tbuckley/cabot-search huggingface dataset:
Noninvasive Ventilation in Acute Cardiogenic Pulmonary Edema
Authors: Josep Masip, Marta Roque, Bernat Sánchez, Rafael Fernández, Mireia Subirana, José Angel Expósito
Journal: JAMA (2005)

In patients with acute cardiogenic pulmonary edema noninvasive ventilation may reduce intubation rate, but the impact on mortality and the superiority of one technique over another have not been clearly established.To systematically review and quantitatively synthesize the short-term effect of noninvasive ventilation on major clinical outcomes.MEDLINE and EMBASE (from inception to October 2005) and Cochrane databases (library issue 4, 2005) were searched to identify relevant randomized controlled trials and systematic reviews published from January 1, 1988, to October 31, 2005.Included trials were all parallel studies comparing noninvasive ventilation to conventional oxygen therapy in patients with acute pulmonary edema. Comparisons of different techniques, either continuous positive airway pressure (CPAP) or bilevel noninvasive pressure support ventilation (NIPSV), were also included.Fifteen trials were selected. Overall, noninvasive ventilation significantly reduced the mortality rate by nearly 45% compared with conventional therapy (risk ratio [RR], 0.55; 95% confidence interval [CI], 0.40-0.78; P = .72 for heterogeneity). The results were significant for CPAP (RR, 0.53; 95% CI, 0.35-0.81; P = .44 for heterogeneity) but not for NIPSV (RR, 0.60; 95% CI, 0.34-1.05; P = .76 for heterogeneity), although there were fewer studies in the latter. Both modalities showed a significant decrease in the "need to intubate" rate compared with conventional therapy: CPAP (RR, 0.40; 95% CI, 0.27-0.58; P = .21 for heterogeneity), NIPSV (RR, 0.48; 95% CI, 0.30-0.76; P = .24 for heterogeneity), and together (RR, 0.43; 95% CI, 0.32-0.57; P = .20 for heterogeneity). There were no differences in intubation or mortality rates in the analysis of studies comparing the 2 techniques.Noninvasive ventilation reduces the need for intubation and mortality in patients with acute cardiogenic pulmonary edema. Although the level of evidence is higher for CPAP, there are no significant differences in clinical outcomes when comparing CPAP vs NIPSV.
Secretory type II phospholipase A2 binds to ischemic myocardium during myocardial infarction in humans
Authors: R Nijmeijer
Journal: Cardiovascular Research (2002)

Objective: An increase of circulating secretory Phospholipase A2 (sPLA2) is a risk factor for coronary artery disease. We hypothesized that this reflects participation of sPLA2 in local inflammatory reactions ensuing in ischemic myocardium. Therefore, we studied the course of circulating sPLA2, in patients with acute myocardial infarction (AMI) or unstable angina pectoris (UAP), and investigated the presence of sPLA2 in infarcted myocardial tissue. Methods: Plasma samples of 107 patients with AMI or UAP, collected on admission and at varying intervals thereafter, were tested for the presence of sPLA2 and C-reactive protein (CRP). Cumulative release values of these parameters were calculated, which allowed for comparison of the results rearranged in time according to the onset of symptoms. By immunohistochemistry we studied the presence of sPLA2 and CRP in myocardial tissue of 30 patients who died subsequent to AMI. Results: Levels of sPLA2 became elevated during the disease course in 66 of the 87 patients with AMI, and were higher than those of the patients with UAP of whom 8 of the 20 had elevated levels. By immunohistochemistry sPLA2 was found to be localized in the infarcted myocardium, particularly in its borderzone, from 12 h after the onset of AMI. Positive staining for sPLA2 was more extensive than that for CRP. Conclusions: The localization pattern of sPLA2 in infarcted myocardium as well as its plasma course, in relation to those of CRP, are in line with a supposed pro-inflammatory role during AMI for sPLA2 as a generator of lysophospholipids serving as ligands for CRP.
Screening for Sickle Cell Disease and Related Disorders
Authors: Fred Rosner
Journal: JAMA (1972)

