tbuckley/cabot-search huggingface dataset:
SACREDNESS OF PROFESSIONAL CONFIDENCE.
Journal: JAMA (1897)

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
Association of Maternal Antidepressant Prescription During Pregnancy and Danish School-aged Children’s Standardized Test Scores
Authors: Alain Braillon
Journal: JAMA (2022)

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
Utilizing the autoantibody immune response to tumor antigens for kidney cancer early detection.
Authors: Christian R Hoerner, Michael Jhatro, Rebecca Waitz, Kathy Kamath, Minlu Zhang, Abhilash Dhal, John Shon, Alice C. Fan
Journal: Journal of Clinical Oncology (2022)

369 Background: Kidney cancer (renal cell carcinoma, RCC), the 8th most common U.S. cancer, is in need for better cure rates through early detection (5-year relative survival for stage I RCC: ̃95%; for stage IV RCC ̃19%). Autoantibodies are common in cancer and result from the altered expression, localization, or post-translational modification of endogenous proteins in tumor cells (autoantigens) and from the expression of mutated genes that give rise to new proteins (neoantigens). In contrast to cellular immune responses in cancer, autoantibodies are less well characterized, yet hold promise to enable cancer early detection by immune amplification of the ‘cancer signal’ while retaining specificity to cancer types including RCC. Autoantibodies may therefore be useful for kidney cancer early detection and diagnosis. Our goal was to profile the autoantibody repertoire in blood from patients with clear cell RCC (ccRCC), the most common form of RCC, in order to: 1) determine if autoantibodies can be detected in patients with early-stage and late-stage ccRCC; 2) identify common epitopes amongst ccRCC patients that could suggest common RCC antigens; and 3) determine specificity and sensitivity of potential autoantibody biomarkers for ccRCC vs. other non-cancer conditions. Methods: We use the SERA platform (https://serimmune.com/publications/) to compare putative autoantibody signal in blood from 177 patients with ccRCC, 23 with benign kidney lesions, and ̃800 healthy controls. SERA utilizes a random bacterial display 12mer peptide library of 1010 diversity in conjunction with next-generation sequencing to ascertain epitope enrichment across the entire human proteome. Results: We find significant differences in epitope repertoires in ccRCC compared to the healthy human cohort. Patients with ccRCC exhibit a rich repertoire of rare, enriched epitopes which may comprise putative autoantibody signal. This epitope signal is present with high abundance in all ccRCC stages, including stage I ccRCC. In contrast, healthy controls and patients with benign kidney lesions demonstrate more restricted repertoires. However, we do not find evidence of common ccRCC antigens: epitopes are not conserved across large subsets of ccRCC patients. Conclusions: Our initial results suggest that each patient may develop an individualized tumor-associated antibody response. Whether assessing a select epitope panel in a patient’s blood could be useful for ccRCC early detection, or even epitope diversity without needing to identify specific epitopes, warrants further study.
Comparison of major adverse cardiovascular events risk after androgen deprivation therapy initiation by body mass index.
Authors: Lucio N. Gordan, Stuart Atkinson, Deborah Boldt-Houle, Andrew K. Lee
Journal: Journal of Clinical Oncology (2022)

44 Background: The association between androgen deprivation therapy (ADT) and increased cardiovascular (CV) risk in prostate cancer (PCa) patients is controversial. 1-2 Major adverse cardiovascular events (MACE) occurred in 3-6% of patients in a 48-week ADT trial, 2 but meta-analysis from a 2011 study found no association between ADT and increased risk of CV death. 1 Body mass index (BMI) is a potential risk factor; Lee et al. found a lower risk of MACE in patients with high BMI than those with a normal weight, and patients with low BMI had a higher risk of all-cause mortality. 3 This study evaluates the association between BMI and MACE risk in PCa patients on ADT using real-world data. Methods: Analyses of US electronic medical records (2010 to 2020) of PCa patients (n=36,249) receiving LHRH agonist/antagonist injections were conducted to calculate the risk of MACE since ADT initiation for the following BMI groups: &lt;18.5, 18.5 to &lt;25, 25 to &lt;30, 30 to &lt;35, and &gt;35. BMI groups were based on the standard weight status associated with each BMI range (underweight, normal or healthy weight, overweight, obese, and severely obese, respectively). 4 The database contained 178,388 LHRH agonist/antagonist injection entries and 965 documented MACE events. Exclusion criteria included lack of ADT initiation date, lack of BMI data, and MACE within 6 months prior to ADT initiation. MACE was defined as myocardial infarction, stroke, and death from any cause based on a recent study in this field. 2 Kaplan-Meier event-free survival curves were constructed to compare the risk of MACE between BMI groups. Statistical significance between survival curves was evaluated by log-rank test. Results: Differences in MACE incidence between BMI groups were not significant. (Table). Conclusions: MACE risk was similar across BMI subgroups after ADT initiation. This is consistent with the literature that higher BMIs do not confer additional CV/MACE risk as might be expected (a lower risk of MACE in patients with high BMI than those with normal weight). 3 This 10-year analysis in &gt;35,000 patients is likely reflective of the real world, but further study is recommended to evaluate whether BMI should be considered a predisposing risk factor for CV disease in PCa patients undergoing ADT. As the association between ADT and increased CV risk in PCa patients is controversial, future studies evaluating the role of co-morbidities on MACE risk for PCa patients during ADT may be helpful to identify other CV predictors.[Table: see text]
Hyperprolactinaemia.
Authors: M. Hartog, M. G. Hull
Journal: BMJ (1988)

