tbuckley/cabot-search huggingface dataset:
Bleeding into a baboon
Journal: JAMA (1969)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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 journal
Book Review Infant Nutrition: A textbook of infant feeding for students and practitioners of medicine . By William McK. Marriott, M.D. Revised by P. C. Jeans, M.D. Third edition. 8°, cloth, 475 pp., with 31 illustrations. St. Louis: The C. V. Mosby Company, 1941. $5.50.
Journal: New England Journal of Medicine (1942)
Tuberculosis Treatment
Authors: V. Alton Dohner
Journal: JAMA (1973)

<h3>To the Editor.—</h3> The letter by Ostrow and Miller regarding twice weekly therapy for tuberculosis (224:1530, 1973) is misleading because of several neglected items. The alcoholic patients chosen for the Denver program were mainly Caucasian, known to live in the area surrounding the satellite clinic, and were a highly selected group. There was considerable cooperation from hotel and boarding house managers in keeping these selected patients attending clinic. The managers informed the nurse when patients were unable to attend clinic due to illness and always helped in locating patients who missed an appointment. The nurse who operated the "shot" clinic was especially selected for her lack of bias toward the alcoholic and indigent population. She was known for her cheerful attitudes and her acceptance of these patients as individuals. Most deserving of critical comment is the statement that the poorest cooperation was received from Native Americans. I believe there are
Erratum: A Toll-like receptor–independent antiviral response induced by double-stranded B-form DNA
Authors: Ken J Ishii, Cevayir Coban, Hiroki Kato, Ken Takahashi, Yuichi Torii, Fumihiko Takeshita, Holger Ludwig, Gerd Sutter, Koichi Suzuki, Hiroaki Hemmi, Shintaro Sato, Masahiro Yamamoto, Satoshi Uematsu, Taro Kawai, Osamu Takeuchi, Shizuo Akira
Journal: Nature Immunology (2006)
β-Blockers and Depression
Authors: Roselie A. Bright
Journal: JAMA (1992)

<h3>Objective.</h3> —To evaluate the relationship between β-blockers and depression. <h3>Design.</h3> —Case-control study. <h3>Setting.</h3> —New Jersey Medicaid recipients during July 1980 to December 1983. <h3>Participants.</h3> —New depression case patients (N = 4302) were identified from Medicaid claims for depression markers (antidepressant drugs, in-hospital depression diagnosis, or electroconvulsive therapy). Control patients were randomly selected and matched on the basis of Medicaid enrollment on the case patients' date for first depression marker (index date), birth year, sex, race, and nursing home residency status. <h3>Main Exposure Measure.</h3> —β-Blocker use as evidenced by prescription claims in the year before the index date. <h3>Results.</h3> —Case patients overall were more likely to have taken β-blockers (simple, matched odds ratio [OR] of 1.45; 95% confidence interval [CI], 1.29 to 1.62). Controlling for confounders (benzodiazepine use, frequent outpatient visits, and frequent use of medications other than β-blockers) resulted in a null effect (OR=0.98; 95% CI, 0.87 to 1.12). The ORs were consistently lower for case patients with a depression diagnosis or electroconvulsive therapy than for cases with only antidepressant use as a marker. These results did not vary by age, sex, race, nursing home status, or use of other selected specific medications. <h3>Conclusions.</h3> —Ongoing β-blocker use was not causally related to markers of depression. The difference between this study and those it contradicts is that this one identified certain confounding variables that accounted for the apparent relationship. (<i>JAMA</i>. 1992;267:1783-1787)
Long-term safety profile of cenicriviroc in adults with non-alcoholic steatohepatitis: rollover study
Authors: Sven Francque, Alex Hodge, Jerome Boursier, Sam Moussa, Ziad H. Younes, Grace S. Park, Gerardo Rodriquez, Karen Lai, Eduardo Bruno Martins, Naim Alkhouri, Manal Abdelmalek
Journal: Journal of Hepatology (2020)
THE ELECTIVE LOCALIZATION OF BACTERIA IN MUSCLE
Journal: JAMA (1921)

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
心理压力和银屑病:系统性评述和元分析
Authors: I. Snast, O. Reiter, L. Atzmony, Y.A. Leshem, E. Hodak, D. Mimouni, L. Pavlovsky
Journal: British Journal of Dermatology (2018)

