tbuckley/cabot-search huggingface dataset:
Monitoring approaches for health-care workers during the COVID-19 pandemic
Authors: Julia A Bielicki, Xavier Duval, Nina Gobat, Herman Goossens, Marion Koopmans, Evelina Tacconelli, Sylvie van der Werf
Journal: The Lancet Infectious Diseases (2020)

Health-care workers are crucial to any health-care system. During the ongoing COVID-19 pandemic, health-care workers are at a substantially increased risk of becoming infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and could come to considerable harm as a result. Depending on the phase of the pandemic, patients with COVID-19 might not be the main source of SARS-CoV-2 infection and health-care workers could be exposed to atypical patients, infected family members, contacts, and colleagues, or live in communities of active transmission. Clear strategies to support and appropriately manage exposed and infected health-care workers are essential to ensure effective staff management and to engender trust in the workplace. These management strategies should focus on risk stratification, suitable clinical monitoring, low-threshold access to diagnostics, and decision making about removal from and return to work. Policy makers need to support health-care facilities in interpreting guidance during a pandemic that will probably be characterised by fluctuating local incidence of SARS-CoV-2 to mitigate the impact of this pandemic on their workforce.
Molecular basis of <i>ETV6</i>-mediated predisposition to childhood acute lymphoblastic leukemia
Authors: Rina Nishii, Rebekah Baskin-Doerfler, Wentao Yang, Ninad Oak, Xujie Zhao, Wenjian Yang, Keito Hoshitsuki, Mackenzie Bloom, Katherine Verbist, Melissa Burns, Zhenhua Li, Ting-Nien Lin, Maoxiang Qian, Takaya Moriyama, Julie M. Gastier-Foster, Karen R. Rabin, Elizabeth Raetz, Charles Mullighan, Ching-Hon Pui, Allen Eng-Juh Yeoh, Jinghui Zhang, Monika L. Metzger, Jeffery M. Klco, Stephen P. Hunger, Scott Newman, Gang Wu, Mignon L. Loh, Kim E. Nichols, Jun J. Yang
Journal: Blood (2020)
Serologic characterization of anti-p200 pemphigoid: Epitope spreading as a common phenomenon
Authors: Maike M. Holtsche, Stephanie Goletz, Anabelle von Georg, Nina van Beek, Franziska Hübner, Manuela Pigors, Detlef Zillikens, Enno Schmidt
Journal: Journal of the American Academy of Dermatology (2020)

retrospective design, use of claims data, and lack of correlation with clinical outcomes.
Medical leaders write to PM calling for “decisive action” against obesity and health inequalities
Authors: Gareth Iacobucci
Journal: BMJ (2020)

The government’s plans for tackling obesity must be part of a wider strategy to reduce health inequalities that have widened further since the covid-19 pandemic, medical royal colleges have told the prime minister.

In a letter to Boris Johnson, shared with The BMJ , the Royal College of Physicians, the Royal College of Child and Paediatric Health, and the Royal College of General Practitioners said that anything less …
FRI0165 Serum levels of interleukin-12 in behcet’s disease
Authors: A Canataroglu, E Erken, R Gunesacar
Journal: Annals of the Rheumatic Diseases (2001)

<h3>Background</h3> Behcet's disease (BD) is a vasculitis with unknown aetiology. Previous studies have reported that T cell mediated immune response may play role in the pathogenesis of BD. Various cytokines have been demonstrated to be elevated in the serum of patients with BD. Interleukin-12 (IL-12) has been shown to have multiple effects on T cells and is a central mediator of the cell mediated immune response by its actions on the development, proliferation and activities of T helper 1 (TH1) cells. <h3>Objectives</h3> The purpose of this study was to assess the serum levels of IL-12 in patients with BD. <h3>Methods</h3> Serum IL-12 levels were investigated in 36 BD patients (13 active BD and 23 inactive BD patients), in 23 rheumatoid arthritis (RA) patients and in 22 healthy controls (HC) using sandwich ELISA method. <h3>Results</h3> The mean IL-12 levels in the serum of the patients with BD, RA and HC were 3.023 ± 0.732 (mean ± standard error) pg/ml, 4.189 ± 0.991 pg/ml, 0.126 ± 0.091 pg/ml, respectively. The serum IL-12 level of BD patients was significantly higher from that of HC (p = 0.000), but no statistical difference was observed between the serum IL-12 levels of BD patients and RA patients (p = 0.335). Active BD (5.617 ± 1.588 pg/ml) and inactive BD (1.557 ± 0.534 pg/ml) patients had higher serum levels of IL-12 when compared to those of HC (p = 0.000 and p = 0.004, respectively). <h3>Conclusion</h3> Our results suggest involvement of IL-12 in the pathogenesis of BD.
THU0076 SONIC HEDGEHOG PROMOTES SYNOVIAL HYPERPLASIA AND BONE DAMAGE THROUGH P38 MAPK SIGNALING IN EXPERIMENTAL ARTHRITIS
Authors: S. Zhu, Y. Shi, Y. Ye, X. Feng, J. Huang
Journal: Annals of the Rheumatic Diseases (2020)

