tbuckley/cabot-search huggingface dataset:
A prospective observational study to determine the adequacy of 6 months antitubercular therapy in tubercular mediastinal lymphadenopathy
Authors: Akanksha Jha, Nirmal Jain, Rohan Aurangabadwalla, Nitin Jain, Mehul Thakkar, Nalin Joshi
Journal: European Respiratory Journal (2011)

Background:  The present study was designed to evaluate adequacy of 6months antituberculosis therapy (ATT), Revised National Tuberculosis Control Programme (RNTCP) Cat I with isoniazid (H), rifampicin (R), pyrazinamide (Z), ethambutol (E) followed by HR thrice weekly in patients with tubercular mediastinal lymphadenopathy (TML).   Material & methods:  75 cases of significant mediastinal lymphadenopathy on contrast enhanced CT chest (CECT Chest) and diagnosis of Tuberculosis on transbronchial needle aspiration were included. All patients were given 6months ATT [2(HRZE) 3 /4(HR) 3 ]as per RNTCP and followed up at the end of 2,5 and 6 months for clinico-radiological assessment. CECT Chest done at the end of 6months and treatment was extended with (HR) 3  in patients with persistent significant lymphadenopathy (>1 cm) on CT Chest. Repeat CECT Chest was done 3 monthly till complete radiological response.   Results:  Mean age of patients was 27.5±14.38 years with M:F ratio of 3:2. Common symptoms were fever (88%), dry cough (70%) and anorexia (60%). Right paratracheal (73%), Pretracheal (67%) were commonest lymph node groups involved. Only 15 out of 75 patients (20%) showed evidence of complete clinico-radiological improvement at end of 6 months while 5 (6.67%) patients were lost to follow up. Remaining 55 patients needed extended treatment (HR) 3 . 46 (61.33%) patients had complete clinico-radiological improvement at end of 9 months, while 9 (12%) patients required 12 months ATT.   Conclusion:  74% of the patients with TML required ATT for more than 6months (9-12 months) compared to 20% of the patients in whom 6 months ATT was adequate.The results suggest that 6months RNTCP CAT I is inadequate for treating TML.
Ward Nine (Male Geriatric)
Authors: Rob Burnside
Journal: JAMA (2004)

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
Still Life With Profile of Laval
Authors: M Therese Southgate
Journal: JAMA (2005)

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
Abstract 20396: Induction of Ischemia-Reperfusion Injury by Extracellular RNA: A case for Tumor Necrosis Factor (TNF-α) - Shedding
Authors: Hector A Cabrera-Fuentes, Klaus T Preissner
Journal: Circulation (2014)

Introduction: During acute myocardial infarction, cardiomyocyte death has a great impact on the quality of life and survival of patients. Despite reopening/reperfusion of stenosed vessels, a major organ damage remains. The initial mechanistic triggers of this myocardial “ischemia/reperfusion (I/R) injury” remain greatly unexplained. Hypothesis: We hypothesized that extracellular RNA (eRNA), derived from damaged tissue, and tumor-necrosis-factor-a (TNF-α), may dictate cardiac I/R injury. Methods and Results: Following myocardial I/R in mice or I/R induced in the isolated Langendorff rat heart, increased eRNA levels were found together with cardiac injury markers. Likewise, eRNA was released from cardiomyocytes under hypoxia and subsequently induced TNF-α liberation by activation of TNF-α converting enzyme (TACE) to provoke cardiomyocyte death. Conversely, TNF-α promoted eRNA release especially under hypoxia, feeding a vicious cell damaging cycle during I/R. Administration of RNase1 or TAPI (a TACE-inhibito...
LOCULATED AZYGOS FISSURE EFFUSION IN CARDIAC FAILURE
Authors: R L FRIEDMAN
Journal: Annals of Internal Medicine (1953)

