tbuckley/cabot-search huggingface dataset:
2022 American College of Rheumatology/European Alliance of Associations for Rheumatology Classification Criteria for Microscopic Polyangiitis
Authors: Ravi Suppiah, Joanna C. Robson, Peter C. Grayson, Cristina Ponte, Anthea Craven, Sara Khalid, Andrew Judge, Andrew Hutchings, Peter A. Merkel, Raashid A. Luqmani, Richard A. Watts
Journal: Arthritis & Rheumatology (2022)

Objective To develop and validate classification criteria for microscopic polyangiitis (MPA). Methods Patients with vasculitis or comparator diseases were recruited into an international cohort. The study proceeded in 5 phases: 1) identification of candidate items using consensus methodology, 2) prospective collection of candidate items present at the time of diagnosis, 3) data‐driven reduction of the number of candidate items, 4) expert panel review of cases to define the reference diagnosis, and 5) derivation of a points‐based risk score for disease classification in a development set using least absolute shrinkage and selection operator logistic regression, with subsequent validation of performance characteristics in an independent set of cases and comparators. Results The development set for MPA consisted of 149 cases of MPA and 408 comparators. The validation set consisted of an additional 142 cases of MPA and 414 comparators. From 91 candidate items, regression analysis identified 10 items for MPA, 6 of which were retained. The final criteria and their weights were as follows: perinuclear antineutrophil cytoplasmic antibody (ANCA) or anti–myeloperoxidase‐ANCA positivity (+6), pauci‐immune glomerulonephritis (+3), lung fibrosis or interstitial lung disease (+3), sino‐nasal symptoms or signs (−3), cytoplasmic ANCA or anti–proteinase 3 ANCA positivity (−1), and eosinophil count ≥1 × 10 9 /liter (−4). After excluding mimics of vasculitis, a patient with a diagnosis of small‐ or medium‐vessel vasculitis could be classified as having MPA with a cumulative score of ≥5 points. When these criteria were tested in the validation data set, the sensitivity was 91% (95% confidence interval [95% CI] 85–95%) and the specificity was 94% (95% CI 92–96%). Conclusion The 2022 American College of Rheumatology/European Alliance of Associations for Rheumatology classification criteria for MPA are now validated for use in clinical research.
Transdermal nicotine for smoking cessation. Six-month results from two multicenter controlled clinical trials. Transdermal Nicotine Study Group
Authors: Arden Christen, Bradley Beiswanger, Melissa Mau, Cheryl Walker, Dorothy Hatsukami, Sharon Allen, Marguerite Huber, Joni Jensen, Stephen Rennard, David Daughton, Ronald Cheney, Kathleen Hatlelid, Austin Thompson, Edward Lichtenstein, Anthony Biglan, Linda Ochs, Scott Heatley, Lawrence Repsher, William Schones, Dara Stlllman, Cheryl Casey, Bonnie Poole, Jennifer Leitch, Stephen Fortmann, Joel Killen, Mark Hansen, L. Rasenick Douss, John Hughes, William Valliere, Laura Solomon, William Wadland, Elbert Glover, Penny Glover, Donna Causey, Mark Knowles, Katherine Voss-Roberts, Della Prather, Nancy Trunnell, Diane Moos, Clyde Rolf, Robert Nowak, Phillip Ackerman, Neil Malone
Journal: JAMA (1991)

