tbuckley/cabot-search huggingface dataset:
Children’s Exposure to Volatile Organic Compounds as Determined by Longitudinal Measurements in Blood
Authors: Ken Sexton, John L. Adgate, Timothy R. Church, David L. Ashley, Larry L. Needham, Gurumurthy Ramachandran, Ann L. Fredrickson, Andrew D. Ryan
Journal: Environmental Health Perspectives (2004)

Blood concentrations of 11 volatile organic compounds (VOCs) were measured up to four times over 2 years in a probability sample of more than 150 children from two poor, minority neighborhoods in Minneapolis, Minnesota. Blood levels of benzene, carbon tetrachloride, trichloroethene, and m-/p-xylene were comparable with those measured in selected adults from the Third National Health and Nutrition Examination Survey (NHANES III), whereas concentrations of ethylbenzene, tetrachloroethylene, toluene, 1,1,1-trichloroethane, and o-xylene were two or more times lower in the children. Blood levels of styrene were more than twice as high, and for about 10% of the children 1,4-dichlorobenzene levels were greater than or equal to 10 times higher compared with NHANES III subjects. We observed strong statistical associations between numerous pairwise combinations of individual VOCs in blood (e.g., benzene and m-/p-xylene, m-/p-xylene and o-xylene, 1,1,1-trichloroethane and m-/p-xylene, and 1,1,1-trichloroethane and trichloroethene). Between-child variability was higher than within-child variability for 1,4-dichlorobenzene and tetrachloroethylene. Between- and within-child variability were approximately the same for ethylbenzene and 1,1,1-trichloroethane, and between-child was lower than within-child variability for the other seven compounds. Two-day, integrated personal air measurements explained almost 79% of the variance in blood levels for 1,4-dichlorobenzene and approximately 20% for tetrachloroethylene, toluene, m-/p-xylene, and o-xylene. Personal air measurements explained much less of the variance (between 0.5 and 8%) for trichloroethene, styrene, benzene, and ethylbenzene. We observed no significant statistical associations between total urinary cotinine (a biomarker for exposure to environmental tobacco smoke) and blood VOC concentrations. For siblings living in the same household, we found strong statistical associations between measured blood VOC concentrations.
5-Fr vs. 3-Fr pancreatic stents for the prevention of post-ERCP pancreatitis in high-risk patients: a systematic review and network meta-analysis
Authors: Elham Afghani, Venkata Akshintala, Mouen Khashab, Joanna Law, Susan Hutfless, Katherine Kim, Anne Lennon, Anthony Kalloo, Vikesh Singh
Journal: Endoscopy (2014)

<b>Background and study aims:</b> Placement of a pancreatic stent is recommended for the prevention of pancreatitis after endoscopic retrograde cholangiopancreatitis (ERCP) among high-risk patients. However, it is not known whether there is a particular feature of the pancreatic stent that is associated with a lower incidence of post-ERCP pancreatitis (PEP). This systematic review and network meta-analysis (NMA) aimed to examine whether a particular feature of pancreatic stents is associated with lower incidence of PEP. <b>Patients and methods:</b> The MEDLINE, Embase, and Cochrane Library databases were searched for randomized controlled trials (RCTs) that evaluated the efficacy of pancreatic stents in the prevention of PEP from September 1993 to June 2013. Trials that reported the incidence of PEP in high-risk patients randomized to one vs. another type of pancreatic stent or vs. no stent at all were included in the analysis. <b>Results:</b> Among the 1377 citations identified from the database searches, 6 RCTs involving 561 patients were included. Three RCTs evaluated 5-Fr straight, flanged pancreatic stents, two RCTs evaluated 5-Fr single-pigtail, unflanged stents, and three RCTs evaluated 3-Fr single-pigtail, unflanged stents. The probability of being ranked the best was 50.3 % (SD = 0.5, Markov chain error = 0.003) for 5-Fr single-pigtail, unflanged pancreatic stents, 46.5 % for 5-Fr straight, flanged stents, and 3.1 % for 3-Fr single-pigtail, unflanged stents. <b>Conclusion:</b> The 5-Fr pancreatic stent is superior to the 3-Fr pancreatic stent for the prevention of PEP in high-risk patients. The 5-Fr single-pigtail, unflanged pancreatic stent and 5-Fr straight, flanged pancreatic stent performed similarly and both performed better than the 3-Fr pancreatic stent in preventing PEP, suggesting that stent diameter is more important for the prevention of PEP than type of stent or the presence of flanges.
The ICMJE's definition of authorship is illogical and unethical
Authors: D. Shaw
Journal: BMJ (2011)

In recent years there have been many revelations about ghost authors, who contribute to publications but are not credited, and guest authors, who do not contribute but are credited. Most medical and many other journals adhere to the authorship standards set by the International Committee of Medical Journal Editors (ICMJE), which were designed in part to combat the phenomena of ghost and guest authorship. However, the current criteria set for authorship by the ICMJE have their own problems.