Case Reports1 March 1953LOCULATED AZYGOS FISSURE EFFUSION IN CARDIAC FAILUREROBERT L. FRIEDMAN, M.D.ROBERT L. FRIEDMAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-38-3-582 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptInterlobar effusions are not uncommon in cardiac failure. Most frequently they are loculated in the right lesser fissure, rarely in the azygos fissure. The rarity of this latter localization prompts the present report.A point to be noted in considering the rarity of loculated effusion in the azygos fissure in cardiac failure is the incidence of the azygos fissure in routine chest surveys. In 50,000 examinations, Etter1found an incidence of 0.26 per cent; Litten,20.07 per cent in 8,000 cases; Minehart,30.13 per cent in 10,000 cases; and Pendley,41.05 per cent in 150,000 cases. Since the average incidence...Bibliography1. Etter LE: Variations in position of the azygos septum and its incidence in 50,000 x-ray examinations, Am. J. Roentgenol. 58: 726-729, 1947. Google Scholar2. Litten F: Zur Rontgendiagnose des Lobus venue azygos, insbesondere seine Erkennbarkeit durch das stereoskoptische Verfahren, Deutsche med. Wchnschr. 55: 400-401, 1929. CrossrefGoogle Scholar3. Minehart VL: Azygos lobe of the lung, M. Bull. 5, pp. 112-113, U. S. Veterans Bureau, 1929. Google Scholar4. Pendley WO: The azygos lobe in photofluorography, U. S. Nav. M. Bull. 46: 1920-1927, 1946. MedlineGoogle Scholar5. Robertson RF: Interlobar hydrothorax in cardiac failure, Brit. Heart J. 13: 112-114, 1951. CrossrefMedlineGoogle Scholar6. SteinSchwedel LDJB: Interlobar effusions in patients with heart disease, Am. Heart J. 10: 230-239, 1934. CrossrefGoogle Scholar7. Stivelman BP: Interlobar pleural effusions, Am. J. Roentgenol. 34: 475-481, 1935. Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Richmond, Virginia*Received for publication July 12, 1952.From the Department of Radiology, McGuire Veterans Hospital, Richmond, Virginia.Sponsored by the Veterans Administration with the approval of the Chief Medical Director. Statements and conclusions published by the author are a result of his own study and do not necessarily reflect the opinion or policy of the Veterans Administration. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byRespiratory System 1 March 1953Volume 38, Issue 3Page: 582-585KeywordsDiagnostic radiologyHeart failureThorax ePublished: 1 December 2008 Issue Published: 1 March 1953 PDF downloadLoading ...
Turnover at the Top
Authors: Phil Gunby
Journal: JAMA (2000)

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
Abstract 3688: Arctigenin induced immunogenic cell death through a reactive oxygen species/endoplasmic reticulum stress pathway in lung cancer
Authors: Chih-Hsin Kuo, Ya-Ling Hsu, Ming-Shyan Huang
Journal: Cancer Research (2014)

Abstract Induction of immunogenic cell death (ICD) is characterized by surface exposure of damage-associated molecular pattern molecules, which can induce a tumor-specific immune response. ICD are promising treatments for cancer by restoring efficient anti-tumor immunity. Here we reported that the arctigenin, an anti-inflammation and anti-cancer agent, elicits a potent anticancer immunity effect by inducing the translocation of calreticulin (CRT) to cell membrane and the release of high-mobility group protein 1 (HMGB1) in lung cancer. Treatment of A549 cells with arctigenin increased the production of ROS generation, which in turn triggered an endoplasmic reticulum (ER) stress response, including the phosphorylation of PERK (PKR-like endoplasmic reticulum kinase and IRE1 (inositol-requiring 1). The antioxidant, EUK8, significantly decreased CRT translocation and HMGB release by inhibiting the ER stress (PERK phosphorylation). Taken together, the production of ROS induced CRT translocation and HMGB1 release, mediating arctigenin-induced enhancement of tumor immunity. This indicated that arctigenin is a potential immunetherapeutic agent against lung tumor. Citation Format: Chih-Hsin Kuo, Ya-Ling Hsu, Ming-Shyan Huang. Arctigenin induced immunogenic cell death through a reactive oxygen species/endoplasmic reticulum stress pathway in lung cancer. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3688. doi:10.1158/1538-7445.AM2014-3688
Annual Report Cites Improvements in Access to Health Care
Authors: Tracy Hampton
Journal: JAMA (2015)

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
Abstract 13963: Hyperamylinemia, a Potential Therapeutic Target in Diabetic Cardiorenal Syndrome
Authors: Sarah Srodulski, Analia Loria, Sanda Despa, Florin Despa
Journal: Circulation (2014)

Background: Recent studies show that hyperamylinemia, which is common in humans with prediabetic insulin resistance, promotes accumulation of oligomeric amylin not only in pancreatic islets, but also in kidneys and heart. The oligomerized amylin is a potent source of oxidative stress and inflammation.

Hypothesis: Controlling hyperamylinemia may improve cardiac and renal function in type-2 diabetes (T2D).