cardiology, haematology, neurology, and rheumatology clinics as well as in obstetrics.Treatment depends on careful anticoagulation, but the value of steroids, immunosuppressive agents, and plasma exchange is still not clear.In obstetrics, although claims of therapeutic success with various anticoagulation or immunosuppressive regimens increase each year, the data remain anecdotal and the overall results poor.
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Journal: JAMA (1989)

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
Apolipoprotein A-IV inhibits experimental colitis
Authors: Thorsten Vowinkel, Mikiji Mori, Christian F. Krieglstein, Janice Russell, Fumito Saijo, Sulaiman Bharwani, Richard H. Turnage, W. Sean Davidson, Patrick Tso, D. Neil Granger, Theodore J. Kalogeris
Journal: Journal of Clinical Investigation (2004)

The antiatherogenic properties of apoA-IV suggest that this protein may act as an anti-inflammatory agent. We examined this possibility in a mouse model of acute colitis. Mice consumed 3% dextran sulfate sodium (DSS) in their drinking water for 7 days, with or without daily intraperitoneal injections of recombinant human apoA-IV. apoA-IV significantly and specifically delayed the onset, and reduced the severity and extent of, DSS-induced inflammation, as assessed by clinical disease activity score, macroscopic appearance and histology of the colon, and tissue myeloperoxidase activity. Intravital fluorescence microscopy of colonic microvasculature revealed that apoA-IV significantly inhibited DSS-induced leukocyte and platelet adhesive interactions. Furthermore, apoA-IV dramatically reduced the upregulation of P-selectin on colonic endothelium during DSS-colitis. apoA-IV knockout mice exhibited a significantly greater inflammatory response to DSS than did their WT littermates; this greater susceptibility to DSS-induced inflammation was reversed upon exogenous administration of apoA-IV to knockout mice. These results provide the first direct support for the hypothesis that apoA-IV is an endogenous anti-inflammatory protein. This anti-inflammatory effect likely involves the inhibition of P-selectin–mediated leukocyte and platelet adhesive interactions.
Alectinib Superior to Crizotinib for ALK+ NSCLC
Journal: Cancer Discovery (2017)

Findings from the global phase III ALEX trial unequivocally show that alectinib is superior to crizotinib as first-line therapy for ALK+ non-small cell lung cancer. Alectinib more than doubled progression-free survival, significantly reduced the incidence of brain and CNS metastases, and should be considered the new standard of care.
Clinical Methods: A Guide to the Practical Study of Medicine
Journal: JAMA (1952)

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
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Journal: JAMA (1985)

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
SPARC, a Novel Regulator of Vascular Cell Function in Pulmonary Hypertension
Authors: Christine Veith, Ipek Vartürk-Özcan, Magdalena Wujak, Stefan Hadzic, Cheng-Yu Wu, Fenja Knoepp, Simone Kraut, Aleksandar Petrovic, Marija Gredic, Oleg Pak, Monika Brosien, Marie Heimbrodt, Jochen Wilhelm, Friederike C. Weisel, Kathrin Malkmus, Katharina Schäfer, Henning Gall, Khodr Tello, Djuro Kosanovic, Akylbek Sydykov, Akpay Sarybaev, Andreas Günther, Ralf P. Brandes, Werner Seeger, Friedrich Grimminger, Hossein A. Ghofrani, Ralph T. Schermuly, Grazyna Kwapiszewska, Natascha Sommer, Norbert Weissmann
Journal: Circulation (2022)

