tbuckley/cabot-search huggingface dataset:
What Influences Early Hypothyroidism After Radioiodine Treatment for Graves' Hyperthyroidism?
Authors: Vani Vijayakumar, Seham Ali, Thomas Nishino, Martin Nusynowitz
Journal: Clinical Nuclear Medicine (2006)

The objective of this study was to evaluate the factors influencing the occurrence of early hypothyroidism after radioiodine treatment of Graves' hyperthyroidism.Of 147 patients with Graves' disease (GD) treated with radioactive I-131 (RAI) in our thyroid clinic between July 2003 and December 2004, 84 were followed at 2 and 4 to 5 months after treatment. The age range was 12 to 75 years and the dosage range in these patients was 7.4 to 29.9 mCi. Twenty-four were males and 60 were females. Factors possibly contributing to post-RAI hypothyroidism are: dosage of I-131, age, gender, size of the gland, initial serum free T4, free T3, thyroid-stimulating hormone (TSH) levels, pretreatment with antithyroid drugs, radioactive iodine uptake, and duration of disease.All patients had low TSH, elevated FT4, and elevated radioactive iodine uptake (RAIU) at 4 and/or 24 hours. Of the 84 patients followed, 46% of the males and 62% of the females became hypothyroid at 4 to 5 months (57% of the total). Twenty-one patients remained hyperthyroid and 14 patients became euthyroid. Multivariate analysis of these 84 patients showed no statistically significant single contributing factor for the development of early hypothyroidism.The early onset of hypothyroidism after RAI in GD is very common (57%) and unpredictable. Thus, after RAI treatment, all patients must be closely monitored for the development of this disorder.
Abstract 5196: CDF inhibits cell migration by inactivating cancer stem cell markers, and expression of VEGF, IL-6 and miR-21 in human pancreatic and prostate cancer cells under hypoxic condition
Authors: Bin Bao, Shadan Ali, Aamir Ahmad, Asfar S. Azmi, Sanjeev Banerjee, Dejuan Kong, Yiwei Li, Subhash Padhye, Fazlul H. Sarkar
Journal: Cancer Research (2012)

Abstract Hypoxia has been well recognized to cause therapeutic resistance associated with solid tumors and considered to play critical roles in other of biological events including cell growth and proliferation, cell survival, angiogenesis, immunosurveillance, tumor invasion and metastasis. Hypoxia-inducible factor (HIF) 1α, a master transcription factor that regulates hypoxia responsive genes, plays critical roles in the adaptation of tumor cells to a hypoxic microenvironment. Tumor hypoxia and over-expression of HIF-1α have been reportedly associated with resistance to radiation therapy and chemotherapy, increased risk of invasion and metastasis and poor clinical prognosis, all of which leads to higher mortality of patients diagnosed with solid tumors. Emerging evidence suggest that hypoxia and HIF signaling pathways leads to the acquisition of epithelial-to-mesenchymal transition (EMT), maintenance of cancer stem cell (CSC) functions, and causing inflammatory tumor microenvironment, which contributes to therapeutic resistance; however, the exact mechanisms by which hypoxia/HIF regulates these events are not fully understood. Here, we demonstrates that hypoxia increases the productions of VEGF and IL-6, and increased expression of CSC marker genes such as Nanog, Oct4, EZH2 as well as miR-21, an oncogenic miRNA, in human pancreatic cancer (AsPC-1 and MiaPaCa-2) and prostate cancer (PC-3 and LNCaP) cells. The treatment of these cells with CDF, a novel curcumin analog that was previously shown to be biologically superior than curcumin as an anti-tumor agent both in vitro and in vivo, inhibited the productions of VEGF, IL-6, Nanog, Oct4 and EZH2 mRNAs, as well as down regulated the expression of miR-21 in these cells under hypoxic condition. CDF also decreased cell migration in pancreatic and prostate cancer cells under hypoxic condition as documented by wound healing assay. Taken together, these data suggest for the first time that the anti-tumor effect of CDF could in part be due to inhibition of tumor hypoxic pathways including the inhibition of CSC markers and thereby reconditioning the tumor microenvironment, which would be useful for overcoming therapeutic resistance. 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 5196. doi:1538-7445.AM2012-5196
Varenicline and suicidal behaviour: a cohort study based on data from the General Practice Research Database
Authors: D Gunnell, D Irvine, L Wise, C Davies, R M Martin
Journal: BMJ (2009)

