tbuckley/cabot-search huggingface dataset:
Pitfalls of liver stiffness measurement: A 5-year prospective study of 13,369 examinations
Authors: Laurent Castéra, Juliette Foucher, Pierre-Henri Bernard, Françoise Carvalho, Daniele Allaix, Wassil Merrouche, Patrice Couzigou, Victor de Lédinghen
Journal: Hepatology (2009)

Liver stiffness measurement (LSM) based on transient elastography (TE, FibroScan) is gaining in popularity for noninvasive assessment of liver fibrosis. However, LSM has limitations, which have not yet been thoroughly evaluated. We prospectively investigated the frequency and determinants of LSM failure and unreliable results over a 5-year period, based on 13,369 examinations (134,239 shots). LSM failure was defined as zero valid shots, and unreliable examinations were defined as fewer than 10 valid shots, an interquartile range (IQR)/LSM greater than 30%, or a success rate less than 60%. LSM failure occurred in 3.1% of all examinations (4% at first examination [n = 7261]) and was independently associated at first examination with body mass index (BMI) greater than 30 kg/m2 (odds ratio [OR], 7.5; 95% confidence interval [CI], 5.6-10.2; P = 0.0001), operator experience fewer than 500 examinations (OR 2.5 [1.6-4.0]; P = 0.0001); age greater than 52 years (OR 2.3 [1.6-3.2]; P = 0.0001), and type 2 diabetes (OR 1.6 [1.1-2.2]; P = 0.009). Unreliable results were obtained in a further 15.8% of cases (17% at first examination) and were independently associated at first examination with BMI greater than 30 kg/m2 (OR 3.3 [2.8-4.0]; P = 0.0001), operator experience fewer than 500 examinations (OR 3.1 [2.4-3.9]; P = 0.0001), age greater than 52 years (OR 1.8 [1.6-2.1]; P = 0.0001), female sex (OR 1.4 [1.2-1.6], P = 0.0001), hypertension (OR 1.3 [1.1-1.5]; P = 0.003), and type 2 diabetes (OR 1.2 [1.0-1.5]; P = 0.05). When metabolic syndrome and waist circumference were taken into account in a subgroup of 2835 patients, waist circumference was the most important determinant of LSM failure and unreliable results. Conclusion: In our experience, liver stiffness measurements are uninterpretable in nearly one in five cases. The principal reasons are obesity, particularly increased waist circumference, and limited operator experience. These results emphasize the need for adequate operator training and for technological improvements in specific patient subpopulations. (Hepatology 2010.)
Ambulatory Medical Care Records
Authors: Matthew C. Gleason
Journal: JAMA (1976)

<h3>To the Editor.—</h3> The article, "Ambulatory Care Medical Records" (234:1245, 1975), should be a warning to all physicians. It came from the Harvard Center for Community Health and was written by one physician and two nonphysicians. Of the seven paragraphs, four of them had nothing to do with patient care but were only to give third parties information. It is part of any federally run national health scheme that everything is known about every physician. I would strongly urge that a private practitioner determine for himself whether or not this information will improve the health of his individual patient.
Pesticides in Surface Drinking-Water Supplies of the Northern Great Plains
Authors: David B. Donald, Allan J. Cessna, Ed Sverko, Nancy E. Glozier
Journal: Environmental Health Perspectives (2007)

