tbuckley/cabot-search huggingface dataset:
Is progesterone elevation on the day of human chorionic gonadotrophin administration associated with the probability of pregnancy in in vitro fertilization? A systematic review and meta-analysis
Authors: C.A. Venetis, E.M. Kolibianakis, E. Papanikolaou, J. Bontis, P. Devroey, B.C. Tarlatzis
Journal: Human Reproduction Update (2007)

The role of progesterone elevation on in vitro fertilization (IVF) outcome has remained a debatable issue for several years. The aim of this systematic review and meta-analysis was to evaluate whether progesterone elevation on the day of human chorionic gonadotrophin (hCG) administration is associated with the probability of pregnancy. Eligible studies were considered those in which patients did not participate more than once. A literature search in MEDLINE, EMBASE and CENTRAL identified 12 eligible studies, 10 of which were retrospective. The majority (n = 10) of these studies did not detect a statistically significant association between progesterone elevation and the probability of pregnancy. Meta-analysis was performed only for the studies (n = 5) that provided data on clinical pregnancy per patient reaching hCG administration for final oocyte maturation. No statistically significant association between progesterone elevation and the probability of clinical pregnancy was detected (Odds ratio: 0.75, 95% confidence interval 0.53-1.06; P = 0.10). This finding persisted in the sensitivity analyses performed, which excluded the studies that did not report clearly that measurement of progesterone did not affect patients' management and those that did not report definition of clinical pregnancy. In addition, subgroup analyses were conducted on the basis of type of gonadotrophin-releasing hormone GnRH analogue used and on the value of serum threshold used to classify patients in those with or without progesterone elevation. These analyses, however, did not materially change the results obtained. In conclusion, the best available evidence does not support an association between progesterone elevation on the day of hCG administration and the probability of clinical pregnancy in women undergoing ovarian stimulation with GnRH analogues and gonadotrophins for IVF.
Profiling Three-Dimensional Nuclear Telomeric Architecture of Myelodysplastic Syndromes and Acute Myeloid Leukemia Defines Patient Subgroups
Authors: Macoura Gadji, Julius Adebayo Awe, Prerana Rodrigues, Rajat Kumar, Donald S. Houston, Ludger Klewes, Tandakha Ndiaye Dièye, Eduardo Magalhães Rego, Roberto Falcão Passetto, Fábio Morato de Oliveira, Sabine Mai
Journal: Clinical Cancer Research (2012)

Myelodysplastic syndromes (MDS) are a group of disorders characterized by cytopenias, with a propensity for evolution into acute myeloid leukemias (AML). This transformation is driven by genomic instability, but mechanisms remain unknown. Telomere dysfunction might generate genomic instability leading to cytopenias and disease progression.We undertook a pilot study of 94 patients with MDS (56 patients) and AML (38 patients). The MDS cohort consisted of refractory cytopenia with multilineage dysplasia (32 cases), refractory anemia (12 cases), refractory anemia with excess of blasts (RAEB)1 (8 cases), RAEB2 (1 case), refractory anemia with ring sideroblasts (2 cases), and MDS with isolated del(5q) (1 case). The AML cohort was composed of AML-M4 (12 cases), AML-M2 (10 cases), AML-M5 (5 cases), AML-M0 (5 cases), AML-M1 (2 cases), AML-M4eo (1 case), and AML with multidysplasia-related changes (1 case). Three-dimensional quantitative FISH of telomeres was carried out on nuclei from bone marrow samples and analyzed using TeloView.We defined three-dimensional nuclear telomeric profiles on the basis of telomere numbers, telomeric aggregates, telomere signal intensities, nuclear volumes, and nuclear telomere distribution. Using these parameters, we blindly subdivided the MDS patients into nine subgroups and the AML patients into six subgroups. Each of the parameters showed significant differences between MDS and AML. Combining all parameters revealed significant differences between all subgroups. Three-dimensional telomeric profiles are linked to the evolution of telomere dysfunction, defining a model of progression from MDS to AML.Our results show distinct three-dimensional telomeric profiles specific to patients with MDS and AML that help subgroup patients based on the severity of telomere dysfunction highlighted in the profiles.
Inhibition of Platelet-Dependent Thrombosis by Local Delivery of Heparin With a Hydrogel-Coated Balloon
Authors: Gilberto L. Nunes, Clifford N. Thomas, Stephen R. Hanson, James J. Barry, Spencer B. King, Neal A. Scott
Journal: Circulation (1995)