Background: Abnormal activation of sonic hedgehog (SHH) signaling has been found in synovium from patients with rheumatoid arthritis (RA). Inhibition of SHH signaling is reported to attenuate inflammation and cartilage damage in adjuvant-induced arthritis (AIA). Previously we have demonstrated that SHH signaling promoted the tumor-like behavior of fibroblast-like synoviocytes (FLSs) through p38 MAPK in vitro . Objectives: In the current study, we aim to further explore the role of SHH-p38 MAPK signaling in regulating synovial hyperplasia and bone erosion in experimental arthritis. Methods: Collagen-induced arthritis (CIA) mouse model was induced and the mice were injected with adenovirus associated virus (AAV) overexpressing SHH or treated with small molecule inhibitors GDC-0449. SB203580 was administrated for the inhibition of p38 MAPK. The severity of paw inflammation was graded and serum levels of TNFα, IL-6 were detected. The histological features of arthritis were evaluated by H&amp;E staining. The bone erosion was identified by micro-CT assessment and the number and function of osteoclasts were determined. Results: Blockade of SHH by GDC-0449 significantly alleviated the symptoms and decreased the synovial hyperplasia, inflammatory infiltration, cartilage and bone damage in ankles of CIA. The bone erosions in the area of the metatarsophalangeal and ankle joints and production of TNFα, IL-6 were decreased by SHH inhibition. In addition, the administration of GDC-0449 significantly decreased the number of TRAP positive cells and the expression of NFATc1. On the contrary, SHH overexpression led to increased severity of arthritis and pathological changes. We also observed the accelerated bone injury accompanied with increased number and activity of osteoclasts and increased production of serum IL-6 in mice with upregulation of SHH expression. Of note, the administration of p38 MAPK inhibitor reversed the effects of SHH overexpression, with a reduction of joint swelling and histological scores. Inhibition of p38 MAPK prevented the bone erosion and decreased the number of TRAP positive cells and the expression of NFATc1, which were promoted by SHH overexpression. Conclusion: The study indicates that SHH promotes the synovial hyperplasia and bone erosion of CIA in a p38 MAPK-dependent manner. SHH-p38 MAPK signaling could be a potential target for the treatment of RA. Acknowledgments: This work was supported by grants from the National Natural Science Foundation of China (81571584, 81701609). Disclosure of Interests: None declared
Modulation of the Astrocyte-Neuron Lactate Shuttle System contributes to Neuroprotective action of Fibroblast Growth Factor 21
Authors: Yan Sun, Yue Wang, Su-Ting Chen, Ying-Jie Chen, Jie Shen, Wen-Bing Yao, Xiang-Dong Gao, Song Chen
Journal: Theranostics (2020)

