tbuckley/cabot-search huggingface dataset:
Neurological Soft Signs in First-Episode Schizophrenia: A Follow-Up Study
Authors: Silke Bachmann, Christina Bottmer, Johannes Schröder
Journal: American Journal of Psychiatry (2005)

Neurological soft signs are frequently found in schizophrenia. They are indicators of both genetic liability and psychopathological symptoms. To further differentiate "trait" and "state" relations the authors compared the 1-year course of neurological soft signs in schizophrenia patients and comparison subjects.Thirty-nine patients with first-episode schizophrenia spectrum disorders were examined after remission of acute symptoms and 14 months later. Established instruments assessed diagnoses, psychopathological symptoms, predictors of outcome, handedness, and neurological soft signs. Twenty-two age- and gender-matched comparison subjects were also examined twice.Neurological soft sign scores in patients were significantly elevated relative to comparison subjects at both measurement points. Whereas neurological soft signs remained stable in comparison subjects (time 1: mean=4.8, SD=3.3; time 2: mean=4.6, SD=3.9), they significantly decreased in patients (time 1: mean=15.7, SD=7.1; time 2: mean=10.1, SD=7.9). This effect was more pronounced in patients with a favorable versus a chronic course and was mainly accounted for by motor signs. Predictors of follow-up neurological soft sign scores were neurological soft sign levels at remission and compliance with treatment.Although neurological soft signs are intrinsic to schizophrenia, their level varies with the clinical course. Thus, neurological soft signs may correspond to both genetic liability and the activity of the disease process and may be considered as potential predictors of outcome.
Overexpression and Mislocalization of the Chromosomal Segregation Protein Separase in Multiple Human Cancers
Authors: Rene Meyer, Viacheslav Fofanov, AnilK. Panigrahi, Fatima Merchant, Nenggang Zhang, Debananda Pati
Journal: Clinical Cancer Research (2009)

Separase, an endopeptidase, plays a pivotal role in chromosomal segregation by separating sister chromatids during the metaphase to anaphase transition. Using a mouse mammary tumor model we have recently shown that overexpression of Separase induces aneuploidy and tumorigenesis (Zhang et al., Proc Natl Acad Sci 2008;105:13033). In the present study, we have investigated the expression level of Separase across a wide range of human tumors.
Absence of Association between Organic Solvent Exposure and Risk of Chronic Renal Failure
Authors: C. Michael Fored, Gun Nise, Elisabeth Ejerblad, Jon P. Fryzek, Per Lindblad, Joseph K. McLaughlin, Carl-Gustaf Elinder, Olof Nyre[Combining Acute Accent]n
Journal: Journal of the American Society of Nephrology (2004)

ABSTRACT. Exposure to organic solvents has been suggested to cause or exacerbate renal disease, but methodologic concerns regarding previous studies preclude firm conclusions. We examined the role of organic solvents in a population-based case-control study of early-stage chronic renal failure (CRF). All native Swedish residents aged 18 to 74 yr, living in Sweden between May 1996 and May 1998, formed the source population. Incident cases of CRF in a pre-uremic stage (n = 926) and control subjects (n = 998), randomly selected from the study base, underwent personal interviews that included a detailed occupational history. Expert rating by a certified occupational hygienist was used to assess organic solvent exposure intensity and duration. Relative risks were estimated by odds ratios (OR) in logistic regression models, with adjustment for potentially important covariates. The overall risk for CRF among subjects ever exposed to organic solvents was virtually identical to that among never-exposed (OR, 1.01; 95% confidence interval [CI], 0.81 to 1.25). No dose-response relationships were observed for lifetime cumulative solvent exposure, average dose, or exposure frequency or duration. The absence of association pertained to all subgroups of CRF: glomerulonephritis (OR, 0.96; 95% CI, 0.68 to 1.34), diabetic nephropathy (OR, 1.02; 95% CI, 0.74 to 1.41), renal vascular disease (OR, 1.16; 95% CI, 0.76 to 1.75), and other renal CRF (OR, 0.92; 95% CI, 0.66 to 1.27). The results from a nationwide, population-based study do not support the hypothesis of an adverse effect of organic solvents on CRF development, in general. Detrimental effects from subclasses of solvents or on specific renal diseases cannot be ruled out. E-mail: [email protected]
Initial and late results of balloon angioplasty of restenosis lesions within Wiktor stent: a comparison with Palmaz-Schatz stent
Authors: M. Toma, H. Tamai, Y.-S. Hsu, K. Kosuga, A. Kawashima, S. Matsui, T. Hata, T. Nakamura, M. Minami, S. Motohara, H. Uehata
Journal: Journal of the American College of Cardiology (1998)
Family History of Cancer in Patients With Gastric Cancer
Authors: Vincenzo Formica, Enrico Vasile, Mario Roselli
Journal: Journal of Clinical Oncology (2012)

