tbuckley/cabot-search huggingface dataset:
Call for emergency action to limit global temperature increases, restore biodiversity, and protect health
Authors: Lukoye Atwoli, Abdullah H. Baqui, Thomas Benfield, Raffaella Bosurgi, Fiona Godlee, Stephen Hancocks, Richard Horton, Laurie Laybourn-Langton, Carlos Augusto Monteiro, Ian Norman, Kirsten Patrick, Nigel Praities, Marcel GM Olde Rikkert, Eric J. Rubin, Peush Sahni, Richard Smith, Nick Talley, Sue Turale, Damián Vázquez
Journal: PLoS Medicine (2021)

> Wealthy nations must do much more, much faster.

The United Nations General Assembly in September 2021 will bring countries together at a critical time for marshalling collective action to tackle the global environmental crisis. They will meet again at the biodiversity summit in Kunming, China, and the climate conference (Conference of the Parties (COP)26) in Glasgow, UK. Ahead of these pivotal meetings, we—the editors of health journals worldwide—call for urgent action to keep average global temperature increases below 1.5°C, halt the destruction of nature and protect health.

Health is already being harmed by global temperature increases and the destruction of the natural world, a state of affairs health professionals have been bringing attention to for decades.1 The science is unequivocal; a global increase of 1.5°C above the preindustrial average and the continued loss of biodiversity risk catastrophic harm to health that will be impossible to reverse.2 3 Despite the world’s necessary preoccupation with COVID-19, we cannot wait for the pandemic to pass to rapidly reduce emissions.

Reflecting the severity of the moment, this editorial appears in health journals across the world. We are united in recognising that only fundamental and equitable changes to societies will reverse our current trajectory.

The risks to health of increases above 1.5°C are now well established.2 Indeed, no temperature rise is ‘safe’. In the past 20 years, heat-related mortality among people aged over 65 has increased by more than 50%.4 Higher temperatures have brought increased dehydration and renal function loss, dermatological malignancies, tropical infections, adverse mental health outcomes, pregnancy complications, allergies, and cardiovascular and pulmonary morbidity and mortality.5 6 Harms disproportionately affect the most vulnerable, including children, older populations, ethnic minorities, poorer communities and those with underlying health problems.2 4 

Global heating is also contributing to the decline in …
Initiation of migraine-related cortical spreading depolarization by hyperactivity of GABAergic neurons and NaV1.1 channels
Authors: Oana Chever, Sarah Zerimech, Paolo Scalmani, Louisiane Lemaire, Lara Pizzamiglio, Alexandre Loucif, Marion Ayrault, Martin Krupa, Mathieu Desroches, Fabrice Duprat, Isabelle Léna, Sandrine Cestèle, Massimo Mantegazza
Journal: Journal of Clinical Investigation (2021)