To the Editor.—  Nalbandian and coworkers have certainly made a valuable contribution in their critical evaluation of the Sickledex  for hemoglobin S ( 218 :1679, 1971) and in their introduction of an automated system for screening large numbers of individuals for sickle cell disease ( 218 :1680, 1971). The following comments seem pertinent.  Their statement that it is pointless to attempt to screen black babies for the presence of hemoglobin S before 6 months of age by any test is a dogmatic misrepresentation of the true situation. Schneider et al 1 have demonstrated that citrate agar electrophoresis can readily detect sickle hemoglobin on cord blood samples.  The discovery of 165 cases of sickle cell hemoglobin among 23,000 troops screened at Fort Knox, Kentucky, indicates that a large number of white soldiers were screened. One might question the need for devoting effort, time, and expense to such a screening program, and reserve
Case 21-1988
Authors: Richard C. Cabot, Robert E. Scully, Eugene J. Mark, William F. McNeely, Betty U. McNeely, Leonard Zinman, Richard C. Pfister, Robert H. Young
Journal: New England Journal of Medicine (1988)

Presentation of CaseA 77-year-old man was admitted to the hospital because of a question of a right enterocutaneous fistula with a right inguinal abscess.There was a long history of diabetes mellitus, which recently was managed by diet alone. An appendectomy and right inguinal herniorrhaphy were performed in the past. Thirteen years before entry the patient underwent a surgical procedure at another hospital for a right renal calculus. Seven years before admission a computed tomographic (CT) scan of the abdomen was performed at another hospital because of chronic abdominal pain and revealed a fluid collection of considerable length and . . .
Herpesvirus-like DNA sequences in patients with Mediterranean Kaposi's sarcoma
Authors: N. Dupin, M. Grandadam, V. Calvez, J.T. Aubin, J.M. Huraux, H. Agut, N. Dupin, I. Gorin, S. Havard, F. Lamy, M. Leibowitch, J.P. Escande
Journal: The Lancet (1995)
Increased sensitivity of melanocytes to oxidative stress and abnormal expression of tyrosinase-related protein in vitiligo
Authors: K. Jimbow, H. Chen, J-S. Park, P.D. Thomas
Journal: British Journal of Dermatology (2001)

Background Vitiligo is a depigmenting disease of the skin, which may derive from programmed melanocyte death or destruction due to inherent sensitivity to oxidative stress arising from either toxic intermediates of melanin, a melanocyte‐specific protein, or other sources. Tyrosinase‐related protein (TRP) ‐1 has been shown to be involved not only in melanin biosynthesis but also in the prevention of premature melanocyte death in animals. Objectives To clarify the biological role of human TRP‐1 in melanocyte survival. Methods Cultured melanocyte strains from an active advancing border of vitiligo were established and studied. Results The established ‘vitiligo melanocytes’ showed large perikaryon and stubby dendrites. They showed early cell death when exposed to oxidative stress (ultraviolet B) and increased and abnormal immunostaining and immunoprecipitation by antibodies against human and mouse TRP‐1, indicating an altered synthesis and processing of TRP‐1. In pulse–chase and sequential immunoprecipitation experiments, vitiligo melanocytes revealed abnormal protein–protein interaction with calnexin, a melanogenesis‐associated chaperone, suggesting altered folding and maturation of nascent TRP‐1 polypeptides. Northern blot analysis indicated a decreased expression of TRP‐1 mRNA, but heteroduplex analysis and verification of the mutation at the carboxy terminus of TRP‐1 by restriction enzyme analysis did not show any abnormality. Conclusions Our study suggests that the early cell death of vitiligo melanocytes is related to their increased sensitivity to oxidative stress, which may arise from complex processes of abnormal synthesis and processing of TRP‐1 and its interaction with calnexin.
P314Ontogenetic contribution of mesodermal pro/epicardial cell lineages to coronary endothelium
Authors: E Cano, R Carmona Megias, A Ruiz, YY Chau, ND Hastie, R Munoz-Chapuli, JM Perez Pomares
Journal: Cardiovascular Research (2014)