Some aspects of the results were also somewhat disconcerting, probably as a result of the low effective number of patients.The effects of family history were observed in only 48 patients with stage III and IV disease, of whom approximately 40% (fewer than 20 patients) died.Among these patients, the effects were limited to those with exactly one relative with gastric cancer; if the patient had two or more family members diagnosed with gastric cancer, the adjusted hazard ratios were 1.12 (95% CI, 0.39 to 3.24), 1.17 (95% CI, 0.40 to 3.39), and 0.91 (95% CI, 0.27 to 3.08) for disease-free survival, recurrence-free survival, and overall survival, respectively.The advantages of the study by Han et al 1 are the large size and detailed clinical data, which in principle may allow analyses of subgroups with distinct biologic behavior.However, the extensive literature on the attempts to associate familial risk with survival has remained largely inconclusive, which we have assumed to depend on different genetic and environmental risk factors for cancer susceptibility and survival. 4,13The data summarized for 13 different cancers analyzed using the Swedish Family-Cancer Database found consistent association between family history and survival for ovarian cancer only; the hazard ratio for survival was 1.4 in women with a family history of ovarian cancer.
Abstract 3204: Novel, rapid and sensitive technology to analyze gene expression directly from archived FFPE clinical oncology specimens without sample preparation
Authors: Chang Hee Kim, Arpad Gerstner, Majid R. Abedi, John R. Childers, Robert Terbrueggen
Journal: Cancer Research (2012)

Abstract Formalin-Fixed Paraffin Embedded (FFPE) tissue samples are the standard for clinical oncology tissue sample archiving worldwide. It is estimated that there are approximately a billion FFPE tissue cancer samples archived in hospitals and tissue banks around the world, and many of these samples have full clinical annotation including long term follow-up data. Current methods of analyzing gene expression in these samples involve laborious and expensive sample preparation protocols and long turnaround times (2 days or longer). We have developed a novel, rapid (3 hours), sample-to-answer technology to analyze gene expression from clinical FFPE tissues without the need for RNA extraction. The technique is highly sensitive and requires only 2 mm x 5 mm x 10 microns of FFPE material scraped from a pathology slide. The gene expression data obtained directly from FFPE without sample preparation correlates highly with data obtained on RNA extracted from the same FFPE sample using conventional methods. Importantly, the gene expression data obtained from prostate and breast FFPE samples correlate highly with microarray data, and with data from matching mirrored FF (Fresh Frozen) samples. The assay can be developed for detection using Luminex instrument or Capillary Electrophoresis instrument (Caliper GX or ABI 3500). Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 3204. doi:1538-7445.AM2012-3204
B Lymphocyte Antigen D8/17 and Repetitive Behaviors in Autism
Authors: Eric Hollander, Gina DelGiudice-Asch, Lorraine Simon, James Schmeidler, Charles Cartwright, Concetta M. DeCaria, Jee Kwon, Charlotte Cunningham-Rundles, Floresta Chapman, John B. Zabriskie
Journal: American Journal of Psychiatry (1999)

