tbuckley/cabot-search huggingface dataset:
V. Meta-Analysis of the Efficacy of Hormone Replacement Therapy in Treating and Preventing Osteoporosis in Postmenopausal Women
Authors: George Wells, Peter Tugwell, Beverley Shea, Gordon Guyatt, Joan Peterson, Nicole Zytaruk, Vivian Robinson, David Henry, Diane O’Connell, Ann Cranney
Journal: Endocrine Reviews (2002)

To review the effect of hormone replacement therapy (HRT) on bone density and fractures in postmenopausal women.We searched MEDLINE and EMBASE from 1966 to 1999, the Cochrane Controlled Register, citations of relevant articles, and proceedings of international meetings for eligible randomized controlled trials. We contacted osteoporosis investigators to identify additional studies, and primary authors for unpublished data.We included 57 studies that randomized postmenopausal women to HRT or a control (placebo or calcium/vitamin D) and were of at least 1 yr in duration. Seven of these studies reported fractures.For each study, three independent reviewers assessed the methodological quality and abstracted the data.HRT showed a trend toward reduced incidence of vertebral fractures [relative risk (RR) 0.66, 95% confidence interval (CI) 0.41-1.07; 5 trials] and nonvertebral fractures (RR 0.87, 95% CI 0.71-1.08; 6 trials). HRT had a consistent effect on bone mineral density (BMD) at all sites. The difference between HRT and control in the percent change in bone density at 2 yr was 6.76 (5.83, 7.89; 21 trials) at the lumbar spine and 4.53 (3.68, 5.36; 14 trials) and 4.12 (3.45, 4.80; 9 trials) at the forearm and femoral neck, respectively.HRT has a consistent, favorable and large effect on bone density at all sites. The data show a nonsignificant trend toward a reduced incidence in vertebral and nonvertebral fractures.
Platelets are not degranulated by a nonionic dimeric contrast agent during diagnostic coronary angiography and coronary interventions
Authors: Eríc F. Grabowski, Susan E. Boor, Louis J. Rodino, Charles Dow, Robert Holt, Herman Gold, Ik-Kyung Jang, Alan D. Michelson
Journal: Journal of the American College of Cardiology (1996)
Association between human leukocyte antigen DP gene polymorphisms and chronic hepatitis B in a Chinese population
Authors: Chibo Liu
Journal: Hepatology (2011)

We read with great interest the article by Guo et al.,1 which suggested that 11 polymorphisms of human leukocyte antigen DP genes were significantly associated with chronic hepatitis B in a Chinese population. These significant associations were first reported by a genome-wide association study in Japanese and Thai populations.2 Since then, besides the study by Guo et al,1 two studies further confirmed the significant associations.3, 4 These studies are very important, because the findings would help us more deeply understand the genetic mechanism of chronic hepatitis B. However, after carefully inspecting the article by Guo et al.,1 we noted four issues that should be considered. First, the authors stated that the Bonferroni correction was the current P value times 4. In my opinion, it is not true. On the basis of data in Table 2, the P value should be multiplied by 8 [(2 haplotype blocks + 2 variants (rs3135021+rs11752643)) × 2 group comparisons]; in Table 3, the multiplication should be by 12 [((2 haplotype blocks + 1 variant (rs3135021)) × 2 genotype comparisons for each variant × 2 group comparisons)]. Therefore, the P value for statistical significance in Table 2 should be 0.05/8 = 0.00625 and that in Table 3 should be 0.05/12 = 0.00417. On the basis of the new P values, the association between rs2395309 and chronic hepatitis B is not statistically significant after Bonferroni correction (Table 3). Second, the authors did not provide the statistical powers of their studied sample for each variant. Therefore, I am not certain whether the statistically significant results are the true ones or are due to chance. It is always better to present the statistical powers. Third, it is more proper to move the notes of Armitage's trend test in Table 2 to the notes in Table 3, because the three genotypes for each variant in Table 3, rather than those in Table 2, showed the trends. Fourth, the order in which the three genotypes are listed under each SNP variant, namely rs9277341, rs9277535, rs3117222, and rs9380343, is not uniform in Table 2 and Table 3, and this would confuse the readers. Therefore, we suggest that the authors should keep odds ratios with 95% confidence intervals in the same direction in order to present their results more clearly. Chibo Liu M.B.*, * Department of Clinical Laboratory Taizhou Municipal Hospital Taizhou, China.
Anxiety During MRI-Reply
Authors: Carlos Mélendez
Journal: JAMA (1994)