Purpose: The embryonic origin of coronary endothelium remains controversial.Whereas studies using avian embryos support a critical contribution of epicardial progenitor/epicardium-derived cells to coronary endothelium, genetic tagging experiments in mice suggest that proepicardial/epicardial cell differentiation into coronary endothelial cells is a rare event.Methods : Using proepicardial/epicardial Cre drivers and different reporter lines (R26R-eYFP/R26R-eGFP) we have traced proepicardial/epicardial-derived cells.Results: We have identified a significant contribution of these cells to coronary endothelium from embryonic to postnatal stages.Genetically-tagged coronary endothelial cells express vascular markers (FACS and sqPCR) similar to those characterizing proepicardial angioblasts (ED9.5).Our spatio-temporal map shows that Wt1Cre-YFP+ and eGata4Cre-YFP cells incorporate to the coronary endothelium.Moreover, Wt1Cre-YFP+ and eGata4Cre-YFP cells display a preferential incorporation to presumptive coronary arteries and capillaries rather than to coronary veins.Such patterned distribution is especially evident on the left ventricular side.Conclusion: Cells from a Wt1+ and an eGata4+ cell lineage incorporate to coronary endothelium along mouse embryogenesis.Although the contribution of proepicardial/epicardial cells to the mouse coronary endothelium is not as massive as in avian embryos, this study unambiguously confirms a significant contribution of these cells to coronary development and identifies a potential role for these cells in the patterning and organization of the coronary arterial vasculature.
Methylprednisolone treatment fails to protect mice from the H5N1 influenza A virus-induced proinflammatory response and mortality
Authors: Lin Pu, Tao Jiang, Jing-Yuan Liu, Yong-Qiang Deng, Peng Wang, Qing-Gong Nian, Xue-Dong Yu, Shun-Ya Zhu, Yong-Li Zhang, Cheng-Feng Qin
Journal: Journal of Infection (2014)
Mitogen-activated Protein Kinase Kinase Antagonized Fas-associated Death Domain Protein–mediated Apoptosis by Induced FLICE-inhibitory Protein Expression
Authors: Jung-Hua Yeh, Shu-Ching Hsu, Shou-Hwa Han, Ming-Zong Lai
Journal: The Journal of Experimental Medicine (1998)

Fas and Fas-associated death domain (FADD) play a critical role in the homeostasis of different cell types. The regulation of Fas and FADD-mediated cell death is pivotal to many physiological functions. The activation of T lymphocytes by concanavalin A (Con A) inhibited Fas-mediated cell death. We identified that among the several activation signals downstream of Con A stimulation, mitogen-activated protein (MAP) kinase kinase (MKK) was the major kinase pathway that antagonized Fas-triggered cell death. MKK1 suppressed FADD- but not caspase-3– induced apoptosis, indicating that antagonism occurred early along the Fas-initiated apoptotic cascade. We further demonstrated that activation of MKK1 led to expression of FLIP, a specific inhibitor of FADD. MKK1 inhibition of FADD-induced cell death was abrogated if induction of FLIP was prevented, indicating that FLIP mediates MKK1 suppression of FADD-mediated apoptosis. Our results illustrate a general mechanism by which activation of MAP kinase attenuates apoptotic signals initiated by death receptors in normal and transformed cells.
STUDIES ON THE PATHOGENESIS OF FEVER
Authors: Helmut H. Hahn, S. Fai Cheuk, C. Dianne S. Elfenbein, W. Barry Wood
Journal: The Journal of Experimental Medicine (1970)

Only intact exudate granulocytes from rabbits generated large amounts of endogenous pyrogen when incubated in 0.15 M NaCl. No matter how whole-cell lysates or combinations of subcellular fractions were incubated, their yields of pyrogen never approached those of whole cells; at most, only minimal amounts of pyrogen were formed, once the integrity of the cells had been destroyed. Some pyrogen could be extracted from disrupted cells, but never more than a fraction (&amp;lt;25%) of that released from incubated whole cells. The yield could be slightly improved by lowering the pH (to 3.5) and by increasing the volume of extraction fluid. Virtually all of the preformed pyrogen that could be extracted from sucroselysed cells was found in their cytoplasmic fraction. Contrary to the results of Herion et al. (3), none could be detected in the granular (or lysosomal) fraction. Likewise, all efforts to recover pyrogen from the membrane-nuclear fraction were unsuccessful. In keeping with the finding that preformed pyrogen is contained in the cytoplasmic fraction were the observations that practically all of the aldolase, a cytoplasmic enzyme, and very little of the acid phosphatase, a granular enzyme, were lost from the cells during the release of pyrogen. Lysozyme, an enzyme stored in both the granules and the cytoplasm, was partially released from the cells under the same circumstances. Neither the release of pyrogen nor its slight intracellular buildup that precedes release (4) were affected by concentrations of puromycin that block protein synthesis in the cells and prevent their activation. Hence, it is concluded that the release process, which also involves the formation of active pyrogen (4), does not require protein synthesis, whereas activation of the cells, which may involve the synthesis of an inactive precursor (2), does.
Improving decision accuracy where base rates matter: The prediction of violent recidivism
Authors: Vernon L. Quinsey
Journal: Behavioral and Brain Sciences (1996)