Methods: To test this hypothesis, we used a rat model of T2D overexpressing human amylin in the pancreas (HIP rat). Cardiac function (M-mode echocardiography), intra-arterial blood pressure and kidney function (metabolic cage) were assessed in diabetic HIP vs. age-matched control rats. To reduce amylin deposition, we pharmacologically elevated the endogenous blood levels of eicosanoids, molecules with anti-aggregation properties, by blocking the soluble epoxide hydrolase.

Results: We found that amylin begins to accumulate in the cardiovascular system in the pre-diabetic state (i.e. non-fasted blood glucose level in the 150-200 mg/dl domain). Oligomerized amylin was identified in the blood vessel wall, glomeruli and cardiac myocytes suggesting that hyperamylinemia may directly affect cardiac and renal function. Compared to wild-type littermates, HIP rats develop cardiac hypertrophy (~75% increase in heart to body weight ratio; P<0.01), systolic dysfunction (fractional shortening of 36.9±2.0% vs. 44.7±1.6% in wild-type; P<0.05), hypertension (mean arterial blood pressure was increased by ~20%; P<0.05) and typical signs nephropathy, including increased diuresis (by ~500/%; P<0.001), natriuresis (by ~120%; P<0.001), creatinine clearance (by~70%; P<0.01) and microalbuminuria (by 300%; P<0.001). Treatment doubled the blood level of eicosanoids, which drastically reduced incorporation of aggregated amylin in heart and kidneys. Animals in the treated group showed reduced cardiac hypertrophy and hypertension. The protective mechanisms included the mitigation of amylin-induced oxidative stress and inflammation.

Conclusions: Accumulation of oligomerized amylin affects cardiac and renal function in T2D. This pathological process is reduced by elevating the blood levels of anti-aggregation eicosanoids.
632. Retrovirally Transduced Muscle-Derived Stem Cells Facilitate Repair of Osteochondral Defects
Authors: Ryosuke Kuroda, Arvydas Usas, Hairong Peng, Masamitsu Sakamoto, Johnny Huard
Journal: Molecular Therapy (2004)

Due to their limited intrinsic ability for self-repair, articular cartilage defects caused by inflammation or articular fractures do not fully heal. Skeletal muscle represents a potential source of cells for use in cartilage tissue engineering applications. Subpopulation of muscle-derived stem cells isolated from mouse skeletal muscle (MDSCs), possess the ability of multipotent differentiation and have been found capable to enhance bone healing, when genetically engineered to express bone morphogenetic proteins (BMP-2, BMP-4)1,2. BMP-4 also appears to be a good candidate for enhancing the production of chondrogenic components in vitro. The goal of this study was to test whether we could induce early progenitor cells derived from skeletal muscle to differentiate into chondrocytes and repair osteochondral defects. MDSCs were transduced with retroviral vectors CLBMP-4, CLLacZ and the level of functional BMP-4 was determined by bioassay and Western blot analysis. A full-thickness articular cartilage defects were created in the trochlear grooves of the femora in thirty-nine 12-week-old athymic rats, and treated in three different ways. Rats in Group 1 received transplantation of cells expressing LacZ (MDSC-LacZ) embedded in fibrin glue, rats in Group 2 received transplantation of cells expressing LacZ and BMP-4 (MDSC-LacZ-B4) embedded in fibrin glue, and rats in Group 3 received fibrin glue without cells (control). We sacrificed the rats 4, 8, 12, and 24 weeks after surgery and monitored healing by using histology and immunohistochemistry. Four weeks after transplantation repaired tissues treated with MDSC-LacZ-B4 contained hypertrophic chondrocytes, which stained positive for LacZ and Alcian blue. These cells expressed both β-galactosidase and Type II collagen, suggesting possible donor cell differentiation into chondrocytes after stimulation with BMP-4. MDSC-LacZ-B4-treated defects received a significantly higher histological grading (O'Driscoll et al. 1988) score than did the controls 8, 12, and 24 weeks after transplantation. The MDSC-LacZ group also scored significantly higher than controls at the 8- and 12-week time points. More importantly, the MDSC-LacZ-B4 treatment group scored significantly higher than the MDSC-LacZ group 24 weeks after transplantation. We detected LacZ-positive cells in the repaired tissues for up to 12 weeks after transplantation, a finding that suggests improved muscle-derived stem cell survivability (relative to less purified myoblast transplantation reported previously by Adachi, et al.3) and continuous gene expression within the lesions in the MDSC-LacZ and MDSC-LacZ-B4 groups. Thus muscle-derived stem cells appear to be good candidates as both gene delivery vehicles to deliver BMP-4 and as a cell source for cartilage repair. This simple technique could constitute an attractive strategy for future orthopaedic tissue engineering applications.
An unusual approach to manage a bronchopleural fistula following carinal pneumonectomy
Authors: Samir Naik, Brendan Madden, Robin Kanagasaby
Journal: European Respiratory Journal (2012)