Background Systemic administration of heparin can decrease mortality and morbidity of acute ischemic coronary syndromes such as unstable angina and myocardial infarction. Hemorrhage is the major limiting factor in the clinical use of systemic heparin. The objective of the present study was to determine whether local delivery of heparin could inhibit platelet-dependent thrombosis without altering systemic bleeding parameters. Methods and Results Hydrogel-coated angioplasty balloon catheters were dipped in a heparin solution, dried, and applied to a platelet-rich mural thrombus in a chronic ex vivo porcine arteriovenous shunt. 111 In-labeled platelet deposition was quantified by gamma camera imaging. In a separate series of experiments, 3 H-heparin was used to estimate the amount of heparin delivered to the thrombus with the coated balloon. Systemic heparin administration produced a dose-dependent decrease in platelet-dependent thrombus formation that was maximal at 200 units/kg. Bleeding times and activated partial thromboplastin times were prolonged at this dose. An equal inhibition of thrombus formation was achieved after the coated balloon was dipped in a heparin solution (10 000 units/mL) and deployed at the mural thrombus. In contrast to systemic heparin administration, there was no alteration in bleeding parameters associated with local heparin delivery. The estimated amount of heparin delivered with the coated balloon was 40 units. Conclusions Local delivery of heparin in amounts sufficient to inhibit platelet-dependent thrombosis can be accomplished with a hydrogel-coated coronary angioplasty balloon catheter. Local heparin delivery can inhibit thrombus formation in amounts that are several orders of magnitude lower than the required systemic dose. Local delivery of heparin was not associated with prolongation of bleeding parameters.
Randomized phase II study of docetaxel plus estramustine and single-agent docetaxel in patients with metastatic hormone-refractory prostate cancer
Authors: J-C Eymard, F. Priou, A. Zannetti, A. Ravaud, D. Lepillé, P. Kerbrat, P. Gomez, B. Paule, D. Genet, P. Hérait, E. Ecstein-Fraïssé, F. Joly
Journal: Annals of Oncology (2007)
Chromosomal Instability (CIN) Phenotype, CIN High or CIN Low, Predicts Survival for Colorectal Cancer
Authors: Toshiaki Watanabe, Takashi Kobunai, Yoko Yamamoto, Keiji Matsuda, Soichiro Ishihara, Keijiro Nozawa, Hideki Yamada, Tamuro Hayama, Eisuke Inoue, Junko Tamura, Hisae Iinuma, Takashi Akiyoshi, Tetsuichiro Muto
Journal: Journal of Clinical Oncology (2012)

Purpose To examine whether chromosomal instability (CIN) phenotype, determined by the severity of CIN, can predict survival for stages II and III colorectal cancer (CRC). Patients and Methods We determined microsatellite instability (MSI) and loss of heterozygosity (LOH) status in 1,103 patients (training [n = 845] and validation [n = 258] sets with stages II and III CRC). The LOH ratio was defined as the frequency of LOH in chromosomes 2p, 5q, 17p, and 18q. According to the LOH ratio, non–MSI high tumors were classified as CIN high (LOH ratio ≥ 33%) or CIN low (LOH ratio &lt; 33%). CIN-high tumors were subclassified as CIN high (mild type; LOH ratio &lt; 75%) or CIN high (severe type; LOH ratio ≥ 75%). We used microarrays to identify a gene signature that could classify the CIN phenotype and evaluated its ability to predict prognosis. Results CIN high showed the worst survival (P &lt; .001), whereas there was no significant difference between CIN low and MSI high. CIN high (severe type) showed poorer survival than CIN high (mild type; P &lt; .001). Multivariate analysis revealed that CIN phenotype was an independent risk factor for disease-free and overall survival, respectively, in both the training (P &lt; .001 and P = .0155) and validation sets (P &lt; .001 and P = .0076). Microarray analysis also revealed that survival was significantly poorer in those with the CIN-high than in the CIN-low gene signature (P = .0203). In a validation of 290 independent CRCs (GSE14333), the CIN-high gene signature showed significantly poorer survival than the CIN-low signature (P = .0047). Conclusion The CIN phenotype is a predictive marker for survival and may be used to select high-risk patients with stages II and III CRC.
Dietary Manipulation of Histone Structure and Function
Authors: Barbara Delage, Roderick H. Dashwood
Journal: Annual Review of Nutrition (2008)