Human health anomalies have been associated with pesticide exposure for people living in rural landscapes in the northern Great Plains of North America.The objective of this study was to investigate the occurrence of 45 pesticides in drinking water from reservoirs in this area that received water primarily from snowmelt and rainfall runoff from agricultural crop lands.Water from 15 reservoirs was sampled frequently during the spring pesticide application period (early May to mid-August) and less frequently for the remainder of the year. Drinking water was sampled in early July. Sample extracts were analyzed for pesticide content using mass spectrometric detection.We detected two insecticides and 27 herbicides in reservoir water. Consistent detection of a subset of 7 herbicides suggested that atmospheric deposition, either directly or in rain, was the principal pathway from fields to the reservoirs. However, the highest concentrations and number of herbicides in drinking water were associated with runoff from a localized 133-mm rainfall over 15 days toward the end of spring herbicide application. Water treatment removed from 14 to 86% of individual herbicides. Drinking water contained 3-15 herbicides (average, 6.4).We estimated the mean annual calculated concentration of herbicides in drinking water to be 75 ng/L (2,4-dichlorophenoxy)acetic acid, 31 ng/L (2-chloro-4-methylphenoxy)acetic acid, 24 ng/L clopyralid, 11 ng/L dichlorprop, 4 ng/L dicamba, 3 ng/L mecoprop, and 1 ng/L bromoxynil. The maximum total concentration of herbicides in drinking water was 2,423 ng/L. For the seven herbicides with established drinking water guidelines, all concentrations of the individual chemicals were well below their respective guideline. However, guidelines have not been established for the majority of the herbicides found in drinking water or for mixtures of pesticides.
Human Health Effects of Tetrachloroethylene: Key Findings and Scientific Issues
Authors: Kathryn Z. Guyton, Karen A. Hogan, Cheryl Siegel Scott, Glinda S. Cooper, Ambuja S. Bale, Leonid Kopylev, Stanley Barone, Susan L. Makris, Barbara Glenn, Ravi P. Subramaniam, Maureen R. Gwinn, Rebecca C. Dzubow, Weihsueh A. Chiu
Journal: Environmental Health Perspectives (2014)

The U.S. Environmental Protection Agency (EPA) completed a toxicological review of tetrachloroethylene (perchloroethylene, PCE) in February 2012 in support of the Integrated Risk Information System (IRIS).We reviewed key findings and scientific issues regarding the human health effects of PCE described in the U.S. EPA's Toxicological Review of Tetrachloroethylene (Perchloroethylene).The updated assessment of PCE synthesized and characterized a substantial database of epidemiological, experimental animal, and mechanistic studies. Key scientific issues were addressed through modeling of PCE toxicokinetics, synthesis of evidence from neurological studies, and analyses of toxicokinetic, mechanistic, and other factors (tumor latency, severity, and background rate) in interpreting experimental animal cancer findings. Considerations in evaluating epidemiological studies included the quality (e.g., specificity) of the exposure assessment methods and other essential design features, and the potential for alternative explanations for observed associations (e.g., bias or confounding).Toxicokinetic modeling aided in characterizing the complex metabolism and multiple metabolites that contribute to PCE toxicity. The exposure assessment approach-a key evaluation factor for epidemiological studies of bladder cancer, non-Hodgkin lymphoma, and multiple myeloma-provided suggestive evidence of carcinogenicity. Bioassay data provided conclusive evidence of carcinogenicity in experimental animals. Neurotoxicity was identified as a sensitive noncancer health effect, occurring at low exposures: a conclusion supported by multiple studies. Evidence was integrated from human, experimental animal, and mechanistic data sets in assessing adverse health effects of PCE.PCE is likely to be carcinogenic to humans. Neurotoxicity is a sensitive adverse health effect of PCE.
Sodium Chloride Preference in Essential Hypertension
Authors: Paul J. Schechter
Journal: JAMA (1973)

Sodium chloride preference was determined in ten patients with essential hypertension and in 12 normal volunteers. All exhibited normal detection and recognition thresholds for the taste of sodium chloride. All were placed on a constant dry diet containing 9 mEq of Na+ and given, as their only source of fluids, a choice of drinking either distilled water or 0.15 M sodium chloride. Patients with essential hypertension consumed a markedly greater proportion of their total fluid intake as saline (38.2% vs 10.6%, average daily preference over one week) and also showed a greater total fluid intake (1,269 ml vs 668 ml, average daily intake over one week). The hypertensive patients consumed more than four times as much salt as did the normal volunteers.
The short consensus repeats 1 and 2, not the cytoplasmic domain, of human CD46 are crucial for infection of subgroup B adenovirus serotype 35
Authors: Fuminori Sakurai, Sayaka Murakami, Kenji Kawabata, Naoki Okada, Akira Yamamoto, Tsukasa Seya, Takao Hayakawa, Hiroyuki Mizuguchi
Journal: Journal of Controlled Release (2006)
Acid-base abnormalities in infants with congenital heart disease.
Authors: V. R. Kamath, R. S. Jones
Journal: BMJ (1966)

