tbuckley/cabot-search huggingface dataset:
OP0132-HPR Predictors and Outcome of Avoidance of Activities in Persons with Early Symptomatic Knee Osteoarthritis: A 5-Year Follow-Up Study in the CHECK Cohort
Authors: J.F.M. Holla, M. van der Leeden, D.L. Knol, L.D. Roorda, W.K. Hilberdink, W.F. Lems, M.P. Steultjens, J. Dekker
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> It has been hypothesized (i) that pain and low vitality lead to an increase in avoidance of activities in persons with early symptomatic knee osteoarthritis (OA), and (ii) that avoidance of activities leads to an increase in activity limitations. <h3>Objectives</h3> The present study aimed to evaluate these hypotheses in a cross-sectional and longitudinal design. <h3>Methods</h3> Baseline, 2-year and 5-year follow-up data of 828 participants from the Cohort Hip and Cohort Knee (CHECK) study with early symptomatic knee OA were used. Knee pain, vitality, avoidance of activities and activity limitations were measured with reliable and validated instruments. Regression and autoregressive generalized estimating equations (GEE) models analyzed the cross-sectional and longitudinal associations between pain, vitality, avoidance of activities and activity limitations. The models were adjusted for age, gender, education level, body-mass index, comorbidity, and radiographic severity. <h3>Results</h3> (i) In cross-sectional analyses, greater knee pain and lower vitality were associated with higher levels of avoidance of activities. In longitudinal analyses, pain and vitality predicted a subsequent increase in avoidance of activities. (ii) In cross-sectional analyses, a higher level of avoidance of activities was associated with greater activity limitations. In longitudinal analyses, this relationship was marginally significant. <h3>Conclusions</h3> Knee pain and low vitality lead to a subsequent increase in avoidance of activities, already at an early stage of knee OA. Avoidance of activities is related to activity limitations: alternative measurement instruments and a longer follow-up may be required to establish the longitudinal relationship. <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.1194
Catastrophic injuries in the Olympic styles of wrestling in Iran
Authors: R Kordi, A Akbarnejad, W A Wallace
Journal: British Journal of Sports Medicine (2008)

In this study, a profile of direct catastrophic injuries in international styles of wrestling was developed, and the possible risk factors were described.Survey and retrospective review.Catastrophic injuries that occurred in wrestling clubs in Iran from July 1998 to June 2005 were identified by contacting several sources. The cases were retrospectively reviewed.The injuries included were 29 direct injuries (12 fatalities, 11 non-fatal and 6 serious).The injury rate was 1.99 direct catastrophic injuries/100 000 wrestlers/year. The majority of direct injuries occurred during training sessions, with a trend towards more injuries in the low-weight and middle-weight classes and those who were competing at high performance and experience levels. The takedown position, especially for the attacking wrestler who faces a counterattack, was the most common activity at the time of injury. A list of risk factors was suggested, of which "performing the wrestling manoeuvre incorrectly", "inappropriate management of the injury", "lack of the coach supervision", "mat problems" and "lack of restraining the wrestlers in a precarious position" were the most common risk factors.Catastrophic wrestling injuries are rare and preventable. Coaches have an essential role in the prevention of these injuries.
Thyroid Hormone–Induced Alterations in Phospholamban-Deficient Mouse Hearts
Authors: Eva Kiss, Angie G. Brittsan, Istvan Edes, Ingrid L. Grupp, Gunter Grupp, Evangelia G. Kranias
Journal: Circulation Research (1998)