<h3>Objective.</h3> —To evaluate the efficacy of a new transdermal nicotine system for smoking cessation. <h3>Design.</h3> —Two 6-week, randomized, double-blind, placebo-controlled, parallel group trials were conducted. Successful abstainers from both trials enrolled in a third trial for blinded downtitration from medications (6 weeks) and subsequent off-drug follow-up (12 weeks). <h3>Setting.</h3> —Nine outpatient clinics specializing in the treatment of smoking cessation. <h3>Patients.</h3> —Healthy volunteers who smoked one or more packs of cigarettes daily and wanted to participate in a smoking cessation program. <h3>Intervention.</h3> —Patients were randomly assigned to a transdermal nicotine system delivering nicotine at rates of 21,14, or 7 mg (in trial 1 only) over 24 hours or to placebo. Group counseling sessions were provided to all participants. <h3>Main Outcome Measure.</h3> —Rates of continuous smoking abstinence were determined during 6 weeks of full-dose treatment, a 6-week weaning period (through week 12), and a 3-month follow-up receiving no therapy (through week 24). Abstinence was defined by patient diary reports of no smoking during the designated periods, confirmed by expired-breath carbon monoxide levels of 8 ppm or lower. <h3>Results.</h3> —The centers enrolled 935 patients. Cessation rates during the last 4 weeks of the two 6-week trials (pooled data) were 61%, 48%, and 27% for 21-and 14-mg transdermal nicotine and placebo, respectively (<i>P</i>≤.001 for each active treatment vs placebo). Six-month abstinence rates for 21-mg transdermal nicotine and placebo were 26% and 12%, respectively (<i>P</i>≤.001). All transdermal nicotine doses significantly decreased the severity of nicotine withdrawal symptoms and significantly reduced cigarette use by patients who did not stop smoking. Compliance was excellent, and no serious systemic adverse effects were reported. <h3>Conclusions.</h3> —Transdermal nicotine systems show considerable promise as an aid to smoking cessation. (<i>JAMA</i>. 1991;266:3133-3138)
Adverse Events of Immune Checkpoint Inhibitors Therapy for Urologic Cancer Patients in Clinical Trials: A Collaborative Systematic Review and Meta-analysis
Authors: Zhenjie Wu, Qi Chen, Le Qu, Mingmin Li, Linhui Wang, Maria C. Mir, Umberto Carbonara, Savio D. Pandolfo, Peter C. Black, Asit K Paul, Giuseppe Di Lorenzo, Francesco Porpiglia, Andrea Mari, Andrea Necchi, Morgan Rouprêt, Sarah P. Psutka, Riccardo Autorino
Journal: European Urology (2022)

Therapies based on immune checkpoint inhibitors (ICIs) are transforming the treatment landscape of urologic oncology. Nevertheless, an exhaustive overview of the toxicity spectrum of these novel therapies has yet to be provided.To comprehensively investigate the incidence and profile of ICI therapy-related adverse events (AEs) across urologic cancers.We searched for all clinical trials investigating the role of ICI therapy published between January 2010 and September 2021. Studies involving urologic cancers with reported overall incidence or tabulated data of treatment-related AEs (trAEs) or immune-related AEs (irAEs) were included. A systematic review and meta-analysis was performed after protocol registration in PROSPERO (CRD42021276435).We identified 2638 records, of which 92 studies (including 22942 participants) met the inclusion criteria. The pooled overall incidence was 81.6% (95% confidence interval [CI] 78.0-84.7) for any-grade trAEs and 29.3% (95% CI 24.9-34.1) for grade ≥3 trAEs. The pooled overall incidence was 34.3% (95% CI 28.5-40.7) for any-grade irAEs and 10.2% (95%CI 8.2-12.7) for grade ≥3 irAEs. On a multivariable analysis, cancer type, therapy combination, clinical settings (perioperative vs advanced/metastatic), and drug exposure were independently associated with the occurrence of trAEs or irAEs. The overall rate of treatment-related mortality was 0.94% (140 of 14 899 participants), with pneumonitis (9.3%), pneumonia (7.9%), and respiratory failure (7.1%) being the most common causes. Immune-related mortality occurred in 0.26% (28 of 10 723) patients, with pneumonitis (35.7%), hepatic failure (10.7%), and hepatitis (7.1%) being most common.Our study provides a comprehensive overview of ICI-associated AEs in urologic cancer patients. The spectrum and incidence of AEs vary across cancer types, ICI types, clinical settings, and therapy combinations. These findings provide important guidance to clinicians in counseling and management of patients with urologic cancers.A high proportion of patients experience immune checkpoint inhibitor-associated toxicity. Physician and patient education is critical for early recognition and proper management.
Correction in Article Information
Journal: JAMA Network Open (2022)