Imagine that Andrew, Michael, and Chris decide to collaborate on some research. Andrew has had a brilliant idea for a study, and he and Chris carry it out successfully. Michael writes a paper based on their results and analysis, and Chris checks and corrects it. All three approve the final draft. They are aware that their paper is of great importance, so they decide to submit it to the BMJ . All goes well until they reach the authorship statement stage of the submission process, where they must agree with the statement, “We all meet the definition …
Detection of pancreatic islet 64,000 M(r) autoantigens in insulin-dependent diabetes distinct from glutamate decarboxylase.
Authors: M R Christie, J A Hollands, T J Brown, B K Michelsen, T L Delovitch
Journal: Journal of Clinical Investigation (1993)

Patients with insulin-dependent diabetes (IDDM) possess antibodies to islet proteins of M(r)-64,000. Potential autoantigens of this M(r) include glutamate decarboxylase (GAD) and 65 kD heat shock protein. We have detected two distinct antibody specificities in IDDM that bind 50,000 M(r) or 37,000/40,000 M(r) proteolytic fragments of 64,000 M(r) proteins. In this study, we investigated relationships of these proteolytic fragments to GAD and heat shock proteins. Polyclonal antibodies to GAD bound 50,000 M(r) fragments of islet antigen. Recombinant GAD65, but not GAD67, blocked binding to this antigen, suggesting that 50,000 M(r) fragments are derived from islet GAD65. In contrast, GAD antibodies did not recognize 37,000/40,000 M(r) fragments, and neither GAD isoforms blocked autoantibody binding to precursors of these fragments. The 37,000/40,000 M(r) fragments, but not the 50,000 M(r) fragments, were detected after trypsin treatment of immunoprecipitates from insulinoma cells that lacked expression of major GAD isoforms. Antibodies in IDDM did not bind native or trypsinized islet heat shock proteins. Thus, IDDM patients possess antibodies to GAD, but also distinct antibodies to a 64,000 M(r) protein that is not related to known GAD isoforms or heat shock proteins.
Hypersecretion of glucagon and gastrin in severely burnt patients.
Authors: C I Orton, A W Segal, S R Bloom, J Clarke
Journal: BMJ (1975)

Hyperglucagonaemia and hypergastrinaemia were observed in some severely burnt patients during their illness. Hyperglucagonaemia seemed to be related to the severity of illness rather than to the burn itself, and the close correlation of glucagon concentrations with glucose and urea and its inverse correlation with bicarbonate concentrations suggest that glucagon might contribute to the hypercatabolic state. One patient developed high levels of gastrin and massive bleeding from a stress ulcer of the duodenum. Possibly gastrin hypersecretion may have a role in the pathogenesis of Curling9s ulcer.
Targeting Akt3 Signaling in Malignant Melanoma Using Isoselenocyanates
Authors: Arati Sharma, Arun K. Sharma, SubbaRao V. Madhunapantula, Dhimant Desai, Sung Jin Huh, Paul Mosca, Shantu Amin, Gavin P. Robertson
Journal: Clinical Cancer Research (2009)