银屑病是一种慢性炎症性皮肤病。银屑病患者及其医生都知道,心理压力会导致疾病恶化;但是,缺乏有效证据证实这一关系。该评述调查了评估先前心理压力与银屑病恶化和发病之间的相互作用。作者评述了包含32537名银屑病患者的39项不同研究。第一类研究在特定时间点评估银屑病患者。研究发现,约有一半的患者认为压力导致其病情恶化,并能够记住发病或恶化之前的压力事件。但是,这些研究得出的证据难以证明压力和银屑病之间的显著相关性,因为患者并未与对照组(接触压力事件的非银屑病患者)进行对比,并且也不清楚银屑病恶化/发病与患者回忆压力事件之间的时间间隔。第二类研究评估了银屑病患者对比非银屑病患者在疾病发作或恶化前回忆起压力事件的频率。这些研究得出了相矛盾的结果:某些研究发现银屑病患者与非银屑病患者相比,更频繁地想起压力事件,而其他研究则未发现显著差异。有趣的是,不基于患者回忆、而是审核所记录的应激障碍诊断的唯一一项研究发现,银屑病患者与非银屑病患者之间的比率相似。某个研究采用的第三种方法评估了某个时间点的压力大小与一个月后的银屑病严重性之间的相互作用,发现仅有微弱的联系。作者们未发现有力证据证实,心理压力与银屑病恶化和发作的密切关联。要更好地了解心理压力对银屑病发作和病情的影响,需要更多研究,尤其是长期记录心理压力并评估病情的研究。
Hydrops of the gallbladder in an adult with Kawasaki disease
Authors: L. I. Liebmann
Journal: JAMA (1982)

An acute, febrile, self-limited disease process occurred in an otherwise healthy young adult that satisfies accepted criteria for the diagnosis of Kawasaki disease. Unusual features of this case include the patient's age and the documentation of notable, acute noncalculous distention of the gallbladder, a recognized complication of the condition. Evidence of cystic-duct obstruction during the acute phase of distention and subsequent establishment of patency during the convalescent stage is provided with the use of serial ultrasonographic and radioisotopic studies. Discussion of the possible mechanisms for acute hydrops of the gallbladder in Kawasaki disease is included and the need to consider this diagnosis in young adults with the appropriate clinical manifestations is underscored. (<i>JAMA</i>1982;247:827-829)
Abstract LB-325: Developmental hierarchy in Langerhans cell histiocytosis
Authors: Florian Halbritter, Matthias Farlik, Christoph Bock, Caroline Hutter
Journal: Cancer Research (2019)

Abstract Langerhans Cell Histiocytosis (LCH) is a neoplastic disease characterized by the accumulation of CD1a+CD207+ cells of unknown origin. Constitutive activation of the ERK signaling pathway is a common feature of LCH, but the pathogenesis of this disease remains unclear. Here we present a comprehensive analysis of the composition of LCH lesions that provides new insight into the development and molecular mechanisms of this disease. We used a multilayered approach employing immunohistochemistry, flow cytometry, single- cell RNA-sequencing, and ATAC- sequencing of LCH biopsies obtained from different patients. Based on the single- cell RNA expression data, we identified different LCH cell populations within LCH lesions that display distinct pathway signatures, including a stem-cell-like, proliferative state. Computational analysis discovered a hierarchy between these cells that suggest a directed developmental program in each tumor. Finally, functional chromatin mapping inferred distinct regulatory signatures discriminating the different cell states. Taken together, our study shows at single-cell resolution that there is considerable intra-tumoral heterogeneity in LCH and provides detailed insight into the molecular framework underlying tumor development. Our transcriptomic and epigenomic analyses have generated a reference map of subpopulations of LCH cells with distinct functional and phenotypic properties. We propose that the lesions are comprised of different LCH cell subsets that arise in an intrinsic developmental process. This work can serve as a template for the analysis of tumorigenesis beyond LCH. Citation Format: Florian Halbritter, Matthias Farlik, Christoph Bock, Caroline Hutter. Developmental hierarchy in Langerhans cell histiocytosis [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr LB-325.
From the Institute of Medicine
Authors: M. J. Field
Journal: JAMA (1993)

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
ETIOLOGY OF DEVIATIONS OF THE NASAL SEPTUM: ANATOMIC THEORY
Journal: JAMA (1920)

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
Fatal virus‐associated hemophagocytic syndrome associated with coexistent chronic active hepatitis B and acute hepatitis C virus infection
Authors: Mikkel Faurschou, Ove Juul Nielsen, Per Boye Hansen, Birgitte Ravn Juhl, Hans Hasselbalch
Journal: American Journal of Hematology (1999)

A 28-year-old man was admitted to our department with intermittent fever, hepatosplenomegaly and pancytopenia. Liver parameters and serum ferritin were markedly elevated. Bone marrow biopsy showed hypocellularity, histiocytic hyperplasia, and hemophagocytosis consistent with a virus-associated hemophagocytic syndrome (VAHS). There was serological evidence of chronic active hepatitis B and acute hepatitis C virus infection. The patient died despite aggressive immunosuppressive and supportive treatment. Autopsy revealed signs of acute viral hepatitis with cholestasis. Histiocytes engaged in hemophagocytosis were observed in bone marrow and spleen. The condition was interpreted as VAHS associated with chronic active hepatitis B and acute hepatitis C virus infection. To our knowledge this is the first report of a hemophagocytic syndrome in that setting. Am. J. Hematol. 61:135–138, 1999. © 1999 Wiley-Liss, Inc.
Anna Donald
Authors: R. Smith, M. Gray
Journal: BMJ (2009)

