tbuckley/cabot-search huggingface dataset:
Helicobacter pylori infection in children: relation with current household living conditions.
Authors: W A McCallion, L J Murray, A G Bailie, A M Dalzell, D P O'Reilly, K B Bamford
Journal: Gut (1996)

BACKGROUND: Studies demonstrating that deprived household living conditions during childhood are risk factors for acquisition of Helicobacter pylori infection have been performed mainly in adults, who probably acquired the infection several decades ago. This study investigates whether deprived household living conditions remain important risk factors for infection in subjects (children) with recently acquired infection. AIMS: To examine the relation between current household living conditions and acquisition of H pylori infection in childhood. SUBJECTS/SETTING: Opportunistically recruited group of 367 children, aged 3 to 15 years, undergoing routine non-gastrointestinal day surgery. METHODS: Anti-H pylori IgG antibodies measured by a commercial enzyme linked immunosorbent assay validated for use in children. Postal questionnaire collecting sociodemographic data and data on household living conditions. RESULTS: Infection was associated with social class and overcrowding in the household. After adjustment for age, social class, and household density, a positive association remained between infection with H pylori and bed-sharing between children and parents on one or two nights per week, odds ratio for infection (95% CI), 2.29 (1.21, 4.32) or more frequently, odds ratio for infection (95% CI), 2.95 (1.35, 6.45). CONCLUSIONS: The continuing importance of household living conditions in the acquisition of H pylori infection is confirmed and household crowding and sharing a bed with a parent are identified as risk factors for infection.
464 INFECTIVITY RATIO COULD EXPLAIN WHY SUBJECTS WITH FAVORABLE ILE-28B GENOTYPE HAD LOWER RATES OF SUSTAINED VIROLOGICAL RESPONSE
Authors: F.M. Jiménez Macías, P.G. Casado Monge, F. Barrero Alor, M. Ramos Lora, E. Pujol de la Llave, C. Ruíz-Frutos, J.L. Robles Rodríguez, L. Galisteo Almeda, J. Conde-García, M.V. Salinas-Martín, C. Bocanegra Martín, S. Grutzmancher Saiz, C. Contreras Mazuelos, D. Merino Muñoz
Journal: Journal of Hepatology (2013)
Changing Concepts Of Suicide
Authors: Alden W. Squires
Journal: JAMA (1967)

<h3>To the Editor:—</h3> Your editorial entitled "Changing Concepts of Suicide" (<b>199</b>:752, 1967) illustrates the almost fanatical preoccupation with mere survival which pervades medical philosophy and "ethics" today. The logical and valid views of suicide expressed by Pliny the Elder and Thomas Browne, having long since been stultified by medieval dogmatists, legalists, and theologians, now are being further debased by "the dominant current approach" in Medicine. The latter asserts flatly that every prospective suicide is invariably an emotionally disturbed individual, with whose purposes and act a physician is obligated to interfere. As the editorial states, many great writers and themes of the past have recognized the possibility that deliberate, self-sacrificial self-destruction may be an act so honorable and dignified that it can transcend all philosophical, religious, legal, and social strictures. To this list of ancient taboos, contemporary psychiatry now presumes to add another. A statement by Dr. Rubin on page
Diabetes, Asymptomatic Hyperglycemia, and 22-Year Mortality in Black and White Men: The Chicago Heart Association Detection Project in Industry Study
Authors: Lynn P Lowe, Kiang Liu, Philip Greenland, Boyd E Metzger, Alan R Dyer, Jeremiah Stamler
Journal: Diabetes Care (1997)

OBJECTIVE To assess relationships of diabetes and asymptomatic hyperglycemia at baseline to the risk of cardiovascular disease (CVD) and all-cause (ALL) mortality in employed, white and black middle-aged men. RESEARCH DESIGN AND METHODS A prospective cohort study of 11,554 white men and 666 black men between the ages 35 and 64 from 1967 to 1973 was conducted using data from the Chicago Heart Association (CHA) Detection Project in Industry 22-year mortality follow-up. cox proportional hazards models, adjusted fro age and other CVD risk factors, were used to estimate the relative risk (RR) and the 95% CI of mortality associated with baseline glycemic status. RESULTS Age-adjusted baseline prevalence of clinical diabetes was similar in white (3.7%) and black (4.3%) men; asymptomatic hyperglycemia (glucose post–50-g load ≥ 11.1 mmol/l) was present in 11.1% of whites and 7.8% of blacks. After controlling for age, lifestyle, and other CVD risk factors, mortality risk was increased among white men with clinical diabetes (CVD: RR 2.51, CI 2.08−3.02; ALL: RR 1.88, CI 1.63−2.17) and asymptomatic hyperglycemia (CVD: RR 1.18, CI 1.01−1.37; ALL: RR 1.24, CI 1.11−1.37), compared with men with postload glucose &amp;lt; 8.9 mmol/l. Risks were similarly, though nonsignificantly (owing to low statistical power), increased among black men with clinical diabetes (CVD: RR 1.60, CI 0.60−4.29; ALL: RR 1.78, CI 0.97−3.25) and asymptomatic hyperglycemia (CVD: RR 1.29, CI 0.61−2.72; ALL: RR 1.37, CI 0.85−2.20). CONCLUSIONS Asymptomatic hyperglycemia and clinical diabetes appear to confer increased mortality risk in both white and black men. In addition, mortality risk is increased with increased severity of glycemia. These findings indicate the importance of applying efforts to reduce risk factors and prevent diabetes in both blacks and whites.
Family History of Hematopoietic Malignancy and Risk of Lymphoma
Authors: Ellen T. Chang, Karin Ekström Smedby, Henrik Hjalgrim, Anna Porwit-MacDonald, Göran Roos, Bengt Glimelius, Hans-Olov Adami
Journal: JNCI Journal of the National Cancer Institute (2005)