A viewpoint considering Alzheimer's disease (AD) as "type 3 diabetes" emphasizes the pivotal role of dysfunctional brain energy metabolism in AD. The hormone fibroblast growth factor 21 (FGF21) is a crucial regulator in energy metabolism; however, our understanding of the therapeutic potential and mechanisms underlying the effect of FGF21 on neurodegeneration of AD is far from complete. Methods: To further elucidate the effect of FGF21 on AD-related neurodegeneration, we used APP/PS1 transgenic mice to assess the effects of FGF21 on memory dysfunction, amyloid plaque pathology and pathological tau hyperphosphorylation. We also established an in vitro system to mimic astrocyte-neuron communication and an in vivo model of acute injury. Based on the in vivo and in vitro models, we analyzed the neuroprotective actions of FGF21 and pathways related to astrocyte-neuron communication and further focused on the astrocyte-neuron lactate shuttle system. Results: Here, we report that FGF21 can ameliorate Alzheimer-like neurodegeneration in APP/PS1 transgenic mice. We detected defects in the astrocyte-neuron lactate shuttle system in the in vivo and in vitro models of AD and identified FGF21 as a neuroprotective molecule that can rescue these deficits. Administration of FGF21 can alleviate memory dysfunction, amyloid plaque pathology and pathological tau hyperphosphorylation, and the function of FGF21 in neurodegeneration is mediated in part by monocarboxylate transporters (MCTs). In vivo evidence also suggests that FGF21 acts centrally in mice to exert its effects on neurodegeneration and energy metabolism via its regulation of MCTs. Conclusions: These results suggest that FGF21 alters metabolic parameters to mediate its neuroprotective functions. Modulation of the astrocyte-neuron lactate shuttle system can be one of the most efficient strategies for FGF21 in Alzheimer-like degeneration and contributes to improvements in brain metabolic defects and amyloid β-induced cytotoxicity. Our findings provide insights into the mechanisms underlying the effects of FGF21 on neurodegeneration and brain energy metabolism and suggest that FGF21 may have therapeutic value in the treatment of AD and other neurodegenerative diseases.
An International Multicenter Evaluation of Inheritance Patterns, Arrhythmic Risks, and Underlying Mechanisms of <i>CASQ2</i> -Catecholaminergic Polymorphic Ventricular Tachycardia
Authors: Kevin Ng, Erron W. Titus, Krystien V. Lieve, Thomas M. Roston, Andrea Mazzanti, Frederick H. Deiter, Isabelle Denjoy, Jodie Ingles, Jan Till, Tomas Robyns, Sean P. Connors, Christian Steinberg, Dominic J. Abrams, Benjamin Pang, Melvin M. Scheinman, J. Martijn Bos, Stephen A. Duffett, Christian van der Werf, Alice Maltret, Martin S. Green, Julie Rutberg, Seshadri Balaji, Julia Cadrin-Tourigny, Kate M. Orland, Linda M. Knight, Caitlin Brateng, Jeremy Wu, Anthony S. Tang, Allan C. Skanes, Jaimie Manlucu, Jeff S. Healey, Craig T. January, Andrew D. Krahn, Kathryn K. Collins, Kathleen R. Maginot, Peter Fischbach, Susan P. Etheridge, Lee L. Eckhardt, Robert M. Hamilton, Michael J. Ackerman, Ferran Rosés I. Noguer, Christopher Semsarian, Natalia Jura, Antoine Leenhardt, Michael H. Gollob, Silvia G. Priori, Shubhayan Sanatani, Arthur A.M. Wilde, Rahul C. Deo, Jason D. Roberts
Journal: Circulation (2020)

Genetic variants in calsequestrin-2 (
Authors’ response: Estimating the generation interval for COVID-19 based on symptom onset data
Authors: Cécile Kremer, Tapiwa Ganyani, Dongxuan Chen, Andrea Torneri, Christel Faes, Jacco Wallinga, Niel Hens
Journal: Eurosurveillance (2020)

Preview this article: Authors' response: Estimating the generation interval for COVID-19 based on symptom onset data, Page 1 of 1 < Previous page | Next page > /docserver/preview/fulltext/eurosurveillance/25/29/eurosurv-25-29-4-1.gif
METTL14 aggravates endothelial inflammation and atherosclerosis by increasing FOXO1 N6-methyladeosine modifications
Authors: Dongdong Jian, Ying Wang, Liguo Jian, Hao Tang, Lixin Rao, Ke Chen, Zhen Jia, Wanjun Zhang, Yiran Liu, Xu Chen, Xiwen Shen, Chuanyu Gao, Shuai Wang, Muwei Li
Journal: Theranostics (2020)

Aims: The N6-methyladenosine (m6A) modification plays an important role in various biological processes, but its role in atherosclerosis remains unknown. The aim of this study was to investigate the role and mechanism of m6A modification in endothelial cell inflammation and its influence on atherosclerosis development. Methods: We constructed a stable TNF-α-induced endothelial cell inflammation model and assessed the changes in the expression of m6A modification-related proteins to identify the major factors involved in this process. The m6A-modified mRNAs were identified by methylated RNA immunoprecipitation (RIP) sequencing and forkhead box O1 (FOXO1) was selected as a potential target. Through cytological experiments, we verified whether methyltransferase-like 14 (METTL14) regulates FOXO1 expression by regulating m6A-dependent mRNA and protein interaction. The effect of METTL14 on atherosclerosis development in vivo was verified using METTL14 knockout mice. Results: These findings confirmed that METTL14 plays major roles in TNF-α-induced endothelial cell inflammation. During endothelial inflammation, m6A modification of FOXO1, an important transcription factor, was remarkably increased. Moreover, METTL14 knockdown significantly decreased TNF-α-induced FOXO1 expression. RIP assay confirmed that METTL14 directly binds to FOXO1 mRNA, increases its m6A modification, and enhances its translation through subsequent YTH N6-methyladenosine RNA binding protein 1 recognition. Furthermore, METTL14 was shown to interact with FOXO1 and act directly on the promoter regions of VCAM-1 and ICAM-1 to promote their transcription, thus mediating endothelial cell inflammatory response. In vivo experiments showed that METTL14 gene knockout significantly reduced the development of atherosclerotic plaques. Conclusion: METTL14 promotes FOXO1 expression by enhancing its m6A modification and inducing endothelial cell inflammatory response as well as atherosclerotic plaque formation. Decreased expression of METTL14 can inhibit endothelial inflammation and atherosclerosis development. Therefore, METTL14 may serve as a potential target for the clinical treatment of atherosclerosis.
Next‐Generation Immunosequencing Reveals Pathological T‐Cell Architecture in Autoimmune Hepatitis
Authors: Christoph Schultheiß, Donjete Simnica, Edith Willscher, Anna Oberle, Lorenzo Fanchi, Nicola Bonzanni, Nils H. Wildner, Julian Schulze Zur Wiesch, Christina Weiler‐Normann, Ansgar W. Lohse, Mascha Binder
Journal: Hepatology (2020)