Abstract Purpose: Melanoma is the most invasive and deadly form of skin cancer. Few agents are available for treating advanced disease to enable long-term patient survival, which is driving the search for new compounds inhibiting deregulated pathways causing melanoma. Akt3 is an important target in melanomas because its activity is increased in ∼70% of tumors, decreasing apoptosis in order to promote tumorigenesis. Experimental Design: Because naturally occurring products can be effective anticancer agents, a library was screened to identify Akt3 pathway inhibitors. Isothiocyanates were identified as candidates, but low potency requiring high concentrations for therapeutic efficacy made them unsuitable. Therefore, more potent analogs called isoselenocyanates were created using the isothiocyanate backbone but increasing the alkyl chain length and replacing sulfur with selenium. Efficacy was measured on cultured cells and tumors by quantifying proliferation, apoptosis, toxicity, and Akt3 pathway inhibition. Results: Isoselenocyanates significantly decreased Akt3 signaling in cultured melanoma cells and tumors. Compounds having 4 to 6 carbon alkyl side chains with selenium substituted for sulfur, called ISC-4 and ISC-6, respectively, decreased tumor development by ∼60% compared with the corresponding isothiocyanates, which had no effect. No changes in animal body weight or in blood parameters indicative of liver-, kidney-, or cardiac-related toxicity were observed with isoselenocyanates. Mechanistically, isoselenocyanates ISC-4 and ISC-6 decreased melanoma tumorigenesis by causing an ∼3-fold increase in apoptosis. Conclusions: Synthetic isoselenocyanates are therapeutically effective for inhibiting melanoma tumor development by targeting Akt3 signaling to increase apoptosis in melanoma cells with negligible associated systemic toxicity.
The Nature and Function of Putative Gonadotropin Surge-Attenuating/Inhibiting Factor (GnSAF/IF)
Authors: PAUL A. FOWLER, ALLAN TEMPLETON
Journal: Endocrine Reviews (1996)

REGULATION of the ovarian cycle is by a complex series of positive and negative feedback mechanisms between ovary, hypothalamus, and pituitary. The role of steroidal feedback between ovary, pituitary, and hypothalamus has been known for many years, and our knowledge of the mechanisms involved continues to expand. Nonsteroidal ovarian secretagogues also have endocrine regulatory function, some acting centrally. The best known of these is inhibin, although its central function is now uncertain. Since the late 1970s it has become evident that there are ovarian nonsteroidal products with specific inhibitory effects on pituitary responsiveness to GnRH. As early as 1979 (1) it was suggested that follicular fluid contained a factor other than inhibin that suppressed GnRH-induced LH secretion in vitro. Recent reviews of a novel ovarian factor, which has been called gonadotropin surge-attenuating factor (GnSAF) or gonadotropin surge-inhibiting factor (GnSIF), have supported the evidence for its existence and possible physiological role (2–6). Reviews of the LH surge itself have begun to include reference to this ovarian product (7). In this review we concentrate on the nature, activity, and probable role of GnSAF/IF in the regulation of LH secretion during the ovarian cycle.
TOPICAL IODINE-CONTAINING ANTISEPTICS AND NEONATAL HYPOTHYROIDISM IN VERY-LOW-BIRTHWEIGHT INFANTS
Authors: P. Smerdely, S.C. Boyages, D. Wu, G. Leslie, E. John, A. Lim, K. Waite, V. Roberts, J. Arnold, C.J. Eastman
Journal: The Lancet (1989)
Abstract 5188: Altering cell attachment to growth substrate up-regulates growth differentiation factor 15 (GDF15) expression
Authors: Koh Meng Aw Yong, Yu Zeng, Donald Vindivich, Robert Getzenberg
Journal: Cancer Research (2012)

Abstract Cell attachment to the extracellular environment is critical in determining cell fate. When normal cells lose attachment, they undergo anoikis. Cancer cells develop resistance to anoikis which results in metastasis. While there are many known genes alterations that can alter cell adhesion, less is known about how such a loss of cell adhesion may influence gene expression. We believe that a change in cell adhesion could trigger changes to gene expression, and the resulting changes play an important role in prostate cancer metastasis. Using prostate cancer cell lines, we examined gene expression changes in cancer cells brought about by loss of attachment to their growth substrate through chemical and physical means and how these changes play a role in prostate cancer. Microarray analysis was performed on LNCaP cells treated with latrunculin B, an actin cytoskeleton disrupting agent for 8 hours. Using quantitative real time PCR and immunoblot analysis, a member of the tumor growth factor beta superfamily, GDF15 was found to be consistently up-regulated when the cells were treated with either latrunculin B or other drugs that disrupt the actin cytoskeleton. These findings were observed not only in LNCaP but in PC3 and DU145 as well. GDF15 expression was rapidly increased in these three cell lines when cells were prevented from attaching to tissue culture plastic and the levels of GDF15 expression could be maintained as long as the cells were not allowed to re-attach. This up-regulation was reversed when cells were allowed to re-attach to growth substrate, or by regaining cell shape when the drugs were removed. GDF15 has been shown to be associated with metastatic prostate cancer as well as contributing to disease associated cachexia. In our study, we demonstrated that loss of cell adhesion was sufficient to increase GDF15 expression in a rapid and sustainable manner. This finding is novel and different from other reports that increased GDF15 led to altered cell shape and adhesion. We believe that our findings may provide a picture of the initial stages in metastasis when a cancer cell loses adhesion to the extracellular environment. Furthermore, our results reinforce the potential utility of GDF15 as a prognostic marker in prostate cancer, as well as the intricate relationship between the cell and the physical environment in cancer. 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 5188. doi:1538-7445.AM2012-5188
Phylogenetic Analysis of Nitrite, Nitric Oxide, and Nitrous Oxide Respiratory Enzymes Reveal a Complex Evolutionary History for Denitrification
Authors: Christopher M. Jones, Blaž Stres, Magnus Rosenquist, Sara Hallin
Journal: Molecular Biology and Evolution (2008)

