQR increase in traffic particle exposure on the day before death is associated with a 2.3% increase [95% confidence interval (CI), 1.2 to 3.4%] in all-cause mortality risk. Stroke deaths were particularly elevated (4.4%; 95% CI, −0.2 to 9.3%), as were diabetes deaths (5.7%; 95% CI, −1.7 to 13.7%). Sulfate particles are spatially homogeneous, and using a central monitor, we found that an IQR increase in sulfate levels on the day before death is associated with a 1.1% (95% CI, 0.1 to 2.0%) increase in all-cause mortality risk.ConclusionsBoth traffic and powerplant particles are associated with increased deaths in Boston, with larger effects for traffic particles.
Nickel allergy following EU regulation - more action is needed
Authors: C. Lidén
Journal: British Journal of Dermatology (2013)

ORIGINAL ARTICLE, p 854 The occurrence of nickel allergy is decreasing in the young female population following a European Union regulation limiting nickel release. This is shown in the study by Garg et al.1 in this issue of the British Journal of Dermatology. Patch‐test data from more than 180 000 patients with dermatitis in Denmark, Germany, Italy and the U.K., between 1985 and 2010, are analysed. The trend of nickel allergy is described by country, sex and age groups. The overall frequency of nickel allergy during the period was lowest in Denmark (17·4% in women and 3·1% in men) and highest in Italy (31·9% in women and 10·8% in men). The authors conclude that the downward trend is encouraging, but also that more work is needed for reduction of nickel allergy. This is fully agreed. Scientific surveys in many countries show that the market is full of articles that release too much nickel, and that adaptation to the regulation is generally poor. This is the responsibility of manufacturers, importers and retailers, while authorities have the role of controlling compliance with the regulation. Efficient control and enforcement would most likely result in reduced risks to consumers. Contact dermatitis experts can influence authorities and their priorities by informing them about nickel allergy and its consequences.
M1 macrophages act as LTβR-independent lymphoid tissue inducer cells during atherosclerosis-related lymphoid neogenesis
Authors: Kevin Guedj, Jamila Khallou-Laschet, Marc Clement, Marion Morvan, Anh-Thu Gaston, Giulia Fornasa, Jianping Dai, Marianne Gervais-Taurel, Gerard Eberl, Jean-Baptiste Michel, Giuseppina Caligiuri, Antonino Nicoletti
Journal: Cardiovascular Research (2013)

AimsThe goal of this study was to characterize the role of inflammatory macrophages in the induction of the vascular smooth muscle cell (VSMC)-mediated formation of aortic tertiary lymphoid organs (TLOs).
Switch to a raltegravir-based regimen versus continuation of a lopinavir-ritonavir-based regimen in stable HIV-infected patients with suppressed viraemia (SWITCHMRK 1 and 2): two multicentre, double-blind, randomised controlled trials
Authors: Joseph J Eron, Benjamin Young, David A Cooper, Michael Youle, Edwin DeJesus, Jaime Andrade-Villanueva, Cassy Workman, Roberto Zajdenverg, Gerd Fätkenheuer, Daniel S Berger, Princy N Kumar, Anthony J Rodgers, Melissa A Shaughnessy, Monica L Walker, Richard JO Barnard, Michael D Miller, Mark J DiNubile, Bach-Yen Nguyen, Randi Leavitt, Xia Xu, Peter Sklar
Journal: The Lancet (2010)
PPAR Agonists Amplify iNOS Expression While Inhibiting NF-κB
Authors: Eva Cernuda-Morollón, Fernando Rodríguez-Pascual, Peter Klatt, Santiago Lamas, Dolores Pérez-Sala
Journal: Journal of the American Society of Nephrology (2002)