A family history of hematopoietic malignancy is associated with an increased risk of non-Hodgkin lymphoma (NHL) and Hodgkin lymphoma (HL), although the magnitude of the relative risk is unclear. We estimated the association between familial hematopoietic cancer and risk of lymphoma using validated, registry-based family data, and we also investigated whether associations between some environmental exposures and risk of lymphoma vary between individuals with and without such a family history.In a population-based case-control study of malignant lymphoma, 1506 case patients and 1229 control subjects were linked to the Swedish Multi-Generation Register and then to the Swedish Cancer Register to ascertain history of cancer in first-degree relatives of patients with malignant lymphoma. Multiple logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations with the risk of lymphoma.A history of hematopoietic malignancy in any first-degree relative was associated with an increased risk of all NHL (OR = 1.8, 95% CI = 1.2 to 2.5), common B-cell NHL subtypes, and HL. Relative risks were generally stronger in association with sibling hematopoietic cancer (OR for all NHL = 3.2, 95% CI = 1.3 to 7.6) than with parental hematopoietic cancer (OR = 1.6, 95% CI = 1.1 to 2.3). A family history of NHL or chronic lymphocytic leukemia (CLL) was associated with an increased risk of several NHL subtypes and HL, whereas familial multiple myeloma was associated with a higher risk of follicular lymphoma. There was no statistically significant heterogeneity in NHL risk associations with environmental factors between individuals with and without familial hematopoietic malignancy.The increased risk of NHL and HL among individuals with a family history of hematopoietic malignancy was approximately twofold for both lymphoma types. There was no evidence that etiologic associations varied between familial NHL and nonfamilial NHL.
Case Report: CT negative Malignant Otitis Externa Diagnosed with Tc-99m Fanolesomab (NeutroSpec??) WBC Scan &amp; Gallium-67 Imaging
Authors: Ruby Chadha, Dana Mathews, William Erdman, Philip Shie, David Brandon
Journal: Clinical Nuclear Medicine (2006)

Scientific Abstracts: Nine Poster Presentations for the 51st Annual Meeting of the Southwestern Chapter of the Society of Nuclear Medicine April 7-9, 2006, Hyatt Regency, Albuquerque, New Mexico http: //www.swcsnm.org: PDF Only
REGULATION OF DRUG-METABOLIZING ENZYMES AND TRANSPORTERS IN INFLAMMATION
Authors: Alison E. Aitken, Terrilyn A. Richardson, Edward T. Morgan
Journal: The Annual Review of Pharmacology and Toxicology (2005)

Inflammation and infection have long been known to downregulate the activity and expression of cytochrome P450 (CYP) enzymes involved in hepatic drug clearance. This can result in elevated plasma drug levels and increased adverse effects. Recent information on regulation of human CYP enzymes is presented, as are new developments in our understanding of the mechanisms of regulation. Experiments to study the effects of modulating CYP activities on the inflammatory response have yielded possible insights into the physiological consequences, if not the purpose, of the downregulation. Regulation of hepatic flavin monooxygenases, UDP-glucuronosyltransferases, sulfotransferases, glutathione S-transferases, as well as of hepatic transporters during the inflammatory response, exhibits similarities and differences with regulation of CYPs.
Genetic evidence for a novel gene(s) involved in urogenital development on 10q26
Authors: Tsutomu Ogata, Koji Muroya, Isoji Sasagawa, Tomoki Kosho, Keiko Wakui, Satoru Sakazume, Katsumi Ito, Nobutake Matsuo, Hirofumi Ohashi, Toshiro Nagai
Journal: Kidney International (2000)
Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults.
Authors: D S Celermajer, K E Sorensen, D Georgakopoulos, C Bull, O Thomas, J Robinson, J E Deanfield
Journal: Circulation (1993)