NK cells recognize and kill tumor cells and normal cells, and these play an important role in immune defense in cancer, infectious disease, and autoimmunity. NK killing is regulated by positive or negative signals derived from the interaction of surface receptors with ligands on the target cells. However, the mechanisms controlling the proliferation and maintenance of NK cells in normal human individuals are less clearly defined. In this study, using an entirely autologous system, we demonstrate that human peripheral blood CD3<sup>−</sup>CD56<sup>+</sup>, killer cell-inhibitory receptor (KIR)-expressing cells proliferate and expand in response to LPS. These responses are enhanced in the presence of anti-IL-10 receptor-blocking Abs or on the removal of CD14<sup>+</sup> cells from the cultures. This enhancement is also reflected in substantial increases in cytolytic activity and IFN-γ production. The negative effect of CD14<sup>+</sup> cells may also be IL-10 mediated, IL-10 being lost from the culture supernatants of CD14-depleted PBMC and rIL-10 reversing the effect of this depletion. On the other hand, mRNA for the p35 and p40 subunits of IL-12 is still induced in CD14-depleted cultures. The expansion of CD3<sup>−</sup>CD56<sup>+</sup> cells was also inhibited by CTLA4-Ig, indicating a role for CD80/86. B lymphocytes were not required for the expansion of CD3<sup>−</sup>CD56<sup>+</sup> cells, whereas removal of MHC class II<sup>+</sup> cells from CD14-depleted cultures resulted in a complete abrogation of these responses. Expansion of CD3<sup>−</sup>CD56<sup>+</sup> cells was reconstituted in MHC class II-depleted cell cultures by adding back monocyte-derived dendritic cells. These results indicate that the responses of CD3<sup>−</sup>CD56<sup>+</sup> NK cells to LPS may be driven by a MHC class II<sup>+</sup> B7<sup>+</sup> CD14<sup>−</sup> peripheral population, most likely blood dendritic cells.
Membrane cation and anion transport activities in erythrocytes of hereditary spherocytosis: Effects of different membrane protein defects
Authors: Lucia De Franceschi, Oliviero Olivieri, Emanuele Miraglia del Giudice, Silverio Perrotta, Vincenzo Sabato, Roberto Corrocher, Achille Iolascon
Journal: American Journal of Hematology (1997)

Hereditary spherocytosis (HS) is due to different membrane protein defects (i.e., deficiency of spectrin and ankyrin, band 3, or band 4.2). In order to gain new insight into the relationships between band 3 function and proteins associated with the cytoskeleton, we studied erythrocyte anion transport activity in HS characterized by different membrane protein defects. Anion transport activity was increased in HS due to partial band 4.2 deficiency or to band 4.2 absence, while in HS associated with deficiency of spectrin + ankyrin or band 3, the anion transport results were normal or decreased, respectively. Moreover, since HS erythrocytes are characterized by an increased Na and a decreased K, we studied the principal membrane cation transport pathways. Activity of the Na/K pump was increased in all HS studied, while no changes in Na/K/2Cl cotransport and Na/Li exchange were evident between control and HS as well as between forms of HS associated with different membrane protein defects. K/Cl cotransport activity was decreased in all HS studied compared to normal red cells. In all HS, passive membrane permeability to Na and K was increased compared to normal erythrocytes. The increased Na and the low K content can be attributed to the abnormal membrane permeability to cations, which is not related to a specific membrane protein defect. Am. J. Hematol. 55:121–128, 1997. © 1997 Wiley-Liss, Inc.
PTU-049 Modulation of toll-like receptor genes with selective gut decontamination in cirrhotic animals prevents the development of acute-on chronic liver failure (ACLF)
Authors: N Shah, D Dhar, N A Davies, R P Mookerjee, R Jalan
Journal: Gut (2012)