Post-translational modifications of histones are the subject of intensive investigations with the aim of decoding how they regulate, alone or in combination, chromatin structure, genomic stability, and gene expression. Major epigenetic programming events take place during gametogenesis and fetal development and are thought to have long-lasting consequences on adult health. Epidemiological and experimental studies have pointed toward maternal nutrition as a major player during prenatal development in influencing disease susceptibility later in life. Although the mechanisms underlying such observations are not well elucidated, epigenetic alterations of histones by particular maternal diets might be of central importance. Moreover, as much as dietary sources can influence epigenetic programming during pregnancy, they have started to be implicated in cancer chemoprevention, via the targeting of reversible epigenetic deregulations at the level of the histones.
Relations Between Carotid Artery Wall Thickness and Liver Histology in Subjects With Nonalcoholic Fatty Liver Disease
Authors: Giovanni Targher, Lorenzo Bertolini, Roberto Padovani, Stefano Rodella, Giacomo Zoppini, Luciano Zenari, Massimo Cigolini, Giancarlo Falezza, Guido Arcaro
Journal: Diabetes Care (2006)

OBJECTIVE—Nonalcoholic fatty liver disease (NAFLD) is closely associated with several metabolic syndrome features. We assessed whether NAFLD is associated with carotid artery intima-media thickness (IMT) as a marker of subclinical atherosclerosis and whether such an association is independent of classical risk factors, insulin resistance, and metabolic syndrome features. RESEARCH DESIGN AND METHODS—We compared carotid IMT, as assessed by ultrasonography, in 85 consecutive patients with biopsy-proven NAFLD and 160 age-, sex-, and BMI-matched healthy control subjects. RESULTS—NAFLD patients had a markedly greater carotid IMT (1.14 ± 0.20 vs. 0.82 ± 0.12 mm; P &amp;lt; 0.001) than control subjects. The metabolic syndrome (according to Adult Treatment Panel III criteria) and its individual components were more frequent in those with NAFLD (P &amp;lt; 0.001). The marked differences in carotid IMT observed between the groups were only slightly weakened after adjustment for age, sex, BMI, smoking history, LDL cholesterol, insulin resistance (by homeostasis model assessment), and metabolic syndrome components. Notably, carotid IMT was strongly associated with degree of hepatic steatosis, necroinflammation, and fibrosis among NAFLD patients (P &amp;lt; 0.001 for all). Similarly, by logistic regression analysis, the severity of histological features of NAFLD independently predicted carotid IMT (P &amp;lt; 0.001) after adjustment for all potential confounders. CONCLUSIONS—These results suggest that the severity of liver histopathology among NAFLD patients is strongly associated with early carotid atherosclerosis, independent of classical risk factors, insulin resistance, and the presence of metabolic syndrome.
Choice cuts for patients with AIDS?
Authors: B T Goh, G E Forster
Journal: BMJ (1990)

lactic acid (the fatigue substance) which reduce performance capacity."4Incubation with physiological concentrations of lactic acid reduced the filterability oferythrocytes,' and more than 40 years ago high blood concentrations of lactate after moderate exercise in subjects with neurocirculatory asthenia were considered to suggest deficient aerobic metabolism.6In New Zealand members of the Dunedin Myalgic Encephalomyelitis Support Group were found to have reduced blood filterability when they were acutely unwell,7 and analysis of red cell shape has shown that subjects with the symptoms of myalgic encephalomyelitis have appreciably in- creased percentages of non-discocytic red cells.89As such cells will impair capillary blood flow the chronic tiredness of subjects with the symptoms of myalgic encephalomyelitis and a reduced per- centage of normal discocytes is probably explicable in terms of inadequate energy generation.'Observations made on red cell shape in other disorders that have chronic tiredness as a common symptom provide support for the statement by Ffrench that "there is no doubt that oxygen lack is the first cause of tissue cell exhaustion which is manifested early by clinical tiredness.""Without disputing that central fatigue exists in some patients with chronic tiredness it is suggested that studies of those factors that influence capillary blood flow and oxygen delivery could be ofvalue in separating those whose problem is an affective disorder.
Spleen Cells from Young but Not Old Immunized Mice Eradicate Large Established Cancers
Authors: Karin Schreiber, Ainhoa Arina, Boris Engels, Michael T. Spiotto, John Sidney, Alessandro Sette, Theodore G. Karrison, Ralph R. Weichselbaum, Donald A. Rowley, Hans Schreiber
Journal: Clinical Cancer Research (2012)

