tbuckley/cabot-search huggingface dataset:
Evaluation of In Vivo Breast Fine Needle Aspirates by Flow Cytometry: An Efficacy Study
Authors: J. E. Fuhr, A. A. Kattine, H. S. Nelson
Journal: JNCI Journal of the National Cancer Institute (1992)

Background : Malignancy of the breast is frequently diagnosed through fine needle aspiration. in the hands of a skilled aspirator and Cytopathologist, this can be a highly accurate procedure. Purpose : This study was undertaken to evalate whether sufficient resedual cells in the bore of the needle could be harvested and analyzed efficiently by flow cytopmetry analysis. The goal was then to determine the value of routine flow cytometry as an adjuctive technology in the interpretation of breast fine needle aspirations. Methods : Cells were rinsed from tthe neddles of 83 consecutive diagnostic fine needle aspirates after preliminary inspection had confirmed adquate material was obntained for cytopathology. Cells were washed, and nuclei prepared by detergent treatment. Afger ribonuclease treatment, DNA was stained with the fluorescent marler propodoium iodide. DNA content per cell was determined by flow cytometry by measurement of right angle fluorescence. Results . Less then 4% of the sample were rejcted for inadequate cell numbers. Flow cytometry criteria for evidence of malignancy included the presence of a DNA aneuploid population or an elevated rate of proliferation(13% or higher) of a diploid population. Accuracy of flow cytometry was based on cytopathologic interpretation in all cases except tow whcih were based on results of excisional biopsy. The sensitivity of the flow cytometry analysis was 76% the specificity was 100, with results from flow cytometry pivotal in the correct diagnoses for two patients whose cytopathologic results were equivocal. Analyusis of histograms indicateded acceptable coefficients of variation for all populations. Gating analysis indicated the suitability of the material for this type of study, with an average of 85% of the events selected, or “ gated in. ” Low recoveries were associated with the presence of necrotic debris in the sample. Conclusion : Flow cytometry can be a valuable adjunctive technology, Capable of providing the cytopathologist with additional information regarding the character of cells an; yzed. [ J Natl Cancer Inst 84: 1272–1276, 1992]
Hyponatremia During ACTH Infusions
Authors: MICHAEL GEHEB
Journal: Annals of Internal Medicine (1979)

Letters and Corrections1 November 1979Hyponatremia During ACTH InfusionsMICHAEL GEHEB, M.D., MALCOLM COX, M.D., IRWIN SINGER, M.D.MICHAEL GEHEB, M.D.Search for more papers by this author, MALCOLM COX, M.D.Search for more papers by this author, IRWIN SINGER, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-91-5-792_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: Sheeler and Schumacher report in the May issue (1) three cases of severe hyponatremia (101, 109, and 116 meq/L) associated with infusions of ACTH in which a limited volume of 5% dextrose in water was given intravenously as the carrier. Even assuming that renal water excretion was negligible, serum antidiuretic hormone (ADH) levels were maximal, and all three patients were small in size, the decrease in serum sodium concentration cannot be accounted for by the amount of water infused in any of these cases. Assuming a body weight of 50 kg, which is small for an adult,...Reference1. SHEELERSCHUMACHER LO. Hyponatremia during ACTH infusions. Ann Intern Med. 1979;90:798-9. LinkGoogle Scholar1. MCDONALDMILLERANDERSONBERLSCHRIER KPRTR. Hormonal control of renal water excretion. Kidney Int. 1976;10:38-45. CrossrefMedlineGoogle Scholar2. BOYKINDETORRENTEERICKSONROBERTSONSCHRIER JAAGR. Role of plasma vasopressin in impaired water excretion of glucocorticoid deficiency. J Clin Invest. 1978;62:738-44. CrossrefMedlineGoogle Scholar3. ROSEWILLIAMSJAGGERLAULER LGPD. The 48-hour adrenocorticotrophin infusion test for adrenocortical insufficiency. Ann Intern Med. 1970;73:49-54. LinkGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Philadelphia Veterans Administration Medical Center Hospital of the University of Pennsylvania Philadelphia, PA 19104 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byCorticotrophins and corticosteroids 1 November 1979Volume 91, Issue 5Page: 792-792KeywordsAdrenocorticotropic hormoneAntidiuretic hormoneAttentionBody weightExcretionGlucoseHyponatremiaSodium Issue Published: 1 November 1979 PDF downloadLoading ...
WHICH VIRTUAL HISTOLOGY INTRAVASCULAR ULTRASOUND PROPERTIES DISCRIMINATE BETTER BETWEEN STABLE ANGINA PECTORIS AND TROPONIN POSITIVE ACUTE CORONARY SYNDROME - ASSESSMENT OF PLAQUES OR ANALYSIS OF THE WHOLE CORONARY ARTERY VASCULATURE?
Authors: Patrick A. Calvert, Daniel Obaid, Nick E. West, Leonard M. Shapiro, Duncan McNab, Cameron G. Densem, Peter M. Schofield, Denise Braganza, Sarah C. Clarke, Michael O’Sullivan, Kausik K. Ray, Martin R. Bennett
Journal: Journal of the American College of Cardiology (2010)
Cloning and regulation of expression of the rat kidney urea transporter (rUT2).
Authors: C P Smith, W S Lee, S Martial, M A Knepper, G You, J M Sands, M A Hediger
Journal: Journal of Clinical Investigation (1995)