Spreading depolarizations (SDs) are involved in migraine, epilepsy, stroke, traumatic brain injury, and subarachnoid hemorrhage. However, the cellular origin and specific differential mechanisms are not clear. Increased glutamatergic activity is thought to be the key factor for generating cortical spreading depression (CSD), a pathological mechanism of migraine. Here, we show that acute pharmacological activation of NaV1.1 (the main Na+ channel of interneurons) or optogenetic-induced hyperactivity of GABAergic interneurons is sufficient to ignite CSD in the neocortex by spiking-generated extracellular K+ build-up. Neither GABAergic nor glutamatergic synaptic transmission were required for CSD initiation. CSD was not generated in other brain areas, suggesting that this is a neocortex-specific mechanism of CSD initiation. Gain-of-function mutations of NaV1.1 (SCN1A) cause familial hemiplegic migraine type-3 (FHM3), a subtype of migraine with aura, of which CSD is the neurophysiological correlate. Our results provide the mechanism linking NaV1.1 gain of function to CSD generation in FHM3. Thus, we reveal the key role of hyperactivity of GABAergic interneurons in a mechanism of CSD initiation, which is relevant as a pathological mechanism of Nav1.1 FHM3 mutations, and possibly also for other types of migraine and diseases in which SDs are involved.
Early treatment of COVID-19 with anakinra guided by soluble urokinase plasminogen receptor plasma levels: a double-blind, randomized controlled phase 3 trial
Authors: Evdoxia Kyriazopoulou, Garyfallia Poulakou, Haralampos Milionis, Simeon Metallidis, Georgios Adamis, Konstantinos Tsiakos, Archontoula Fragkou, Aggeliki Rapti, Christina Damoulari, Massimo Fantoni, Ioannis Kalomenidis, Georgios Chrysos, Andrea Angheben, Ilias Kainis, Zoi Alexiou, Francesco Castelli, Francesco Saverio Serino, Maria Tsilika, Petros Bakakos, Emanuele Nicastri, Vassiliki Tzavara, Evangelos Kostis, Lorenzo Dagna, Panagiotis Koufargyris, Katerina Dimakou, Spyridon Savvanis, Glykeria Tzatzagou, Maria Chini, Giulio Cavalli, Matteo Bassetti, Konstantina Katrini, Vasileios Kotsis, George Tsoukalas, Carlo Selmi, Ioannis Bliziotis, Michael Samarkos, Michael Doumas, Sofia Ktena, Aikaterini Masgala, Ilias Papanikolaou, Maria Kosmidou, Dimitra-Melia Myrodia, Aikaterini Argyraki, Chiara Simona Cardellino, Katerina Koliakou, Eleni-Ioanna Katsigianni, Vassiliki Rapti, Efthymia Giannitsioti, Antonella Cingolani, Styliani Micha, Karolina Akinosoglou, Orestis Liatsis-Douvitsas, Styliani Symbardi, Nikolaos Gatselis, Maria Mouktaroudi, Giuseppe Ippolito, Eleni Florou, Antigone Kotsaki, Mihai G. Netea, Jesper Eugen-Olsen, Miltiades Kyprianou, Periklis Panagopoulos, George N. Dalekos, Evangelos J. Giamarellos-Bourboulis
Journal: Nature Medicine (2021)

Abstract Early increase of soluble urokinase plasminogen activator receptor (suPAR) serum levels is indicative of increased risk of progression of coronavirus disease 2019 (COVID-19) to respiratory failure. The SAVE-MORE double-blind, randomized controlled trial evaluated the efficacy and safety of anakinra, an IL-1α/β inhibitor, in 594 patients with COVID-19 at risk of progressing to respiratory failure as identified by plasma suPAR ≥6 ng ml −1 , 85.9% ( n = 510) of whom were receiving dexamethasone. At day 28, the adjusted proportional odds of having a worse clinical status (assessed by the 11-point World Health Organization Clinical Progression Scale (WHO-CPS)) with anakinra, as compared to placebo, was 0.36 (95% confidence interval 0.26–0.50). The median WHO-CPS decrease on day 28 from baseline in the placebo and anakinra groups was 3 and 4 points, respectively (odds ratio (OR) = 0.40, P &lt; 0.0001); the respective median decrease of Sequential Organ Failure Assessment (SOFA) score on day 7 from baseline was 0 and 1 points (OR = 0.63, P = 0.004). Twenty-eight-day mortality decreased (hazard ratio = 0.45, P = 0.045), and hospital stay was shorter.
Information Blocking and Oncology
Authors: Najeff Waseem, Sheetal Kircher, Josephine L. Feliciano
Journal: JAMA Oncology (2021)