Denitrification is a facultative respiratory pathway in which nitrite (NO2−), nitric oxide (NO), and nitrous oxide (N2O) are successively reduced to nitrogen gas (N2), effectively closing the nitrogen cycle. The ability to denitrify is widely dispersed among prokaryotes, and this polyphyletic distribution has raised the possibility of horizontal gene transfer (HGT) having a substantial role in the evolution of denitrification. Comparisons of 16S rRNA and denitrification gene phylogenies in recent studies support this possibility; however, these results remain speculative as they are based on visual comparisons of phylogenies from partial sequences. We reanalyzed publicly available nirS, nirK, norB, and nosZ partial sequences using Bayesian and maximum likelihood phylogenetic inference. Concomitant analysis of denitrification genes with 16S rRNA sequences from the same organisms showed substantial differences between the trees, which were supported by examining the posterior probability of monophyletic constraints at different taxonomic levels. Although these differences suggest HGT of denitrification genes, the presence of structural variants for nirK, norB, and nosZ makes it difficult to determine HGT from other evolutionary events. Additional analysis using phylogenetic networks and likelihood ratio tests of phylogenies based on full-length sequences retrieved from genomes also revealed significant differences in tree topologies among denitrification and 16S rRNA gene phylogenies, with the exception of the nosZ gene phylogeny within the data set of the nirK-harboring genomes. However, inspection of codon usage and G + C content plots from complete genomes gave no evidence for recent HGT. Instead, the close proximity of denitrification gene copies in the genomes of several denitrifying bacteria suggests duplication. Although HGT cannot be ruled out as a factor in the evolution of denitrification genes, our analysis suggests that other phenomena, such gene duplication/divergence and lineage sorting, may have differently influenced the evolution of each denitrification gene.
Bullied children are picked on for their vulnerability
Authors: S. Leff
Journal: BMJ (1999)

EDITOR—All school doctors and nurses in the South Downs Health Trust were asked to record, over two months in 1997, details of health contacts with children aged 8-14 in which bullying was assessed as an important factor affecting the health consultation. Staff (eight doctors, 14 nurses) logged 97 contacts. As in Salmon et al's study,1half the children were …
Subacute Bacterial Endocarditis Caused by Gaffkya Tetragena
Authors: Robert D. Boynton
Journal: New England Journal of Medicine (1950)

GAFFKY1 first described Micrococcus tetragena, now known as Gaffkya tetragena,2 in 1881. Reimann,3 in 1935, reported a case of septicemia and reviewed the literature. He found more than 170 cases of G. tetragena infections reported from other countries and 2 in the American literature. Subsequently, he reported extensive bacteriologic and immunological studies of this organism.4 5 6 7 8 Since then, at least 6 cases of tetragena infections have been reported in this country, including septicemia, meningitis, pneumonia, penile ulcer and ulcerative stomatitis.9 10 11 12 13 14 To date, in the entire literature, only 10 authenticated cases of subacute bacterial endocarditis caused by G. tetragena have been . . .
Proteasome inhibitor bortezomib-induced apoptosis in natural killer (NK)–cell leukemia and lymphoma: an in vitro and in vivo preclinical evaluation
Authors: Lijun Shen, Wing-Yan Au, Tianhuan Guo, Kai-Yau Wong, Michelle L. Wong, Junjiro Tsuchiyama, Po-Wing Yuen, Yok-Lam Kwong, Raymond H. Liang, Gopesh Srivastava
Journal: Blood (2007)
A PROSPECTIVE STUDY OF SLEEP DURATION AND THE RISK OF INCIDENT ATRIAL FIBRILLATION IN AN URBAN POPULATION: THE SUITA STUDY
Authors: Yoshihiro Kokubo, Takashi Kobayashi, Makoto Watanbe, Kengo Kusano, Shiro Kamakura, Yoshihiro Miyamoto
Journal: Journal of the American College of Cardiology (2014)
The Incidence and Etiology of the Ventilation/Perfusion Reverse Mismatch Defect
Authors: PRESTON CARVALHO, J PETER LAVENDER
Journal: Clinical Nuclear Medicine (1989)