In mammals, urea is the predominant end-product of nitrogen metabolism and plays a central role in the urinary-concentrating mechanism. Urea accumulation in the renal medulla is critical to the ability of the kidney to concentrate urine to an osmolality greater than systemic plasma. Regulation of urea excretion and accumulation in the renal medulla depends on the functional state of specialized phloretin-sensitive urea transporters. To study these transporters and their regulation of expression we isolated a cDNA which encodes the rat homologue (rUT2) of rabbit UT2 (You, G., C.P. Smith, Y. Kanai, W.-S. Lee, M. Stelzner, and M.A. Hediger, et al. Nature (Lond.). 1993. 365:844-847). Rat UT2 has 88% amino acid sequence identity to rabbit UT2 and 64% identity to the recently cloned human erythrocyte urea transporter, HUT11 (Olives, B., P. Neav, P. Bailly, M.A. Hediger, G. Rousselet, J.P. Cartron, and P. Ripoch J. Biol. Chem. 1994. 269:31649-31652). Analysis of rat kidney mRNA revealed two transcripts of size 2.9 and 4.0 kb which had spatially distinct distributions. Northern analysis and in situ hybridization showed that the 4.0-kb transcript was primarily responsive to changes in the protein content of the diet whereas the 2.9-kb transcript was responsive to changes in the hydration state of the animal. These studies reveal that the expression levels of the two rUT2 transcripts are modulated by different pathways to allow fluid and nitrogen balance to be regulated independently. Our data provide important insights into the regulation of the renal urea transporter UT2 and provide a basis on which to refine our understanding of the urinary concentrating mechanism and its regulation.
New NHS IT system will preserve patient confidentiality
Authors: Madeleine Brettingham
Journal: BMJ (2005)

New NHS information technology (IT) systems will save lives, the health minister, John Hutton, claimed last week, when he launched a new phase of publicity for the NHS's national programme for information technology. He also insisted that only staff with a legitimate relationship to a patient would be able to view their details.

Mr Hutton was adamant that fears that the new systems might cause further delays and complications for staff and patients were misplaced: “This is the biggest civil IT project underway anywhere in the world today. Not everything is going to go smoothly all of the time, and we're …
Meth Use Linked to Risk of Parkinson Disease
Authors: Bridget M. Kuehn
Journal: JAMA (2011)

Abuse of methamphetamine may increase a person's risk of developing Parkinson disease, according to a new study (Callaghan RC et al. Drug Alcohol Depend. doi: 10.1016/j.drugalcdep.2011.06.013 [published online ahead of print July 26, 2011]).
Murderer can be forced to take medication to become sane enough to be executed
Authors: S. Gottlieb
Journal: BMJ (2003)

The US Supreme Court has let stand a ruling by a federal appeals court in February that officials in the state of Arkansas had the right to force a convicted murderer to take drug treatment to make him sane enough to be executed.

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Charles Singleton

Credit: AP PHOTO/DANNY JOHNSTON

In 1986 the Supreme Court proclaimed it illegal to execute people unless they understood that they were being put to death and why.

An appeals court based in St Louis ruled in February this year that the constitution's prohibition against cruel and unusual punishment would not be violated if the authorities forcibly gave antipsychotic medication to …

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Targeting miR-21 for the Therapy of Pancreatic Cancer
Authors: Flavie Sicard, Marion Gayral, Hubert Lulka, Louis Buscail, Pierre Cordelier
Journal: Molecular Therapy (2013)