Alexander R. Zheutlin, MD, MS; Favel L. Mondesir, PhD, MSPH; Catherine G. Derington, PharmD, MS; Jordan B. King, PharmD, MS; Chong Zhang, MS; Jordana B. Cohen, MD, MSCE; Dan R. Berlowitz, MD, MPH; D. Edmund Anstey, MD, MPH; William C. Cushman, MD; Tom H. Greene, PhD; Olugbenga Ogedegbe, MD, MPH; Adam P. Bress, PharmD, MS
TCTAP A-028 Procedural and 1-year Outcomes Following Large Vessel Coronary Artery Perforation Treated by Covered Stents Implantation: Multicenter CRACK Registry
Authors: Wojciech Wańha, Rafał Januszek, Łukasz Kuźma, Tomasz Figatowski, Michalina Kołodziejczak, Magdalena Żak, Malwina Smolarek, Monika Monika Gruz-Kwapisz, Maciej Wybraniec, Mateusz Tajstra, Brunon Tomasiewicz, Andrzej Łoś, Dariusz Jagielak, Tomasz Roleder, Adrian Wlodarczak, Jakub Kulczycki, Damian Hudziak, Pawel Stachowiak, Krzysztof Reczuch, Miłosz Jaguszewski, Sławomir Dobrzycki, Grzegorz Smolka, Stanisław Bartuś, Andrzej Ochala, Mariusz Gąsior, Wojciech Wojakowski
Journal: Journal of the American College of Cardiology (2021)
Predictive coding of natural images by V1 firing rates and rhythmic synchronization
Authors: Cem Uran, Alina Peter, Andreea Lazar, William Barnes, Johanna Klon-Lipok, Katharine A. Shapcott, Rasmus Roese, Pascal Fries, Wolf Singer, Martin Vinck
Journal: Neuron (2022)

Predictive coding is an important candidate theory of self-supervised learning in the brain. Its central idea is that sensory responses result from comparisons between bottom-up inputs and contextual predictions, a process in which rates and synchronization may play distinct roles. We recorded from awake macaque V1 and developed a technique to quantify stimulus predictability for natural images based on self-supervised, generative neural networks. We find that neuronal firing rates were mainly modulated by the contextual predictability of higher-order image features, which correlated strongly with human perceptual similarity judgments. By contrast, V1 gamma (γ)-synchronization increased monotonically with the contextual predictability of low-level image features and emerged exclusively for larger stimuli. Consequently, γ-synchronization was induced by natural images that are highly compressible and low-dimensional. Natural stimuli with low predictability induced prominent, late-onset beta (β)-synchronization, likely reflecting cortical feedback. Our findings reveal distinct roles of synchronization and firing rates in the predictive coding of natural images.
Lack of Reliability of a Single Peripheral Blood Eosinophil Count as Biomarker for High Th2 Asthma
Authors: Ruchi Patel, Brian Patchett, Granit Mavraj, Bede Nriagu, Edward Schulman
Journal: Journal of Allergy and Clinical Immunology (2022)

A peripheral blood eosinophil count (PBEC) of 300 cells/μl is regarded as a major marker of the high Th2 (HTh2) asthma subtype. We hypothesized that analyzing the stability of PBECs over multiple years would demonstrate limitations of a single PBEC ≤ or ≥ 300 cells/μl as a predictable marker of Th2 status. A retrospective chart review was conducted of severe asthma patients seen at the Drexel Severe Asthma Clinic. We included 116 patients having at least 5 yearly PBECs (mean = 9.8 PBECs over 7.1 years). For each patient, individual counts were compared to mean PBECs over multiple yearly repeats. To assess predictability of PBECs, the following measurements of validity were taken: sensitivity, specificity, false discovery rate, false omission rate, false negative rate, false positive rate, predictive values, and likelihood ratios. The sensitivity of a single PBEC of ≥ 300 cells/μl in classifying HTh2 compared to a mean ≥ 300 cells/μl was 46.7%, while the specificity was 96.1%. The false discovery rate was 26.1%; false omission rate was 11.7%; false negative rate was 53.3%; false positive rate was 3.9%; positive predictive value was 73.9%; negative predictive value was 88.3%; positive likelihood ratio was 11.9; negative likelihood ratio was 0.6. In a severe asthma patient, a single PBEC of ≥ 300 cells/μl may inaccurately represent the mean over multiple years, and may mislead clinicians to prescribe expensive and potentially inappropriate biologic treatments for “high Th2” asthma.
MUC1 deficiency induces the nasal epithelial barrier dysfunction <i>via</i> RBFOX3 shortage augment ubiquitin–proteasomal degradation in allergic rhinitis pathogenesis
Authors: Chunyi Zhang, Yiyan Wang, Wenjing Liao, Tianhao Liang, Weixing Liu, Junyang Xie, Xiaofen Wang, Pingchang Yang, Wenju Lu, Xiaowen Zhang
Journal: Allergy (2022)