Abstract —Alterations in the expression levels of the sarcoplasmic reticulum (SR) Ca 2+ -ATPase and its regulator, phospholamban, have been implicated in the effects of thyroxine hormone on cardiac function. To determine the role of phospholamban in these effects, hypothyroidism and hyperthyroidism were induced in phospholamban-deficient mice and their isogenic wild types. Hypothyroidism resulted in significant decreases of left ventricular contractility, which could be moderately stimulated by increases in preload or afterload, in both phospholamban-deficient and wild-type mice. However, the basal contractile parameters in hypothyroid phospholamban-deficient hearts were at least as high as those exhibited by hyperthyroid wild-type hearts. In hyperthyroidism, there was no further enhancement of the hyperdynamic contractile parameters in phospholamban-deficient hearts, although the wild-type hearts exhibited significantly increased contractile function compared with their respective euthyroid groups. Furthermore, increases in preload or afterload did not enhance contractility in either phospholamban-deficient or wild-type hyperthyroid hearts. Examination of the relative tissue levels of cardiac SR Ca 2+ -ATPase revealed increases in hyperthyroidism and decreases in hypothyroidism compared with euthyroidism, and these changes were similar between phospholamban-deficient and wild-type hearts. An opposite trend was observed for phospholamban expression levels in the wild-type group, which were depressed in hyperthyroid hearts but increased in hypothyroid hearts. These findings indicate that (1) thyroid hormones induce similar changes in the cardiac SR Ca 2+ -ATPase levels in either the presence or absence of phospholamban, (2) the thyroxine-induced increases in SR Ca 2+ -ATPase levels are not associated with any further stimulation of the hyperdynamic cardiac function in phospholamban-deficient mice, and (3) the decreased contractile parameters in hypothyroid phospholamban-deficient hearts associated with decreases in SR Ca 2+ -ATPase levels and myosin heavy chain isoform switches are at least as high as those of the stimulated hyperthyroid wild-type hearts. Thus, alterations in the phospholamban level or its activity may be a critical determinant of the contractile responses to altered thyroid states in the mammalian heart.
The Houston Citywide Policy on Medical Futility-Reply
Authors: Amir Halevy
Journal: JAMA (1996)

<h3>In Reply.</h3> —We are pleased that Drs Bauman and Vawter support the general direction of the Houston policy and that their groups are in the process of developing similar policies. We agree with Bauman that society as a whole needs to address the issues of resource allocation and rationing. However, that does not free institutions from their duty as responsible stewards of the resources made available to them, to consider the allocation of those resources as they decide whether providing demanded interventions is appropriate. Institutional integrity, we have argued, demands that this be considered. We also believe, in disagreement with Bauman, that a failure to provide the intervention unless the patient ultimately agrees is not abandonment. It must be remembered that all appropriate care would, according to step 7 of our protocol, continue to be provided, and abandonment is only the failure to provide appropriate care. A failure to provide inappropriate care
Dissection of T-cell Antigen Specificity in Human Melanoma
Authors: Rikke Sick Andersen, Charlotte Albæk Thrue, Niels Junker, Rikke Lyngaa, Marco Donia, Eva Ellebæk, Inge Marie Svane, Ton N. Schumacher, Per thor Straten, Sine Reker Hadrup
Journal: Cancer Research (2012)

Tumor-infiltrating lymphocytes (TIL) isolated from melanoma patients and expanded in vitro by interleukin (IL)-2 treatment can elicit therapeutic response after adoptive transfer, but the antigen specificities of the T cells transferred have not been determined. By compiling all known melanoma-associated antigens and applying a novel technology for high-throughput analysis of T-cell responses, we dissected the composition of melanoma-restricted T-cell responses in 63 TIL cultures. T-cell reactivity screens against 175 melanoma-associated epitopes detected 90 responses against 18 different epitopes predominantly from differentiation and cancer-testis antigens. Notably, the majority of these responses were of low frequency and tumor-specific T-cell frequencies decreased during rapid expansion. A further notable observation was a large variation in the T-cell specificities detected in cultures established from different fragments of resected melanoma lesions. In summary, our findings provide an initial definition of T-cell populations contributing to tumor recognition in TILs although the specificity of many tumor-reactive TILs remains undefined.
Early experience with percutaneous transcatheter implantation of heart valve prosthesis for the treatment of end-stage inoperable patients with calcific aortic stenosis
Authors: Alain Cribier, Hélène Eltchaninoff, Christophe Tron, Fabrice Bauer, Carla Agatiello, Laurent Sebagh, Assaf Bash, Danielle Nusimovici, P.Y Litzler, Jean-Paul Bessou, Martin B Leon
Journal: Journal of the American College of Cardiology (2004)
<i>ATG16L1</i>Crohn's disease risk stresses the endoplasmic reticulum of Paneth cells
Authors: Arthur Kaser, Richard S Blumberg
Journal: Gut (2013)