Solid tumors that have grown two weeks or longer in mice and have diameters larger than 1 cm are histologically indistinguishable from autochthonous human cancers. When experimental tumors reach this clinically relevant size, they are usually refractory to most immunotherapies but may be destroyed by adoptive T-cell transfer. However, TCR-transgenic T cells and/or tumor cells overexpressing antigens are frequently used in these experiments. Here we studied the requirements for destroying clinical size, unmanipulated 8101 tumors by adoptive cell therapy.8101 arose in an old mouse after chronic exposure to UV light. A cancer line was established, which was never serially transplanted. The immunodominant CD8(+) T cell-recognized antigen of this tumor is caused by a somatic tumor-specific mutation in the RNA helicase p68. 8101 tumors were treated with spleen cells from young naive, or young and old immunized mice to ascertain the characteristics of immune cells that lead to rejection.Here we show that the mutant p68 peptide has an exceptionally high affinity to the presenting MHC class I molecule K(b) and that spleen cells from immunized young syngeneic mice adoptively transferred to Rag(-/-) or cancer-suppressed euthymic mice eradicate 8101 tumors larger than 1 cm in average diameter and established for several weeks. Spleen cells from naive young mice or from old and boosted (reimmunized) mice were ineffective.Relapse-free destruction of large and long-established tumors expressing a genuine very high-affinity tumor-specific antigen can be achieved by using adoptive transfer of lymphocytes from immunized young individuals.
A randomized trial comparing endoscopic ligation with nadolol plus isosorbide-5-mononitrate for the prevention of variceal rebleeding, preliminary results
Authors: A. Gallego, C. Villanueva, J. Ortiz, J. Miñana, G. Soriano, E. Ricart, X. Torras, S. Sáinz, L. Kolle, C. Guarner, J. Balanzó
Journal: Journal of Hepatology (1998)
G-Protein–Coupled Receptor Kinase 2–Mediated Desensitization of Adiponectin Receptor 1 in Failing Heart
Authors: Yajing Wang, Erhe Gao, Wayne Bond Lau, Yang Wang, Gaizheng Liu, Jing-Jing Li, Xiaoliang Wang, Yuexing Yuan, Walter J. Koch, Xin-Liang Ma
Journal: Circulation (2015)

Background— Phosphorylative desensitization of G-protein–coupled receptors contributes significantly to post–myocardial infarction (MI) remodeling and heart failure (HF). Here, we determined whether adiponectin receptors (AdipoRs) 1 and 2 (the 7-transmembrane domain–containing receptors mediating adiponectin functions) are phosphorylatively modified and functionally impaired after MI. Methods and Results— Post-MI HF was induced by coronary artery occlusion. Receptor phosphorylation, kinase expression, and adiponectin function were determined via in vivo, ex vivo, and in vitro models. AdipoR1 and AdipoR2 are not phosphorylated in the normal heart. However, AdipoR1 was significantly phosphorylated after MI, peaking at 7 days and remaining significantly phosphorylated thereafter. The extent of post-MI AdipoR1 phosphorylation positively correlated with the expression level of GPCR kinase (GRK) 2, the predominant GRK isoform upregulated in the failing heart. Cardiac-specific GRK2 knockout virtually abolished post-MI AdipoR1 phosphorylation, whereas virus-mediated GRK2 overexpression significantly phosphorylated AdipoR1 and blocked adiponectin metabolic-regulatory/anti-inflammatory signaling. Mass spectrometry identified serine-7, threonine-24, and threonine-53 (residues located in the n-terminal intracellular AdipoR1 region) as the GRK2 phosphorylation sites. Ex vivo experiments demonstrated that adenosine monophosphate–activated protein kinase activation and the anti–tumor necrosis factor-α effect of adiponectin were significantly inhibited in cardiomyocytes isolated from nonischemic area 7 days after MI. In vivo experiments demonstrated that acute adiponectin administration–induced cardiac GLUT4 translocation and endothelial nitric oxide synthase phosphorylation were blunted 7 days after MI. Continuous adiponectin administration beginning 7 days after MI failed to protect the heart from adverse remodeling and HF progression. Finally, cardiac-specific GRK2 knockdown restored the cardioprotective effect of adiponectin. Conclusion— AdipoR1 is phosphorylatively modified and desensitized by GRK2 in failing cardiomyocytes, contributing to post-MI remodeling and HF progression.
Asthma: prevalence and cost of illness
Authors: S. Stock, M. Redaelli, M. Luengen, G. Wendland, D. Civello, K. W. Lauterbach
Journal: European Respiratory Journal (2005)

