tbuckley/cabot-search huggingface dataset:
Influenza A Infections in Infants of Vaccinated and Unvaccinated Mothers—Reply
Authors: Anders Hviid, Henrik Svanström
Journal: JAMA Pediatrics (2017)

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 Pediatrics 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 Pediatrics journal
Carcinogenic Effectiveness of Ultraviolet Radiation of Wavelength 2537A
Authors: Harold F. Blum, Stuart W. Lippincott
Journal: JNCI Journal of the National Cancer Institute (1942)

Journal Article Carcinogenic Effectiveness of Ultraviolet Radiation of Wavelength 2537A Get access Harold F. Blum, Harold F. Blum senior pharmacologist Search for other works by this author on: Oxford Academic PubMed Google Scholar Stuart W. Lippincott Stuart W. Lippincott passed assistant surgeon National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 3, Issue 2, October 1942, Pages 211–216, https://doi.org/10.1093/jnci/3.2.211 Published: 01 October 1942
脂質代謝:低温誘導性リポカイン12,13‐diHOMEは褐色脂肪組織への脂肪酸輸送を促進する
Authors: Lynes Matthew D, Leiria Luiz O, Lundh Morten, Shamsi Farnaz, Huang Tian Lian, Takahashi Hirokazu, Hirshman Michael F, Goodyear Laurie J, Tseng Yu‐Hua, Bartelt Alexander, Schlein Christian, Lee Alexandra, Hotamisligil Goekhan S, Baer Lisa A, May Francis J, Stanford Kristin I, Gao Fei, Narain Niven R, Chen Emily Y, Kiebish Michael A, Cypess Aaron M, Blueher Matthias
Journal: Nature Medicine (2017)
A STUDY ON MEDICATION USE AND INJURIES IN OVER 1500 NOVICE RUNNERS
Authors: Henk van der Worp, Marienke van Middelkoop, Fred Hartgens, Bionka Huisstede, Per Wilms, Bas Kluitenberg, Evert Verhagen, Nadine Rasenberg, Ron Diercks
Journal: British Journal of Sports Medicine (2017)