With 163 genetic loci identified to date, genome wide association studies have revealed the significant genetic complexity associated with risk for IBD.1 Autophagy, pinpointed through the discovery of risk variants in ATG16L1 2 and other autophagy genes,1 remains one of the most interesting disease-specific revelations of Crohn’s disease genetics. Around a fifth of the overall genetic risk yet known for Crohn's disease may lie in genes that are directly involved in autophagy,1 including NOD2 , which has recently been exposed as an autophagy inducer,3 a decade after it was reported as the first Crohn's disease risk gene.4 Given this, chances are that further autophagy regulators might hide in the many currently unexplored genetic risk loci. As an ostensibly disease-specific, genetically affected biological process, autophagy stands out within all the genetic heterogeneity of IBD,1 where the vast majority of risk loci (and computationally inferred genes and pathways) is shared between Crohn's disease and UC,1 and with other immune-related diseases that have phenotypically little in common with Crohn's disease.5 Understanding how autophagy risk genes and their variants contribute to Crohn's disease pathogenesis holds the promise of unravelling some of the secrets of this disease.

Autophagy (or ‘self-eating’) represents a basic function of all cell types wherein it serves an essential homeostatic function or is induced by the needs associated with metabolic changes such as starvation or the removal of microbes (xenophagy) (reviewed …
Reduced bronchial CD4+ T-cell density in smokers with occupational asthma
Authors: T. Sjåheim, J. Kongerud, Ø. Bjørtuft, P. A. Drabløs, D. Malterud, T. S. Halstensen
Journal: European Respiratory Journal (2006)

Cigarette smoking may alter bronchial inflammation in asthma. Multicolour immunohistofluorescent examination on bronchial cryosections was used to examine bronchial inflammatory cell infiltrate in patients with occupational asthma. Monoclonal antibodies to CD3, CD4, CD8, T-cell receptor-δ1, CD68 and human leukocyte antigen-DR were combined to identify T-cell subsets and macrophages in bronchial biopsies from 20 workers with occupational asthma (12 smokers and eight nonsmokers), 15 healthy workers (seven smokers and eight nonsmokers) and 10 nonsmoking, nonexposed controls. The increased subepithelial CD4+ T-cell density in nonsmoking asthmatics was not present in smoking asthmatics, who had the lowest CD4+ T-cell density of all groups. The decreased subepithelial CD4+ and CD8+ T-cell density correlated with a reduction in lung function, as measured by percentage predicted forced expiratory volume in one second, in smoking asthmatics only. Although smoking asthmatics had a significantly increased number of intraepithelial CD8+ T-cells and macrophages compared with nonsmoking asthmatics, the proportion of γδ-T-cells was significantly decreased in both asthmatic groups. Smoking asthmatics had a distinctly different distribution of T-cell subsets compared with nonsmoking asthmatics. The accumulation of subepithelial CD4+ T-cells, which was observed in nonsmoking asthmatics, appeared to be inhibited in smoking asthmatics, suggesting a smoking-induced bronchial immune modulation, at least in occupational asthma in the aluminium industry.
Letter: Interspersed advertising
Authors: I. Heisler
Journal: JAMA (1974)

<h3>To the Editor.—</h3> Several communications with officers of the American Medical Association and the chief editor of the<i>Archives of Psychiatry</i>regarding the matter of pagination in AMA journals, ie, permitting obverse sides of pages to carry scientific material and advertising, have not yielded satisfactory answers to the questions that I raised. This practice compels the binding of journals with advertising matter included. Perusal of a number of journals from this country and abroad indicates that this practice is limited to the AMA journals! Quite a few colleagues have raised objection to this practice, and thus far it has not been openly acknowledged or corrected. I believe it essential that you publish this letter to encourage a wider membership to offer their views.
Basal-Like Breast Cancer: A Critical Review
Authors: Emad A. Rakha, Jorge S. Reis-Filho, Ian O. Ellis
Journal: Journal of Clinical Oncology (2008)