All authors declare that there is no competing interest in relation to this work. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Neurological associations of COVID-19
Authors: Mark A Ellul, Laura Benjamin, Bhagteshwar Singh, Suzannah Lant, Benedict Daniel Michael, Ava Easton, Rachel Kneen, Sylviane Defres, Jim Sejvar, Tom Solomon
Journal: The Lancet Neurology (2020)

SummaryBackgroundThe COVID-19 pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is of a scale not seen since the 1918 influenza pandemic. Although the predominant clinical presentation is with respiratory disease, neurological manifestations are being recognised increasingly. On the basis of knowledge of other coronaviruses, especially those that caused the severe acute respiratory syndrome and Middle East respiratory syndrome epidemics, cases of CNS and peripheral nervous system disease caused by SARS-CoV-2 might be expected to be rare.Recent developmentsA growing number of case reports and series describe a wide array of neurological manifestations in 901 patients, but many have insufficient detail, reflecting the challenge of studying such patients. Encephalopathy has been reported for 93 patients in total, including 16 (7%) of 214 hospitalised patients with COVID-19 in Wuhan, China, and 40 (69%) of 58 patients in intensive care with COVID-19 in France. Encephalitis has been described in eight patients to date, and Guillain-Barré syndrome in 19 patients. SARS-CoV-2 has been detected in the CSF of some patients. Anosmia and ageusia are common, and can occur in the absence of other clinical features. Unexpectedly, acute cerebrovascular disease is also emerging as an important complication, with cohort studies reporting stroke in 2–6% of patients hospitalised with COVID-19. So far, 96 patients with stroke have been described, who frequently had vascular events in the context of a pro-inflammatory hypercoagulable state with elevated C-reactive protein, D-dimer, and ferritin.Where next?Careful clinical, diagnostic, and epidemiological studies are needed to help define the manifestations and burden of neurological disease caused by SARS-CoV-2. Precise case definitions must be used to distinguish non-specific complications of severe disease (eg, hypoxic encephalopathy and critical care neuropathy) from those caused directly or indirectly by the virus, including infectious, para-infectious, and post-infectious encephalitis, hypercoagulable states leading to stroke, and acute neuropathies such as Guillain-Barré syndrome. Recognition of neurological disease associated with SARS-CoV-2 in patients whose respiratory infection is mild or asymptomatic might prove challenging, especially if the primary COVID-19 illness occurred weeks earlier. The proportion of infections leading to neurological disease will probably remain small. However, these patients might be left with severe neurological sequelae. With so many people infected, the overall number of neurological patients, and their associated health burden and social and economic costs might be large. Health-care planners and policy makers must prepare for this eventuality, while the many ongoing studies investigating neurological associations increase our knowledge base.
Loco-regional radiosensitizing nanoparticles-in-gel augments head and neck cancer chemoradiotherapy
Authors: Prateek Bhardwaj, Vikram Gota, Komal Vishwakarma, Venkatesh Pai, Pradip Chaudhari, Bhabani Mohanty, Rahul Thorat, Subhash Yadav, Murari Gurjar, Jayant Sastri Goda, Rinti Banerjee
Journal: Journal of Controlled Release (2022)
Long-Term Efficacy of Dupilumab in Quadrants of Elevated- vs Low- Type 2 Biomarker Patients With Uncontrolled, Moderate-to-Severe Asthma: LIBERTY ASTHMA TRAVERSE
Authors: Michael Wechsler, Ian Pavord, Alberto Papi, Kenneth Chapman, Xuezhou Mao, Benjamin Ortiz, Michel Djandji, Juby Jacob-Nara, Paul Rowe, Yamo Deniz, Elizabeth Laws, Bolanle Akinlade, Nikhil Amin, David Lederer, Megan Hardin
Journal: Journal of Allergy and Clinical Immunology (2022)
Cortisol Absorption in Man
Journal: JAMA (1963)

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 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) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Amyloidosis
Authors: Mark B. Pepys
Journal: Annual Review of Medicine (2005)

