tbuckley/cabot-search huggingface dataset:
Primary Pulmonary Hypertension
Authors: Stephen Archer, Stuart Rich
Journal: Circulation (2000)

Abstract —Primary pulmonary hypertension (PPH) is a syndrome of dyspnea, chest pain, and syncope defined by increased pulmonary vascular resistance and the absence of a known cause. It also occurs in a familial form, which is linked to unidentified genes on chromosome 2. This syndrome is characterized by abnormalities of pulmonary vascular biology in each compartment of the blood vessel. The lumen has a prothrombotic diathesis, the endothelium displays an excessive production of vasoconstrictors relative to vasodilators, and the smooth muscle cells are depolarized and calcium-overloaded, which is due in part to reduced expression of voltage-gated potassium channels (Kv). This causes vasoconstriction and may promote cell proliferation. The adventitia displays excessive remodeling, which is associated with exaggerated metalloproteinase and elastase activity. Conceptually, PPH seems to require a permissive genotype, a susceptible phenotype (eg, endothelial dysfunction) and, in many cases, an exogenous trigger (eg, an anorexigen). Although there is not a generally accepted, unifying hypothesis regarding its cause, impaired function and the expression of vascular and platelet Kv channels suggest PPH may be a disease of the ion channels. Abnormal matrix metalloproteinase and elastase activity could also explain the abnormal vascular tone, platelet activation, and remodeling in PPH. Although calcium-channel blockers and prostacyclin, particularly when coadministered with warfarin, improve survival, PPH has a 5-year mortality rate of ≈50%. Pharmacological and gene therapies aimed at enhancing the activity of prostacyclin, nitric oxide synthases, and Kv channels or at inhibiting endothelin and matrix metalloproteinases are promising areas for future development.
ACTIVEDEP: a randomised, controlled trial of a home-based exercise intervention to alleviate depression in middle-aged and older adults
Authors: Jon J Pfaff, Helman Alfonso, Robert U Newton, Moira Sim, Leon Flicker, Osvaldo P Almeida
Journal: British Journal of Sports Medicine (2013)

Objective To evaluate the efficacy of a home-based exercise programme added to usual medical care for the treatment of depression. Design Prospective, two group parallel, randomised controlled study. Setting Community-based. Patients 200 adults aged 50 years or older deemed to be currently suffering from a clinical depressive illness and under the care of a general practitioner. Interventions Participants were randomly allocated to either usual medical care alone (control) or usual medical care plus physical activity (intervention). The intervention consisted of a 12-week home-based programme to promote physical activity at a level that meets recently published guidelines for exercise in people aged 65 years or over. Main outcome measurements Severity of depression was measured with the structured interview guide for the Montgomery-Asberg Depression Rating Scale (SIGMA), and depression status was assessed with the Structured Clinical Interview for DSM-IV Axis I Disorders (SCID-I). Results Remission of depressive illness was similar in both the usual care (59%) and exercise groups (63%; OR = 1.18, 95% CI 0.61 to 2.30) at the end of the 12-week intervention, and again at the 52-week follow-up (67% vs 68%) (OR=1.07, 95% CI 0.56 to 2.02). There was no change in objective measures of fitness over the 12-week intervention among the exercise group. Conclusions This home-based physical activity intervention failed to enhance fitness and did not ameliorate depressive symptoms in older adults, possibly due to a lack of ongoing supervision to ensure compliance and optimal engagement.
Atrioventricular Block in a Long-Term Dialysis Patient
Authors: William Dreher
Journal: JAMA (1975)