Monoclonal antibody D8/17 identifies a B lymphocyte antigen with expanded expression in rheumatic fever, Sydenham's chorea, and subgroups of obsessive-compulsive disorder and Tourette's syndrome with repetitive behaviors. The authors examined the rate of D8/17 expression in children with autism and its correlation with severity of repetitive behaviors.Blood samples from 18 patients with autism and 14 comparable medically ill children were evaluated for percentage of D8/17-positive B cells by immunofluorescence and for streptococcal antibodies. Severity of repetitive behaviors was also determined.The frequency of individuals with > or =11% D8/17-positive cells was significantly higher in the autistic patients (78%) than the comparison subjects (21%), severity of repetitive behaviors significantly correlated with D8/17 expression, and D8/17-positive patients had significantly higher compulsion scores than D8/17-negative patients.D8/17 expression is high in patients with autism and may serve as a marker for compulsion severity within autism.
Cancer Patients' Roles in Treatment Decisions: Do Characteristics of the Decision Influence Roles?
Authors: Nancy L. Keating, Mary Beth Landrum, Neeraj K. Arora, Jennifer L. Malin, Patricia A. Ganz, Michelle van Ryn, Jane C. Weeks
Journal: Journal of Clinical Oncology (2010)

Purpose Patients with more active roles in decisions are more satisfied and may have better health outcomes. Younger and better educated patients have more active roles in decisions, but whether patients' roles in decisions differ by characteristics of the decision itself is unknown. Patients and Methods We surveyed a large, population-based cohort of patients with recently diagnosed lung or colorectal cancer about their roles in decisions regarding surgery, radiation therapy, and/or chemotherapy. We used multinomial logistic regression to assess whether characteristics of the decision, including evidence about the treatment's benefit, whether the decision was likely preference-sensitive (palliative therapy for metastatic cancer), and treatment modality, influenced patients' roles in that decision. Results Of 10,939 decisions made by 5,383 patients, 38.9% were patient controlled, 43.6% were shared, and 17.5% were physician controlled. When there was good evidence to support a treatment, shared control was greatest; when evidence was uncertain, patient control was greatest; and when there was no evidence for or evidence against a treatment, physician control was greatest (overall P &lt; .001). Decisions about treatments for metastatic cancers tended to be more physician controlled than other decisions (P &lt; .001). Conclusion Patients making decisions about treatments for which no evidence supports benefit and decisions about noncurative treatments reported more physician control, which suggests that patients may not want the responsibility of deciding on treatments that will not cure them. Better strategies for shared decision making may be needed when there is no evidence to support benefit of a treatment or when patients have terminal illnesses that cannot be cured.
Localization and alteration of mono-, di-, and trifucosyl alpha 1----3 type 2 chain structures during human embryogenesis and in human cancer.
Authors: Y Fukushi, S Hakomori, T Shepard
Journal: The Journal of Experimental Medicine (1984)

Distribution patterns of specific fucose-containing antigens having X determinant (Gal beta 1----4[Fuc alpha 1----3]GlcNAc) as well as the di- or trimeric X determinants (Gal beta 1----4[Fuc alpha 1----3]GlcNAc beta 1----3Gal beta 1----4[Fuc alpha 1----3]-GlcNAc) in the developing human embryo and fetus and in human cancer have been examined using immunohistological techniques. Tissue sections were stained with monoclonal antibody FH3, which defines X determinant, and with monoclonal antibody FH4, which defines di- or trimeric X determinant. The following general trends in the expression of the antigens defined by FH3 and FH4 have been observed: (a) A well-organized, orderly appearance and disappearance of the antigens was observed during the histogenesis of various epithelia of gastrointestinal and other organs. The developmental stage exhibiting the maximum antigen expression is different for each organ. (b) The X determinant defined by FH3 was expressed approximately 2 wk earlier than the di- or trimeric X determinant defined by FH4, and the antigen defined by FH4 regressed more rapidly and more completely than the X determinant defined by FH3 on further development of epithelial tissue. Thus, expression of the FH4 antigen is highly limited to specific types of cells in newborn and adult epithelial tissues. (c) The antigen defined by FH4 was strongly expressed in the majority of tubular and papillary adenocarcinoma of stomach, adenocarcinoma of colon, and infiltrating ductal carcinoma of breast and its metastatic lesions. No antigen was found in poorly differentiated stomach adenocarcinoma, squamous lung carcinoma, and many other types of tumors from ovary, testis, prostate, skin, and muscle. The presence of the antigen defined by FH4 is therefore limited to carcinoma of the stomach, colon, and breast and can be regarded as a retrograde expression of the antigen to a certain stage of fetal development in which expression of this antigen was maximal.
Identification of citrullinated vimentin peptides as T cell epitopes in HLA-DR4 positive RA patients
Authors: A L Feitsma, E I H van der Voort, K L M C Franken, H Bannoudi, B G Elferink, J W Drijfhout, T W J Huizinga, R R P de Vries, R E M Toes, A Ioan-Facsinay
Journal: Annals of the Rheumatic Diseases (2010)

