tbuckley/cabot-search huggingface dataset:
Response to Measles Vaccine in Haitian Infants 6 to 12 Months Old
Authors: Neal A. Halsey, Reginald Boulos, Frantz Mode, Jean Andre, Linda Bowman, Robert G. Yaeger, Serge Toureau, Jon Rohde, Carlo Boulos
Journal: New England Journal of Medicine (1985)

To study the factors affecting the serologic response to measles vaccination, we evaluated 595 Haitian infants from 6 through 12 months of age, and their mothers, at the beginning of an immunization program. Thirty-four per cent of the infants had preexisting serologic evidence of measles infections by 11 months of age. Among infants more than nine months of age, those who had had measles had a significantly lower nutritional status than those who had not (P less than 0.01). After vaccination, seroconversion rates increased from 45 per cent at 6 months to 100 per cent at 12 months. The lowest rate of vaccine failure compatible with acceptably low rates of natural infections could be achieved by vaccination after eight months of age. Infants born to mothers with low levels of antibody to measles (hemagglutination-inhibition antibody titers less than 1:40) were significantly more likely to have had natural measles (P less than 0.01) or to have seroconversion after vaccination (P less than 0.001) at 6 to 10 months of age than were infants born to mothers with higher of age than were infants born to mothers with higher titers. Malnutrition and acute infections did not affect seroconversion rates. These data support the World Health Organization recommendation to administer measles vaccine in under-developed countries as soon after nine months of age as possible, regardless of nutritional status or the presence of minor illnesses.
622. PhiC31 Integrase as a Tool: Gene Therapy for Angiogenesis
Authors: Joylette L. Portlock, Sohail Jarrahian, Carmen Bertoni, Thomas A. Rando, Michele P. Calos, Michael Chorny, Ilia Fishbein, Ivan Alferiev, Robert J. Levy
Journal: Molecular Therapy (2005)

622. PhiC31 Integrase as a Tool: Gene Therapy for Angiogenesis Joylette L. Portlock, Sohail Jarrahian, Carmen Bertoni, Thomas A. Rando, Michele P. Calos. Genetics Department, Stanford University School of Medicine, Stanford, CA; Departments of Neurology and Neurological Sciences, Stanford University School of Medicinee, Stanford, CA; Neurology Service and GRECC, Veterans Affairs Palo Alto Health Care System, Palo Alto, CA.
Human leukocyte antigen B27 selects for rare escape mutations that significantly impair hepatitis C virus replication and require compensatory mutations
Authors: Christoph Neumann-Haefelin, Cesar Oniangue-Ndza, Thomas Kuntzen, Julia Schmidt, Katja Nitschke, John Sidney, Célia Caillet-Saguy, Marco Binder, Nadine Kersting, Michael W. Kemper, Karen A. Power, Susan Ingber, Laura L. Reyor, Kelsey Hills-Evans, Arthur Y. Kim, Georg M. Lauer, Volker Lohmann, Alessandro Sette, Matthew R. Henn, Stéphane Bressanelli, Robert Thimme, Todd M. Allen
Journal: Hepatology (2011)

Human leukocyte antigen B27 is associated with spontaneous viral clearance in hepatitis C virus (HCV) infection. Viral escape within the immunodominant, HLA-B27-restricted, HCV-specific, cluster of differentiation (CD)8(+) T-cell epitope, nonstructural protein (NS)5B(2841-2849) (ARMILMTHF), has been shown to be limited by viral fitness costs as well as broad T-cell cross-recognition, suggesting a potential mechanism of protection by HLA-B27. Here, we studied the subdominant HLA-B27-restricted epitope, NS5B(2936-2944) (GRAAICGKY), to further define the mechanisms of protection by HLA-B27. We identified a unique pattern of escape mutations within this epitope in a large cohort of HCV genotype 1a-infected patients. The predominant escape mutations represented conservative substitutions at the main HLA-B27 anchor residue or a T-cell receptor contact site, neither of which impaired viral replication capacity, as assessed in a subgenomic HCV replicon system. In contrast, however, in a subset of HLA-B27(+) subjects, rare escape mutations arose at the HLA-B27 anchor residue, R(2937) , which nearly abolished viral replication. Notably, these rare mutations only occurred in conjunction with the selection of two equally rare, and structurally proximal, upstream mutations. Coexpression of these upstream mutations with the rare escape mutations dramatically restored viral replication capacity from <5% to ≥ 70% of wild-type levels.The selection of rare CTL escape mutations in this HLA-B27-restricted epitope dramatically impairs viral replicative fitness, unless properly compensated. These data support a role for the targeting of highly constrained regions by HLA-B27 in its ability to assert immune control of HCV and other highly variable pathogens.
Pertussis Vaccine Encephalopathy
Authors: James E. Lewis
Journal: JAMA (1990)