Information about the frequency, nature, and extent of acid base abnormalities in infants with congenital heart disease is limited. Gootman et al. (1963) reported four cases with Fallot's tetralogy, pulmonary atresia, transposition of the great vessels, and severe pulmonary stenosis. All were cyanosed at the time of investigation and had a low pH (7.05-7.28) due to base depletion. Rudolph and Danilowicz (1963) reported the case of a 10J-month-old infant with pulmonary atresia and ventricular septal defect in a severe cyanotic attack with an arterial pH of 7.08. Conventional treatment did not produce any improvement, whereas an infusion of sodium bicarbonate brought about dramatic improvement in the level of conscious ness and the pH rose to 7.38. Talner et al. (1965) reported 20 infants with congenital heart disease in cardiac failure with increased pulmonary blood-flow and/or pulmonary venous hypertension. They demonstrated the existence of raised arterial Pco2 levels in those with failure. Sunico et at. (1960) had previously reported similar findings. In this paper the acid-base abnormalities in a group of 85 infants with congenital heart disease are examined and corre lated with the clinical state. The therapeutic implications are discussed.
Arteritis and Infarction of the Intestine in Rheumatoid Arthritis
Authors: Richard H. Adler
Journal: JAMA (1962)

Two patients with rheumatoid arthritis developed an acute fulminating form of mesenteric arteritis and intestinal necrosis that required surgical resection. Only one had been receiving adrenal corticosteroid treatment. Both were operated upon twice and have been maintained on anticoagulant and steroid treatment. Neither patient has had any recurrence of abdominal symptoms. Immediate treatment with anticoagulants after surgery appeared to be beneficial. An awareness of the occurrence of necrotizing mesenteric arteritis in patients with rheumatoid arthritis who develop signs of an acute condition within the abdomen is essential if a fatality from unsuspected bowel gangrene is to be avoided. The nature of the acute arteritis and its relationship to adrenal corticosteroid treatment, rheumatoid arthritis, and connective tissue disease are discussed.
Mass Fatality Management following the South Asian Tsunami Disaster: Case Studies in Thailand, Indonesia, and Sri Lanka
Authors: Oliver W Morgan, Pongruk Sribanditmongkol, Clifford Perera, Yeddi Sulasmi, Dana Van Alphen, Egbert Sondorp
Journal: PLoS Medicine (2006)

Background Following natural disasters, mismanagement of the dead has consequences for the psychological well-being of survivors. However, no technical guidelines currently exist for managing mass fatalities following large natural disasters. Existing methods of mass fatality management are not directly transferable as they are designed for transport accidents and acts of terrorism. Furthermore, no information is currently available about post-disaster management of the dead following previous large natural disasters. Methods and Findings After the tsunami disaster on 26 December 2004, we conducted three descriptive case studies to systematically document how the dead were managed in Thailand, Indonesia, and Sri Lanka. We considered the following parameters: body recovery and storage, identification, disposal of human remains, and health risks from dead bodies. We used participant observations as members of post-tsunami response teams, conducted semi-structured interviews with key informants, and collected information from published and unpublished documents. Refrigeration for preserving human remains was not available soon enough after the disaster, necessitating the use of other methods such as dry ice or temporary burial. No country had sufficient forensic capacity to identify thousands of victims. Rapid decomposition made visual identification almost impossible after 24–48 h. In Thailand, most forensic identification was made using dental and fingerprint data. Few victims were identified from DNA. Lack of national or local mass fatality plans further limited the quality and timeliness of response, a problem which was exacerbated by the absence of practical field guidelines or an international agency providing technical support. Conclusions Emergency response should not add to the distress of affected communities by inappropriately disposing of the victims. The rights of survivors to see their dead treated with dignity and respect requires practical guidelines and technical support. Mass fatality management following natural disasters needs to be informed by further field research and supported by a network of regional and international forensic institutes and agencies.
B7-H1–expressing antigen-presenting cells mediate polarization of protumorigenic Th22 subsets
Authors: Dong-Ming Kuang, Xiao Xiao, Qiyi Zhao, Min-Min Chen, Xue-Feng Li, Rui-Xian Liu, Yuan Wei, Fang-Zhu Ouyang, Dong-Ping Chen, Yan Wu, Xiang-Ming Lao, Hong Deng, Limin Zheng
Journal: Journal of Clinical Investigation (2014)