Background In sedentary subjects use of medication is expected to be high which may cause problems when taking up exercise as several types of medication have been linked to musculoskeletal disorders. Objective To study the relation between medication use and the incidence of running-related injuries in novice runners. Design Prospective cohort study with propensity score matching analysis. Setting A nationwide start to run program for novice runners (N=7,660). Patients (or Participants) Novice runners (N=1,696) aged between 18–65 years taking part in a start to run program. Interventions (or Assessment of Risk Factors) Self-reported medication use was assessed with a questionnaire at baseline. Medication was categorized according to (1) condition and (2) chemical properties. Subjects who used medication were matched to controls using propensity score matching. Main Outcome Measurements Incidence rate differences were calculated between subjects that used medication and matched controls for each medication category. Results Women who took contraceptives had lower incidence densities of running-related injuries compared to matched controls both when medication was categorized according to condition (all contraceptives: incidence rate difference=−21.2 injuries/1000 h, 95% CI −41.9−−0.5) and according to chemical properties (hormonal contraceptives: incidence rate difference=−35.7 injuries/1000 h, 95% CI −61.3−−10.1). For other medication types no relation with injuries was established. Conclusions The study gives an overview of the influence of medication use on injuries in novice runners. Only for contraceptive use a relation with injuries was found. The use of contraceptives seems to have a preventive effect on the occurrence of injuries. An explanation for this finding may be the direct hormonal effect of contraceptives, for example on neuromuscular control and joint laxity, or an indirect effect through personal characteristics related to contraceptive use, such as health behaviour or risk-taking behaviour.
01.03 Ttp/s100a9 deficient mice promote a tnf-dependent psoriatic arthritis phenotype triggered by the bacterial environment
Authors: Athanasios Stratis, Mareike Fröhling, Thomas Vogl, Karin Loser, Peter Paruzel, Perry Blackshear, Debbie Stumpo, Johannes Roth, Thomas Pap
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Psoriatic-Arthritis (PsA) is a type of inflammatory chronic arthritis with a seronegative spondyloarthropathy and associated psoriasis. The Danger-Associated Molecular Pattern molecules (DAMPs) S100A8 and S100A9 are both antimicrobial proteins with chemotactic activity and are the most abundant DAMPs expressed during many inflammatory disorders. The expression of the S100A8/S100A9-complex is highly elevated in psoriasis and psoriatic arthritis. However, the mechanisms that regulate S100A8/S100A9-complex-activities are poorly understood, which has led us to examine the role of S100A8 and S100A9 under chronic inflammatory conditions. <h3>Material and methods</h3> We crossed S100A9-deficient mice with TTP (tristetraprolin)-deficient mice into a systemic inflammatory model featuring high levels of TNF with an arthritic joint destruction phenotype. Disease progression in TTP<sup>-/-</sup> x S100A9<sup>-/-</sup> mice was analysed by immunostaining, immunohistochemistry and the adapted PASI-score. To neutralise TNF in TTP<sup>-/-</sup> x S100A9<sup>-/-</sup> mice we used an aTNF-inhibiting monoclonal antibody already in clinical use for therapy of arthritis and psoriasis. To measure altered protein levels we used Western blot analysis. Primary keratinocytes were isolated of the skin from newborn mice and infected with E.coli isolated from the faeces of mice. <h3>Results</h3> TTP/S100A9 deficiency led to highly elevated levels of the S100A9 complex partner S100A8 in the epidermis and to a severe psoriatic phenotype of TTP-/- x S100A9-/- mice. Furthermore the mice showed an accelerated course of arthritis compared to TTP-/- mice, including increased articular cartilage loss and bone destruction. Inhibition of TNF by application of anti-TNF clearly reduced the psoriatic phenotype of TTP-/- x S100A9-/- mice. Additionally, the reduction of the environmental bacterial levels led to a milder phenotype and decelerated pathogenesis. The <i>in vitro</i> infection of isolated keratinocytes with isolated E.coli resulted in a high expression of S100A8. <h3>Conclusions</h3> The data reveal that the S100A8/S100A9-complex acts not only as a systemic danger signal molecule, but is also TNF dependent and is essential for the regulation of inflammation. The loss of S100A9 led to a disregulated inflammatory response and this to a severe psoriasis with enhanced cartilage and bone destruction. Furthermore, an exogenic bacterial factor, such as E. coli, is also demonstrated to be important in the activation of the disease.
Epidemiology and burden of systemic lupus erythematosus in a Southern European population: data from the community-based lupus registry of Crete, Greece
Authors: Irini Gergianaki, Antonis Fanouriakis, Argyro Repa, Michalis Tzanakakis, Christina Adamichou, Alexandra Pompieri, Giorgis Spirou, Antonios Bertsias, Eleni Kabouraki, Ioannis Tzanakis, Leda Chatzi, Prodromos Sidiropoulos, Dimitrios T Boumpas, George K Bertsias
Journal: Annals of the Rheumatic Diseases (2017)

Several population-based studies on systemic lupus erythematosus (SLE) have been reported, yet community-based, individual-case validated, comprehensive reports are missing. We studied the SLE epidemiology and burden on the island of Crete during 1999-2013.Multisource case-finding included patients ≥15 years old. Cases were ascertained by the ACR 1997, SLICC 2012 criteria and rheumatologist diagnosis, and validated through synthesis of medical charts, administrative and patient-generated data.Overall age-adjusted/sex-adjusted incidence was 7.4 (95% CI 6.8 to 7.9) per 100 000 persons/year, with stabilising trends in women but increasing in men, and average (±SD) age of diagnosis at 43 (±15) years. Adjusted and crude prevalence (December 2013) was 123.4 (113.9 to 132.9) and 143 (133 to 154)/105 (165/105 in urban vs 123/105 in rural regions, p<0.001), respectively. Age-adjusted/sex-adjusted nephritis incidence was 0.6 (0.4 to 0.8) with stable trends, whereas that of neuropsychiatric SLE was 0.5 (0.4 to 0.7) per 100 000 persons/year and increasing. Although half of prevalent cases had mild manifestations, 30.5% developed organ damage after 7.2 (±6.6) years of disease duration, with the neuropsychiatric domain most frequently afflicted, and 4.4% of patients with nephritis developed end-stage renal disease. The ACR 1997 and SLICC 2012 classification criteria showed high concordance (87%), yet physician-based diagnosis occurred earlier than criteria-based in about 20% of cases.By the use of a comprehensive methodology, we describe the full spectrum of SLE from the community to tertiary care, with almost half of the cases having mild disease, yet with significant damage accrual. SLE is not rare, affects predominantly middle-aged women and is increasingly recognised in men. Neuropsychiatric disease is an emerging frontier in lupus prevention and care.
SEQUENCING JUDGEMENT SKILLS AND DECISIONS-MADE ON RUGBY ATHLETES: AN ANALYSIS ON INJURY PREVENTION
Authors: Henare R Broughton
Journal: British Journal of Sports Medicine (2017)