<h3>In Reply.</h3> —We are grateful to Dr Persili and colleagues for drawing our attention to three additional published articles concerning anxiety-related reactions during MRI examinations. We apologize for not having captured these references with our search strategy. The 12% incidence of "motor unrest or claustrophobia" reported by Oberstein et al<sup>1</sup>is within the range found in our review. Of special interest was the correlation shown between final diagnosis and claustrophobic reactions in 21 633 subjects undergoing MRI examinations. This observation may be helpful in screening for subjects at risk. The article by Nozzolillo et al,<sup>2</sup>based on 28 subjects, is also in keeping with findings reported in the publications reviewed in our article. The article by Ellis et al<sup>3</sup>describes a handheld air bellows communication device that may be useful to facilitate patient communication during the test, though modern scanners have built-in voice communication systems.
Incidence of Non-A, Non-B Hepatitis after Screening Blood Donors for Antibodies to Hepatitis C Virus and Surrogate Markers
Authors: Josep M. Barrera, Miquel Bruguera, M. Guadalupe Ercilla, José M. Sánchez-Tapias, María P. Gil, Cristina Gil, Josep Costa, Antonio Gelabert, Joan Rodés, Ricardo Castillo
Journal: Annals of Internal Medicine (1991)

▪Objective: To compare the effect of screening blood donors for antibodies to hepatitis C virus (anti-HCV) on the incidence of non-A, non-B hepatitis in recipients with that of screening blood donors for antibodies to hepatitis B core antigen (anti-HBc) and elevated alanine aminotransferase levels. ▪Design: Cohort analysis of serum samples from donors and recipients. Recipients were followed for 12 months to determine the occurrence of non-A, non-B hepatitis. ▪Setting: The blood-transmitted viruses unit and the liver unit of a university teaching hospital. ▪Subjects: A total of 250 patients who had open heart surgery and their 3142 blood donors. ▪Measurements: Donor sera were tested for anti-HCV by enzyme-linked immunosorbent assay (ELISA) and, in the event of a positive result, by recombinant immunoblot assay (RIBA). Antibodies to anti-HBc and serum alanine aminotransferase (ALT) levels were also measured. Measurements of anti-HCV and ALT activity in recipients were done before transfusion and at regular intervals during follow-up. ▪Main Results: Of the 250 transfusion recipients, 40 developed non-A, non-B hepatitis. Of the 3142 donors, 70 were positive for anti-HCV by ELISA, 440 were positive for anti-HBc, and 177 had alanine aminotransferase levels between 0.67 and 1.33 µkat/L. The sensitivity (87%), specificity (89%), positive predictive value (59%), and negative predictive value (97%) of blood-donor screening were higher for anti-HCV than for anti-HBc (82%, 36%, 21%, and 91%, respectively) and for elevated alanine aminotransferase levels (65%, 70%, 29%, and 91%, respectively). The expected number of donors excluded because of the presence of anti-HCV was considerably smaller than that of donors with positive results for surrogate markers of hepatitis. ▪Conclusion: Screening blood donors for the presence of anti-HCV is more accurate than screening for surrogate markers (anti-HBc and ALT) and protects more effectively against post-transfusion non-A, non-B hepatitis.
Mechanism of ST Elevation and Ventricular Arrhythmias in an Experimental Brugada Syndrome Model
Authors: Masaomi Kimura, Takao Kobayashi, Shingen Owada, Keiichi Ashikaga, Takumi Higuma, Shingo Sasaki, Atsushi Iwasa, Shigeru Motomura, Ken Okumura
Journal: Circulation (2003)