Despite tremendous efforts worldwide from clinicians and cancer scientists, pancreatic ductal adenocarcinoma (PDA) remains a deadly disease for which no cure is available. Recently, microRNAs (miRNAs) have emerged as key actors in carcinogenesis and we demonstrated that microRNA-21 (miR-21), oncomiR is expressed early during PDA. In the present study, we asked whether targeting miR-21 in human PDA-derived cell lines using lentiviral vectors (LVs) may impede tumor growth. We demonstrated that LVs-transduced human PDA efficiently downregulated miR-21 expression, both in vitro and in vivo. Consequently, cell proliferation was strongly inhibited and PDA-derived cell lines died by apoptosis through the mitochondrial pathway. In vivo, miR-21 depletion stopped the progression of a very aggressive model of PDA, to induce cell death by apoptosis; furthermore, combining miR-21 targeting and chemotherapeutic treatment provoked tumor regression. We demonstrate herein for the first time that targeting oncogenic miRNA strongly inhibit pancreatic cancer tumor growth both in vitro and in vivo. Because miR-21 is overexpressed in most human tumors; therapeutic delivery of miR-21 antagonists may still be beneficial for a large number of cancers for which no cure is available. Despite tremendous efforts worldwide from clinicians and cancer scientists, pancreatic ductal adenocarcinoma (PDA) remains a deadly disease for which no cure is available. Recently, microRNAs (miRNAs) have emerged as key actors in carcinogenesis and we demonstrated that microRNA-21 (miR-21), oncomiR is expressed early during PDA. In the present study, we asked whether targeting miR-21 in human PDA-derived cell lines using lentiviral vectors (LVs) may impede tumor growth. We demonstrated that LVs-transduced human PDA efficiently downregulated miR-21 expression, both in vitro and in vivo. Consequently, cell proliferation was strongly inhibited and PDA-derived cell lines died by apoptosis through the mitochondrial pathway. In vivo, miR-21 depletion stopped the progression of a very aggressive model of PDA, to induce cell death by apoptosis; furthermore, combining miR-21 targeting and chemotherapeutic treatment provoked tumor regression. We demonstrate herein for the first time that targeting oncogenic miRNA strongly inhibit pancreatic cancer tumor growth both in vitro and in vivo. Because miR-21 is overexpressed in most human tumors; therapeutic delivery of miR-21 antagonists may still be beneficial for a large number of cancers for which no cure is available.
In Vivo Gene Transfer of Prepro-Calcitonin Gene–Related Peptide to the Lung Attenuates Chronic Hypoxia-Induced Pulmonary Hypertension in the Mouse
Authors: Hunter C. Champion, Trinity J. Bivalacqua, Kazunori Toyoda, Donald D. Heistad, Albert L. Hyman, Philip J. Kadowitz
Journal: Circulation (2000)

Background —Calcitonin gene–related peptide (CGRP) is believed to play an important role in maintaining low pulmonary vascular resistance (PVR) and in modulating pulmonary vascular responses to chronic hypoxia; however, the effects of adenovirally mediated gene transfer of CGRP on the response to hypoxia are unknown. Methods and Results —In the present study, an adenoviral vector encoding prepro-CGRP (AdRSVCGRP) was used to examine the effects of in vivo gene transfer of CGRP on increases in PVR, right ventricular mass (RVM), and pulmonary vascular remodeling that occur in chronic hypoxia in the mouse. Intratracheal administration of AdRSVCGRP, followed by 16 days of chronic hypoxia (F io 2 0.10), increased lung CGRP and cAMP levels. The increase in pulmonary arterial pressure (PAP), PVR, RVM, and pulmonary vascular remodeling in response to chronic hypoxia was attenuated in animals overexpressing prepro-CGRP, whereas systemic pressure was not altered while in chronically hypoxic mice, angiotensin II and endothelin-1–induced increases in PAP were reduced, whereas decreases in PAP in response to CGRP and adrenomedullin were not changed and decreases in PAP in response to a cAMP phosphodiesterase inhibitor were enhanced by AdRSVCGRP. Conclusions —In vivo CGRP lung gene transfer attenuates the increase in PVR and RVM, pulmonary vascular remodeling, and pressor responses in chronically hypoxic mice, suggesting that CGRP gene transfer alone and with a cAMP phosphodiesterase inhibitor may be useful for the treatment of pulmonary hypertensive disorders.
The Chemistry of Life: Eight Lectures on History of Biochemistry
Authors: Lester S. King
Journal: JAMA (1970)