<b>Objective</b> To determine whether varenicline, a recently licensed smoking cessation product, is associated with an increased risk of suicide and suicidal behaviour compared with alternative treatments bupropion and nicotine replacement therapy. <b>Design</b> Cohort study nested within the General Practice Research Database. <b>Setting</b> Primary care in the United Kingdom. <b>Participants</b> 80 660 men and women aged 18-95 years were prescribed a new course of a smoking cessation product between 1 September 2006 and 31 May 2008; the initial drugs prescribed during follow-up were nicotine replacement products (n=63 265), varenicline (n=10 973), and bupropion (n=6422). <b>Main outcome measures</b> Primary outcomes were fatal and non-fatal self harm, secondary outcomes were suicidal thoughts and depression, all investigated with Cox's proportional hazards models. <b>Results</b> There was no clear evidence that varenicline was associated with an increased risk of fatal (n=2) or non-fatal (n=166) self harm, although a twofold increased risk cannot be ruled out on the basis of the upper limit of the 95% confidence interval. Compared with nicotine replacement products, the hazard ratio for self harm among people prescribed varenicline was 1.12 (95% CI 0.67 to 1.88), and it was 1.17 (0.59 to 2.32) for people prescribed bupropion. There was no evidence that varenicline was associated with an increased risk of depression (n=2244) (hazard ratio 0.88 (0.77 to1.00)) or suicidal thoughts (n=37) (1.43 (0.53 to 3.85)). <b>Conclusion</b> Although a twofold increased risk of self harm with varenicline cannot be ruled out, these findings provide some reassurance concerning its association with suicidal behaviour.
10-year survey of 485 sterilizations. Part II: patients' views on their sterilization.
Authors: R G Whitelaw
Journal: BMJ (1979)

As part of a study of the complications after sterilisation 485 of the 547 women who had been sterilised by a modified Pomeroy procedure in one unit over 10 years were interviewed. They were asked whether they regretted being sterilised and about the quality of their sex lives, mental health, social relationships, and marriages. Most women were pleased to have been sterilised, only 24 regretting it. Regret was more pronounced among women who had been sterilised in association with a third caesarean section, those sterilised for medical reasons, and those whose marriages had ended in divorce. In each case where a woman regretted a sterilisation that had been performed on the recommendation of a psychiatrist, the psychiatrists were still prepared to defent their opinions. On their sex lives, mental health, social relationships, and marriages, more women reported improvement than deterioration, and in most cases the deterioration could not be attributed to the sterilisation. The overall benefits from sterilisation to the women in this series therefore seemed to outweigh substantially the adverse consequences experienced by a few.
Characterization of a novel <i>Candida albicans</i> 29 kDa IgE‐binding protein – purification, cDNA isolation and heterologous expression of Cand a 3
Authors: H. Chou, M. F. Tam, C.‐Y. Chang, H.‐Y. Lai, M.‐H. Huang, C.‐T. Chou, S.‐S. Lee, H.‐D. Shen
Journal: Allergy (2003)

Background: Candida albicans has been implicated in human allergic disorders. However, many of its immunoglobulin E (IgE)‐reacting components have not yet been identified. The purpose of the present study is to characterize a novel 29 kDa IgE‐binding protein from C. albicans . Methods: The 29 kDa protein was partially purified and its tryptic digests subjected to mass spectrometric analysis. The cDNA encoding this protein was isolated and heterologously expressed in Escherichia coli. Monoclonal antibodies (MoAbs) were raised against the 29 kDa protein purified from C. abicans extracts. Results: We isolated a 29 kDa IgE‐reacting component from C. albicans . The protein was digested on‐gel with trypsin and the masses of the resulting fragments were determined in a MALDI‐TOF mass spectrometer. The data were searched against protein sequences deduced from the C. albicans genome. An open reading frame that possibly encodes the 29 kDa IgE‐reacting component was identified. The cDNA corresponding to the open reading frame was isolated. It encodes a 236 residues protein that has 62% sequence identity to that of a hypothetical protein (YDR533c) from Saccharomyces cerevisiae . Conserved domain search suggests that the encoded protein belongs to the ThiJ/PfpI family. The cDNA isolated was inserted into a pQE‐30 vector for protein expression in Escherichia coli . The recombinant protein can react with IgE antibodies in sera from asthmatic patients and two MoAbs that were generated against the purified native 29 kDa protein from C. albicans . Conclusions: We identified and cloned a novel 29 kDa IgE‐reacting component (Cand a 3) from C. albicans . The recombinant proteins produced from this clone and the MoAbs prepared may be useful in the standardization of diagnostic extracts. They are also instrumental in elucidating the role of C. albicans in clinical allergy.
ME-09 * DYNAMIC EVIDENCE OF TUMOR INDUCED MICROGLIA ACTIVATION AT THE INFILTRATIVE MARGINS OF GLIOMA
Authors: J. Juliano, O. Gil, A. Hawkins-Daarud, R. Rockne, J. Gallaher, S. Massey, A. Anderson, J. Bruce, P. Canoll, K. Swanson
Journal: Neuro-Oncology (2014)