Objective To analyse rugby athletes' judgement knowledge and decisions-made where there is the potential to minimise error and prevent injury. Material and methods A prospective cohort of 300 rugby athletes participated in the Division 2A Senior Rugby All-Ireland Championships in the period of 2010–2011. The athletes came from the Dublin University Football Club and opposing Clubs and the ten match fixtures videoed, injury data were collated with informed consent obtained. Results Time durations for the scrum had a mean throw in – clearance of 3.128 s (SD 2.109), the tackle, mean clearance time 4.135 s (SD 3.0320) and the lineout, mean throw in – clearance 4.072 s (SD 3.2584). On space dimensions the scrum, short-arm binding was preferred, Fisher's exact test: p-value=0.094 and variations in alignment, p-value=0.056. Of the injury data a Chi-squared test, confirmed significant differences p&lt;0.05 with the hooker compared to the locks in the scrum 33.156 for cervical and lumbar spinal injuries respectively. In open play, loose forwards sustained cervical injuries, p&lt;0.05 due to the tackle compared to midfield backs 28.917 with lower limb injuries attributed to running and being tackled. Conclusions Judgement analysis on the scrum, tackle, and lineout showed consistent delays in recovery and completion from ball clearances respectively. Variations in alignments occurred with inconsistencies at the post-set in the scrum. In contrast applying Judgement knowledge with reference to the Laws of the Game there is the potential to minimise error and prevent injury.
心疾患:心‐脳‐腎ネットワークは組織マクロファージの活性化を介して心臓負荷への適応を制御している
Authors: Fujiu Katsuhito, Shibata Munehiko, Nakayama Yukiteru, Ogata Fusa, Matsumoto Sahohime, Komuro Issei, Iwami Shingo, Nakae Susumu, Noshita Koji, Nagai Ryozo, Manabe Ichiro
Journal: Nature Medicine (2017)
04.16 Tnf/tnfr2 signalling in mesenchymal cells of joints and aortic heart valves is aetiopathogenic for comorbid arthritis and heart valve disease developing in the tnf<sup>Δare/+</sup> mouse model
Authors: Maria Sakkou, Maria C Denis, Panagiotis Chouvardas, Alejandro Prados, Niki E Karagianni, Lydia Ntari, George Kollias
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Background</h3> Chronic inflammatory diseases, such as Rheumatoid arthritis (RA) and Inflammatory Bowel Disease (IBD) are often co-manifested with additional comorbidities. Studies performed in the established TNF<sup>ΔARE/+</sup> mouse model of TNF dependent RA and Crohn's-like IBD, have demonstrated that stromal cells in the joint and the gut are primary and sufficient targets of TNF leading to the development of these two pathologies. Valvular heart disease (VHD) is one of the most common comorbid conditions in RA patients, that frequently leads to heart failure and premature death. We have recently observed that VHD is also displayed in the TNF<sup>ΔARE/+</sup> mouse model and our current aim has been to identify whether TNF signalling in stromal cells of the heart play also a role in regulating the VHD pathology similarly to what has been shown in the joint-gut axis. To this end we have used ColVI-Cre mice (specific for mesenchymal cells) and dissected genetically the role of TNFR2 in the stroma of the TNF<sup>ΔARE/+</sup> mouse model by assessing its function in RA and the VHD comorbidity. <h3>Materials and methods</h3> Mesenchymal cells specific deletion of TNFR2 was achieved by crossing TNF<sup>ΔARE/+</sup> to ColVICre/p75<sup>f/f</sup>. We further used histopathological analysis and cell isolation, characterisation, signalling analysis and RNAseq expression profiling analysis to decipher the pathologic mechanisms. <h3>Results</h3> Interestingly, we found that stroma-specific TNFR2 deletion leads to amelioration of RA and VHD pathologies. These results point to a common role of stroma-expressing TNFR2 in RA and VHD. Furthermore, we identified that isolated stromal cells from joint (SFs) and aortic heart valve (VICs) lacking TNFR2, failed to acquire pathogenic 'activated phenotypes' and display increased expression of the anti-inflammatory IL1RA which correlated with increased AKT signalling. Comparative RNAseq experiments performed in SFs and VICs lacking TNFR2 showed that the majority of deregulated pathways in TNF<sup>ΔARE/+</sup> are reversed to normal levels. <h3>Conclusion</h3> Taken together, our data demonstrate that the RA and VHD comorbidities developing in the TNF<sup>ΔARE/+</sup> mouse model, share common cellular mechanisms converging at the TNF/TNFR2 dependent activation of their mesenchymal stroma.
Arrhythmogenic cardiomyopathy: pathology, genetics, and concepts in pathogenesis
Authors: Edgar T. Hoorntje, Wouter P. te Rijdt, Cynthia A. James, Kalliopi Pilichou, Cristina Basso, Daniel P. Judge, Connie R. Bezzina, J. Peter van Tintelen
Journal: Cardiovascular Research (2017)