WITH THE advent of hemodialysis for patients with end-stage renal disease, medical complications not previously encountered, including advanced secondary hyperparathyroidism with resultant metastatic calcifications, have developed.<sup>1-6</sup>Cardiac calcifications have been reported previously as an autopsy finding, with some leading to refractory fatal cardiac arrhythmias.<sup>1-5</sup>Our patient had first-degree heart block, possibly as a result of metastatic cardiac calcification that completely reversed to normal sinus rhythm two months after a total parathyroidectomy. <h3>Report of a Case</h3> A 20-year-old man with end-stage renal disease secondary to chronic pyelonephritis and vesicoureteral reflux began hemodialysis treatments in July 1971. On Aug 2, 1973, he was admitted to the hospital for the revision of an arteriovenous fistula because of recurrent episodes of high-output cardiac failure. An electrocardiogram on Aug 3 demonstrated first-degree heart block with a PR interval of 0.24 seconds. The ventricular rate was 100 beats per minute, and there was evidence
Campylobacter Enteritis: Clinical and Epidemiologic Features
Authors: MARTIN J. BLASER
Journal: Annals of Internal Medicine (1979)

Campylobacter fetus subspecies (ssp.) jejuni has been recently recognized to cause diarrheal disease in man. To assess its importance as an enteric pathogen, we prospectively studied 514 patients with diarrhea. Campylobacter fetus ssp. jejuni was isolated from the feces of 26 patients (5%) and seven of 11 of their symptomatic household contacts. This organism was isolated from the feces of only one of 18 asymptomatic household contacts and not at all from 157 other healthy persons. Seventeen of 20 patients from whom C. fetus ssp. jejuni was isolated from fecal culture showed at least a fourfold rise in specific IgG titers. Review of 35 cases of Campylobacter enteritis identified a typical clinical syndrome with acute onset of diarrhea, abdominal pain, fever, and constitutional symptoms. Stool examination revealed blood in 60% and polymorphonuclear leukocytes in 78% of patients. Epidemiologic investigation strongly suggested an external source for the infection in 22 of 35 patients.
IgE-mediated hypersensitivity in human heart !tissue: Histamine release and functional c,hanges
Authors: L.Michael Graver, Donna A. Robertson, Roberto Levi, Carl G. Becker, Babette B. Weksler, William A. Gay
Journal: Journal of Allergy and Clinical Immunology (1986)

In experiments described herein, it was observed that IRE-mediated hypersensitivity can result in significant histamine and thromboxane release from human myocardium, suggesting that the human heart may participate as a target organ in allergic reactions.Muscle units (pectinate muscles) were isolated from human atria1 appendages, removed routinely during corrective cardiac surgery, and were allowed to beat spontaneously in a tissue bath.Remnants of each atria1 specimen were chopped and added to the tissue bath, Challenge of the atrial tissue with goat antiserum to human myeloma IgE caused histamine and thromboxane B2 release and marked increases in contractility and spontaneous rate.In contrast, challenge with nonspeciJic goat antiserum or with antiserum from which anti-IgE antibodies had been removed caused neither mediator release nor changes in rate or contractility.The histamine HI-receptor antagonist cimetidine inhibited the inotropic and chronotropic changes but not the histamine release.(J ALURGYCLIN IMMUNOL 77:709-14, 1986.)Data from our laboratory indicate that the heart reacts as a target organ in immediate hypersensitivity reactions.'-' Cardiac dysfunctions observed during anaphylaxis in the guinea pig'.* resemble those reported in humans4-' and are caused by mediators released intracardially and reaching the heart from the lung.*In the guinea pig cardiac anaphylaxis' is characterized by tachycardia, a brief increase in contractile force followed by a prolonged decrease, coronary vasoconstriction, arrhythmias, and mediator release.', 3, '"." The increases in rate and contractility
Tolbutamide-Associated Hyponatremia
Authors: L. Lichtenberg
Journal: JAMA (1978)

To the Editor.—  It is known that the use of chlorpropamide in diabetics may result in hyponatremia.1Less well appreciated and only once described before is a similar phenomenon with the use of tolbutamide.  Report of a Case.—  A 64-year-old man, diabetic for ten years, was admitted to Hines Veterans Administration Hospital, Surgical Service, for bilateral nonhealing ulcers on the stumps of his below-the-knee amputations, performed four years earlier for gangrene. Diabetes had been controlled (fasting blood glucose levels averaged 100 mg/dl) with oral tolbutamide, 500 mg daily, for two years.  Physical examination showed an oriented, cooperative, chronically ill man. There was no edema, evidence of heart failure, or cirrhosis. Necrotic ulcers were present on both stumps. Chest x-ray film was normal. Serum sodium level was 114 mEq/liter; chloride level, 83 mEq/liter; BUN level, 12 mg/dl; creatinine level, 0.7 mg/dl; cholesterol level, 150 mg/dl; and albumin level, 2.9 g/dl.
William L. Webb, Jr, MD
Authors: Charles W. Boren
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
Colon Cancer Update Triggers Changes in Practice
Authors: C. Vanchieri
Journal: JNCI Journal of the National Cancer Institute (1990)