Kr-81m ventilation and Tc-99m perfusion images of 392 patients were examined retrospectively for the incidence and etiology of the reverse mismatch defect, which is characterized by a region of lung where the perfusion defect exceeds the ventilation defect. Forty-six patients (11.7%) showed such defects. The most frequent causes were pneumonia (15%), atelactasis (15%), pleural effusions (15%), chronic obstructive airway disease (24%), and bronchial obstruction (31%). The significance of the reverse mismatch defect is discussed.
Aldehyde Dehydrogenase in Combination with CD133 Defines Angiogenic Ovarian Cancer Stem Cells That Portend Poor Patient Survival
Authors: Ines A. Silva, Shoumei Bai, Karen McLean, Kun Yang, Kent Griffith, Dafydd Thomas, Christophe Ginestier, Carolyn Johnston, Angela Kueck, R. Kevin Reynolds, Max S. Wicha, Ronald J. Buckanovich
Journal: Cancer Research (2011)

Abstract Markers that reliably identify cancer stem cells (CSC) in ovarian cancer could assist prognosis and improve strategies for therapy. CD133 is a reported marker of ovarian CSC. Aldehyde dehydrogenase (ALDH) activity is a reported CSC marker in several solid tumors, but it has not been studied in ovarian CSC. Here we report that dual positivity of CD133 and ALDH defines a compelling marker set in ovarian CSC. All human ovarian tumors and cell lines displayed ALDH activity. ALDH+ cells isolated from ovarian cancer cell lines were chemoresistant and preferentially grew tumors, compared with ALDH− cells, validating ALDH as a marker of ovarian CSC in cell lines. Notably, as few as 1,000 ALDH+ cells isolated directly from CD133− human ovarian tumors were sufficient to generate tumors in immunocompromised mice, whereas 50,000 ALDH− cells were unable to initiate tumors. Using ALDH in combination with CD133 to analyze ovarian cancer cell lines, we observed even greater growth in the ALDH+CD133+ cells compared with ALDH+CD133− cells, suggesting a further enrichment of ovarian CSC in ALDH+CD133+ cells. Strikingly, as few as 11 ALDH+CD133+ cells isolated directly from human tumors were sufficient to initiate tumors in mice. Like other CSC, ovarian CSC exhibited increased angiogenic capacity compared with bulk tumor cells. Finally, the presence of ALDH+CD133+ cells in debulked primary tumor specimens correlated with reduced disease-free and overall survival in ovarian cancer patients. Taken together, our findings define ALDH and CD133 as a functionally significant set of markers to identify ovarian CSCs. Cancer Res; 71(11); 3991–4001. ©2011 AACR.
Serum Vascular Endothelial Growth Factor and COX-2/5-LOX Inhibition in Advanced Non-small Cell Lung Cancer: Cancer and Leukemia Group B 150304
Authors: Martin J. Edelman, Lydia Hodgson, Xiaofei Wang, Robert Christenson, Scott Jewell, Everett Vokes, Robert Kratzke
Journal: Journal of Thoracic Oncology (2011)
A False Positive Space-Occupying Lesion Appearance in Colloid Liver Scintigraphy due to Chilaiditiʼs Syndrome
Authors: EMEL ÖZTÜRK, YAVUZ NARIN, YÜKSEL PABUÇÇLU, MEHMET ÖZGÜVEN, BENGÜL GÜNALP, HIKMET BAYHAN
Journal: Clinical Nuclear Medicine (1993)

A 77-year-old man, diagnosed as having prostate adenocarcinoma, was admitted to the hospital for therapy. Prior to the therapy, the patient underwent abdominal ultrasound for the evaluation of liver metastasis. However, the liver was obscured with high-density shadows suggesting intestinal structures. For further evaluation, colloid liver-spleen scintigraphy was performed and a large photon-deficient area was found in the anterior portion of right hepatic lobe. An abdominal CT scan performed to determine the nature of the lesion revealed Chilaiditi's syndrome.