tbuckley/cabot-search huggingface dataset:
Early Invasive vs Conservative Treatment Strategies in Women and Men With Unstable Angina and Non–ST-Segment Elevation Myocardial Infarction
Authors: Michelle O’Donoghue, William E. Boden, Eugene Braunwald, Christopher P. Cannon, Tim C. Clayton, Robbert J. de Winter, Keith A. A. Fox, Bo Lagerqvist, Peter A. McCullough, Sabina A. Murphy, Rudolf Spacek, Eva Swahn, Lars Wallentin, Fons Windhausen, Marc S. Sabatine
Journal: JAMA (2008)

Although an invasive strategy is frequently used in patients with non-ST-segment elevation acute coronary syndromes (NSTE ACS), data from some trials suggest that this strategy may not benefit women.To conduct a meta-analysis of randomized trials to compare the effects of an invasive vs conservative strategy in women and men with NSTE ACS.Trials were identified through a computerized literature search of the MEDLINE and Cochrane databases (1970-April 2008) using the search terms invasive strategy, conservative strategy, selective invasive strategy, acute coronary syndromes, non-ST-elevation myocardial infarction, and unstable angina.Randomized clinical trials comparing an invasive vs conservative treatment strategy in patients with NSTE ACS.The principal investigators for each trial provided the sex-specific incidences of death, myocardial infarction (MI), and rehospitalization with ACS through 12 months of follow-up.Data were combined across 8 trials (3075 women and 7075 men). The odds ratio (OR) for the composite of death, MI, or ACS for invasive vs conservative strategy in women was 0.81 (95% confidence interval [CI], 0.65-1.01; 21.1% vs 25.0%) and in men was 0.73 (95% CI, 0.55-0.98; 21.2% vs 26.3%) without significant heterogeneity between sexes (P for interaction = .26). Among biomarker-positive women, an invasive strategy was associated with a 33% lower odds of death, MI, or ACS (OR, 0.67; 95% CI, 0.50-0.88) and a nonsignificant 23% lower odds of death or MI (OR, 0.77; 95% CI, 0.47-1.25). In contrast, an invasive strategy was not associated with a significant reduction in the triple composite end point in biomarker-negative women (OR, 0.94; 95% CI, 0.61-1.44; P for interaction = .36) and was associated with a nonsignificant 35% higher odds of death or MI (OR, 1.35; 95% CI, 0.78-2.35; P for interaction = .08). Among men, the OR for death, MI, or ACS was 0.56 (95% CI, 0.46-0.67) if biomarker-positive and 0.72 (95% CI, 0.51-1.01) if biomarker-negative (P for interaction = .09).In NSTE ACS, an invasive strategy has a comparable benefit in men and high-risk women for reducing the composite end point of death, MI, or rehospitalization with ACS. In contrast, our data provide evidence supporting the new guideline recommendation for a conservative strategy in low-risk women.
Essential role for CD103 in the T cell–mediated regulation of experimental colitis
Authors: Oliver Annacker, Janine L. Coombes, Vivianne Malmstrom, Holm H. Uhlig, Tim Bourne, Bengt Johansson-Lindbom, William W. Agace, Christina M. Parker, Fiona Powrie
Journal: The Journal of Experimental Medicine (2005)

The integrin CD103 is highly expressed at mucosal sites, but its role in mucosal immune regulation remains poorly understood. We have analyzed the functional role of CD103 in intestinal immune regulation using the T cell transfer model of colitis. Our results show no mandatory role for CD103 expression on T cells for either the development or CD4+CD25+ regulatory T (T reg) cell–mediated control of colitis. However, wild-type CD4+CD25+ T cells were unable to prevent colitis in immune-deficient recipients lacking CD103, demonstrating a nonredundant functional role for CD103 on host cells in T reg cell–mediated intestinal immune regulation. Non–T cell expression of CD103 is restricted primarily to CD11chighMHC class IIhigh dendritic cells (DCs). This DC population is present at a high frequency in the gut-associated lymphoid tissue and appears to mediate a distinct functional role. Thus, CD103+ DCs, but not their CD103− counterparts, promoted expression of the gut-homing receptor CCR9 on T cells. Conversely, CD103− DCs promoted the differentiation of IFN-γ–producing T cells. Collectively, these data suggest that CD103+ and CD103− DCs represent functionally distinct subsets and that CD103 expression on DCs influences the balance between effector and regulatory T cell activity in the intestine.
The Art of 'HAART': Researchers Probe the Potential and Limits of Aggressive HIV Treatments
Authors: Joan Stephenson
Journal: JAMA (1997)