Journal Article Colon Cancer Update Triggers Changes in Practice Get access Cori Vanchieri Cori Vanchieri Search for other works by this author on: Oxford Academic PubMed Google Scholar JNCI: Journal of the National Cancer Institute, Volume 82, Issue 11, 6 June 1990, Page 898, https://doi.org/10.1093/jnci/82.11.898 Published: 06 June 1990
Identification of PML/RARα rearrangements in suspected acute promyelocytic leukemia using fluorescence in situ hybridization of bone marrow smears: a comparison with cytogenetics and RT-PCR in MRC ATRA trial patients
Authors: S Iqbal, D Grimwade, A Chase, A Goldstone, A Burnett, JM Goldman, D Swirsky
Journal: Leukemia (2000)
The diabetes-susceptible gene SLC30A8/ZnT8 regulates hepatic insulin clearance
Authors: Motoyuki Tamaki, Yoshio Fujitani, Akemi Hara, Toyoyoshi Uchida, Yoshifumi Tamura, Kageumi Takeno, Minako Kawaguchi, Takahiro Watanabe, Takeshi Ogihara, Ayako Fukunaka, Tomoaki Shimizu, Tomoya Mita, Akio Kanazawa, Mica O. Imaizumi, Takaya Abe, Hiroshi Kiyonari, Shintaro Hojyo, Toshiyuki Fukada, Takeshi Kawauchi, Shinya Nagamatsu, Toshio Hirano, Ryuzo Kawamori, Hirotaka Watada
Journal: Journal of Clinical Investigation (2013)

Recent genome-wide association studies demonstrated that common variants of solute carrier family 30 member 8 gene (SLC30A8) increase susceptibility to type 2 diabetes. SLC30A8 encodes zinc transporter-8 (ZnT8), which delivers zinc ion from the cytoplasm into insulin granules. Although it is well known that insulin granules contain high amounts of zinc, the physiological role of secreted zinc remains elusive. In this study, we generated mice with β cell-specific Slc30a8 deficiency (ZnT8KO mice) and demonstrated an unexpected functional linkage between Slc30a8 deletion and hepatic insulin clearance. The ZnT8KO mice had low peripheral blood insulin levels, despite insulin hypersecretion from pancreatic β cells. We also demonstrated that a substantial amount of the hypersecreted insulin was degraded during its first passage through the liver. Consistent with these findings, ZnT8KO mice and human individuals carrying rs13266634, a major risk allele of SLC30A8, exhibited increased insulin clearance, as assessed by c-peptide/insulin ratio. Furthermore, we demonstrated that zinc secreted in concert with insulin suppressed hepatic insulin clearance by inhibiting clathrin-dependent insulin endocytosis. Our results indicate that SLC30A8 regulates hepatic insulin clearance and that genetic dysregulation of this system may play a role in the pathogenesis of type 2 diabetes.
Plasma alpha natriuretic peptide in cardiac impairment.
Authors: A M Richards, J G Cleland, G Tonolo, G D McIntyre, B J Leckie, H J Dargie, S G Ball, J I Robertson
Journal: BMJ (1986)