<h3>7b the Editor. —</h3> In his editorial proclaiming the "myth" of pertussis vaccine encephalopathies, Cherry<sup>1</sup>fails to recognize the paucity of conceptually and methodologically sound research on the insidious neurotoxic effects of the "whole cell" pertussis vaccine. There is little scientific dispute that the pertussis toxin can produce acute local and systemic reactions. The more heated controversy has focused on whether these acute symptoms also involve lasting central nervous system effects, or, as Cherry's referenced studies describe, "permanent brain damage" and "serious neurologic illness." At a minimum, a conceptually sound cause-and-effect study of hypothesized pertussis vaccine encephalopathies would specify and operationally define the full range of potential sequelae, ie, mild, moderate, and severe pertussis vaccine encephalopathies. An animal experimental paradigm employed by Goh and Pennefather<sup>2</sup>recently identified a significant neuropathologic mechanism of pertussis toxin, the functional "uncoupling" of G-type proteins in a hippocampal region, effecting disruption of long-term
From a Parkinson's disease expert: Rasagiline and the Future of Therapy
Authors: Shaheen E Lakhan
Journal: Molecular Neurodegeneration (2007)

John Finberg is a professor of pharmacology at the Faculty of Medicine, Technion – Israel Institute of Technology, home of Israel's two Nobel laureates. He and his colleague Prof. Moussa Youdim were instrumental in the early clinical development of the anti-Parkinson drug rasagiline, which gained UK- and EU-marketing authorization in 2005 and US FDA approval in 2006. In our interview, Finberg reflects on his clinical research to develop rasagiline as a commercial drug and its proposed pharmacological mechanisms of action. Moreover, he elucidates the current state of anti-Parkinson drug discovery and offers direction for future research.
Stem cell deficiencies and thymic abnormalities in fetal mouse trisomy 16.
Authors: C J Epstein, B G Hofmeister, D Yee, S A Smith, R Philip, D R Cox, L B Epstein
Journal: The Journal of Experimental Medicine (1985)

Mouse fetuses with trisomy 16 have severe abnormalities of several hematopoietic stem cell and precursor populations. The thymus is extremely hypoplastic, with a greater than or equal to 80% reduction in the number of thymocytes. This cellular deficiency appears to be the result of a deficiency in the number of precursor cells in the early thymus, since the rate of proliferation of thymocytes in explanted day-14 thymuses was normal. However, the functional maturation of thymocytes was delayed in vitro in day-17 organ explants, although the maximal response to the mitogenic and interleukin 2-stimulating effects of concanavalin A are quantitatively normal. B cells and pre-B cells in the fetal liver were moderately decreased, but the ability of fetal liver cells to be transformed by Abelson murine leukemia virus was nearly totally lost. There were also significant relative and absolute decreases in the number of spleen, culture, and erythroid colony-forming units (CFU-S, CFU-C, CFU-E) and of erythroid burst-forming units (BFU-E) in the trisomic liver, and the trisomic animals were anemic with small spleens and livers. However, unlike other genetically caused anemias, there was no reduction in the number of germ cells. The hematopoietic abnormalities in the trisomy 16 mouse, involving the lymphoid, myeloid, and erythroid cell lineages, are much more generalized than the abnormalities in any of the other described genetically caused immunodeficiencies or anemias in the mouse. They are also more severe than those in human trisomy 21 (Down syndrome), for which mouse trisomy 16 is a genetic model, but there does exist an interesting parallel between the thymic abnormalities in the two species.
What does London need from its ambulance service?
Authors: R A Cocks, E Glucksman
Journal: BMJ (1993)

count to return to an acceptable value, usually within a fortnight.In the first two years since the drug's introduction 2337 patients have received clozapine in Britain.Seventy four of the patients (3-2%) have developed neutropenia induced by clozapine.Of these 74 patients, 11 developed agranulocytosis, of whom one died-a patient who had received clozapine for eight weeks.Although neutropenia is the most important side effect of clozapine, other clinically important side effects occur in over
US National Institutes of Health proposes new rules on researchers' ties to industry
Authors: J. H. Tanne
Journal: BMJ (2010)

Senior figures at the US National Institutes of Health (NIH) have proposed new, stricter rules for funded researchers on showing their ties with industry.