PURPOSE: Microglia are a major cellular component of malignant glioma, and in some cases, compose up to 40% of the mass of the tumor. Previous studies have shown that microglia can decrease T-cell response to glioma, and their abundance is correlated with increased histologic grade. These studies suggest that microglia facilitate the progression and infiltration of glioma, however the dynamics of the relationship between tumor cells and microglia are not well characterized. METHODS: In this work, we examined the dynamic migratory behavior of glioma and microglia cells using two-color time-lapse fluorescence microscopy of brain slices from a PDGF-driven rat model of glioma in which glioma cells and microglia were labeled with separate fluorescent markers. We quantified glioma cells and microglia motility through single cell tracking and particle image velocimetry. RESULTS: We found that microglia were predominately abundant within the tumor mass and that microglia motility was strongly correlated with the presence of glioma cells. This provides the first dynamic evidence that glioma induces microglial motility. We found that motility of glioma cells and microglia were variably correlated. Our results also show that microglia and glioma cells exhibit stark differences in migratory behavior. Microglia move by a simple random walk, while glioma cells exhibit highly persistent motion, characterized as super diffusion, within the same microenvironment indicating intrinsic differences in response to migratory cues. CONCLUSION: These results provide the first dynamic evidence of glioma cells stimulating the activation of microglia, by means of increasing motility and localization in and around the infiltrative edge of glioma. Further, these results show dynamic interactions between glioma and microglia and suggest that glioma cells and microglia are either responding to different migratory cues, or are responding to the same cues in different ways.
Cell death mechanisms of acute and lethal cell injury. Edited by W.J. Mergner, R. T. Jones and B. F. Trump, 263 pp. New York: W.W. Morton, 1990. $110
Authors: Raymond S. Koff, Melissa P. Upton
Journal: Hepatology (1991)

This small volume is a multiauthored work summarizing mechanisms of cell injury and death as they are currently understood.The editors are internationally recognized for extensive experimental work in the areas of acute cell injury, shock and cell death, and are eminently qualified to edit this work.The text is organized as chapters under two major headings.The first, induction of cell injury, includes chapters on membranes in cell injury, cellular ion regulation, mechanisms of complement-mediated membrane damage, plasma membrane and mitochondria1 changes in cell injury and cell metabolism and microcirculation during ischemia and reflow.The second heading, mechanisms propagating cell injury, includes pathobiology of lysosomes; biochemical mechanisms of oxidative cell injury in isolated hepatocytes; phospholipids, phospholipases and cell injury; and cardiac adenine nucleotide metabolism in cell injury and restitution.As a summary of the cellular events in injury.both at the membrane and organellular levels, the book succinctly and clearly outlines the physiological events associated with reversible and irreversible cell injury.Particularly well summarized in a fluently written chapter by Mohammed M. Sayeed, is the role of ion flux in membrane destabilizat.ion.Sayeed discusses the normal physiology of cellular ion regulation; this is followed by a presentation of ion dysregulation associated with various models of shock (including sepsis and hemorrhagic shock) with particular reference to experimental models using skeletal muscle and liver slices.I found this chapter particularly helpful as a review and overview of the subject and as a useful reference for other chapters in the text.As a reviewer, I have striven for objectivity in evaluating this book, but I feel that I must caution the reader that my bias as a practicing surgical and anatomical pathologist undoubtedly colors my evalu-
Clusters of differential gene expression of structural proteins between failing and nonfailing hearts: preliminary insights from oligonucleotide microarrays
Authors: W.H.Wilson Tang, Fen-Lai Tan, Gary S. Francis, Christine S. Moravec, Jianbo Li, Carolyn Apperson-Hansen, Patrick M. McCarthy, James B. Young, Meredith Bond
Journal: Journal of the American College of Cardiology (2002)
Deficiencies in proposed new EU regulation of clinical trials
Authors: P. C. Gotzsche
Journal: BMJ (2012)