IN THE space of less than 2 years, some AIDS researchers have moved from the early flush of success with new, aggressive drug regimens that battle the human immunodeficiency virus (HIV) to cautious speculation that they may be on the right track to developing a viruseradicating strategy for at least some HIV-infected patients. However, mindful of a roller-coaster history of dashed hopes in treating HIV infection and AIDS, many investigators point out that formidable hurdles must be cleared before such hopes can be realized. These include the familiar specter of drug resistance, toxic adverse effects and rigorous dosing regimens that make tolerance of the drugs difficult and compliance problematic, treatment histories that render some patients unsuitable candidates for the aggressive new therapies, the possibility that sanctuary sites (such as the brain) contain a reservoir of virus that is beyond the drugs' reach, and the fear that the HIV-ravaged immune systems
Do non-steroidal anti-inflammatory drugs adversely affect stress fracture healing? A short review
Authors: P Wheeler, M E Batt
Journal: British Journal of Sports Medicine (2005)

A literature search was performed to determine whether non-steroidal anti-inflammatory drugs (NSAIDs) adversely affect the healing of stress fractures. Evidence exists from laboratory studies and animal subjects that NSAIDs can affect fracture healing. This link has not been proved or disproved in human subjects, particularly for stress fractures. In view of the high usage of NSAIDs in treating musculoskeletal disorders, research is required to investigate whether the healing of stress fractures is affected by these drugs.
IFNL3 polymorphisms predict response to therapy in chronic hepatitis C genotype 2/3 infection
Authors: Mohammed Eslam, Reynold Leung, Manuel Romero-Gomez, Alessandra Mangia, William L. Irving, David Sheridan, Ulrich Spengler, Lindsay Mollison, Wendy Cheng, Elisabetta Bugianesi, Duncan McLeod, Abed M. Zaitoun, Vito Attino, Diane Goeltz, Jacob Nattermann, Mark Douglas, David R. Booth, Jacob George, Golo Ahlenstiel
Journal: Journal of Hepatology (2014)
A SPREADING FACTOR IN CERTAIN SNAKE VENOMS AND ITS RELATION TO THEIR MODE OF ACTION
Authors: F. Duran-Reynals
Journal: The Journal of Experimental Medicine (1939)

The venom of several species of poisonous snakes acts to spread India ink through the skin as do the spreading factors procurable from certain tissues and elaborated by invasive bacteria. The factor is most abundant in the venom of the Viperidae (rattlesnake) family and relatively scant in the venom of Colubridae proteroglypha (cobra) family, and it is absent from toad venom. Extracts of the supralabial glands of harmless snakes contain only negligible amounts of the factor. Rattlesnake venom heated at 65 degrees to 100 degrees loses a large proportion of its toxicity but retains the ability to spread ink. Rattlesnake venom that has lost its toxicity on standing or on heating markedly enhances the infection produced by bacterial or virus suspension in the rabbit skin. Antivenine serum inactivates both the toxic and spreading factors of venom.
Study did a good job
Authors: J. P. Vandenbroucke
Journal: BMJ (2010)

The BMJ and several Dutch national newspapers published many criticisms of the methods of the Utrecht study on perinatal mortality in the Netherlands.1 These include: the numbers in Utrecht differ from those in another study, and therefore can’t be right; there was no correction for confounders; the number of midwife deliveries with live births was underestimated; the study wasn’t really …
Gastrointestinal Hormones in Clinical Disease: Recent Developments
Authors: JOHN H. WALSH
Journal: Annals of Internal Medicine (1979)

With the advent of radioimmunoassay and immunocytochemical methods, the peptides of the gastrointestinal tract have been identified and measured. Gastrinoma and insulinoma syndromes have been well characterized. The pancreatic cholera syndrome and some of the evidence that the major manifestations of this disease may be mediated by vasoactive intestinal peptide have been re-examined. Pancreatic polypeptide seems to be an ideal peptide for study of vagal-cholinergic mechanisms that regulate hormone release; it also appears to be a tumor marker for several types of pancreatic endocrine tumors, particularly those of pancreatic cholera. Secretin and cholecystokinin are important regulators of pancreatic exocrine secretion and have been used to test pancreatic function, but there is little evidence that they account for clinical disease. Glucagon-secreting tumors produce a clinical syndrome of diabetes mellitus and distinctive skin lesions, which can be cured by tumor resection. Hormone-secreting tumors may provide insight into normal gut physiology.
AMERICAN PHYSICIANS ARE WELCOME IN THE HUNGARIAN CLINICS
Authors: Donald Guthrie
Journal: JAMA (1931)