Amyloidosis is a clinical disorder caused by extracellular deposition of insoluble abnormal fibrils, derived from aggregation of misfolded, normally soluble, protein. About 23 different unrelated proteins are known to form amyloid fibrils in vivo, which share a pathognomonic structure although they are associated with clinically distinct conditions. Systemic amyloidosis, with amyloid deposits in the viscera, blood vessel walls, and connective tissue, is usually fatal and is the cause of about one per thousand deaths in developed countries. This rarity and the variable involvement of different organs and tissues are often responsible for missed or delayed diagnosis, and amyloidosis remains a considerable clinical challenge. However, recent elucidation of important aspects of pathogenesis, as well as developments in diagnosis, monitoring, and treatment, have greatly improved outcomes, especially when patients are managed in specialist centers.
Ueber Feuerbestattung.
Journal: JAMA (1890)

In this small monograph we have a critical review of the subject of cremation from a hygienic as well as historical standpoint. The author first considers the various methods of disposing of the dead: mummification, embalming, and various other methods of preserving bodies, as well as earth burial, and their rapid destruction by chemical means. Then follows a lengthy review of cremation in ancient times, as well as its progress of late years in different parts of the world. The volume closes with an excellent chronological list of the publications relating to cremation. It has been said that "comparisons are odious," and it would be invidious to say aught against this work, especially as it has been written with a charitable object; as we are informed on the title page the net receipts of the sale of the work are to be devoted to maintaining the vacation colony for poor
P1.07-010 Peripheral Blood Biomarkers Associated with Clinical Outcome in Non–Small Cell Lung Cancer Patients Treated with Nivolumab
Authors: J. Tanizaki, K. Haratani, H. Hayashi, Y. Chiba, K. Yonesaka, K. Kudo, H. Kaneda, Y. Hasegawa, K. Tanaka, M. Takeda, K. Nakagawa
Journal: Journal of Thoracic Oncology (2017)
Overexpression of wild type RRAS2, without oncogenic mutations, drives chronic lymphocytic leukemia
Authors: Alejandro M. Hortal, Clara L. Oeste, Claudia Cifuentes, Miguel Alcoceba, Isabel Fernández-Pisonero, Laura Clavaín, Rut Tercero, Pilar Mendoza, Verónica Domínguez, Marta García-Flores, Belén Pintado, David Abia, Carmen García-Macías, Almudena Navarro-Bailón, Xosé R. Bustelo, Marcos González, Balbino Alarcón
Journal: Molecular Cancer (2022)

Chronic lymphocytic leukemia (CLL) is the most frequent, and still incurable, form of leukemia in the Western World. It is widely accepted that cancer results from an evolutionary process shaped by the acquisition of driver mutations which confer selective growth advantage to cells that harbor them. Clear examples are missense mutations in classic RAS genes (KRAS, HRAS and NRAS) that underlie the development of approximately 13% of human cancers. Although autonomous B cell antigen receptor (BCR) signaling is involved and mutations in many tumor suppressor genes and oncogenes have been identified, an oncogenic driver gene has not still been identified for CLL.Conditional knock-in mice were generated to overexpress wild type RRAS2 and prove its driver role. RT-qPCR analysis of a human CLL sample cohort was carried out to measure RRAS2 transcriptional expression. Sanger DNA sequencing was used to identify a SNP in the 3'UTR region of RRAS2 in human CLL samples. RNAseq of murine CLL was carried out to identify activated pathways, molecular mechanisms and to pinpoint somatic mutations accompanying RRAS2 overexpression. Flow cytometry was used for phenotypic characterization and shRNA techniques to knockdown RRAS2 expression in human CLL.RRAS2 mRNA is found overexpressed in its wild type form in 82% of the human CLL samples analyzed (n = 178, mean and median = 5-fold) as well as in the explored metadata. A single nucleotide polymorphism (rs8570) in the 3'UTR of the RRAS2 mRNA has been identified in CLL patients, linking higher expression of RRAS2 with more aggressive disease. Deliberate overexpression of wild type RRAS2 in mice, but not an oncogenic Q72L mutation in the coding sequence, provokes the development of CLL. Overexpression of wild type RRAS2 in mice is accompanied by a strong convergent selection of somatic mutations in genes that have been identified in human CLL. R-RAS2 protein is physically bound to the BCR and mediates BCR signals in CLL.The results indicate that overexpression of wild type RRAS2 is behind the development of CLL.