Although phase 2 reentry is said to be responsible for initiation of ventricular tachycardia (VT) in Brugada syndrome, information about the activation sequence during VT is limited.We developed an experimental Brugada syndrome model using a canine isolated right ventricular preparation cross-circulated with arterial blood of a supporter dog and examined the VT mechanism. Two plaque electrodes (35x30 mm) containing 96 bipolar electrodes were attached to the endocardium and epicardium. Saddleback and coved types of ST elevation in transmural ECG were induced by pilsicainide, a pure sodium channel blocker, and pinacidil, a KATP channel opener. Eighteen polymorphic VT episodes were recorded in 9 of the 12 preparations associated with ST elevation. Fourteen episodes spontaneously developed in 5 preparations after an extrasystole during basic drive pacing. Analysis of local recovery times revealed increased dispersion especially in epicardium, and the extrasystole originated from a site with a short recovery time, suggesting that phase 2 reentry was its mechanism. The other 4 VTs in 4 preparations were induced by premature stimulation. Analysis of the activation sequences during VT revealed reentry between epicardium and endocardium or reentry around an arc of a functional block confined to epicardium or endocardium with bystander activation of the other.Electrical heterogeneity in the recovery phase was induced in this experimental Brugada syndrome model, which can be a substrate for the development of phase 2 reentry and the subsequent reentry around an arc of the functional block, resulting in sustained VT.
Randomized trial of balloon angioplasty versus stenting for the treatment of long coronary lesions
Authors: Alfredo Rodriguez, Alexandre A. Abizaid, Rafael Moguel, William Torres, Carlos Fernandez, Vinicius Vaz, Maximo Rodriguez, Rodolfo Staico, Fausto Feres, Jose Eduardo M. Sousa, Igor F. Palacios
Journal: Journal of the American College of Cardiology (2003)
Use of antidepressants among people committing suicide in Sweden
Authors: G Isaccsson, P Holmgren, D Wasserman, U Bergman
Journal: BMJ (1994)

<h3>Abstract</h3> <b>Objective</b>: To analyse the outcome of depression in the Swedish population as reflected by the detection of antidepressants in a national forensic toxicological screening programme of unnatural deaths. <b>Design</b>:Antidepressants detected by the National Laboratory of Forensic Chemistry were related to data on use expressed in person years of exposure. <b>Subjects</b>: All 7000 cases of unnatural death with results from forensic toxicological screening in 1990-1; this included 3400 (85%) of the 4000 cases of suicide in Sweden. <b>Main outcome measures</b>:Number of findings of antidepressants in the screening programme and number of findings of different antidepressants in relation to their use. <b>Results</b>:Antidepressants were found in 585 screening tests, corresponding to 542 subjects or less than 16% of the 3400 cases of suicide. Newer,less toxic antidepressants were found more often than the older compounds. Toxic concentrations of antidepressants were found in only 190 cases (5.6%). <b>Conclusion</b>:A consistent finding in surveys of suicide is that about half of the patients who commit suicide are depressed. The current data suggest that most depressed patients who commit suicide are not taking antidepressants immediately before death.Therapeutic failure may be a greater problem with antidepressants than toxicity as the results did not indicate any advantage of the newer, less toxic antidepressants. All causes of death should be included in risk analyses, thereby providing an estimate of effectiveness as well as toxicity of antidepressants.
Neurofibroma of the trachea: a case report.
Authors: A Thijs-van Nies, B Van de Brekel, H J Buytendijk, F Maesen
Journal: Thorax (1978)

A tracheal tumour was discovered by radiology in a 36-year-old man with haemoptysis, bronchitis, and dyspnoea. The tumour was situated 5 cm below the vocal cords. A frozen section of a bronchoscopic biopsy specimen confirmed it to be a neurofibroma. Resection was performed endoscopically.
CD30 Is a CD40-Inducible Molecule that Negatively Regulates CD40-Mediated Immunoglobulin Class Switching in Non-Antigen-Selected Human B Cells
Authors: Andrea Cerutti, András Schaffer, Shefali Shah, Hong Zan, Hsiou-Chi Liou, Raymond G Goodwin, Paolo Casali
Journal: Immunity (1998)

We used our monoclonal model of germinal center maturation, CL-01 B cells, to investigate the role of CD30 in human B cell differentiation. CL-01 cells are IgM+IgD+CD30+ and switch to IgG, IgA, and IgE when exposed to CD40L and IL-4. Switching is hampered by CD30 coengagement, possibly through interference with the CD40-mediated NF-κB-dependent transcriptional activation of downstream CH genes. The physiological relevance of this phenomenon is emphasized by similar CD30-mediated effects in naive B cells. Expression of CD30 by these cells is induced by CD40L but is inhibited by B cell receptor coengagement and/or exposure to IL-6 and IL-12. Our data suggest that CD30 critically regulates the CD40-mediated differentiation of non-antigen-selected human B cells.
P18. The tumour leukocyte infiltrate is the key predictor for therapeutic response to catumaxomab therapy
Authors: K Weiler, L Rava, M Jäger, I Funke, M Joka, KW Jauch, B Mayer
Journal: Journal for ImmunoTherapy of Cancer (2014)