Recent gene expression profiling of breast cancer has identified specific subtypes with clinical, biologic, and therapeutic implications. The basal-like group of tumors is characterized by an expression signature similar to that of the basal/myoepithelial cells of the breast and is reported to have transcriptomic characteristics similar to those of tumors arising in BRCA1 germline mutation carriers. They are associated with aggressive behavior and poor prognosis, and typically do not express hormone receptors or HER-2 ("triple-negative" phenotype). Therefore, patients with basal-like cancers are unlikely to benefit from currently available targeted systemic therapy. Although basal-like tumors are characterized by distinctive morphologic, genetic, immunophenotypic, and clinical features, neither an accepted consensus on routine clinical identification and definition of this aggressive subtype of breast cancer nor a way of systematically classifying this complex group of tumors has been described. Different definitions are, therefore, likely to produce variable and contradictory results that may hamper consistent identification and development of treatment strategies for these tumors. In this review, we discuss definition, heterogeneity, morphologic spectrum, relation to BRCA1, and clinical significance of this important class of breast cancer.
Osteopontin-mediated myocardial fibrosis in heart failure: a role for lysyl oxidase?
Authors: Begoña López, Arantxa González, Diana Lindner, Dirk Westermann, Susana Ravassa, Javier Beaumont, Idoia Gallego, Amaia Zudaire, Cristina Brugnolaro, Ramón Querejeta, Mariano Larman, Carsten Tschöpe, Javier Díez
Journal: Cardiovascular Research (2013)

We investigated whether the pro-fibrotic matricellular protein osteopontin (OPN) is associated with the enzymes involved in the extracellular synthesis of fibril-forming collagen type I (i.e. procollagen C-proteinase, PCP) and its cross-linking to form insoluble fibrils (i.e. lysyl oxidase, LOX) in heart failure (HF) of hypertensive origin. OPN, PCP, and LOX were assessed by histochemical and molecular methods in the myocardium of 21 patients with hypertensive heart disease (HHD) and HF. Whereas the myocardial expression of OPN was very scarce in control hearts (n = 10), it was highly expressed in HF patients (P < 0.0001). OPN was directly correlated with LOX (r = 0.460, P = 0.041), insoluble collagen (r = 0.534, P = 0.015), pulmonary capillary wedge pressure (r = 0.558; P = 0.009), and left-ventricular (LV) chamber stiffness (r = 0.458, P = 0.037), and inversely correlated with LV ejection fraction (r = −0.513, P = 0.017) in all patients. OPN did not correlate with PCP and other parameters assessing collagen synthesis by fibroblasts or degradation by matrix metalloproteinases. In vitro studies showed that OPN significantly (P < 0.05) increases the expression and activity of LOX in human cardiac and dermal fibroblasts. An excess of OPN is associated with increased LOX and insoluble collagen, as well as with LV stiffness and systolic dysfunction in patients with HHD and HF. In addition, OPN up-regulates LOX in human fibroblasts. It is suggested that the OPN–LOX axis might facilitate the formation of insoluble collagen (i.e. stiff and resistant to degradation) and the subsequent alteration in LV mechanical properties and function in patients with HHD and HF.
Periodontal disease in men
Authors: M. Cenk Haytac, Onur Ozcelik, Angelo Mariotti
Journal: Periodontology 2000 (2012)

In relation to periodontal diseases associated with sex-steroid hormones, men have been the forgotten sex. It is not surprising that there has been less scrutiny of the effects of sex-steroid hormones in men considering the more striking changes that occur in women during different periods of their life. Despite the gingival inflammatory changes reported in women, men have been reported to have a higher prevalence of destructive periodontal diseases. The information presented in this review will provide a contemporary evaluation of male susceptibility to periodontal diseases.
Hepatitis C Virus Infection in Patients with Essential Mixed Cryoglobulinemia
Authors: Rocco Misiani, Piermario Bellavita, Domenico Fenili, Giuseppe Borelli, Donatella Marchesi, Margherita Massazza, Giovanni Vendramin, Benedetto Comotti, Elisabetta Tanzi, Guido Scudeller, Alessandro Zanetti
Journal: Annals of Internal Medicine (1992)