The purpose of this study was to estimate the prevalence and cost of illness of asthma in Germany by retrospectively analysing routine health insurance data. This analysis investigated claims data from all insured persons of six large sickness funds. Insurants with asthma were identified via the International Classification of Diseases (ninth revision) diagnosis and the Anatomical Therapeutic Chemical Classification System Code for regular medication prescriptions. Costs for hospital care, medication and sick benefit were taken from claims data. Costs for rehabilitation, premature death and early retirement were estimated using the human capital approach and data from national statistics. Prevalence of asthma in the German statutory health insurance was 6.34%. Total costs for asthma, including direct and indirect costs, were calculated at \#8364;2.74 billion during 1999. The prevalence of asthma in the German statutory health insurance has previously been estimated to be 4–6%. The results of this large study show the prevalence of asthma in the German social insurance system to be ∼6%. The study also indicates that there is room for substantial savings in the German social insurance system, with indirect costs amounting to 74.8% of total costs and payment of sick benefits through the sickness funds amounting to 58.3% of indirect costs. These costs may be reduced with better asthma control in patients.
IMMUNOLOGICAL MEMORY IN MICE
Authors: G. F. Mitchell, Eva L. Chan, Marion S. Noble, I. L. Weissman, R. I. Mishell, L. A. Herzenberg
Journal: The Journal of Experimental Medicine (1972)

Using anti-allotype sera and AKR anti thetaC3H sera, a requirement for two cell types has been demonstrated in the adoptive secondary response of mice to heterologous erythrocytes. The cell types have been designated B cells [precursors of plaque-forming cells (PFC)] and T cells (thymus-influenced cells, not providing precursors of detectable PFC). The in vivo indirect PFC response of spleen cells from primed mice is markedly reduced by in vitro treatment of the cells with a mixture of anti-theta serum and guinea pig serum (Anti theta + GPS). This B cell response is fully restored to control levels by thymus cells from normal mice which do not themselves provide precursors of indirect PFC. Thus memory is carried by the B cell lineage but the expression of this memory is dependent on the presence of a cell population which is sensitive to Anti theta + GPS and which is replaced functionally by unprimed T cells. When assayed for T cell activity, thoracic duct cells from specifically primed mice are better than cells from nonspecifically primed mice in restoring the B cell response of spleen cells from immunized mice. Moreover, the T cell activity of a reconstitutive cell population from primed mice is reduced by incubation with Anti theta + GPS. We conclude that memory to heterologous erythrocyte antigens is carried by the T cell lineage as well as the B cell lineage even though unprimed T cells are sufficient for expression of B cell memory.
Introduction of Combined CHOP Plus Rituximab Therapy Dramatically Improved Outcome of Diffuse Large B-Cell Lymphoma in British Columbia
Authors: Laurie H. Sehn, Jane Donaldson, Mukesh Chhanabhai, Catherine Fitzgerald, Karamjit Gill, Richard Klasa, Nicol MacPherson, Susan O'Reilly, John J. Spinelli, Judy Sutherland, Kenneth S. Wilson, Randy D. Gascoyne, Joseph M. Connors
Journal: Journal of Clinical Oncology (2005)

For more than two decades, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been the standard therapy for diffuse large B-cell lymphoma (DLBCL). The addition of rituximab to CHOP has been shown to improve outcome in elderly patients with DLBCL. We conducted a population-based analysis to assess the impact of this combination therapy on adult patients with DLBCL in the province of British Columbia (BC).We compared outcomes during a 3-year period; 18 months before (prerituximab) and 18 months after (postrituximab) institution of a policy recommending the combination of CHOP and rituximab for all patients with newly diagnosed advanced-stage (stage III or IV or stage I or II with "B" symptoms or bulky [> 10 cm] disease) DLBCL.A total of 292 patients were evaluated; 140 in the prerituximab group (median follow-up, 42 months) and 152 in the postrituximab group (median follow-up, 24 months). Both progression-free survival (risk ratio, 0.56; 95% CI, 0.39 to 0.81; P = .002) and overall survival (risk ratio, 0.40; 95% CI, 0.27 to 0.61, P < .0001) were significantly improved in the postrituximab group. After controlling for age and International Prognostic Index score, era of treatment remained a strong independent predictor of progression-free survival (risk ratio, 0.59; 95% CI, 0.41 to 0.85; P = .005) and overall survival (risk ratio, 0.43; 95% CI, 0.29 to 0.66; P < .001). The benefit of treatment in the postrituximab era was present regardless of age.The addition of rituximab to CHOP chemotherapy has resulted in a dramatic improvement in outcome for DLBCL patients of all ages in the province of BC.