Abstract Base rates are vital in predicting violent criminal recidivism. However, both lay people given simulated prediction tasks and professionals milking real life predictions appear insensitive to variations in the base rate of violent recidivism. Although there are techniques to help decision makers attend to base rates, increased decision accuracy is better sought in improved actuarial models as opposed to improved clinicians.
Acupunctural Analgesia: Its Explanation by Conditioning Theory, Autogenic Training, and Hypnosis
Authors: WILLIAM S. KROGER
Journal: American Journal of Psychiatry (1973)

Acupunctural analgesia seems to work—but better for the Chinese than for other nationalities. Significant antecedent, intervening, and dependent variables indicate that the technique can best be understood within the paradigm of contemporary conditioning theory. It has not been placed in this framework because scientist-observers have not stressed the effects of shaping and modifying behavior by a kind of operant conditioning that brings about compliant behavior without the necessity for overt cooperation. This compliance can account for the broad spectrum of psychobiologic experiences leading to well-known placebo responses. Another factor not generally recognized is the powerful effect of suggestion, which enhances suggestibility and hypnotizability. The author also discusses the neuropsychophysiologic mechanisms involved in acupunctural analgesia.
Alan MacRae Whittington
Authors: T. Morgan
Journal: BMJ (2002)

General practitioner Ascot, Berkshire, 1950-83 (b Isleworth, Middlesex, 1920; q Cambridge/Middlesex Hospital 1946), d 4 August 2002.

Alan worked in ear, nose, and throat at the Middlesex Hospital and in the Royal Air Force during national service before entering general practice in Longridge, Lancashire. A southerner at heart, he took up a partnership in Ascot and remained in practice there until forced to retire by his first stroke at the age of 63. He retained his patience and sense of humour despite being denied an active retirement—his hobbies had been dinghy sailing, gardening (especially vegetables), cooking, his family, and his dogs. He leaves a wife, Ann; two sons; and five grandchildren.
The Politics of Cancer
Authors: Richard L. Meyer
Journal: JAMA (1981)

<i>The Politics of Cancer</i>is a 600+ page political statement. Starting from the premises that a high percentage of cancers are caused by exposure to environmental agents and that the latent period between exposure and clinical cancer is 15 to 20 years, Dr Epstein discloses major and minor carcinogenic experiences in the workplace, the personal environment, and the general environment. This overwhelming, ubiquitous exposure to one or more carcinogenic agents is the cause of immeasurable avoidable suffering. The proliferation of carcinogenic agents in the future and the uncontrollable use of known carcinogenic agents are leading to an explosion in the incidence of cancer. This scenario must be changed. The cause of cancer has been defined. That cause is man-made or man-controlled, and so must be removed. Past obstacles have been a greedy, crass industry and an inept government. An aroused citizenry with enforceable regulations over possible, probable, potential, or definite
DIFFERING PATTERNS OF MYOSTATIN SIGNALING REGULATE HYPERTROPHY IN SEVERE AORTIC STENOSIS AND HYPERTROPHIC CARDIOMYOPATHY
Authors: Estibaliz Castillero, Hirokazu kashi, Halit Yerebakan, Robert Sorabella, Marc Najjar, Klara Pendrak, Catherine Wang, Ziad Ali, Donna Mancini, Jeannine D'rmiento, H. Lee Sweeney, P. Christian Schulze, Isaac George
Journal: Journal of the American College of Cardiology (2014)
Abstract B4: Chromosome 17p13.1 (KCTD11), a smoking-related susceptible region linked to lung cancer risk in Korean populations
Authors: Yeiwon Lee, Minhyeok Lee, Hyunjung Cho, Jeeyoung Hong, Seonjung Kwon, Chang-Gyo Park, Hoi-Young Lee, Ji-Woong Son, Jaeku Kang, Jeeyoung Hong
Journal: Clinical Cancer Research (2010)