ABSTRACT. In acute inflammation, the transcription factor NF-κB is activated and increases the expression of multiple pro-inflammatory genes. Agonists of peroxisome proliferator activated receptors (PPAR) have been reported to exert antiinflammatory effects in various systems. In keeping with such an antiinflammatory role, it was found that several PPAR agonists, including Wy14,643, clofibrate, carbaprostacyclin, and ciglitazone inhibited NF-κB activity and increased IκBα levels in cytokine-stimulated mesangial cells (MC). Activation of NF-κB has been found to be crucial to the cytokine-elicited expression of inducible nitric oxide synthase (iNOS). Despite the inhibitory effect of PPAR agonists on NF-κB activity, this study provides experimental data demonstrating that these agonists amplify cytokine-elicited NO generation in MC, potentiating iNOS protein expression approximately threefold. The upregulation of iNOS expression occurred at the mRNA level and apparently did not result from iNOS mRNA stabilization. Clofibrate and ciglitazone amplified the cytokine-elicited stimulation of a 16-Kb human iNOS promoter construct in stably transfected MC, suggesting that PPAR agonists potentiate iNOS induction through transcriptional mechanisms. MC express all three PPAR proteins. However, iNOS potentiation did not correlate with increased PPAR activity. In addition, Wy14,643-induced amplification of cytokine-elicited iNOS levels also occurred in RAW264.7 macrophages and in human epithelial Caco-2 and HT-29 cells. The observation that these epithelial cell lines express an inactive, truncated PPARα variant suggests that a classical PPARα agonist, such as Wy14,643, may act through PPARα-independent mechanisms. In conclusion, these results show that, despite reducing NF-κB activity, PPAR agonists may amplify the expression of certain NF-κB–dependent genes that are relevant to the inflammatory process, like iNOS.
It Is Time to Stop Screening for Prostate Cancer
Authors: Vinay Prasad
Journal: JAMA Internal Medicine (2014)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal
Is It Ethical to Assign Medically Underserved African Americans to a Usual-Care Control Group in Community-Based Intervention Research?
Authors: Robert M. Anderson
Journal: Diabetes Care (2005)

The purpose of this commentary is to foster discourse regarding the need to conduct research that is scientifically rigorous while according patients the benefits and protections that they are due as human subjects. These two laudable goals can conflict with one another, leaving researchers, institutional review boards, grant application review groups, and funding agencies with the responsibility of striking an appropriate balance. For the past 14 years, our research (1) has focused on evaluating community-based interventions designed to help urban African Americans in metro Detroit live well with type 2 diabetes. Even if previous research on similar interventions has been promising, it is not possible to know a priori if a particular intervention, with these patients in this setting, will be shown to be effective. Therefore, the ideal design (from a scientific perspective) for many of these studies would be a randomized controlled trial using a usual-care control group. However, we have ethical concerns about assigning the African-American patients recruited in metro Detroit to a true usual-care control group.

### Best-known care control groups.

A well-known type of control group involves comparing a new medication or procedure with the best medical care known (also known as current standard of care). The Diabetes Control and Complications Trial provides a good example of this type of control group (2). To test the glucose hypothesis, patients were randomized to either an intensive treatment intervention group or a “best-known care” (at the time of the study) control group. This type of control group differs from a usual-care control group in two very important respects. First, usual care in diabetes, particularly for medically underserved populations, is likely to be suboptimal when compared with best-known care (3). Second, in the Diabetes Control and Complications Trial, the diabetes care received by patients in the control group was precisely defined and under the …
Expression of SORL1 and a novel SORL1 splice variant in normal and Alzheimers disease brain
Authors: Karrie E Grear, I-Fang Ling, James F Simpson, Jennifer L Furman, Christopher R Simmons, Shawn L Peterson, Frederick A Schmitt, William R Markesbery, Qiang Liu, Julia E Crook, Steven G Younkin, Guojun Bu, Steven Estus
Journal: Molecular Neurodegeneration (2009)

Abstract Background Variations in sortilin-related receptor (SORL1) expression and function have been implicated in Alzheimers Disease (AD). Here, to gain insights into SORL1, we evaluated SORL1 expression and splicing as a function of AD and AD neuropathology, neural gene expression and a candidate single nucleotide polymorphism (SNP). Results To identify SORL1 splice variants, we scanned each of the 46 internal SORL1 exons in human brain RNA samples and readily found SORL1 isoforms that lack exon 2 or exon 19. Quantification in a case-control series of the more abundant isoform lacking exon 2 (delta-2-SORL1), as well as the "full-length" SORL1 (FL-SORL1) isoform containing exon 2 showed that expression of FL-SORL1 was reduced in AD individuals. Moreover, FL-SORL1 was reduced in cognitively intact individuals with significant AD-like neuropathology. In contrast, the expression of the delta-2-SORL1 isoform was similar in AD and non-AD brains. The expression of FL-SORL1 was significantly associated with synaptophysin expression while delta-2-SORL1 was modestly enriched in white matter. Lastly, FL-SORL1 expression was associated with rs661057, a SORL1 intron one SNP that has been associated with AD risk. A linear regression analysis found that rs661057, synaptophysin expression and AD neuropathology were each associated with FL-SORL1 expression. Conclusion These results confirm that FL-SORL1 expression declines in AD and with AD-associated neuropathology, suggest that FL-SORL1 declines in cognitively-intact individuals with AD-associated neuropathology, identify a novel SORL1 splice variant that is expressed similarly in AD and non-AD individuals, and provide evidence that an AD-associated SNP is associated with SORL1 expression. Overall, these results contribute to our understanding of SORL1 expression in the human brain.
Association Between Being Underweight and Outcomes in Breast Cancer: Alternative Explanations
Authors: Min-Han Tan, Nicholas Qijie Leo, En Yun Loy, Wei-Yen Lim, Kee Seng Chia
Journal: Journal of Clinical Oncology (2010)