Background and Aims Autoimmune hepatitis (AIH) is a chronic liver disease that regularly relapses when immunosuppression is tapered. It is thought to be driven by T‐cells, whereas the etiologic impact of an apparently deregulated B lineage system, as evidenced by hypergammaglobulinemia and autoantibodies, remains elusive. We set out to investigate T and B cell repertoires supporting chronic inflammation in AIH. Approach and Results T and B cell receptor (TCR/BCR) and human leukocyte antigen (HLA) next‐generation immunosequencing were used to record immune signatures from a cohort of 60 patients with AIH and disease controls. Blood and liver B lineage immune metrics were not indicative of a dominant directional antigen selection apart from a slight skewing of IGHV ‐J genes. More importantly, we found strong AIH‐specific TRBV‐J skewing not attributable to the HLA‐DRB1 specificities of the cohort. This TCR repertoire bias was generated as a result of peripheral T cell (de)selection and persisted in disease remission. Using a clustering algorithm according to antigenic specificity, we identified liver TCR clusters that were shared between patients with AIH but were absent or deselected in patients with other liver pathologies. Conclusions Patients with AIH show profound and persisting T‐cell architectural changes that may explain high relapse rates after tapering immunosuppression. Liver T‐cell clusters shared between patients may mediate liver damage and warrant further study.
Distinct clinical and immunological features of SARS–CoV-2–induced multisystem inflammatory syndrome in children
Authors: Pui Y. Lee, Megan Day-Lewis, Lauren A. Henderson, Kevin G. Friedman, Jeffrey Lo, Jordan E. Roberts, Mindy S. Lo, Craig D. Platt, Janet Chou, Kacie J. Hoyt, Annette L. Baker, Tina M. Banzon, Margaret H. Chang, Ezra Cohen, Sarah D. de Ferranti, Audrey Dionne, Saddiq Habiballah, Olha Halyabar, Jonathan S. Hausmann, Melissa M. Hazen, Erin Janssen, Esra Meidan, Ryan W. Nelson, Alan A. Nguyen, Robert P. Sundel, Fatma Dedeoglu, Peter A. Nigrovic, Jane W. Newburger, Mary Beth F. Son
Journal: Journal of Clinical Investigation (2020)

BACKGROUND. Pediatric SARS–CoV-2 infection can be complicated by a dangerous hyperinflammatory condition termed multisystem inflammatory syndrome in children (MIS-C). The clinical and immunologic spectrum of MIS-C and its relationship to other inflammatory conditions of childhood have not been studied in detail.
Post Autologous Stem Cell Transplant Light Chain Response Is a Prognostic Marker in Multiple Myeloma Patients in PR/ VGPR after Induction Therapy
Authors: Naresh Bumma, Monica Peravali, Jayadev Mettu, Ghayathri Jeyakumar, Seongho Kim, Divaya Bhutani, Abhinav Deol, Lois Ayash, Voravit Ratanatharathorn, Joseph P. Uberti, Asif Alavi
Journal: Blood (2017)
Calculation Error in Study of Pregnant Women With COVID-19 and Maternal and Neonatal Outcomes in Spain
Authors: David Baud
Journal: JAMA (2020)

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 HomeNew OnlineCurrent IssueFor Authors Journals 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2024 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 journal
Lipids and Lipoproteins in 2020
Authors: Brian A. Ference, John J. P. Kastelein, Alberico L. Catapano
Journal: JAMA (2020)