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 Oncology 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 Oncology journal
Simulation of Ventilator Allocation in Critically Ill Patients with COVID-19
Authors: Sivasubramanium V. Bhavani, Yuan Luo, William D. Miller, Lazaro N. Sanchez-Pinto, Xuan Han, Chengsheng Mao, Burhaneddin Sandıkçı, Monica E. Peek, Craig M. Coopersmith, Kelly N. Michelson, William F. Parker
Journal: American Journal of Respiratory and Critical Care Medicine (2021)
Temporal trends in emergency admissions for diabetic ketoacidosis in people with diabetes in England before and during the COVID-19 pandemic: a population-based study
Authors: Shivani Misra, Emma Barron, Eszter Vamos, Stephen Thomas, Ketan Dhatariya, Partha Kar, Bob Young, Kamlesh Khunti, Jonathan Valabhji
Journal: The Lancet Diabetes & Endocrinology (2021)
Publisher Correction: JunB is a key regulator of multiple myeloma bone marrow angiogenesis
Authors: Fengjuan Fan, Stefano Malvestiti, Sonia Vallet, Judith Lind, Jose Manuel Garcia-Manteiga, Eugenio Morelli, Qinyue Jiang, Anja Seckinger, Dirk Hose, Hartmut Goldschmidt, Andreas Stadlbauer, Chunyan Sun, Heng Mei, Martin Pecherstorfer, Latifa Bakiri, Erwin F. Wagner, Giovanni Tonon, Martin Sattler, Yu Hu, Pierfrancesco Tassone, Dirk Jaeger, Klaus Podar
Journal: Leukemia (2021)
Association of Local Therapy With Quality-of-Life Outcomes in Young Women With Breast Cancer
Authors: Laura Dominici, Jiani Hu, Yue Zheng, Hee Jeong Kim, Tari A. King, Kathryn J. Ruddy, Rulla M. Tamimi, Jeffrey Peppercorn, Lidia Schapira, Virginia F. Borges, Steven E. Come, Ellen Warner, Julia S. Wong, Ann H. Partridge, Shoshana M. Rosenberg
Journal: JAMA Surgery (2021)

Increasing rates of bilateral mastectomy have been most pronounced in young women with breast cancer, but the association of surgery with long-term quality of life (QOL) remains largely unknown.To examine the association of surgery with longer-term satisfaction and QOL in young breast cancer survivors.This multicenter cross-sectional study of a prospective cohort was conducted from October 2016 to November 2017, at academic and community hospitals in North America. Women 40 years or younger enrolled in the Young Women's Breast Cancer Study were assessed. Data analysis was performed from during a 1- to 2-year period after conclusion of the study.Primary breast surgery, reconstruction, and radiotherapy.Mean BREAST-Q breast satisfaction and physical, psychosocial, and sexual well-being scores were compared by type of surgery; higher BREAST-Q scores (range, 0-100) indicate better QOL. Linear regression was used to identify demographic and clinical factors associated with BREAST-Q scores for each domain.A total of 560 women with stage 0 to III breast cancer (median age at diagnosis, 36 years; range, 17-40 years; 484 [86%] with stage 0-II disease) completed the BREAST-Q a median of 5.8 years (range, 1.9-10.4 years) from diagnosis. A total of 290 patients (52%) of patients underwent bilateral mastectomy, 110 patients (20%) underwent unilateral mastectomy, and 160 patients (28%) received breast-conserving therapy. Among mastectomy patients, 357 (89%) had reconstruction and 181 (45%) received radiotherapy. In multivariate analyses, implant-based reconstruction (vs autologous) was associated with decreased breast satisfaction (β = -7.4; 95% CI, -12.8 to -2.1; P = .007) and complex reconstruction (vs autologous) with worse physical well-being (β = -14.0; 95% CI, -22.2 to -5.7; P < .001).These results suggest that local therapy in young breast cancer survivors is persistently associated with poorer scores in multiple QOL domains, particularly among those treated with mastectomy and radiotherapy, irrespective of breast reconstruction. Socioeconomic stressors also appear to play a role.
Regulation of Procoagulant and Fibrinolytic Activity in HL60 Cells by Granulocyte-Macrophage-Colony Stimulating Factor Is Linked to Vascular Endothelial Growth Factor mRNA and Protein Expression
Authors: F. Langer, S. Loges, B. Eifrig, D. K. Hossfeld, W. Fiedler
Journal: Blood (2002)
Small extrachromosomal circular DNA (eccDNA): major functions in evolution and cancer
Authors: Xiaoxuan Ling, Yali Han, Jinxue Meng, Bohuan Zhong, Jialong Chen, He Zhang, Jiheng Qin, Jing Pang, Linhua Liu
Journal: Molecular Cancer (2021)