Francis Collins, who heads the agency, and Sally Rockey, head of its office of extramural research, wrote in a commentary in the Journal of the American Medical Association that the existing 1995 rules “need to be clarified and strengthened to ensure greater transparency and accountability” (doi:10.1001/jama.2010.774).

Members of Congress, in particular Republican Senator Chuck Grassley of Iowa, have been investigating undisclosed …
PRECIPITATION TESTS FOR SYPHILIS
Authors: Israel Weinstein
Journal: JAMA (1933)

<h3>To the Editor:</h3> —On visiting the venereal disease exhibit of the United States Public Health Service at the Chicago Century of Progress Exposition I saw a statement which, in my opinion, is not alone incorrect but, in addition, does a grave injustice to American science. I refer to the statement which lists Meinicke as the originator of the precipitation test for syphilis. Ten years before Meinicke began to write on precipitation with syphilitic serums, Michaelis (1907) published his "Precipitinreaktion bei Syphilis." In 1910, Jacobstahl reported a precipitation test which required the dark field microscope to read the results. In 1911, Bruck and Hidaka showed that, by modifying the technic, the use of the microscope was not necessary. In 1915, Hecht published a precipitation method of his own. In 1917, Meinicke published a "water and salt solution" method based on precipitation. In 1918, Sachs and Georgi published a precipitation test which
Child Survival: Strategies for Research
Authors: Helen M. Wallace
Journal: JAMA (1985)

This book is based on a workshop organized by the Rockefeller and Ford Foundations and consists of 17 chapters. Its focus is on child survival in developing countries. The purposes are (1) to prepare a simple framework for interdisciplinary communication and studies, (2) to identify key determinants of morbidity and mortality and the methods of analyzing them developed by biomedical and social scientists, and (3) to consider research needs and strategies for multidisciplinary studies on child survival. The importance of combining the biomedical and social science approaches to studies of factors influencing child survival is the common thread throughout. The biomedical perspectives discussed in this book include infections and parasitic diseases, nutrition, fertility (including birth interval and birth weight), practices and quality of care during pregnancy, childbirth, infancy, and childhood. The social science perspectives include literacy, income, mothers' ages, parity and education, women's roles, health behavior, and sex differences. The
Diabetes and Hypertension
Authors: Zachary T. Bloomgarden
Journal: Diabetes Care (2001)

This article covers presentations and symposia dealing with the relation between diabetes and hypertension that were given at the 16th Scientific Meeting of the American Society of Hypertension, San Francisco, CA, 15–19 May 2001.

At a symposium at the 16th Scientific Meeting of the American Society of Hypertension (ASH), San Francisco, CA, 15–19 May 2001, Willa Hsueh, Los Angeles, CA, discussed clinical trials in hypertension. The Sixth Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC-VI, 1997, available at http://www.nhlbi.nih.gov/guidelines/hypertension/jnc6.pdf) defined essential hypertension as a blood pressure (BP) >140/90 mmHg, but Hsueh noted that only 25% of patients with hypertension have no complications such as renal disease, cardiac disease, obesity, diabetes, and hyperlipidemia. BP goals are lower for patients with such complications. In the JNC-VI, patients with diabetes were noted to be at high risk and were given a BP goal of  1 g proteinuria, the goal to lessen target organ damage was set at 125/75 mmHg. In the U.K. Prospective Diabetes Study (UKPDS) patients were treated with either an ACE inhibitor (ACEI) or β-blocker (BB) and achieved levels of 144/82 vs. 154/87 mmHg over 8 years. However, at a question-and-answer session after the lecture, it was noted that captopril was given only once or twice daily and therefore may not have had optimal benefit. Both treatments reduced microvascular end points of renal and eye disease, macrovascular end points, and congestive heart failure (CHF), which may in part reflect diabetic cardiomyopathy. The Hypertension Optimal Therapy (HOT) trial of 18,790 patients, of whom 8% had diabetes and were treated with felodipine followed by ACEI and then followed by additional agents, showed a clear relation of BP to cardiovascular disease (CVD) events in the diabetes subgroup when comparing …
Multifocal Uptake of Tc-99m Mebrofenin in Dilated Liver Ductules in a Patient With Cystic Fibrosis
Authors: ROBERT T. MORRISON, ROBERT D. STEUART, HUGH CHAUN
Journal: Clinical Nuclear Medicine (1995)