Pulmonary hypertension (PH) is a life-threatening disease, characterized by excessive pulmonary vascular remodeling, leading to elevated pulmonary arterial pressure and right heart hypertrophy. PH can be caused by chronic hypoxia, leading to hyper-proliferation of pulmonary arterial smooth muscle cells (PASMCs) and apoptosis-resistant pulmonary microvascular endothelial cells (PMVECs). On reexposure to normoxia, chronic hypoxia-induced PH in mice is reversible. In this study, the authors aim to identify novel candidate genes involved in pulmonary vascular remodeling specifically in the pulmonary vasculature.After microarray analysis, the authors assessed the role of SPARC (secreted protein acidic and rich in cysteine) in PH using lung tissue from idiopathic pulmonary arterial hypertension (IPAH) patients, as well as from chronically hypoxic mice. In vitro studies were conducted in primary human PASMCs and PMVECs. In vivo function of SPARC was proven in chronic hypoxia-induced PH in mice by using an adeno-associated virus-mediated Sparc knockdown approach.C57BL/6J mice were exposed to normoxia, chronic hypoxia, or chronic hypoxia with subsequent reexposure to normoxia for different time points. Microarray analysis of the pulmonary vascular compartment after laser microdissection identified Sparc as one of the genes downregulated at all reoxygenation time points investigated. Intriguingly, SPARC was vice versa upregulated in lungs during development of hypoxia-induced PH in mice as well as in IPAH, although SPARC plasma levels were not elevated in PH. TGF-β1 (transforming growth factor β1) or HIF2A (hypoxia-inducible factor 2A) signaling pathways induced SPARC expression in human PASMCs. In loss of function studies, SPARC silencing enhanced apoptosis and reduced proliferation. In gain of function studies, elevated SPARC levels induced PASMCs, but not PMVECs, proliferation. Coculture and conditioned medium experiments revealed that PMVECs-secreted SPARC acts as a paracrine factor triggering PASMCs proliferation. Contrary to the authors' expectations, in vivo congenital Sparc knockout mice were not protected from hypoxia-induced PH, most probably because of counter-regulatory proproliferative signaling. However, adeno-associated virus-mediated Sparc knockdown in adult mice significantly improved hemodynamic and cardiac function in PH mice.This study provides evidence for the involvement of SPARC in the pathogenesis of human PH and chronic hypoxia-induced PH in mice, most likely by affecting vascular cell function.
Sepsis promotes splenic production of a protective platelet pool with high CD40 ligand expression
Authors: Colin Valet, Mélia Magnen, Longhui Qiu, Simon J. Cleary, Kristin M. Wang, Serena Ranucci, Elodie Grockowiak, Rafik Boudra, Catharina Conrad, Yurim Seo, Daniel R. Calabrese, John R. Greenland, Andrew D. Leavitt, Emmanuelle Passegué, Simón Méndez-Ferrer, Filip K. Swirski, Mark R. Looney
Journal: Journal of Clinical Investigation (2022)

Platelets have a wide range of functions including critical roles in hemostasis, thrombosis, and immunity. We hypothesized that during acute inflammation, such as in life-threatening sepsis, there are fundamental changes in the sites of platelet production and phenotypes of resultant platelets. Here, we showed during sepsis that the spleen was a major site of megakaryopoiesis and platelet production. Sepsis provoked an adrenergic-dependent mobilization of megakaryocyte-erythrocyte progenitors (MEPs) from the bone marrow to the spleen, where IL-3 induced their differentiation into megakaryocytes (MKs). In the spleen, immune-skewed MKs produced a CD40 ligandhi platelet population with potent immunomodulatory functions. Transfusions of post-sepsis platelets enriched from splenic production enhanced immune responses and reduced overall mortality in sepsis-challenged animals. These findings identify a spleen-derived protective platelet population that may be broadly immunomodulatory in acute inflammatory states such as sepsis.
Cubic multi-ions-doped Na2TiO3 nanorod-like coatings: Structure-stable, highly efficient platform for ions-exchanged release to immunomodulatory promotion on vascularized bone apposition
Authors: Dongmei Yu, Bo Li, Meng Yu, Shuo Guo, Zheng Guo, Yong Han
Journal: Bioactive Materials (2022)