To the Editor:  —A few months ago there appeared in the American press several articles stating that American physicians were no longer welcome in the  clinics and that the privilege of allowing Americans to enrol as postgraduate students had been withdrawn.  Just at this time an editorial of mine on Hungarian Surgery appeared in one of our medical journals and since then I have received so many letters with regard to the matter that I should like to reiterate here that a genuine and sincere welcome awaits the American surgeons in the clinics of Budapest, and to deny the veracity of the remarks that so garbled the true state of affairs. American physicians are most cordially received as visitors and as postgraduate students. As to permitting the performing of operations by students and inexperienced surgeons, the  surgical profession must protect itself and its people, just as is done
Mercury Induces an Unopposed Inflammatory Response in Human Peripheral Blood Mononuclear Cells <i>in Vitro</i>
Authors: Renee M. Gardner, Jennifer F. Nyland, Sean L. Evans, Susie B. Wang, Kathleen M. Doyle, Ciprian M. Crainiceanu, Ellen K. Silbergeld
Journal: Environmental Health Perspectives (2009)

The human immune response to mercury is not well characterized despite the body of evidence that suggests that Hg can modulate immune responses, including the induction of autoimmune disease in some mouse models. Dysregulation of cytokine signaling appears to play an important role in the etiology of Hg-induced autoimmunity in animal models.In this study, we systematically investigated the human immune response to Hg in vitro in terms of cytokine release.Human peripheral blood mononuclear cells (PBMCs) were isolated from 20 volunteers who donated blood six separate times. PBMCs were cultured with lipopolysaccharide and concentrations of mercuric chloride (HgCl(2)) up to 200 nM. Seven cytokines representing important pathways in physiologic and pathologic immune responses were measured in supernatants. We used multilevel models to account for the intrinsic clustering in the cytokine data due to experimental design.We found a consistent increase in the release of the proinflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha, and concurrent decrease in release of the antiinflammatory cytokines interleukin 1-receptor antagonist (IL-1Ra) and IL-10 in human PBMCs treated with subcytotoxic concentrations of HgCl(2). IL-4, IL-17, and interferon-gamma increased in a concentration-response manner. These results were replicated in a second, independently recruited population of 20 different volunteers.Low concentrations of HgCl(2) affect immune function in human cells by dysregulation of cytokine signaling pathways, with the potential to influence diverse health outcomes such as susceptibility to infectious disease or risk of autoimmunity.
Hospital autopsy: standardised questionnaire survey to determine junior doctors' perceptions
Authors: J N Lund
Journal: BMJ (2001)

Despite the recommendations of the Joint Working Party of the Royal College of Pathologists, the Royal College of Physicians of London, and the Royal College of Surgeons of England, the rate at which hospital postmortem examinations are carried out continues to decline.1 We aimed to find reasons why doctors request an autopsy, whether the findings were communicated to the doctors who requested it, and the effects of such communication on the practice of junior doctors.

In July 2000, we sent a standardised questionnaire to junior doctors working in acute medical and surgical specialties in three hospitals in Mid-Trent. The doctors were …
KENNY METHOD OF TREATMENT OF INFANTILE PARALYSIS
Authors: Sidney V. Haas
Journal: JAMA (1942)

<h3>To the Editor:—</h3> In view of the wide publicity given the Kenny method of treatment of acute poliomyelitis, a copy of the treatment given in the 1906 edition of Osler's Practice of Medicine (p. 917), which I enclose, may prove of interest: The treatment of acute infantile paralysis has a bright and a dark side. In a case of any extent complete recovery cannot be expected; on the other hand, it is remarkable how much improvement may finally take place in a limb which is at first completely flaccid and helpless. The following treatment may be pursued: If seen in the febrile stage, a brisk laxative and a fever mixture may be given. The child should be in bed and the affected limb or limbs wrapped in cotton. As in the great majority of cases the damage is already done when the physician is called and the disease makes no
Multivariate Analysis of Risk Factors for Coronary Heart Disease
Authors: LARS WILHELMSEN, HANS WEDEL, GÖSTA TIBBLIN
Journal: Circulation (1973)