A patient with cystic fibrosis and a previous cholecystectomy, underwent Tc-99m mebrofenin scintigraphy to rule out hepatobiliary disease. The scan revealed multiple focal collections of radiopharmaceutical within the liver parenchyma. This unusual pattern of multiple focal parenchymal activity may be specific for patients with cystic fibrosis. This is the first time this unusual pattern has been confirmed at autopsy.
Disordered leucocyte proliferation in leukaemia.
Authors: J Stuart
Journal: BMJ (1972)

characterizes these diseases.In acute leukaemia a maturation arrest in the leukaemic cell line occurs at the blast-cell stage of development and results in a failure to produce the normal, functional end-cells of that cell line.Extensive replacement with blast cells then leads to a failure to produce the functional units of the other marrow cell lines; this results in the early development of neutropenia, thrombocytopenia, and anaemia, which characterize acute leukaemia.In chronic leukaemia there is on 12 August
Abstract S2-2: Multivariate Analysis of Obesity and Disease Free Survival in Patients with Nodal Positive Primary Breast Cancer — The ADEBAR Trial
Authors: PGM Hepp, B Rack, K Annecke, A Wischnik, S Wolfgang, T Zwingers, N Harbeck, HL Sommer, K Friese, M Kiechle, W. Janni
Journal: Cancer Research (2010)

Abstract Background: The prevalence of obesity increases throughout all evolved civilizations. On the other hand several epidemiological studies have shown not only an increase in breast cancer among obese women but also an adverse impact of obesity on survival of breast cancer patients. This analysis focuses on the impact of obesity on patients (pts) treated within the ADEBAR study protocol. Methods: The ADEBAR Trial compared 4 cycles of EC followed by 4 cycles of Doc vs. 8 cycles of FEC (120) in pts with primary breast cancer (&amp;gt;=4LN). 1500 pts have been accrued from sep/01 through may/05. For this analysis data of 1361 pts has been analyzed about the impact of obesity on disease free survival. Therefore pts have been grouped to either “underweight” (BMI&amp;lt;18.5kg/m2), “normal weight” (BMI18.5-25kg/m2), “overweight” (25kg/m2&amp;lt;BMI&amp;gt;30kg/m2) or “obese” (BMI&amp;gt;30). Results: 13 pts (1.0%) were “underweight”, 557 pts (40.9%) were normal weight, 491 pts (36.1%) were overweight, 300 pts (22.0%) were obese at the time of study enrollment. After a follow up period of 60 months 87.5% of the underweight group, 70.4% of the normal weight group, 70.7% of the overweight group and 58.6% of the obese group were alive with no signs of recurrent disease. This difference was significant (Chi-square=9.355; p&amp;lt; 0.0249). The tumor size at clinical diagnosis was strongly associated to the patient's weight (&amp;lt; 0.0001). There was no significant difference in the number of positive lymph nodes (p = 0.2890), tumor histology (p = 0.9750), grading (p = 0.9520), ER and PR hormone receptors (ER p = 0.9708, PR p = 0.7785) and the expression of HER2 (p = 0.1710) regarding underweight, normal, overweight and obese patients. In a multivariate analysis obesity was an independent prognostic factor with a hazard ratio of 1,007 per 1kg/m2 increase (P&amp;lt;0,0167). Conclusion: This analysis strongly implicates an impact of obesity on disease free survival in patients with early stage node positive breast cancer in the prospectively randomized ADEBAR multicenter trial. It is therefore in line with earlier findings in epidemiological research and raises the question whether a weight reduction might be an additional approach on breast cancer therapy. Figures available in online version. Citation Information: Cancer Res 2010;70(24 Suppl):Abstract nr S2-2.
Hammerhead ribozymes with cleavage site specificity for NUH and NCH display significant anti-hepatitis C viral effect in vitro and in recombinant HepG2 and CCL13 cells
Authors: Maria-Angeles Gonzalez-Carmona, Sabine Schüssler, Matthias Serwe, Michael Alt, János Ludwig, Brian S. Sproat, Robin Steigerwald, Per Hoffmann, Maria Quasdorff, Oliver Schildgen, Wolfgang H. Caselmann
Journal: Journal of Hepatology (2005)
Ischemia–Reperfusion–induced Lung Injury
Authors: Marc de Perrot, Mingyao Liu, Thomas K. Waddell, Shaf Keshavjee
Journal: American Journal of Respiratory and Critical Care Medicine (2003)