The dissolution-derived release of bioactive ions from ceramic coatings on metallic implants, despite improving osseointegration, renders a concern on the interfacial breakdown of the metal/coating/bone system during long-term service. Consequently, persistent efforts to seek alternative strategies instead of dissolution-derived activation are pressingly carrying out. Inspired by bone mineral containing ions as Ca2+, Mg2+, Sr2+ and Zn2+, here we hydrothermally grew the quadruple ions co-doped Na2TiO3 nanorod-like coatings. The co-doped ions partially substitute Na+ in Na2TiO3, and can be efficiently released from cubic lattice via exchange with Na+ in fluid rather than dissolution, endowing the coatings superior long-term stability of structure and bond strength. Regulated by the coatings-conditioned extracellular ions, TLR4-NFκB signalling is enhanced to act primarily in macrophages (MΦs) at 6 h while CaSR-PI3K-Akt1 signalling is potentiated to act predominately since 24 h, triggering MΦs in a M1 response early and then in a M2 response to sequentially secrete diverse cytokines. Acting on endothelial and mesenchymal stem cells with the released ions and cytokines, the immunomodulatory coatings greatly promote Type-H (CD31hiEmcnhi) angiogenesis and osteogenesis in vitro and in vivo, providing new insights into orchestrating insoluble ceramics-coated implants for early vascularized osseointegration in combination with long-term fixation to bone.
Association of cabozantinib dose reductions for toxicity with clinical effectiveness in metastatic renal cell carcinoma (mRCC): Results from the Canadian Kidney Cancer Information System (CKCis).
Authors: Jeffrey Graham, Naveen S. Basappa, Sunita Ghosh, Hanbo Zhang, Aaron Richard Hansen, Aly-Khan A. Lalani, Daniel Yick Chin Heng, Denis Soulieres, Vincent Castonguay, Christian K. Kollmannsberger, Michel Pavic, Lori Wood, Anil Kapoor, Georg A. Bjarnason
Journal: Journal of Clinical Oncology (2022)

316 Background: Cabozantinib (cabo) is an oral multi-targeted tyrosine kinase inhibitor (TKI) with activity in mRCC. TKI toxicity, an indicator of adequate drug exposure, has been associated with clinical effectiveness for sunitinib, pazopanib, and axitinib. We explored whether cabo dose reductions (a surrogate for toxicity) were associated with improved clinical outcomes in mRCC. Methods: Using the CKCis database, we performed an analysis of patients treated with cabo in the second-line or later between 2011-2021. We divided the cohort into those needing a dose reduction (DR, defined as less than the starting dose at time of treatment discontinuation) and those who did not (no-DR). We compared outcomes by dose reduction status, including objective response rate (ORR), time to treatment failure (TTF), and overall survival (OS). Results: We identified 260 patients who received cabo, of which 103 (41.0%) needed a DR. Across all lines, the ORR was similar between the DR and non-DR groups: 19.6% vs. 18.9% (p = 0.903) respectively. The median TTF was 12.75 months (95% CI 10.38 – 17.64) in the DR group vs. 6.44 months (95% CI 5.49 – 8.67) in the no-DR group. After adjusting for IMDC risk, the hazard ratio (HR) for TTF comparing DR vs. no-DR was 0.69 (95% CI 0.50 - 0.97, p-value = 0.03). The median OS was 29.6 months (95% CI 19.58 – 42.64) in the DR group vs. 15.28 (95% CI 11.04 – 22.64) in the no-DR group. After adjusting for IMDC risk, the HR for OS comparing DR vs. no-DR was 0.65 (95% CI 0.43 - 0.98, p = 0.04). Conclusions: Cabozantinib dose reductions, a surrogate for toxicity and adequate drug exposure, appear to be associated with improved TTF and OS in mRCC. Toxicity driven/individualized dosing strategies for cabo alone and in combination with immunotherapy, warrant further investigation.[Table: see text]
Backache.
Authors: J A Mathews
Journal: BMJ (1977)

In recent years there has been a crescendo of interest in the symptom of "low back pain" among epidemiologists, pathologists, radiologists, rheumatologists, and orthopaedic surgeons.Much research is directed at delineating the actual mechanisms by which much common back pain is produced as a preliminary to more efficient prophylaxis, diagnosis, and 7EH