For a prospective study of risk factors for coronary heart disease (CHD), defined as acute nonfatal myocardial infarction and acute fatal CHD, 973 men, all aged 50 years, were recruited from a general Swedish urban population. Of the 855 who agreed to participate, 834 who showed no signs of CHD were selected and observed for nine years and four months. Autopsies were performed on all except two of the 55 patients who died during the study. Forty-four men developed clinical manifestations of CHD during this time; 19 of them died. Using a multiple logistic model, we analyzed nine probable risk factors. The presence of high serum cholesterol, smoking, high systolic blood pressure, dyspnea, and registration by the Temperance Board increased the risk of events related to CHD significantly. The presence of high serum triglycerides, high hematocrit readings, and increased geographic mobility did not cause a significant increase in events related to CHD. Those with sedentary jobs showed a slightly increased tendency to develop manifestations of the disease. The predictive power of the logistic function (with cholesterol, smoking, and systolic blood pressure) was tested in another randomly selected population sample of 5,146 men aged 51-55 years and found to be very accurate. The 10% (decile) of the population that had the highest risk of clinical manifestations of coronary disease and the 10% who had the lowest risk were defined. Manifestations of coronary disease occurred 29 times more frequently in the highest decile than in the lowest decile.
Comparison of adjustable- and fixed-dose budesonide/formoterol pressurized metered-dose inhaler and fixed-dose fluticasone propionate/salmeterol dry powder inhaler in asthma patients
Authors: William W. Busse, Shailen R. Shah, Laura Somerville, Bhash Parasuraman, Paula Martin, Mitchell Goldman
Journal: Journal of Allergy and Clinical Immunology (2008)
Combined Idiopathic Neutropenia and Thrombocytopenia
Authors: CHARLES A. LINKER
Journal: Annals of Internal Medicine (1980)

We report a case of combined idiopathic immune neutropenia and immune thrombocytopenia (thromboneutropenia). Therapy with prednisone was ineffective. Treatment with vincristine raised the patient's platelet count but did not increase the neutrophil count. Splenectomy led to a prompt complete remission. Using radioimmunologic techniques, we have shown both antiplatelet and antineutrophil antibodies and have shown the disappearance of these antibodies after successful treatment.
NHS Scotland orders inquiry into death rates at three hospitals
Authors: B. Christie
Journal: BMJ (2013)

A review has been ordered into patient safety at three Scottish hospitals after concerns about higher than average mortality rates.

Healthcare Improvement Scotland is due to report by the end of the year on any recommendations for improvement at Monklands, Wishaw, and Hairmyres hospitals, which are all in Lanarkshire.

The latest figures on standardised mortality ratios in Scottish hospitals have found Monklands and Wishaw to have higher than average rates, and it has also been decided that the review should be extended to nearby Hairmyres.

This comes at a time when hospital mortality …
A study of the HBV-DNA status before and after liver transplantation
Authors: G. Moraleda, A. Maceda, M.G. Martinz, J. Bartolomé, E. Moreno, J.I. Landa, J. Caballería, N. Gómez, J.M. Jover, V. Carreño
Journal: Journal of Hepatology (1989)
Activation of IL6/IGFIR Confers Poor Prognosis of HBV-Related Hepatocellular Carcinoma through Induction of OCT4/NANOG Expression
Authors: Te-Sheng Chang, Yu-Chih Wu, Ching-Chi Chi, Wei-Chi Su, Pey-Jium Chang, Kam-Fai Lee, Tao-Hsin Tung, Jui Wang, Jun-Jen Liu, Shui-Yi Tung, Liang-Mou Kuo, Hong-Nerng Ho, Thai-Yen Ling, Yen-Hua Huang
Journal: Clinical Cancer Research (2015)