Ischemia-reperfusion-induced lung injury is characterized by nonspecific alveolar damage, lung edema, and hypoxemia occurring within 72 hours after lung transplantation. The most severe form may lead to primary graft failure and remains a significant cause of morbidity and mortality after lung transplantation. Over the past decade, better understanding of the mechanisms of ischemia-reperfusion injury, improvements in the technique of lung preservation, and the development of a new preservation solution specifically for the lung have been associated with a reduction in the incidence of primary graft failure from approximately 30 to 15% or less. Several strategies have also been introduced into clinical practice for the prevention and treatment of ischemia-reperfusion-induced lung injury with various degrees of success. However, only three randomized, double-blinded, placebo-controlled trials on ischemia-reperfusion-induced lung injury have been reported in the literature. In the future, the development of new agents and their application in prospective clinical trials are to be expected to prevent the occurrence of this potentially devastating complication and to further improve the success of lung transplantation.
LAW AND MEDICINE
Authors: Kirke W. Dale
Journal: JAMA (1969)

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Abstract 510: Do adipocytes in the tumor microenvironment influence the growth of pancreatic cancer
Authors: Patrick White, Deborah Swartz-Basile, Kathryn Ziegler, Sue Wang, Henry Pitt, Nicholas Zyromski
Journal: Cancer Research (2011)

Abstract Introduction: Pancreatic cancer develops more frequently and progresses more rapidly in obesity. The mechanisms influencing this association are incompletely understood. Using our murine model of pancreatic cancer in diet-induced obesity, we hypothesized that changes in the immune profile and tumor microenvironment may contribute to accelerated pancreatic cancer growth in obesity. Methods: Thirty male C57BL/6J mice were studied. At 5 weeks of age, 20 mice were fed high fat diet (60% fat; HFD) and 10 were fed low fat (10% fat) diet. At 19 weeks of age all mice were inoculated in the flank with 2.5 x105 Pan02 murine pancreatic cancer cells. After 5 weeks of tumor growth, spleens and tumors were collected, splenic flow cytometry evaluated lymphocyte population, proliferation was determined by PCNA staining, and tumor infiltrating lymphocytes (TIL), both B and T, were scored by immunohistochemistry. Intratumoral adipocyte volume was assessed by H&amp;E staining. Students's t-test and Pearson's correlation were applied where appropriate. P value &amp;lt;0.05 was accepted as statistically significant. Results: Mice were segregated into overweight (OW – heavier than the mean body weight of the HFD mice – 35.5g, n=15) and lean (&amp;lt;35.5g, n=14). OW mice were significantly heavier (37.3±0.2g vs. 33.9±0.3g, p&amp;lt;0.001). Tumors were twice as large in OW mice as in lean mice (1.23±0.2g vs. 0.6±0.1g; p=0.001). The peripheral lymphocyte profile was similar in both OW and lean animals (T cells: 51.2±2.5% vs. 49.2±2.3%, p=0.59; B cells: 32.9±1.0% vs. 32.0±1.9%, p=0.73). TIL were observed in similar numbers in both OW and lean groups (T cell: 1.31±0.18 vs. 1.54±0.16, p=0.35; B cell: 0.63±0.08 vs. 0.91±0.15, p=0.33). Tumor proliferation as measured by PCNA was similar in both groups (139±18 OW vs. 143±14 lean, p=0.85). Interestingly, adipocyte volume was significantly greater in the OW tumor microenvironment than in the lean tumors (3.7%±0.7 vs. 2.2%±0.3, p&amp;lt;0.05). Conclusions: These results demonstrate that: 1) tumor weight was significantly greater in OW mice; 2) peripheral and tumor infiltrating lymphocyte profile was similar in OW and lean animals; and 3) adipocyte volume was significantly greater in the tumor microenvironment of OW mice. We conclude that obesity accelerates the growth of pancreatic cancer, and adipocytes in the tumor microenvironment may directly influence tumor growth. 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 510. doi:10.1158/1538-7445.AM2011-510