The title of this book might sound quite formidable, suggesting bristling formulas and obscure concepts, but the reader need have no fears. The emphasis should rest not on chemistry in the narrower technical sense, but on the word life—ie, biology. The volume gathers together eight lectures given at Cambridge University, sponsored by the History of Science Department, and delivered between 1958 and 1961. Most of the lecturers were, indeed, biochemists, but they direct themselves not to the chemist but to the wider general audience that has interest in medicine, biology, physiology, or history of science.  In his introduction, Joseph Needham emphasizes that our modern development had a long history and grew like plants with roots coming up a very long way from the sub-soil of antiquity. He gives us an interesting—and tantalizing—glimpse of some key concepts of western and Chinese science as they pertain to chemistry.  Then follow eight lectures
Abstract 1361: The clinicopathological significance of LSD1 in esophageal cancers
Authors: Keisuke Kosumi, Yoshifumi Baba, Ryuichi Karashima, Satoshi Ida, Yu Imamura, Takatsugu Ishimoto, Shiro Iwagami, Yasuo Sakamoto, Yuji Miyamoto, Naoya Yoshida, Akihisa Sakamoto, Shinjiro Hino, Mitsuyoshi Nakao, Hideo Baba
Journal: Cancer Research (2014)

Abstract Background: Lysine-specific demethylase 1 (LSD1) is the first discovered histone demethylase which specially removes H3K4me1/2 through a flavin-adenine-dinucleotide (FAD). Previous studies have indicated that LSD1 is associated with cell proliferation, cell invasion and epithelial-mesenchymal transition in human malignant tumors. Recently, it is accepted that LSD1 epigenetically regulates energy-expenditure genes in adipocytes depending on the cellular FAD availability. As a PET scan with a FDG tracer can detect cancers, the method is exceedingly useful for tumor staging or therapeutic effect determination of esophageal cancers. The aim of this study is to investigate the expression and function of LSD1 in esophageal cancer cell-lines and, to analyze the relationships between the LSD1 expression and clinicopathological data including SUVmax (standardized uptake value). Methods: The influence of LSD1 on cell proliferation and invasion was evaluated by knockdown experiments. Using 113 resected esophageal cancer specimens, we evaluated the LSD1 expression by immunohistochemistry and devided them into two groups; a low expression group (LEG) and a high expression group (HEG). We compared these two groups and analyzed the relationships between LSD1 expression and clinicopathological data. Results: In vitro analysis, knockdown of LSD1 did not impact cell proliferation, but suppressed cell invasion. In the immunohistochemical study, the HEG's age was significantly higher (P=0.021), and this group had esophageal cancers at lower locations (P=0.058). HEG was significantly correlated with the T-stage (P=0.020), lymph and blood vessels invasion (P=0.020, P=0.001), and a higher SUVmax (P=0.0088) and lower overall survival (P=0.0017). Conclusions: Our study demonstrated the relationships between the expression of LSD1 and T-stage, lymph and blood vessels invasion, and the SUVmax in esophageal cancers. It is suggested that LSD1 has a potential to impact the malignancy of the esophageal cancer, and may be a therapeutic target in patients with esophageal cancers. Citation Format: Keisuke Kosumi, Yoshifumi Baba, Ryuichi Karashima, Satoshi Ida, Yu Imamura, Takatsugu Ishimoto, Shiro Iwagami, Yasuo Sakamoto, Yuji Miyamoto, Naoya Yoshida, Akihisa Sakamoto, Shinjiro Hino, Mitsuyoshi Nakao, Hideo Baba. The clinicopathological significance of LSD1 in esophageal cancers. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 1361. doi:10.1158/1538-7445.AM2014-1361
Epidemiology: An Introductory Text
Authors: Thomas Mack
Journal: JAMA (1975)

Most textbooks of epidemiology have tended toward poor balance, either because they have been aimed at readers with a narrow purpose, or because the author has been intent on presenting his particular<i>Weltanschauung</i>. This new text by Mausner and Bahn has avoided both of these problems: it is thoroughly eclectic and has been constructed for beginners, regardless of motivation. Much of the book describes the utility of epidemiologic concepts in various practical settings: infectious disease control, etiology of chronic disease, screening, community health evaluation, and the conduct of randomized clinical trials. Each of these sections serves as a properly simplified introduction to the subject from the epidemiologic point of view. Not unexpectedly, the very eclecticism that permits an unrestricted view of epidemiology is partly responsible for the faults of the book. These are concentrated in the first two chapters, which do not provide the clear conceptual foundation necessary for that
Management of lung cancer: Author's reply
Authors: S. G Spiro
Journal: BMJ (1991)