Meeting abstracts Patient stratification for therapeutic response mainly focus on biomarker expression on cancer cells. Contrary, the tumour micromileu is less considered, although stromal cells and leukocytes play a crucial role in tumour progression and drug resistance. The present study
Expression of collagens type I and IV, osteonectin and transforming growth factor beta-1 (TGFβ1) in biliary atresia and paucity of intrahepatic bile ducts during infancy
Authors: Thierry Lamireau, Brigitte Le Bail, Liliane Boussarie, Monique Fabre, Pierre Vergnes, Olivier Bernard, Frédéric Gautier, Paulette Bioulac-Sage, Jean Rosenbaum
Journal: Journal of Hepatology (1999)
Expression of endothelial cell adhesion molecules in human bronchial xenografts.
Authors: J M Pilewski, R A Panettieri, L R Kaiser, S M Albelda
Journal: American Journal of Respiratory and Critical Care Medicine (1994)

The role of endothelial cell adhesion molecules (CAMs) in the selective recruitment of leukocyte subsets to the airway remains unclear. The goal of the present study was to examine the expression of human endothelial CAM in a cytokine-induced airway inflammatory response. To accomplish this, an in vivo model of human bronchus was developed by heterotopically transplanting intact sections of human airway into severe combined immunodeficient (SCID) mice. Three weeks after transplantation, the xenografts closely resembled normal bronchus with little evidence of rejection. Less than 15% of the submucosal vessels expressed E-selectin and vascular cell adhesion molecule-1 (VCAM-1), whereas intercellular adhesion molecule-1 (ICAM-1) was present constitutively on approximately 35% of bronchial microvessels. Intrabronchial instillation of tumor necrosis factor-alpha (TNF-alpha) significantly increased expression of microvascular E-selectin to 40%, ICAM-1 to 65%, and VCAM-1 to 41%, and was accompanied by an influx of murine leukocytes into the bronchial submucosa. These results demonstrate that the human bronchial microvasculature expresses cytokine-inducible adhesion molecules. Mast cells and other resident or migratory cells that secrete TNF-alpha may thus activate the bronchial microvasculature and thereby recruit leukocytes to the airway.
Adefovir for the Treatment of HIV Infection
Authors: John W. Mellors
Journal: JAMA (1999)

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Uncertain premises and Jeffrey's rule
Authors: David E. Over, Constantinos Hadjichristidis
Journal: Behavioral and Brain Sciences (2009)

Abstract Oaksford &amp; Chater (O&amp;C) begin in the halfway Bayesian house of assuming that minor premises in conditional inferences are certain. We demonstrate that this assumption is a serious limitation. They additionally suggest that appealing to Jeffrey's rule could make their approach more general. We present evidence that this rule is not limited enough to account for actual probability judgements.
Rheumatic Mitral Stenosis
Authors: D S Bach
Journal: New England Journal of Medicine (1997)

Figure 1. A 47-year-old woman presented with fatigue and worsening exertional dyspnea. Cardiac auscultation was remarkable for an irregularly irregular rhythm, a loud S1 and accentuated P2, an opening snap, and a III/IV decrescendo diastolic rumble at the apex. Transthoracic echocardiography revealed findings typical of rheumatic mitral stenosis. The mitral leaflets were pliable, with restricted mobility of the leaflet tips (open arrow, panel A), resulting in doming and a “hockey-stick” appearance of the anterior leaflet in diastole (solid arrow, panel A). There was no notable subvalvular thickening. Cross-sectional imaging of the stenotic orifice (Panel B) demonstrated thickening . . .
Exogenous growth hormone inhibits growth hormone-releasing factor-induced growth hormone secretion in normal men.
Authors: S M Rosenthal, J A Hulse, S L Kaplan, M M Grumbach
Journal: Journal of Clinical Investigation (1986)