Regional plasma alpha human atrial natriuretic peptide concentrations were measured, and their relation to intracardiac pressures assessed, in an unselected series of 45 patients undergoing diagnostic cardiac catheterisation. Arteriovenous gradients in plasma concentrations of alpha human atrial natriuretic peptide were consistent with its cardiac secretion and its clearance by the liver and kidneys. Plasma concentrations of the peptide in the pulmonary artery, aorta, and superior vena cava correlated closely with the mean right atrial and pulmonary arterial pressures, and similar, though weaker, positive relations were seen with the left ventricular end diastolic and pulmonary artery wedge pressures. Concentrations of both atrial natriuretic peptide and renin showed significant inverse relations with serum sodium concentrations. Plasma concentrations of alpha human atrial natriuretic peptide are an additional objective indicator of the severity of haemodynamic compromise in patients with cardiac impairment.
Applied Bacteriology for Nurses.
Authors: Charles Frederick Bolduan, Marie. Grund
Journal: JAMA (1930)

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
THE DERIVATION OF TWO DISTINCT ANAPHYLATOXIN ACTIVITIES FROM THE THIRD AND FIFTH COMPONENTS OF HUMAN COMPLEMENT
Authors: C. G. Cochrane, H. J. Müller-Eberhard
Journal: The Journal of Experimental Medicine (1968)

Anaphylatoxin activity was derived from both human C'5 and C'3 molecules. This was achieved in the case of C'5 by interaction with trypsin or with EAC'4, (oxy)2a, 3. The smooth muscle-contracting material obtained from the treated C'5 was found to be a fragment of approximately 9,000-11,000 molecular weight. Its action was inhibited with antihistamine. The trypsinized C'5 also increased vascular permeability in guinea pig skin. When human C'3 was incubated with C'3 inactivator complex, which consists of a cobra venom protein and a beta-globulin of human serum, anaphylatoxin activity was observed. The activity was associated with a fragment cleaved from the C'3 molecule, having a molecular weight of between 6,000 and 15,000 as determined by gel filtration techniques. Similar activity was derived from C'3 by the C'3-converting enzyme in free or in cell-bound form. The C'5 anaphylatoxin failed to cross-desensitize guinea pig ileum to the contracting capacities of C'3 and guinea pig anaphylatoxin and vice versa. Anaphylatoxin prepared from C'3 by all methods mentioned above caused cross-desensitization to the other C'3 derivatives, but failed to desensitize to guinea pig anaphylatoxin.
Multimodal Approaches in the Management of Locally Advanced and Metastatic Renal Cell Carcinoma: Combining Surgery and Systemic Therapies to Improve Patient Outcome
Authors: Christopher G. Wood
Journal: Clinical Cancer Research (2007)

Abstract Patients with locally advanced renal cell carcinoma are at high risk of metastatic relapse following surgery. Patients with metastatic disease have a poor prognosis and few systemic therapy options. Radiation, chemotherapy, hormonal therapy, vaccines, and immunotherapy have all been tested as adjuvant therapy without benefit. Neoadjuvant therapy in the metastatic setting holds promise as a new treatment paradigm. It can serve as a litmus test to allow proper patient selection for aggressive surgical intervention and may provide limited downstaging of primary tumors in selected cases. It can also provide a histologic assessment of the effect of targeted therapy. Application of this paradigm may have merit in the locally advanced setting as well. Effective adjuvant therapy for renal cell carcinoma remains elusive. The benefit of new targeted therapies has yet to be tested in this setting. Neoadjuvant strategies that integrate aggressive surgical intervention with systemic therapy may hold promise as a treatment paradigm.
IFN-β Signaling Positively Regulates Tumorigenesis in Aggressive Fibromatosis, Potentially by Modulating Mesenchymal Progenitors
Authors: Sean S. Tjandra, Claire Hsu, Ingrid Goh, Ananta Gurung, Raymond Poon, Puviindran Nadesan, Benjamin A. Alman
Journal: Cancer Research (2007)