Abstract Lung cancer is the most common cause of cancer death worldwide. Smoking is known as the strongest single factor for the development of lung cancer. However, there are inherited genetic factors that cause different responses to cigarette smoking exposure among individuals. We tried to identify these differences in heavy smokers by examining copy number variations (CNVs) between lung cancer patients and healthy controls. Analysis by array comparative genomic hybridization (aCGH) showed 26 significant (P&amp;lt;0.05) clones with either copy number gains or losses. 3 genes, KCTD11, FGF11, and PTPRH on chromosomal regions 17p13.1 (KCTD11 and FGF11) and 19q13.42 (PTPRH) were selected (P&amp;lt;0.001) and tested by realtime quantitative PCR (qPCR) with 34 healthy controls and 54 lung cancer patients for large-scale analysis. KCTD11, a known tumor suppressor gene, showed copy number losses in cancer patients. In addition, as the years of smoking increased, odds ratios were also increased (0R=0.8,2.2, and 16.0), implying that it is a susceptible gene to lung cancer when an individual smokes. Therefore, KCTD11 is a promising candidate for a predictive marker to identify individuals with high, inherited genetic risk for the development of lung cancer. Citation Information: Clin Cancer Res 2010;16(14 Suppl):B4.
License in Germany.
Authors: B. Becker
Journal: JAMA (1897)

Toledo, Ohio, Dec. 10, 1897. <h3>To the Editor:</h3> —Dr. Blech's answer to the inquiry as to the admission to the practice of medicine in Germany is not quite correct. To be matriculated as a student of medicine, one must be a graduate from a gymnasium covering a classical course of nine years. These graduates are 20 years old on the average. After four semesters, usually during the fifth, the medical student passes the<i>tentamen physicum</i>, an examination in physiology, anatomy, physics, chemistry, physiologic chemistry, botany, mineralogy. Before passing the<i>tentamen physicum</i>the student is not admitted to the clinics. The candidate for<i>State examination</i>must have studied medicine and the allied branches for<i>at least</i>eight semesters, of which not more than three are allowed to be passed at a recognized foreign university. While eight semesters are the required time, it is by no means the average, which may be
Development of allergies and asthma in infants and young children with atopic dermatitis – a prospective follow‐up to 7 years of age
Authors: D. Gustafsson, O. Sjöberg, T. Foucard
Journal: Allergy (2000)

The prognosis of atopic dermatitis is usually good, but the risk of developing asthma and allergic rhinitis is very high. The aim of this study was to follow children with atopic eczema up to school age to chart the course of sensitization and development of clinical allergy, as well as to study risk factors of sensitization.Ninety-four children with atopic dermatitis were followed up to 7 years of age. The children were examined twice a year up to 3 years of age, and thereafter once yearly. At each visit, a clinical examination was performed, and a blood sample was taken. After 3 years of age, skin prick tests (SPTs) with inhalation allergens were performed at each visit. Information was obtained about atopy in the family, feeding patterns during infancy, symptoms of atopic disease, infections, and environmental factors.During the follow-up, the eczema improved in 82 of the 94 children, but 43% developed asthma and 45% allergic rhinitis. The risk of developing asthma was higher in children with a heredity of eczema. Presence of severe eczema at the time of inclusion in the study was associated with an increased tendency to produce food-specific IgE. An early onset of eczema was associated with an increased risk of sensitization to inhalant allergens, and development of urticaria. Early allergic reactions to food were associated with later reactions to food, allergic rhinitis, urticaria, and sensitization to both food and inhalant allergens. Early feeding patterns, time of weaning, and introduction of solid food did not influence the risk of development of allergic symptoms. A large number of periods or days with fever during the follow-up was associated with an increased risk of developing allergic rhinitis and urticaria.Our results confirm the good prognosis for the dermatitis and the increased risk of developing asthma and allergic rhinitis. Development of other allergic symptoms or sensitization was associated with the following factors: a family history of eczema, age at onset of eczema and its severity, early adverse reactions to foods, and proneness to infections.