Arrhythmogenic cardiomyopathy (ACM) is a rare, heritable heart disease characterized by fibro-fatty replacement of the myocardium and a high degree of electric instability. It was first thought to be a congenital disorder, but is now regarded as a dystrophic heart muscle disease that develops over time. There is no curative treatment and current treatment strategies focus on attenuating the symptoms, slowing disease progression, and preventing life-threatening arrhythmias and sudden cardiac death. Identification of mutations in genes encoding desmosomal proteins and in other genes has led to insights into the disease pathogenesis and greatly facilitated identification of family members at risk. The disease phenotype is, however, highly variable and characterized by incomplete penetrance. Although the reasons are still poorly understood, sex, endurance exercise and a gene-dosage effect seem to play a role in these phenomena. The discovery of the genes and mutations implicated in ACM has allowed animal and cellular models to be generated, enabling researchers to start unravelling it's underlying molecular mechanisms. Observations in humans and in animal models suggest that reduced cell–cell adhesion affects gap junction and ion channel remodelling at the intercalated disc, and along with impaired desmosomal function, these can lead to perturbations in signalling cascades like the Wnt/β-catenin and Hippo/YAP pathways. Perturbations of these pathways are also thought to lead to fibro-fatty replacement. A better understanding of the molecular processes may lead to new therapies that target specific pathways involved in ACM.
04.14 Aortic valve disease co-develops with polyarthritis in the tnf-driven models and shares a common mesenchymal cell-mediated causality
Authors: Lydia Ntari, Maria Sakkou, Panagiotis Chouvardas, Alejandro Prados, Anna Katevaini, Niki Karagianni, Maria C Denis, George Kollias
Journal: Annals of the Rheumatic Diseases (2017)

<h3>Introduction and objectives</h3> Rheumatoid arthritis (RA) is a chronic condition characterised by inflammation of the joints as well as destruction of bone and cartilage. Studies on TNF transgenic models of polyarthritis established Tumour Necrosis Factor (TNF) targeting the mesenchymal-origin Synovial Fibroblasts (SFs) as a key event instigating the pathology. RA patients often show higher mortality rates, mainly due to the development of extraarticular disease including cardiovascular, gut and skin manifestations. The Tg197 and Tnf<sup>ΔARE/+</sup> mouse models overexpress TNF and develop spontaneous chronic polyarthritis, fully mimicking human RA pathology. Here, we investigate whether these models develop, similarly to human patients, co-morbid heart pathology. <h3>Materials and methods</h3> We used the Tg197 and Tnf<sup>ΔARE/+</sup> mouse models to evaluate possible arthritis-related cardiovascular disease. For further <i>ex vivo</i> analysis, we isolated Valve Interstitial Cells (VICs), which are the mesenchymal-origin fibroblasts constituting the aortic valve. We used a GFP reporter mouse labelling specifically mesenchymal-origin cells (ColVICre;mTm/mGFP) to target VICs. Similarities of pathogenic VICs and SFs were analysed by comparing their expression profiling with RNA sequencing analysis. <h3>Results</h3> Both arthritis models examined develop TNF-dependent aortic valve thickening, as indicated by the amelioration of the pathology following treatment with anti-TNF biologics. Aortic valves exhibited significant fibrosis with minimal signs of inflammatory cell infiltration and thickened areas, consisting almost entirely of VICs, indicating proliferation of this cell type as a hallmark of the observed phenotype. Isolated VICs from mutant mice exhibited a more proliferative and migratory phenotype and expressed high levels of TNF. Interestingly, VIC activation resembles the activated phenotype of pathogenic SFs isolated from the same mice. A significant functional correlation between these two pathogenic cells of mesenchymal origin was also supported by RNA-seq analysis, suggesting common cellular mechanisms operating in RA and RA-related heart pathology. <h3>Conclusion</h3> TNF-driven arthritis models, apart from their arthritic symptoms, develop co-morbid heart valve disease, similarly to reported comorbidities in RA patients. These two co-morbid diseases are shown here to share common mesenchymal-cell driven aetiopathogenesis.
Global climate is warming rapidly, US draft report warns
Authors: Michael McCarthy
Journal: BMJ (2017)