Classical IL-22-producing T helper cells (Th22 cells) mediate inflammatory responses independently of IFN-γ and IL-17; however, nonclassical Th22 cells have been recently identified and coexpress IFN-γ and/or IL-17 along with IL-22. Little is known about how classical and nonclassical Th22 subsets in human diseases are regulated. Here, we used samples of human blood, normal and peritumoral liver, and hepatocellular carcinoma (HCC) to delineate the phenotype, distribution, generation, and functional relevance of various Th22 subsets. Three nonclassical Th22 subsets constituted the majority of all Th22 cells in human liver and HCC tissues, although the classical Th22 subset was predominant in blood. Monocytes activated by TLR2 and TLR4 agonists served as the antigen-presenting cells (APCs) that most efficiently triggered the expansion of nonclassical Th22 subsets from memory T cells and classical Th22 subsets from naive T cells. Moreover, B7-H1-expressing monocytes skewed Th22 polarization away from IFN-γ and toward IL-17 through interaction with programmed death 1 (PD-1), an effect that can create favorable conditions for in vivo aggressive cancer growth and angiogenesis. Our results provide insight into the selective modulation of Th22 subsets and suggest that strategies to influence functional activities of inflammatory cells may benefit anticancer therapy.
Streptococcal cell wall arthritis. Passive transfer of disease with a T cell line and crossreactivity of streptococcal cell wall antigens with Mycobacterium tuberculosis.
Authors: S Q DeJoy, K M Ferguson, T M Sapp, J B Zabriskie, A L Oronsky, S S Kerwar
Journal: The Journal of Experimental Medicine (1989)

Primary lymph node cells derived from streptococcal cell wall arthritic rats or those derived from adjuvant arthritic rats proliferated in response to cell wall antigens derived from either streptococcal cell walls or those from M. tuberculosis. In addition, two T cell lines have been isolated from lymph nodes of rats during the chronic phase of streptococcal cell wall arthritis. These T cell lines transfered clinical disease to naive syngeneic irradiated recipients, and they proliferated in the presence of cell wall antigens derived from streptococci or antigens derived from Mycobacterium but failed to proliferate in the presence of the 65-kD antigen (containing the sequence TFGLQLELT) derived from Mycobacterium. These observations indicate that T cells play a crucial role in the pathogenesis of streptococcal cell wall arthritis and suggest that antigenic crossreactivity exists between cell walls of group A streptococci and antigens derived from Mycobacterium. The 65-kD Mycobacterium protein is not involved in the observed antigenic crossreactivity.
Cigarette Smoking and Risk of Cataracts
Authors: Hampton Roy
Journal: JAMA (1993)

<h3>To the Editor.</h3> —I read with great interest the two prospective studies demonstrating the relationship between smoking and cataracts.<sup>1,2</sup>I have been studying this relationship since 1984. I coined the term "Roy's syndrome" in 1985 to describe the use of tobacco products causing posterior subcapsular and cortical cataracts, with an earlier onset in one eye.<sup>3</sup> The lens is the only epithelial structure to retain its earliest cells throughout life. Chronic insults can thus cause structural changes (cataracts). For example, a popular ocular differential diagnosis book lists 17 causes of nuclear cataract, 22 causes of cortical cataract, and 72 causes of posterior subcapsular cataract.<sup>4</sup>In upcoming years, I expect additional causes to be demonstrated for cataracts. These two excellent prospective studies suggest an earlier onset of cataract in one eye than in the other eye. In our patient study we tried to identify the cause of onset and
Liver-specific p38α deficiency causes reduced cell growth and cytokinesis failure during chronic biliary cirrhosis in mice
Authors: Ana M. Tormos, Alessandro Arduini, Raquel Talens-Visconti, Ivan del Barco Barrantes, Angel R. Nebreda, Juan Sastre
Journal: Hepatology (2012)