To study the association between hepatitis C virus (HCV) infection and essential mixed cryoglobulinemia.Wards and clinics of the Ospedali Riuniti di Bergamo and Ospedale di Treviglio e Caravaggio, Italy.Fifty-one patients with essential mixed cryoglobulinemia associated with glomerulonephritis and 45 controls with noncryoglobulinemic glomerulopathies.Antibodies to hepatitis C virus (anti-HCV) in sera from patients with essential mixed cryoglobulinemia and from controls, using two enzyme-linked immunosorbent assays (c100 ELISA and c22/c200 ELISA) and a recombinant immunoblot assay (4-RIBA); cryoprecipitate anti-HCV before and after use of dithiothreitol, a substance able to destroy IgM antibodies with rheumatoid factor activity, in patients with essential mixed cryoglobulinemia; serum HCV RNA by polymerase chain reaction in patients with essential mixed cryoglobulinemia.In patients with essential mixed cryoglobulinemia, the c22/c200 ELISA detected anti-HCV in 98% of serum samples (95% CI, 90% to 100%), whereas the rate of reactivity remained at 2% (CI, 0% to 12%) in the control group (P less than 0.0001). These results were confirmed by the 4-RIBA in 66% of patients with essential mixed cryoglobulinemia. The study of cryoprecipitate by c100 ELISA showed anti-HCV in 41% (Cl, 28% to 56%) of patients. After dithiothreitol, the rate of reactivity increased to 94% (CI, 84% to 99%; P less than 0.0001 by the McNemar paired chi-square test), suggesting that the elimination of rheumatoid factor leads to unmasking of anti-HCV in cryoprecipitate. Polymerase chain reaction detected HCV RNA in 13 of 16 sera from patients with essential mixed cryoglobulinemia.The extremely high prevalence of anti-HCV in serum and cryoprecipitate along with the frequently associated serum HCV RNA suggests a close relation between essential mixed cryoglobulinemia and chronic HCV infection.
Lipoproteins containing the truncated apolipoprotein, Apo B-89, are cleared from human plasma more rapidly than Apo B-100-containing lipoproteins in vivo.
Authors: K G Parhofer, P H Barrett, D M Bier, G Schonfeld
Journal: Journal of Clinical Investigation (1992)

We have reported previously on two truncations of apolipoprotein B (apo B-40 and apo B-89) in a kindred with hypobetalipoproteinemia. Premature stop codons were found to be responsible for both apo B-40 and apo B-89, but the physiologic mechanisms accounting for the reduced plasma concentrations of these proteins have not been determined in vivo. This study investigates the metabolism of apo B-89 in two subjects heterozygous for apo B-89/apo B-100 and in one apo B-40/apo B-89 compound heterozygote. In both heterozygotes total apo B concentration is approximately 30% of normal and apo B-89 is present in lower concentrations in plasma than apo B-100. After the administration of [1-13C]leucine as a primed constant infusion over 8 h, 13C enrichments of plasma leucine as well as enrichments of VLDL-, IDL-, and LDL-apo B-89 leucine and VLDL-, IDL-, and LDL-apo B-100 leucine were measured over 110 h. Enrichment values were subsequently converted to tracer/tracee ratios and a multicompartmental model was used to estimate metabolic parameters. In both apo B-89/apo B-100 heterozygotes apo B-89 and apo B-100 were produced at similar rates. Respective transport rates of apo B-89 and apo B-100 for subject 1 were 2.13 +/- 0.18 and 2.56 +/- 0.13 mg.kg-1.d-1, and for subject 2, 6.59 +/- 0.18 and 8.23 +/- 0.39 mg.kg-1.d-1. However, fractional catabolic rates of VLDL, IDL, and LDL particles containing apo B-89 were 1.4-3 times higher than the rates for corresponding apo B-100-containing particles. Metabolic parameters of apo B-89 in the apo B-40/apo B-89 compound heterozygote compared favorably with those established for apo B-89 in apo B-89/apo B-100 heterozygotes. Thus, the enhanced catabolism of VLDL, IDL, and LDL particles containing the truncated apolipoprotein is responsible for the relatively low levels of apo B-89 seen in these subjects.