Abstract Extrachromosomal circular DNA (eccDNA) refers to a type of circular DNA that originate from but are likely independent of chromosomes. Due to technological advancements, eccDNAs have recently emerged as multifunctional molecules with numerous characteristics. The unique topological structure and genetic characteristics of eccDNAs shed new light on the monitoring, early diagnosis, treatment, and prediction of cancer. EccDNAs are commonly observed in both normal and cancer cells and function via different mechanisms in the stress response to exogenous and endogenous stimuli, aging, and carcinogenesis and in drug resistance during cancer treatment. The structural diversity of eccDNAs contributes to the function and numerical diversity of eccDNAs and thereby endows eccDNAs with powerful roles in evolution and in cancer initiation and progression by driving genetic plasticity and heterogeneity from extrachromosomal sites, which has been an ignored function in evolution in recent decades. EccDNAs show great potential in cancer, and we summarize the features, biogenesis, evaluated functions, functional mechanisms, related methods, and clinical utility of eccDNAs with a focus on their role in evolution and cancer.
Non-invasive diagnosis of Pneumocystis jirovecii pneumonia: a systematic review and meta-analysis
Authors: Julien Senécal, Elizabeth Smyth, Olivier Del Corpo, Jimmy M. Hsu, Alexandre Amar-Zifkin, Amy Bergeron, Matthew P. Cheng, Guillaume Butler-Laporte, Emily G. McDonald, Todd C. Lee
Journal: Clinical Microbiology and Infection (2021)
Identification of Allobaculum mucolyticum as a novel human intestinal mucin degrader
Authors: Guus H. van Muijlwijk, Guido van Mierlo, Pascal W.T.C. Jansen, Michiel Vermeulen, Nancy M.C. Bleumink-Pluym, Noah W. Palm, Jos P.M. van Putten, Marcel R. de Zoete
Journal: Gut Microbes (2021)

The human gut microbiota plays a central role in intestinal health and disease. Yet, many of its bacterial constituents are functionally still largely unexplored. A crucial prerequisite for bacterial survival and proliferation is the creation and/or exploitation of an own niche. For many bacterial species that are linked to human disease, the inner mucus layer was found to be an important niche. Allobaculum mucolyticum is a newly identified, IBD-associated species that is thought be closely associated with the host epithelium. To explore how this bacterium is able to effectively colonize this niche, we screened its genome for factors that may contribute to mucosal colonization. Up to 60 genes encoding putative Carbohydrate Active Enzymes (CAZymes) were identified in the genome of A. mucolyticum. Mass spectrometry revealed 49 CAZymes of which 26 were significantly enriched in its secretome. Functional assays demonstrated the presence of CAZyme activity in A. mucolyticum conditioned medium, degradation of human mucin O-glycans, and utilization of liberated non-terminal monosaccharides for bacterial growth. The results support a model in which sialidases and fucosidases remove terminal O-glycan sugars enabling subsequent degradation and utilization of carbohydrates for A. mucolyticum growth. A. mucolyticum CAZyme secretion may thus facilitate bacterial colonization and degradation of the mucus layer and may pose an interesting target for future therapeutic intervention.
Nonbone Marrow CD34 <sup>+</sup> Cells Are Crucial for Endothelial Repair of Injured Artery
Authors: Liujun Jiang, Ting Chen, Shasha Sun, Ruilin Wang, Jiacheng Deng, Lingxia Lyu, Hong Wu, Mei Yang, Xiangyuan Pu, Luping Du, Qishan Chen, Yanhua Hu, Xiaosheng Hu, Yijiang Zhou, Qingbo Xu, Li Zhang
Journal: Circulation Research (2021)

[Figure: see text].
Waistline to the gumline: Relationship between obesity and periodontal disease‐biological and management considerations
Authors: Sukirth M. Ganesan, Stephanie Vazana, Sandra Stuhr
Journal: Periodontology 2000 (2021)