The EU Clinical Trials Directive has been heavily criticised for being bureaucratic, confusing, and leading to a decline in the number of trials conducted in Europe. Although new proposals for regulation are much better, <b>Peter Gøtzsche</b> argues improvements are still needed for patient safety, rational use of drugs, and research planning
Shotgun proteomics implicates protease inhibition and complement activation in the antiinflammatory properties of HDL
Authors: Tomas Vaisar, Subramaniam Pennathur, Pattie S. Green, Sina A. Gharib, Andrew N. Hoofnagle, Marian C. Cheung, Jaeman Byun, Simona Vuletic, Sean Kassim, Pragya Singh, Helen Chea, Robert H. Knopp, John Brunzell, Randolph Geary, Alan Chait, Xue-Qiao Zhao, Keith Elkon, Santica Marcovina, Paul Ridker, John F. Oram, Jay W. Heinecke
Journal: Journal of Clinical Investigation (2007)

HDL lowers the risk for atherosclerotic cardiovascular disease by promoting cholesterol efflux from macrophage foam cells. However, other antiatherosclerotic properties of HDL are poorly understood. To test the hypothesis that the lipoprotein carries proteins that might have novel cardioprotective activities, we used shotgun proteomics to investigate the composition of HDL isolated from healthy subjects and subjects with coronary artery disease (CAD). Unexpectedly, our analytical strategy identified multiple complement-regulatory proteins and a diverse array of distinct serpins with serine-type endopeptidase inhibitor activity. Many acute-phase response proteins were also detected, supporting the proposal that HDL is of central importance in inflammation. Mass spectrometry and biochemical analyses demonstrated that HDL3 from subjects with CAD was selectively enriched in apoE, raising the possibility that HDL carries a unique cargo of proteins in humans with clinically significant cardiovascular disease. Collectively, our observations suggest that HDL plays previously unsuspected roles in regulating the complement system and protecting tissue from proteolysis and that the protein cargo of HDL contributes to its antiinflammatory and antiatherogenic properties.
Radiation Oncology Organization, FDA Announce Radiation Safety Initiatives
Authors: Tracy Hampton
Journal: JAMA (2010)

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1181 EVALUATION OF PROMETHEUS INDEX IN PATIENTS COINFECTED WITH HEPATITIS C VIRUS AND HUMAN IMMUNODEFICIENCY VIRUS
Authors: G.M. Varo, E. Martínez Alfaro, J. Ontañón, M.L. González, A. Puerta García, A. Martínez Motos, L. Navarro
Journal: Journal of Hepatology (2013)
Adrenergic Receptors and the Secretion of Glucagon and Insulin from the Isolated, Perfused Canine Pancreas
Authors: Johan Iversen
Journal: Journal of Clinical Investigation (1973)

During perfusion with a glucose concentration of 150 mg/100 ml, infusions of l-epinephrine, l-norepinephrine, and d-l-isoproterenol at physiological concentrations of 2 ng/ml for 9 min stimulated secretion of glucagon in a monophasic response pattern, in contrast to the biphasic response normally encountered after glucagon releasing stimuli as previously reported from our laboratory (1971. J. Clin. Invest.50: 2123). Glucagon was stimulated in spite of a glucose concentration which in itself effectively inhibits glucagon release. Release of insulin was strongly inhibited after epinephrine and norepinephrine, and strongly stimulated after isoproterenol. During perfusion with a glucose concentration of 25 mg/100 ml, secretion of glucagon was greatly accentuated by the catechols investigated. Secretion of insulin remained unchanged after epinephrine and norepinephrine, but was stimulated by isoproterenol. The catechol induced glucagon release was suppressed or abolished when the beta-blocking agent propanolol was simultaneously infused at a concentration of 1 muM, while the inhibition of insulin became further accentuated. The catechol induced glucagon release remained unchanged when alpha blockade was performed using either phentolamine (1 muM) or dibenzyline (10 mug/ml), while the inhibition of insulin was converted to a stimulation. Evidence is thus presented that both the alpha cells and the bet cells are under the influence of adrenergic substances, the stimulation of glucagon release being mediated through a beta receptor and the inhibition of insulin release being mediated through an alpha receptor.
Sites of particle retention and lung tissue responses to chronically inhaled diesel exhaust and coal dust in rats and cynomolgus monkeys.
Authors: K J Nikula, K J Avila, W C Griffith, J L Mauderly
Journal: Environmental Health Perspectives (1997)