p38α mitogen-activated protein kinases (MAPK) may be essential in the up-regulation of proinflammatory cytokines and can be activated by transforming growth factor β, tumor necrosis factor-α, interleukin-1β, and oxidative stress. p38 MAPK activation results in hepatocyte growth arrest, whereas increased proliferation has been considered a hallmark of p38α-deficient cells. Our aim was to assess the role of p38α in the progression of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, and fibrogenesis. Cholestasis was induced in wildtype and liver-specific p38α knockout mice by bile duct ligation and animals were sacrificed at 12 and 28 days. p38α knockout mice exhibited a 50% decrease in mean life-span after cholestasis induction. MK2 phosphorylation was markedly reduced in liver of p38α-deficient mice upon chronic cholestasis. Hepatocyte growth was reduced and hepatomegaly was absent in p38α-deficient mice during chronic cholestasis through down-regulation of both AKT and mammalian target of rapamycin. Cyclin D1 and cyclin B1 were up-regulated in liver of p38α-deficient mice upon chronic cholestasis, but unexpectedly proliferating cell nuclear antigen was down-regulated at 12 days after cholestasis induction and the mitotic index was very high upon cholestasis in p38α-deficient mice. p38α-knockout hepatocytes exhibited cytokinesis failure evidenced by an enhanced binucleation rate. As chronic cholestasis evolved the binucleation rate decreased in wildtype animals, whereas it remained high in p38α-deficient mice.Our results highlight a key role of p38α in hepatocyte proliferation, in the development of hepatomegaly, and in survival during chronic inflammation such as biliary cirrhosis.
KCa3.1 potassium channels are critical for cAMP-dependent chloride secretion and cyst growth in autosomal-dominant polycystic kidney disease
Authors: Mamdouh Albaqumi, Shekhar Srivastava, Zhai Li, Olga Zhdnova, Heike Wulff, Omar Itani, Darren P. Wallace, Edward Y. Skolnik
Journal: Kidney International (2008)
Intrarenal Resistive Index after Renal Transplantation
Authors: Maarten Naesens, Line Heylen, Evelyne Lerut, Kathleen Claes, Liesbeth De Wever, Filip Claus, Raymond Oyen, Dirk Kuypers, Pieter Evenepoel, Bert Bammens, Ben Sprangers, Björn Meijers, Jacques Pirenne, Diethard Monbaliu, Hylke de Jonge, Christoph Metalidis, Katrien De Vusser, Yves Vanrenterghem
Journal: New England Journal of Medicine (2013)

The intrarenal resistive index is routinely measured in many renal-transplantation centers for assessment of renal-allograft status, although the value of the resistive index remains unclear.In a single-center, prospective study involving 321 renal-allograft recipients, we measured the resistive index at baseline, at the time of protocol-specified renal-allograft biopsies (3, 12, and 24 months after transplantation), and at the time of biopsies performed because of graft dysfunction. A total of 1124 renal-allograft resistive-index measurements were included in the analysis. All patients were followed for at least 4.5 years after transplantation.Allograft recipients with a resistive index of at least 0.80 had higher mortality than those with a resistive index of less than 0.80 at 3, 12, and 24 months after transplantation (hazard ratio, 5.20 [95% confidence interval {CI}, 2.14 to 12.64; P<0.001]; 3.46 [95% CI, 1.39 to 8.56; P=0.007]; and 4.12 [95% CI, 1.26 to 13.45; P=0.02], respectively). The need for dialysis did not differ significantly between patients with a resistive index of at least 0.80 and those with a resistive index of less than 0.80 at 3, 12, and 24 months after transplantation (hazard ratio, 1.95 [95% CI, 0.39 to 9.82; P=0.42]; 0.44 [95% CI, 0.05 to 3.72; P=0.45]; and 1.34 [95% CI, 0.20 to 8.82; P=0.76], respectively). At protocol-specified biopsy time points, the resistive index was not associated with renal-allograft histologic features. Older recipient age was the strongest determinant of a higher resistive index (P<0.001). At the time of biopsies performed because of graft dysfunction, antibody-mediated rejection or acute tubular necrosis, as compared with normal biopsy results, was associated with a higher resistive index (0.87 ± 0.12 vs. 0.78 ± 0.14 [P=0.05], and 0.86 ± 0.09 vs. 0.78 ± 0.14 [P=0.007], respectively).The resistive index, routinely measured at predefined time points after transplantation, reflects characteristics of the recipient but not those of the graft. (ClinicalTrials.gov number, NCT01879124 .).