Abstract Obesity is a pandemic and periodontitis is the sixth most prevalent disease in the world. These two noncommunicable diseases share several risk determinants. Epidemiologic evidence from the last 2 decades has established an increase in periodontitis prevalence in obese and overweight individuals. Biologic mechanisms potentially linking obesity and periodontal disease are adiposity‐associated hyperinflammation, microbial dysbiosis, altered immune response, specific genetic polymorphisms, and increased stress. However, because of the lack of longitudinal interventional studies and randomized clinical trials, there is insufficient evidence to determine the cause‐effect relationship between these two diseases. Despite this, the negative impact of obesity on oral health is well established. Several logistic and physiologic complications are associated with treating obese patients in a dental setting, and it requires an interprofessional team approach. Oral health care professionals need to be aware of the specific management considerations while rendering for this cohort, including modified practice facility and equipment, tailored supportive periodontal therapy, and heightened precaution during conscious sedation and surgical procedures.
リアルワールドでの癌関連静脈血栓塞栓症-COMMAND VTE Registryから-
Authors: Sakamoto Jiro, Yamashita Yugo, Morimoto Takeshi, Amano Hidewo, Takase Toru, Hiramori Seiichi, Kim Kitae, Oi Maki, Akao Masaharu, Kobayashi Yohei, Toyofuku Mamoru, Izumi Toshiaki, Tada Tomohisa, Chen Po-Min, Murata Koichiro, Tsuyuki Yoshiaki, Saga Syunsuke, Nishimoto Yuji, Sasa Tomoki, Kinoshita Minako, Togi Kiyonori, Mabuchi Hiroshi, Takabayashi Kensuke, Yoshikawa Yusuke, Shiomi Hiroki, Kato Takao, Makiyama Takeru, Ono Koh, Tamura Toshihiro, Nakagawa Yoshihisa, Kimura Takeshi
Journal: Circulation (2019)
Sleep Health and Longevity—Considerations for Personalizing Existing Recommendations
Authors: Girardin Jean-Louis, Michael A. Grandner, Seithikurippu R. Pandi-Perumal
Journal: JAMA Network Open (2021)

Thomas Svensson, MD, PhD; Eiko Saito, PhD, MSc, MA; Akiko Kishi Svensson, MD, PhD; Olle Melander, MD, PhD; Marju Orho-Melander, PhD; Masaru Mimura, MD, PhD; Shafiur Rahman, MSc, MHS; Norie Sawada, MD, PhD; Woon-Puay Koh, MBBS, PhD; Xiao-Ou Shu, MPH, PhD; Ichiro Tsuji, MD, PhD; Seiki Kanemura, MD, PhD; Sue K. Park, MD, PhD, MPH; Chisato Nagata, MD, PhD; Shoichiro Tsugane, MD, PhD; Hui Cai, MD, PhD; Jian-Min Yuan, MD, PhD; Sanae Matsuyama, MS; Yumi Sugawara, PhD; Keiko Wada, MD, PhD; Keun-Young Yoo, MD, PhD; Kee Seng Chia, MBBS, MD, MSc; Paolo Boffetta, MD, MPH; Habibul Ahsan, MD, MMedSc; Wei Zheng, MD, PhD; Daehee Kang, MD, PhD; John D. Potter, MBBS, PhD; Manami Inoue, MD, PhD
Review of patient-reported outcomes in multiple myeloma registrational trials: highlighting areas for improvement
Authors: Laura L. Fernandes, Jiaxi Zhou, Bindu Kanapuru, Erica Horodniceanu, Thomas Gwise, Paul G. Kluetz, Vishal Bhatnagar
Journal: Blood Cancer Journal (2021)