A 52-year-old lady was referred with a T4N0M0 lung adenocarcinoma in the right main bronchus with protrusion into the trachea. She was an exsmoker with COPD and hypothyroidism.  She had a right carinal pneumonectomy with anastomosis of left main bronchus on to the trachea. Post discharge she was readmitted with dyspnoea three weeks later. Her post pneumonectomy space was abnormally enlarged which was managed successfully with intercostal tube drainage.  Six weeks later she represented with dyspnoea and sepsis which did not respond to antibiotics. She had a right thoracotomy and bronchoscopy which showed two bronchopleural fistulas (BPF) at the anastomotic site. Unfortunately the BPF persisted. Further surgery was not considered appropriate. She then had a rigid bronchoscopy and a 4cm X 16 mm covered stent deployment to cover the defects. A day later she still had an air leak. Chest X-ray four days later showed that the stent had migrated upwards. She had replacement of the stent with a larger 4cm X 18 mm device. Following day, the air leak stopped completely. Her follow up chest x-ray three months later has been stable with no recurrence of BPF.  This case illustrates the management difficulties of BPF complicating high bronchial to tracheal anastomosis with differing airway diameters. Placement of large stent could have jeopardised the integrity of the airway anastomosis. The first stent migrated because it was preferentially sized with respect to the bronchial diameter. When a larger stent was inserted adequate closure ensued without airway anastomotic dehiscence.  Although surgical treatment of BPF is gold standard carefully selected patients may benefit from endobronchial closure.
Review article: Efficacy of desloratadine in the treatment of allergic rhinitis: a meta‐analysis of randomized, double‐blind, controlled trials
Authors: G. W. Canonica, F. Tarantini, E. Compalati, M. Penagos
Journal: Allergy (2007)

The objective of the study is to assess the efficacy of the nonsedating antihistamine, desloratadine, in the treatment of allergic rhinitis (AR). A search of MEDLINE, EMBASE, LILACS, and CINAHL databases was undertaken from January, 1966 to May, 2006. Double‐blind, randomized, controlled studies of desloratadine in the treatment of AR in adult patients were carried out. The measured outcomes included the total symptoms score, the total nasal symptoms score, nasal airflow, and inflammatory markers (nasal eosinophils, nasal interleukin‐4). The analysis included the calculation of standardized mean difference (SMD). A total of 57 studies were analyzed, and 13 randomized, double‐blind, controlled trials were included in the meta‐analysis. The trials included 3108 subjects who had completed studies involving desloratadine. There was significant heterogeneity among the study results, because of differing study methodologies. Desloratadine was associated with significant reductions in total symptoms scores (SMD −1.63; 95% CI −2.75 to −0.51; P = 0.004) and total nasal symptoms score (SMD −0.66; 95% CI −0.91 to −0.42; P &lt; 0.001), when compared with placebo. Analysis of objective data on nasal blockage demonstrated a significant improvement in nasal airflow with desloratadine, when compared with placebo (SMD 0.32; 95% CI 0.10 to 0.55; P = 0.005). A benefit favoring desloratadine over placebo in terms of nasal eosinophil levels was also noted in the analysis. This meta‐analysis confirms the reduction of AR symptoms and improvement in nasal airflow seen in individual studies of desloratadine. Objective improvements in nasal airflow, total symptoms, and total nasal symptoms seen with desloratadine are supported by Ia evidence.
Maraviroc 150 mg daily plus lopinavir/ritonavir, a nucleoside/nucleotide reverse transcriptase inhibitor-sparing regimen for HIV-infected naive patients: 48-week final results of VEMAN study
Authors: S. Nozza, L. Galli, A. Antinori, S. Chiappetta, F. Mazzotta, M. Zaccarelli, S. Ottou, D. De Battista, M. Pogliaghi, M. Di Pietro, M. Malnati, M. Ripa, S. Bonora, A. Lazzarin
Journal: Clinical Microbiology and Infection (2014)