This JAMA Insights Clinical Update reviews the central role of apolipoprotein B100 molecule (apoB)–containing lipoproteins in the development of atherosclerotic cardiovascular disease (ASCVD), with implications for patient risk assessment and choice of lipid-lowering therapy.
A tumor model of ascites fluid production: Intrahepatic injection of the rabbit with rabbit VX2 tumor cells
Authors: Bonnie L. Ross, Suzanne M. Southward, Mary Richardson, Mark W. Hatton
Journal: Cancer Research (2005)

1049  />From our previous work, approximately 15% of New Zealand White rabbits (NZW; weight range: 2.5 - 3.5 kg), that were injected intravenously with VX2 tumor cells and yielded lung tumors at 28d, accumulated an effusion in the interpleural space. This effusion contained the products and catabolic fragments of hemostasis (e.g. angiostatin, fibrin degradation products (FDPs)) that, when isolated and purified, contributed towards the net anti-angiogenic activity of VX2 effusions as shown by a chick embryo chorioallantoic membrane (CAM) assay. To study the dynamics of tumor effusion formation in vivo, a tumor model has been developed in which an increased proportion of tumor-bearing rabbits accumulate an effusion. Anesthetized NZW rabbits were subjected to a small incision into the abdominal cavity below the xiphoid cartilage. Live tumor cells, from a freshly-harvested lung or liver tumor from a donor rabbit, were injected (2-3 x 105/0.5ml saline) directly into the liver at two sites and the wound closed. After 28d, the rabbit was anesthetized; the abdominal cavity contained an extensive tumor growth associated with the liver, the omentum and the site of incision. Ascites fluid was present in 88% of female rabbits (32 ± 25 ml/rabbit; n = 8) and in 36% of male rabbits (18 ± 45 ml; n = 11). Analyses of total protein content, fibrinolytic factors and FDPs, and anti-angiogenic properties (by the CAM method) indicated that ascites fluid and pleural effusion from VX2-tumor rabbits were similar in many respects. The volume of recovered ascites fluid varied positively with the tumor burden of the liver, whereas the concentration of live VX2 cells/ml of ascites fluid was independent of tumor burden. This rabbit VX2-tumor liver model will be used to study the dynamics of ascites fluid production in the tumor-burdened rabbit, and to investigate more about the changing contents of malignant effusions as tumor growth progresses in vivo.
Markers of Myocardial Stress, Myocardial Injury, and Subclinical Inflammation and the Risk of Sudden Death
Authors: Brendan M. Everett, M.V. Moorthy, Jani T. Tikkanen, Nancy R. Cook, Christine M. Albert
Journal: Circulation (2020)

Background: The majority of sudden cardiac deaths (SCDs) occur in low-risk populations often as the first manifestation of cardiovascular disease (CVD). Biomarkers are screening tools that may identify subclinical cardiovascular disease and those at elevated risk for SCD. We aimed to determine whether the total to high-density lipoprotein cholesterol ratio, high-sensitivity cardiac troponin I, NT-proBNP (N-terminal pro-B-type natriuretic peptide), or high-sensitivity C-reactive protein individually or in combination could identify individuals at higher SCD risk in large, free-living populations with and without cardiovascular disease. Methods: We performed a nested case-control study within 6 prospective cohort studies using 565 SCD cases matched to 1090 controls (1:2) by age, sex, ethnicity, smoking status, and presence of cardiovascular disease. Results: The median study follow-up time until SCD was 11.3 years. When examined as quartiles or continuous variables in conditional logistic regression models, each of the biomarkers was significantly and independently associated with SCD risk after mutually controlling for cardiac risk factors and other biomarkers. The mutually adjusted odds ratios for the top compared with the bottom quartile were 1.90 (95% CI, 1.30–2.76) for total to high-density lipoprotein cholesterol ratio, 2.59 (95% CI, 1.76–3.83) for high-sensitivity cardiac troponin I, 1.65 (95% CI, 1.12–2.44) for NT-proBNP, and 1.65 (95% CI, 1.13–2.41) for high-sensitivity C-reactive protein. A biomarker score that awarded 1 point when the concentration of any of those 4 biomarkers was in the top quartile (score range, 0–4) was strongly associated with SCD, with an adjusted odds ratio of 1.56 (95% CI, 1.37–1.77) per 1-unit increase in the score. Conclusions: Widely available measures of lipids, subclinical myocardial injury, myocardial strain, and vascular inflammation show significant independent associations with SCD risk in apparently low-risk populations. In combination, these measures may have utility to identify individuals at risk for SCD.