Abstract Over the past 13 years, there have been advances in characterizing the patient experience in oncology trials, primarily using patient-reported outcomes (PROs). This review aims to provide details on the PRO measures and analyses used in multiple myeloma (MM) registrational trials. We identified registrational trials supporting MM indications from 2007 to 2020 from FDA databases. Trial protocols, statistical analysis plans, and clinical study reports were reviewed for PRO measures used, collection methods, statistical analyses, baseline and instrument completion definitions, and thresholds for clinical meaningfulness. Twenty-five trials supporting 20 MM indications were identified; 17 (68%) contained submitted PRO data. Of the 17 trials, 14 were randomized controlled trials and the remainder were single-arm trials. All but one trial were open label trials. Seven trials collected data electronically and five in paper format. The majority of trials evaluated at least two PRO measures (82%) with two trials (12%) utilizing four measures. Nine unique PRO measures were used, most commonly the EORTC QLQ-30 (87%), EQ-5D (65%), and QLQ-MY20 (47%). All 17 (100%) trials provided descriptive summaries, 10 (59%) carried out longitudinal mixed model analysis, 9 (53%) conducted responder analysis, and 2 (12%) did a basic inferential test. We noted substantial heterogeneity in terms of PRO collection methods, measures, definitions, and analyses, which may hinder the ability to effectively capture and interpret patient experience in future MM clinical trials. Further research is needed to determine the most appropriate approaches for statistical and analytical methodologies for PRO data in MM trials.
Functional role of sulfotransferase 2B1b in human prostate cancer.
Authors: Dongning He, Andra R. Frost, Charles N. Falany
Journal: Cancer Research (2006)

5342  Human prostate cancer development involves stimulation by several steroid hormones, sulfoconjugation of steroids in the prostate is an important inactivation mechanism. Three major steroid sulfotransferase (SULT) isoforms: SULT2A1, SULT2B1b and SULT1E1 have been reported to conjugate estrogenic and/or hydroxysteroids. Matched human tumor/normal tissue expression arrays showed that SULT2B1b but not SULT2A1, hybridized in both tumor and normal prostate samples. Although RT-PCR found high levels of SULT1E1 message in normal prostate and low levels in BPH and prostate tumor tissues, no detectable SULT1E1 protein was found in prostate tissues by immunoblot analysis. However, immunochemical analysis showed SULT2B1b is localized in the cytosol of epithelial cells of normal and prostate cancer tissues as well as human LNCaP prostate cancer cells. SULT2B1b is selective for the sulfation of 3β-hydroxysteroids such as dihydroepiandrosterone (DHEA), δ 5-androstenediol (5-Adiol) and 5α-androstan-3β-17β-diol (Astane-diol), which are the precursors for androgen or estrogen synthesis and androgen derivatives, respectively. Knock-down of SULT2B1b by short interference RNA (siRNA) resulted in a 92% decrease in SULT2B1b protein expression and a 73% decrease in DHEA sulfation by intact LNCaP cells. SiRNA inhibited and control LNCaP cells were treated with 0.1, 1, 10, 100, 1,000 and 10,000 nM steroids (DHEA, Astane-diol, 5-Adiol) for 48 hours and changes in steroid hormone receptors expression and cell proliferation were analyzed by immunoblot analysis and MTT assay, respectively. DHEA at >= 1000 nM induced androgen receptor (AR) expression in siRNA repressed LNCaP cells, but not in control cells. Instead of no effect on estrogen receptor α (ERα) expression in either cell type, DHEA caused a greater inhibition of ERβ expression in siRNA transfected cells than in control cells. DHEA elicited a greater induction of prostate specific antigen (PSA) expression in siRNA inhibited LNCaP cells than control cells. DHEA also stimulated more cell proliferation in siRNA transfected LNCaP cells. Nevertheless, control LNCaP cells treated with Astane-diol at >=100 nM showed greater proliferation than siRNA transfected cells. Astane-diol had no effect on AR or ERα expressions, however ERβ expression was induced by Astane-diol in the siRNA transfected cells. The induction of PSA expression by Astane-diol in control cells was decreased in the siRNA treated cells. Compared with normal LNCaP cells treated with 5-Adiol, proliferation of siRNA inhibited LNCaP cells was induced at concentrations >= 1nM. PSA expression in siRNA transfected LNCaP cells was also increased at levels >=100 nM although AR or ERα expression was not affected in either cell type. These results indicate that SULT2B1b has an important role in regulating the responsiveness of human prostate cancer cells to stimulation by DHEA, Astane-diol and 5-Adiol (Supported by NIH grant GM38953 to CNF).