<h3>Introduction</h3> Acute deterioration in the liver function following precipitating illness in patients with cirrhosis often lead to multiple organ failure. Inflammation is thought to be a major contributing factor. We hypothesised that toll like receptor9s (TLRs) play a pivotal role in lipopolysaccharide (LPS) mediated cytokine surge in patients with cirrhosis culminating in acute-on-chronic liver failure (ACLF). Selective gut decontamination with Norfloxacin would dampen this inflammatory cascade. <h3>Methods</h3> Global hepatic gene expression was studied in a rodent model of cirrhosis induced by bile duct ligation (BDL) (Agilent microarray) and compared the results to sham animals. TLR related genes were among the differentially expressed genes in the liver. We validated gene expression in the Liver and Kidney in a second set of experiment in Sham, BDL, BDL+LPS, BDL+Norfloxacin, BDL+Norfloxacin+LPS groups using the quantitative real-time PCR. Cytokines (Becton Dickenson) and biochemistry were measured (COBAS Integra 400). <h3>Results</h3> Among the several genes with high expression in the BDL group as detected by the microarray, both TLR 4 and 2 had significantly higher expression in liver and Kidney compared with the sham group. We also found a marked upregulation of the C-C motif ligand 2 (CCl2) and C-X-C motif ligand 2(CxCl2) Furthermore, LPS administration in BDL animals accentuated not only the TLRs (4 and 2) expression in both kidney and liver but also the Cxcl2 and CCl2 in both these organs associated with deterioration organ function as suggested with a rise in the liver enzyme, creatinine and a rise in plasma and tissue cytokines. Norfloxacin pre-treatment in BDL group (BDL+Norfloxacin) attenuated the TLR4 and TLR2 expression in both liver and kidney. Selective decontamination with Norfloxacin in BDL +LPS animals limited the upregulation of TLR4 and TLR2 in the Liver and Kidney. It also prevented the upregulation of the CxcL2 and CCl2 in both these organs. This was associated with significant improvement in liver enzymes, creatinine and cytokines. <h3>Conclusion</h3> This study shows that the liver and kidneys in cirrhotic animals are primed by upregulation of TLR9s and its downstream inflammatory mediators in the Liver and Kidney which make them exquisitely sensitive to the effects of superimposed infection/inflammation leading to organ failure. Selective decontamination with Norfloxacin prevents the progression of ACLF by reducing gene expression of TLR 2 and 4 and its associated inflammatory adaptors. <h3>Competing interests</h3> None declared.
AB0140 Relationship between Expression of Synovial B Cell Survival Factors and Clinical Response to Rituximab Treatment in Rheumatoid Arthritis
Authors: R. Thurlings, M. Boumans, W. de Jager, K. Vos, L. van Baarsen, D. Gerlag, B. Prakken, P.P. Tak
Journal: Annals of the Rheumatic Diseases (2014)

<h3>Background</h3> Rituximab aims to deplete CD20 positive B cells and exerts a significant and often long-lasting clinical effect in a subset of patients with rheumatoid arthritis (RA). The extent of B cell depletion in the inflammatory tissues after rituximab varies between patients and persistence of plasma cells and plasma cell products is associated with clinical non-response. This suggests rituximab may fail to deplete pathogenic B cells. <h3>Objectives</h3> To investigate whether the variable clinical response to rituximab might be explained by differential expression of B cell survival factors in the inflamed synovial tissue of RA patients. <h3>Methods</h3> Twenty-four RA patients underwent an arthroscopic synovial biopsy before, 1 month after and 4 months after treatment with rituximab. Treatment was given via two infusions (1,000 mg on day 1 and 15), both without methylprednisolon premedication to be able to study specific biological effects of rituximab. Clinical response was defined as a response according to the European League Against Rheumatism (EULAR) criteria at week 24. Peripheral blood and synovial tissue were analyzed for expression and levels of B cell survival factors: BLyS, APRIL, IL-1β, IL6, BLyS, VCAM, ICAM, IFNα, CXCL12 and BLIMP1. Correlation between baseline expression and changes in B cell survival factors and clinical response were calculated using logistic regression analysis. <h3>Results</h3> We found no significant correlation between baseline expression level of synovial B cell survival factors and clinical response to treatment. After treatment, the expression levels of BLyS, APRIL, IL-1β, IL6, ICAM and BLIMP1 were unaltered. The expression of IFNα and VCAM decreased after treatment, of which VCAM within one month (<i>P</i> =0.035, <i>P</i> =0.022 and <i>P</i> =0.039, respectively). In contrast, expression of CXCL-12 increased after treatment (<i>P</i> =0.046). In clinical responders VCAM expression decreased further between 1 and 4 months after treatment, although a statistical significant difference with non-responders could not be detected. <h3>Conclusions</h3> Clinical non-response to rituximab is not associated with a higher baseline expression of B cell survival factors in the inflamed synovial tissue of RA patients. However, the persistent expression of survival factors independent of the extent of B cell depletion may promote the persistence of pathogenic B cell subsets in clinical non-responders to treatment. <h3>Acknowledgements</h3> Het Reumafonds <h3>Disclosure of Interest</h3> None declared <h3>DOI</h3> 10.1136/annrheumdis-2014-eular.5312