Abstract Purpose: To unravel the role of interleukin (IL)-6 and insulin-like growth factor (IGF)-I receptor (IGFIR) in expressing stemness-related properties and to evaluate the prognostic values of pluripotent transcription factor OCT4/NANOG, and IGFIR in hepatocellular carcinoma (HCC). Experimental Design: Serum levels of IL6 were detected using ELISA assays (n = 120). The effects of IL6/IGFI on stemness expression in HCC were examined using OCT4/NANOG promoter luciferase reporter, RNA interference, secondary sphere formation, side population, and xenograft animal models. The OCT4/NANOG protein and phospho-IGFI receptor (p-IGFIR) in tissues were detected by Western blotting (n = 8) and immunohistochemical staining (n = 85). OCT4, NANOG, and IGFIR expression levels in tissues (n = 191) were analyzed by real-time qRT-PCR and was correlated with early tumor recurrence using the Kaplan–Meier survival analysis. Results: A high positive correlation between the expression levels of OCT4/NANOG and IGFIR/p-IGFIR in human HCC tissues was observed. The concurrent expression of OCT4/NANOG/IGFIR was mostly confined to hepatitis B virus (HBV)–related HCC (HBV-HCC) and was significantly correlated with early tumor recurrence. High serum levels of IL6 were significantly correlated with high OCT4/NANOG expression. IL6 stimulated an autocrine IGFI/IGFIR expression STAT3 dependently, which stimulated stemness-related properties in both the cell lines and the xenografted mouse tumors. The inhibition of IGFIR activation by either RNA interference or by treatment with the inhibitor picropodophyllin (PPP) significantly suppressed the IL6-induced stemness-related properties both in vitro and in vivo. Conclusions: The expression of pluripotency-related genes is associated with early tumor recurrence and is regulated by IL6-induced IGF/IGFIR activation, particularly in HBV-HCC. Clin Cancer Res; 21(1); 201–10. ©2014 AACR.
Abstract 2050: 2-Deoxy-D-Glucose (2-DG) as a glycolytic inhibitor in the treatment of retinoblastoma
Authors: Christina Decatur, Yolanda Pina, Samuel Houston, Ludimila Cavalcante, Nikesh Shah, Timothy Murray
Journal: Cancer Research (2011)

Abstract Purpose: The aim of the current study is to assess the impact of the glycolytic inhibitor 2-deoxy-D-glucose (2-DG) on tumor burden and hypoxia in the LHBETATAG retinal tumors. Methods: Group A: 17-week-old LHBETATAG transgenic mice (n=30) received periocular injections of saline and 2-DG (62.5, 125, 250, and 500mg/kg). Injections were given 2 times a week for 3 weeks. Group B: 4-week-old mice received oral delivery of 2-DG in custom made food pellets and were treated for either 8 or 18 weeks. 17-week-old mice received oral 2-DG for 8 weeks. At the time of enucleation, all eye samples were snap frozen and analyzed for tumor burden and hypoxic regions using immunohistochemistry. Results: Following injections of 2-DG, tumor control was not different between the control and the lowest two doses (62.5 and 125mg/kg). However, the difference in tumor burden was significant from 250mg/kg dose (p&amp;lt;0.015) and 500mg/kg dose (p&amp;lt;0.001) with 9.7 and 23% tumor burden decrease, respectively. At all doses of periocular 2-DG, the percent hypoxia following drug treatment were lower relative to controls (p&amp;lt;0.001), with a hypoxia decrease in the lowest dose to 2.4% compared to 21% in controls. Following oral delivery of 2-DG, there was a difference between the groups treated with 2-DG and the control groups (p&amp;lt;0.010). A 20% reduction in tumor burden was found in the 8 weeks early treated, a 50% reduction in the 18 weeks early treated, and a 35% reduction in the 8 weeks late treated group. The percent hypoxia was lower relative to controls in the 8 weeks and 18 weeks early treated groups (p&amp;lt;0.001) with a 40% and 50% reduction, respectively. The percent hypoxia did not change following treatment in the treated late group. Conclusions: This study exhibits the efficacy of focal 2-DG as potential therapy to decrease both intratumoral hypoxia and tumor burden. The current study also shows that the non-invasive oral delivery 2-DG treatment has similar or better effects on the tumor depending on the treatment schedule used. In advanced disease of LHBETATAG retinal tumors, hypoxia is increasingly present. The use of glycolytic inhibitors as a therapeutic strategy has the potential to enhance current retinoblastoma treatments. 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 2050. doi:10.1158/1538-7445.AM2011-2050
Pamidronate to Prevent Bone Loss during Androgen-Deprivation Therapy for Prostate Cancer
Authors: Matthew R. Smith, Francis J. McGovern, Anthony L. Zietman, Mary Anne Fallon, Douglas L. Hayden, David A. Schoenfeld, Philip W. Kantoff, Joel S. Finkelstein
Journal: New England Journal of Medicine (2001)

Treatment with a gonadotropin-releasing hormone agonist decreases bone mineral density and increases the risk of fracture in men with prostate cancer. We conducted a controlled study of the prevention of osteoporosis in men undergoing treatment with a gonadotropin-releasing hormone agonist.