Antibodies directed against citrullinated proteins (ACPA) are highly specific for rheumatoid arthritis (RA). The production of ACPA is most likely dependent on the presence of T cells as ACPA have undergone isotype switching and associate with the shared epitope-containing HLA-DRB1 alleles (SE). Vimentin is a likely candidate protein …
Signaling by Myeloid C-Type Lectin Receptors in Immunity and Homeostasis
Authors: David Sancho, Caetano Reis e Sousa
Journal: Annual Review of Immunology (2012)

Myeloid cells are key drivers of physiological responses to pathogen invasion or tissue damage. Members of the C-type lectin receptor (CLR) family stand out among the specialized receptors utilized by myeloid cells to orchestrate these responses. CLR ligands include carbohydrate, protein, and lipid components of both pathogens and self, which variably trigger endocytic, phagocytic, proinflammatory, or anti-inflammatory reactions. These varied outcomes rely on a versatile system for CLR signaling that includes tyrosine-based motifs that recruit kinases, phosphatases, or endocytic adaptors as well as nontyrosine-based signals that modulate the activation of other pathways or couple to the uptake machinery. Here, we review the signaling properties of myeloid CLRs and how they impact the role of myeloid cells in innate and adaptive immunity.
Amygdala Volume Associated With Alcohol Abuse Relapse and Craving
Authors: Jana Wrase, Nicos Makris, Dieter F. Braus, Karl Mann, Michael N. Smolka, David N. Kennedy, Verne S. Caviness, Steven M. Hodge, Lena Tang, Matthew Albaugh, David A. Ziegler, Orin C. Davis, Christian Kissling, Gunter Schumann, Hans C. Breiter, Andreas Heinz
Journal: American Journal of Psychiatry (2008)

Amygdala volume has been associated with drug craving in cocaine addicts, and amygdala volume reduction is observed in some alcohol-dependent subjects. This study sought an association in alcohol-dependent subjects between volumes of reward-related brain regions, alcohol craving, and the risk of relapse.Besides alcohol craving, the authors assessed amygdala, hippocampus, and ventral striatum volumes in 51 alcohol-dependent subjects and 52 age- and education-matched healthy comparison subjects after detoxification. After imaging and clinical assessment, patients were followed for 6 months and alcohol intake was recorded.Alcohol-dependent subjects showed reduced amygdala, hippocampus, and ventral striatum volumes and reported stronger craving in relation to healthy comparison subjects. However, only amygdala volume and craving differentiated between subsequent relapsers and abstainers. A significant decrease of amygdala volume in alcohol-dependent subjects was associated with increased alcohol craving before imaging and an increased alcohol intake during the 6-month follow-up period.These findings suggest a relationship between amygdala volume reduction, alcohol craving, and prospective relapse into alcohol consumption.
Self-Tolerance to the Murine Homologue of a Tyrosinase-Derived Melanoma Antigen
Authors: Teresa A. Colella, Timothy N.J. Bullock, Liane B. Russell, David W. Mullins, Willem W. Overwijk, Chance John Luckey, Richard A. Pierce, Nicholas P. Restifo, Victor H. Engelhard
Journal: The Journal of Experimental Medicine (2000)