The global climate is warming rapidly and will continue to do so even if “greenhouse” gas emissions are reduced substantially, US climate experts conclude in a draft report leaked to the New York Times .1

“Recent data adds to the weight of the evidence for rapid global-scale warming, the dominance of human causes, and the expected continuation of increasing temperatures, including more record-setting extremes,” the report says.

The National Academy of Sciences had signed off on the report, which is mandated by Congress to be prepared every four years, but the draft had not yet been …
THE RELATION BETWEEN LOAD AND PATELLAR TENDON STRUCTURE DURING PRESEASON IN VOLLEYBALL PLAYERS
Authors: Lucas Maciel Rabello, Ruth Ijtsma, Johannes Zwerver, Michel S Brink
Journal: British Journal of Sports Medicine (2017)

Background Patellar tendinopathy is a common overuse injury in jumping sports, with higher prevalence in volleyball players. Different risk factors are associated with patellar tendon problems, including training load. Despite different treatment options, rates of chronicity and recurrence are high. Therefore, the high prevalence and the challenging treatment underlines the importance of prevention. Objective Investigate the relation between tendon load and the response of patellar tendon structure of volleyball players. Design Observational prospective study. Setting The study was performed with elite volleyball players during the preseason. Patients (or Participants) A total of 17 elite male volleyball players from Dutch volleyball league. Interventions (or Assessment of Risk Factors) Training load, including jump frequency and Rating or Perceived Exertion (RPE), were measured every training and match during 7 weeks. Main Outcome Measurements Tendon structure was measured using the Ultrasound Tissue Characterization (UTC), which quantifies the structure of the tendon (percentages of four echo-types). Results On average, players spent 624±215 minutes on training and matches per week with a RPE of 13.9±2.1 indicating 'somewhat hard' intensity. Jump frequency was 278±122 per week. Higher load parameters (volume, intensity and load) resulted all in a higher decrease of echo-type I (p&lt;0.05). Higher volume and load resulted in a higher decrease of echo-type II (p&lt;0.05). Higher cumulative weekly volume and cumulative weekly loads between the first and the last UTC were related to significant higher decreases in echo-type I (p&lt;0.05), but not related for echo-type II. No significant relations were found for jump frequency. None of the load parameters were related to echo-type III and IV. Conclusions The present study showed that load was related to changes in echo-types over a 7 week preseason in elite volleyball players. A higher amount of load was related to greater echo pattern changes.
Comparative Enzymatic Activity of Transplanted Hepatomas and of Normal, Regenerating, and Fetal Liver
Authors: Jesse P. Greenstein, Jesse E. Edwards, Howard B. Andervont, Julius White
Journal: JNCI Journal of the National Cancer Institute (1942)

Journal Article Comparative Enzymatic Activity of Transplanted Hepatomas and of Normal, Regenerating, and Fetal Liver Get access Jesse P. Greenstein, Jesse P. Greenstein senior biochemist Search for other works by this author on: Oxford Academic PubMed Google Scholar Jesse E. Edwards, Jesse E. Edwards research fellow Search for other works by this author on: Oxford Academic PubMed Google Scholar Howard B. Andervont, Howard B. Andervont principal biologist Search for other works by this author on: Oxford Academic PubMed Google Scholar Julius White Julius White senior biochemist National Cancer Institute, National Institute of Health, United States Public Health Service Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 3, Issue 1, August 1942, Pages 7–17, https://doi.org/10.1093/jnci/3.1.7 Published: 01 August 1942