Abstract Aggressive fibromatosis (also called desmoid tumor) is a benign, locally invasive, soft tissue tumor composed of cells with mesenchymal characteristics. These tumors are characterized by increased levels of β-catenin–mediated T-cell factor (TCF)–dependent transcriptional activation. We found that type 1 IFN signaling is activated in human and murine aggressive fibromatosis tumors and that the expression of associated response genes is regulated by β-catenin. When mice deficient for the type 1 IFN receptor (Ifnar1−/−) were crossed with mice predisposed to developing aggressive fibromatosis tumors (Apc/Apc1638N), a significant decrease in aggressive fibromatosis tumor formation was observed compared with littermate controls, showing a novel role for type 1 IFN signaling in promoting tumor formation. Type 1 IFN activation inhibits cell proliferation but does not alter cell apoptosis or the level of β-catenin–mediated TCF-dependent transcriptional activation in aggressive fibromatosis cell cultures. Thus, these changes cannot explain our in vivo results. Intriguingly, Ifnar1−/− mice have smaller numbers of mesenchymal progenitor cells compared with littermate controls, and treatment of aggressive fibromatosis cell cultures with IFN increases the proportion of cells that exclude Hoechst dye and sort to the side population, raising the possibility that type 1 IFN signaling regulates the number of precursor cells present that drive aggressive fibromatosis tumor formation and maintenance. This study identified a novel role for IFN type 1 signaling as a positive regulator of neoplasia and suggests that IFN treatment is a less than optimal therapy for this tumor type. [Cancer Res 2007;67(15):7124–31]
Relax: It's Onlie Sodeyne Death-Reply
Authors: Thomas E. Kottke
Journal: JAMA (1993)

In Reply.  —We regret that Dr Kirkland failed to read or to understand the sentence in the Methods section of our article that defined  unexpected death: The diagnosis of sudden unexpected death was made when a patient who had no previous clinical diagnosis of coronary heart disease died within 24 hours of the onset of symptoms typical or suggestive of acute myocardial infarction.  As wrongly implied by Dr Kirkland, we did not apply the term to any patient who survived more than 24 hours.  We combined the analysis of the group of patients who presented with sudden unexpected death and those who presented with myocardial infarction to avoid the misinterpretation that can occur when the experience of patients with one or the other diagnoses is analyzed in isolation.  Misinterpretation might result, for example, if two different groups of patients have similar survival rates but one group is consistently more
Abstract 1195: EphA4 is a novel tumor suppressor in lung adenocarcinoma
Authors: Shaohua Peng
Journal: Cancer Research (2011)

Abstract Lung cancer is the leading cause of death from cancer, but the mechanisms behind its initiation and progression are not completely understood. Receptor tyrosine kinases (RTKs) are important in normal cellular physiology as well as in the pathogenesis of a variety of tumors. In this study, we explored the roles of the human Eph kinase family in lung adenocarcinoma. The Eph fmaily is the largest RTK superfamily with 14 receptors and 8 ligands (ephrins). Eph receptors have been implicated both as tumor suppressors and oncogenes. To explore the effect of Eph receptors and ephrins on lung cancer, we analyzed gene expression and survival data from 432 lung adenocarcinomas from Director's Challenge Consortium by univariate Cox proportional hazards model. Of the 11 Eph receptors and 8 ephrins analyzed, only the expression of EphA4, EphA5, EphB2, ephrinA1, and ephrinB3 correlated with overall survival. Analysis of an independent dataset confirmed that EphA4 and ephrinA1 expression negatively correlated with survival in lung adenocarcinoma. After adjusting for age, gender and stage, low EphA4 expression remained significantly associated with a poor outcome for both overall and relapse-free survival with a hazard ratio of 1.57. To validate the gene expression profile data, we measured EphA4 expression in 9 NSCLC cell lines and found that the expression levels of EphA4 by microarray were well correlated with expression levels measure by qPCR and Western blotting (R2=0.89, R2=0.79 respectively), which indicate that the tissue microarray probesets are of high quality. To investigate the role of EphA4 as a putative tumor suppressor, we overexpressed EphA4 in NSCLC cell lines with low basal expression and found that the cell migration was inhibited by 38% and E-cadherin expression was increased. Likewise, E-cadherin expression was decreased with EphA4 knockdown in NSCLC cell lines with high basal EphA4 expression. These data are consistent with a role for EphA4 as a tumor suppressor via increased expression of the cell surface adhesion protein E-cadherin and concomitant decreased cell migration. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1195. doi:10.1158/1538-7445.AM2011-1195