Previous studies from this laboratory and by others in rats, monkeys, and humans support the concept that growth hormone (GH) can regulate its own secretion through an autofeedback mechanism. With the availability of human growth hormone-releasing factor (GRF), the possible existence of such a mechanism was reexplored by examining the effect of exogenous GH on the GH response induced by GRF-44-NH2 in six normal men (mean age, 32.4 yr). In all subjects the plasma GH response evoked by GRF-44-NH2 (1 microgram/kg i.v. bolus) was studied before and after 5 d of placebo (1 ml normal saline i.m. every 12 h), and then before and 12 h after 5 d of biosynthetic methionyl human GH (5 U i.m. every 12 h). The GH response to GRF (maximal increment over time 0 value) was significantly inhibited after GH treatment (0-1.3 vs. 2.3-11.2 ng/ml before treatment, P = 0.05), but was not significantly affected by placebo. This impaired pituitary response to GRF persisted for at least 24 h following exogenous GH treatment in two subjects who underwent further study. Serum somatomedin-C concentrations were significantly increased after 5 d of GH treatment (2.66-5.00 vs. 0.92-1.91 U/ml before treatment, P = less than 0.01). The impaired pituitary response to GRF may be mediated indirectly through somatomedin, somatostatin, by a direct effect of GH on the pituitary somatotropes, or by all of these mechanisms. These data suggest that after GH treatment, the blunted GH response to synthetic GRF is not solely a consequence of the inhibition of hypothalamic GRF secretion.
A phase II, multicenter trial of rindopepimut (CDX-110) in newly diagnosed glioblastoma: the ACT III study
Authors: J. Schuster, R. K. Lai, L. D. Recht, D. A. Reardon, N. A. Paleologos, M. D. Groves, M. M. Mrugala, R. Jensen, J. M. Baehring, A. Sloan, G. E. Archer, D. D. Bigner, S. Cruickshank, J. A. Green, T. Keler, T. A. Davis, A. B. Heimberger, J. H. Sampson
Journal: Neuro-Oncology (2015)

The epidermal growth factor receptor variant III deletion mutation, EGFRvIII, is expressed in ∼30% of primary glioblastoma and linked to poor long-term survival. Rindopepimut consists of the unique EGFRvIII peptide sequence conjugated to keyhole limpet hemocyanin. In previous phase II trials (ACTIVATE/ACT II), rindopepimut was well tolerated with robust EGFRvIII-specific immune responses and promising progression-free and overall survival. This multicenter, single-arm phase II clinical trial (ACT III) was performed to confirm these results. Rindopepimut and standard adjuvant temozolomide chemotherapy were administered to 65 patients with newly diagnosed EGFRvIII-expressing (EGFRvIII+) glioblastoma after gross total resection and chemoradiation. Progression-free survival at 5.5 months (∼8.5 mo from diagnosis) was 66%. Relative to study entry, median overall survival was 21.8 months, and 36-month overall survival was 26%. Extended rindopepimut vaccination (up to 3.5+ years) was well tolerated. Grades 1–2 injection site reactions were frequent. Anti-EGFRvIII antibody titers increased ≥4-fold in 85% of patients, and increased with duration of treatment. EGFRvIII was eliminated in 4/6 (67%) tumor samples obtained after >3 months of therapy. This study confirms, in a multicenter setting, the preliminary results seen in previous phase II trials of rindopepimut. A pivotal, double-blind, randomized, phase III trial ("ACT IV") is under way.
Germline TP53 Variants and Susceptibility to Osteosarcoma
Authors: Lisa Mirabello, Meredith Yeager, Phuong L. Mai, Julie M. Gastier-Foster, Richard Gorlick, Chand Khanna, Ana Patiño-Garcia, Luis Sierrasesúmaga, Fernando Lecanda, Irene L. Andrulis, Jay S. Wunder, Nalan Gokgoz, Donald A. Barkauskas, Xijun Zhang, Aurelie Vogt, Kristine Jones, Joseph F. Boland, Stephen J. Chanock, Sharon A. Savage
Journal: JNCI Journal of the National Cancer Institute (2015)

The etiologic contribution of germline genetic variation to sporadic osteosarcoma is not well understood. Osteosarcoma is a sentinel cancer of Li-Fraumeni syndrome (LFS), in which approximately 70% of families meeting the classic criteria have germline TP53 mutations. We sequenced TP53 exons in 765 osteosarcoma cases. Data were analyzed with χ2 tests, logistic regression, and Cox proportional hazards regression models. We observed a high frequency of young osteosarcoma cases (age <30 years) carrying a known LFS- or likely LFS-associated mutation (3.8%) or rare exonic variant (5.7%) with an overall frequency of 9.5%, compared with none in case patients age 30 years and older (P < .001). This high TP53 mutation prevalence in young osteosarcoma cases is statistically significantly greater than the previously reported prevalence of 3% (P = .0024). We identified a novel association between a TP53 rare variant and metastasis at diagnosis of osteosarcoma (rs1800372, odds ratio = 4.27, 95% confidence interval = 1.2 to 15.5, P = .026). Genetic susceptibility to young onset osteosarcoma is distinct from older adult onset osteosarcoma, with a high frequency of LFS-associated and rare exonic TP53 variants.