The usefulness of pulmonary carcinogenicity data from rats exposed to high concentrations of particles for quantitatively predicting lung cancer risk in humans exposed to much lower environmental or occupational concentrations has been questioned. The results of several chronic inhalation bioassays of poorly soluble, nonfibrous particles have suggested that rats may be more prone than other rodent species to develop persistent pulmonary epithelial hyperplasia, metaplasia, and tumors in response to the accumulation of inhaled particles. In addition, rats and primates differ in their pulmonary anatomy and rate of particle clearance from the lung. This paper reviews results of recent Lovelace Respiratory Research Institute (Albuquerque, NM) investigations that directly compared the anatomical patterns of particle retention and the lung tissue responses of rats and monkeys exposed chronically to high occupational concentrations of poorly soluble particles. Lung sections from male cynomolgus monkeys and F344 rats exposed 7 hr/day, 5 days/week for 24 months to filtered ambient air, diesel exhaust (2 mg soot/m3), coal dust (2 mg respirable particulate material/m3), or diesel exhaust and coal dust combined (1 mg soot and 1 mg respirable coal dust/m3) were obtained from a study conducted at the U.S. National Institute for Occupational Safety and Health and examined histopathologically and morphometrically. Within each species, the sites of particle retention and lung tissue responses were the same for diesel soot, coal dust, and combined material. Rats retained a significantly greater portion of the particulate material in the lumens of alveolar ducts and alveoli than monkeys. Conversely, monkeys retained a significantly greater portion of the particulate material in the interstitium than rats. Rats, but not monkeys, had significant alveolar epithelial hyperplastic, inflammatory, and septal fibrotic responses to the retained particles. These results suggest that anatomic patterns of particle retention and lung tissue reactions in rats may not be predictive of retention patterns and tissue responses in primates that inhale poorly soluble particles at concentrations representing high occupational exposures.
Rapidly Increasing Incidence of Ocular Non-Hodgkin Lymphoma
Authors: Roxana Moslehi, Susan S. Devesa, Catherine Schairer, Joseph F. Fraumeni
Journal: JNCI Journal of the National Cancer Institute (2006)

A recent report suggesting that ocular adnexal non-Hodgkin lymphoma (NHL) may be related to Chlamydia psittaci infection underscores the need for reliable epidemiologic data for this malignancy. We examined population-based incidence data from the Surveillance, Epidemiology, and End Results (SEER) Program. During 1992–2001 in the 12 SEER areas, ocular (i.e., eye and adnexa) NHL rates per 100 000 person-years for both sexes were highest among Asians/Pacific Islanders, lower in whites, and lower still in blacks. Incidence increased with advancing age and showed little difference by sex, in contrast to other (extranodal and nodal) NHLs, which occurred predominantly in males. From 1975–2001, there was a rapid and steady increase in incidence of ocular NHL, with annual increases of 6.2% and 6.5% among white males and females, respectively, with no evidence of peaking. By contrast, other NHLs showed evidence of peaking in recent years. The distinctive patterns of ocular NHL call for further studies to identify risk factors and mechanisms, including the potential role of C. psittaci or other infections.
Interaction between IL13 genotype and environmental factors in the risk for allergic rhinitis in Korean children
Authors: Woo Kyung Kim, Ji-Won Kwon, Ju-Hee Seo, Hyung Young Kim, Jinho Yu, Byoung-Ju Kim, Hyo-Bin Kim, So Yeon Lee, Kyung Won Kim, Mi-Jin Kang, Yee-Jin Shin, Soo-Jong Hong
Journal: Journal of Allergy and Clinical Immunology (2012)