Caenorhabditis elegans possesses two classes of inhibitory locomotory neurons, the DD and VD motoneurons (mns), and they form complementary components of a cross-inhibitory neuronal network innervating dorsal and ventral body muscles. The DD and VD mns (collectively called the D mns) share a number of morphological and neurochemical features, and mutations in a number of different genes disrupt both cell types in identical ways; however, the DD and VD mns have different lineal origins and different synaptic patterns. Given the number of phenotypic features shared by the D mns, it was of interest to determine what is responsible for the synaptic patterns that distinguish them. An analysis of the locomotory defect along with a genetic epistasis test suggested that unc-55 mutations alter the function of the VD but not the DD mns. Correlated with the defective locomotory behavior of unc-55 mutants was an alteration in the distribution of varicosities, structures associated with presynaptic elements, on the VD mns. The pattern of varicosities of the unc-55 VD mns resembled that of the wild- type DD mns. Moreover, the selective removal of the DD mns revealed that unc-55 VD mns had adopted a functional role appropriate for the DD mns. Thus, unc-55 appears to be involved in producing the synaptic patterns that distinguish the two D mn classes from one another; when the gene is mutated the VD and DD mns become structurally similar and functionally equivalent.
Sebastian syndrome: Case report and review of the literature
Authors: Guy Young, Naomi L.C. Luban, James G. White
Journal: American Journal of Hematology (1999)

Macrothromboctyopenias (MTCP) are a heterogeneous group of disorders associated with thrombocytopenia and giant platelets, and may include other clinical or laboratory findings such as hereditary nephritis, sensorineural deafness, leukocyte inclusions, and cataracts. Patients with MTCP may have mild to moderate bleeding symptoms or be completely asymptomatic. The most recently described MTCP is the Sebastian syndrome (SS), which consists of thrombocytopenia with giant platelets and leukocyte inclusions. Only three previous reports about this syndrome have been published. Herein, we report the first African-American family with SS. The propositus is a 4-week-old male born to a mother carrying the diagnosis of chronic idiopathic thrombocytopenia purpura (ITP). His 4-year-old brother also has thrombocytopenia. There is no history of bleeding symptoms in any of the family members. The diagnosis was established by demonstrating thrombocytopenia with giant platelets and leukocyte inclusions on both peripheral smear and by electron microscopy. This report illustrates the importance of obtaining a family history when evaluating thrombocytopenia with special emphasis on a history of thrombocytopenia, renal disease, deafness, and cataracts. It is important to differentiate between MTCP and chronic ITP to avoid the unnecessary diagnostic studies, and, more critically, unneeded and potentially harmful therapy. Am. J. Hematol. 61:62–65, 1999. © 1999 Wiley-Liss, Inc.
Probiotic bacteria prevent hepatic damage and maintain colonic barrier function in a mouse model of sepsis
Authors: Julia Ewaschuk, Ryan Endersby, David Thiel, Hugo Diaz, Jody Backer, Mang Ma, Thomas Churchill, Karen Madsen
Journal: Hepatology (2007)

A breakdown in intestinal barrier function and increased bacterial translocation are key events in the pathogenesis of sepsis and liver disease. Altering gut microflora with noninvasive and immunomodulatory probiotic organisms has been proposed as an adjunctive therapy to reduce the level of bacterial translocation and prevent the onset of sepsis. The purpose of this study was to determine the efficacy of a probiotic compound in attenuating hepatic and intestinal injury in a mouse model of sepsis. Wild-type and interleukin-10 (IL-10) gene–deficient 129 Sv/Ev mice were fed the probiotic compound VSL#3 for 7 days. To induce sepsis, the mice were injected with lipopolysaccharide (LPS) and d-galactosamine (GalN) in the presence and absence of the peroxisome proliferator-activated receptor gamma (PPARγ) inhibitor GW9662. The mice were killed after 6 hours, and their colons were removed for the measurement of the cytokine production and epithelial function. The functional permeability was assessed by the mannitol movement and cyclic adenosine monophosphate–dependent chloride secretion in tissue mounted in Ussing chambers. The livers were analyzed for bacterial translocation, cytokine production, histological injury, and PPARγ levels. The tissue levels of tumor necrosis factor alpha, interferon gamma, IL-6, and IL-12p35 ribonucleic acid were measured by semiquantitative reverse transcription polymerase chain reaction. Mice injected with LPS/GalN demonstrated a breakdown in colonic barrier function, which correlated with enhanced proinflammatory cytokine secretion, bacterial translocation, and significant hepatic injury. A pretreatment with oral probiotics prevented the breakdown in intestinal barrier function, reduced bacterial translocation, and significantly attenuated liver injury. The inhibition of PPARγ with GW9662 abrogated the protection induced by probiotics. Conclusion: Orally administered probiotics prevented liver and intestinal damage in a mouse model of sepsis through a PPARγ-dependent mechanism. (Hepatology 2007.)