erable interest. The authors are to be commended for an interesting analysis from a national multicenter data set, concluding that being underweight should be considered as a risk factor for death and recurrence after breast cancer surgery. A possible alternative explanation for the observed association between being underweight and breast cancer outcomes may be the contribution of mammographic screening in older women. Given that the authors present data showing weight increases from younger to older age groups, it seems possible that a higher proportion of mammographic screening among older women will result in a survival bias and stage shifting for older individuals. Mammographic screening is commonly recommended for women in Asia older than age 40 years. This threshold is based on the observation that the proportion of patients diagnosed at a younger age is higher than in the West. Although the authors have controlled for age and histologic grade, it is established that the length and lead time bias contributed by mammographic screening are obvious even after controlling for these effects. 2 In addition, the apparent increase in breast cancer–specific mortality associated with being underweight may be confounded by a cohort effect. These cohort effects in breast cancer incidence have been observed in other Asian countries such as Singapore, where rapid industrialization has resulted in dramatic changes in lifestyle. 3 In Korea, where the study took place over a period of 15 years, increases in average body mass index and obesity have been observed over recent years for each cohort. 4 Further, with the introduction of the Korean National Cancer Screening program for breast cancer from 1999 onward, 3 there is a clear potential for a cohort effect. To control for possible cohort effects, the authors could examine 5-year relative survival against birth cohort using a 3-year central moving average 5
Genetic Risk Score Associations With Cardiovascular Disease and Mortality in the Diabetes Heart Study
Authors: Amanda J. Cox, Fang-Chi Hsu, Maggie C.Y. Ng, Carl D. Langefeld, Barry I. Freedman, J. Jeffrey Carr, Donald W. Bowden
Journal: Diabetes Care (2014)

OBJECTIVE Given the high rates of cardiovascular disease (CVD) and associated mortality in individuals with type 2 diabetes, identifying and understanding predictors of CVD events and mortality could help inform clinical management in this high-risk group. Recent large-scale genetic studies may provide additional tools in this regard. RESEARCH DESIGN AND METHODS Genetic risk scores (GRSs) were constructed in 1,175 self-identified European American (EA) individuals comprising the family-based Diabetes Heart Study based on 1) 13 single nucleotide polymorphisms (SNPs) and 2) 30 SNPs with previously documented associations with CVD in genome-wide association studies. Associations between each GRS and a self-reported history of CVD, coronary artery calcified plaque (CAC) determined by noncontrast computed tomography scan, all-cause mortality, and CVD mortality were examined using marginal models with generalized estimating equations and Cox proportional hazards models. RESULTS The weighted 13-SNP GRS was associated with prior CVD (odds ratio [OR] 1.51 [95% CI 1.22-1.86]; P = 0.0002), CAC (β-coefficient [β] 0.22 [0.02-0.43]; P = 0.04) and CVD mortality (hazard ratio [HR] 1.35 [1.10-1.81]; P = 0.04) when adjusting for the other known CVD risk factors: age, sex, type 2 diabetes affection status, BMI, current smoking status, hypertension, and dyslipidemia. The weighted 30-SNP GRS was also associated with prior CVD (OR 1.33 [1.08-1.65]; P = 0.008), CAC (β 0.29 [0.08-0.50]; P = 0.006), all-cause mortality (HR 1.28 [1.05-1.56]; P = 0.01), and CVD mortality (HR 1.46 [1.08-1.96]; P = 0.01). CONCLUSIONS These findings support the utility of two simple GRSs in examining genetic associations for adverse outcomes in EAs with type 2 diabetes.