The human tyrosinase-derived peptide YMDGTMSQV is presented on the surface of human histocompatibility leukocyte antigen (HLA)-A*0201+ melanomas and has been suggested to be a tumor antigen despite the fact that tyrosinase is also expressed in melanocytes. To gain information about immunoreactivity and self-tolerance to this antigen, we established a model using the murine tyrosinase-derived homologue of this peptide FMDGTMSQV, together with transgenic mice expressing the HLA-A*0201 recombinant molecule AAD. The murine peptide was processed and presented by AAD similarly to its human counterpart. After immunization with recombinant vaccinia virus encoding murine tyrosinase, we detected a robust AAD-restricted cytotoxic T lymphocyte (CTL) response to FMDGTMSQV in AAD transgenic mice in which the entire tyrosinase gene had been deleted by a radiation-induced mutation. A residual response was observed in the AAD+tyrosinase+ mice after activation under certain conditions. At least some of these residual CTLs in AAD+tyrosinase+ mice were of high avidity and induced vitiligo upon adoptive transfer into AAD+tyrosinase+ hosts. Collectively, these data suggest that FMDGTMSQV is naturally processed and presented in vivo, and that this presentation leads to substantial but incomplete self-tolerance. The relevance of this model to an understanding of the human immune response to tyrosinase is discussed.
Gene Regulation Divergence Is a Major Contributor to the Evolution of Dobzhansky–Muller Incompatibilities between Species of Drosophila
Authors: Wilfried Haerty, Rama S. Singh
Journal: Molecular Biology and Evolution (2006)

The Dobzhansky–Muller model denotes incompatible gene interactions between diverging populations/species and is recognized as the basis of postzygotic reproductive isolation. Little is known about the molecular nature of such gene interactions. We have carried out comparative gene expression analyses in the testes of 3 closely related species of the Drosophila melanogaster subgroup and their hybrids (all of which are sterile). We show that in hybrids 1) a higher proportion of male-biased genes (i.e., genes with a higher level of expression in males) are underexpressed (or not expressed) compared with non–sex-biased genes, 2) the majority of the underexpressed genes appear to be under stabilizing selection by virtue of showing similar levels of expression in the parental species, and only a small proportion of genes show signs of directional selection, 3) very few of the misexpressed genes are shared between species pairs, suggesting that there may not be a "common" set of "speciation genes," and 4) expression of non–testes-specific genes is observed in the testes of interspecific hybrids, and the number of such genes is positively correlated with divergence time. These results suggest that gene regulation divergence of sex- and reproduction-related genes is a major contributor to the evolution of Dobzhansky–Muller incompatibilities between species of Drosophila.
Nonvalidation of Reported Genetic Risk Factors for Acute Coronary Syndrome in a Large-Scale Replication Study
Authors: Thomas M. Morgan, Harlan M. Krumholz, Richard P. Lifton, John A. Spertus
Journal: JAMA (2007)

Given the numerous, yet inconsistent, reports of genetic variants being associated with acute coronary syndromes (ACS), there is a need for comprehensive validation of ACS susceptibility genotypes.To perform an extensive validation of putative genetic risk factors for ACS.Through a systematic literature search of articles published before March 10, 2005, we identified genetic variants previously reported as significant susceptibility factors for atherosclerosis or ACS. Restricting our analysis to white patients to reduce confounding from racial admixture, we identified 811 patients who presented from March 2001 through June 2003 with ACS at 2 Kansas City, Mo, university-affiliated hospitals. During 2005-2006, we genotyped the 811 patients along with 650 age- and sex-matched controls for 85 variants in 70 genes and attempted to replicate previously reported associations. We further explored possible associations without prior assumption of specific risk models and used the Sign test to search for weak associations.Compare each prespecified gene variant associated with ACS risk among cases and controls. A surplus of associations would imply that some are associated with ACS.Of 85 variants tested, only 1 putative risk genotype (-455 promoter variant in beta-fibrinogen) was nominally statistically significant (P = .03). Only 4 additional genes were positive in model-free analysis. Neither number of associations was more frequent than expected by chance, given the number of comparisons. Finally, only 41 of 84 predefined risk variants were even marginally more frequent in cases than in controls (with 1 tie), representing a 48.8% "win rate" (95% confidence interval, 38.1%-59.5%) for the collective risk genotypes (P = .91, Sign test).Our null results provide no support for the hypothesis that any of the 85 genetic variants tested is a susceptibility factor for ACS. These results emphasize the need for robust replication of putative genetic risk factors before their introduction into clinical care.