BACKGROUND Cigarette smoking is the most important modifiable risk factor for atherosclerosis. Endothelial dysfunction is an early event in atherogenesis, and we hypothesized that smoking might be associated with endothelial damage in the systemic arteries of otherwise healthy young adults. METHODS AND RESULTS We studied noninvasively the brachial arteries of 200 subjects aged 15 to 57 years, all normotensive, nondiabetic with cholesterol level &lt; or = 240 mg/dL and no family history of premature vascular disease: 80 control subjects aged 16 to 56 years (mean, 35), 80 current smokers aged 15 to 55 years (mean, 33), and 40 former smokers aged 25 to 57 years (mean, 38). Total lifetime amount smoked varied from 1 to 75 pack years in the smokers. Using high-resolution ultrasound, vessel diameter was measured at rest, during reactive hyperemia (with flow increase causing endothelium-dependent dilation), and after sublingual glyceryl trinitrate (GTN, an endothelium-independent vasodilator). Flow-mediated dilation (FMD) was observed in all the control subjects (10 +/- 3.3%; range, 4% to 22%) but was impaired or absent in the smokers (4 +/- 3.9%; range, 0% to 17%; P &lt; .0001). FMD in the smokers was inversely related to lifetime dose smoked (6.6 +/- 4.0% in very light smokers, 4.0 +/- 3.1% in light smokers, 3.2 +/- 3.2% in moderate smokers, and 2.6 +/- 1.2% in heavy smokers; P &lt; .01). FMD for the former smokers was 5.1 +/- 4.1% (range, 0% to 15%). In a multivariate model adjusting for age, sex, cholesterol, smoking history, and vessel size, former smoking was associated with a higher FMD than current smoking (P = .07); when only male former and current smokers were considered, the higher FMD was significant (P = .0001) but not for female smokers (P = .24). GTN caused dilation in all subjects (control subjects, 20 +/- 5.2%; smokers, 17 +/- 5.8%; former smokers, 17.4 +/- 5.4%). Vessel diameter, baseline flow, and degree of reactive hyperemia (Doppler estimated) were similar in all groups. CONCLUSIONS Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent arterial dilation in asymptomatic young adults, consistent with endothelial dysfunction.
Ninjurin1 increases p21 expression and induces cellular senescence in human hepatoma cells
Authors: Takashi Toyama, Yutaka Sasaki, Masayoshi Horimoto, Kenya Iyoda, Takayuki Yakushijin, Kazuyoshi Ohkawa, Tetsuo Takehara, Akinori Kasahara, Toshiyuki Araki, Masatsugu Hori, Norio Hayashi
Journal: Journal of Hepatology (2004)
Bowel Functions, Fecal Unconjugated Primary and Secondary Bile Acids, and Colonic Transit in Patients With Irritable Bowel Syndrome
Authors: Andrea Shin, Michael Camilleri, Priya Vijayvargiya, Irene Busciglio, Duane Burton, Michael Ryks, Deborah Rhoten, Alan Lueke, Amy Saenger, Adam Girtman, Alan R. Zinsmeister
Journal: Clinical Gastroenterology and Hepatology (2013)
Fingernail White Spots: Possible Zinc Deficiency
Authors: Carl C. Pfeiffer
Journal: JAMA (1974)

<h3>To the Editor.—</h3> Many children and teen-agers and a few adults have white spots in the fingernails. These occur more frequently in the nails of the index and little finger of the dominant hand, ie, right hand for the right-handed individuals. Trauma is thus a factor, but not the primary cause, since patients with numerous white nail spots will also have such spots in the toenails. White banding may occur in the nails of both hands. Attention was called to these spots or paired bands by Muerhcke<sup>1</sup>(1956) who ascribed the phenomenon to a serum albumin level lower than 2.2 gm/100 ml. His largest group of patients suffered from nephrosis, and those of the second group had hepatic cirrhosis. All had low serum albumin levels. Two patients responded to cortisone therapy with disappearance of the white banding, and several patients responded to albumin-replacement therapy. We now find, in a
Think tank calls for new GP contracts to encourage innovation
Authors: G. Iacobucci
Journal: BMJ (2014)

General practice contracts should be remodelled to encourage practices to work together alongside hospital specialists, pharmacists, and social care staff, a leading UK healthcare think tank has urged.

The recommendation from the Nuffield Trust is given in a briefing paper proposing solutions to the current pressure facing UK general practice.1 The pressure has prompted fears that the primary care system may collapse under the weight of growing demand and shrinking resources.2

The trust’s paper, Is General Practice in Crisis? argues that although standards of care in general practice have remained high, a workforce crisis is emerging, and access to care is falling because funding isn’t enough to cope with current demand.

NHS England has acknowledged the need to increase primary care funding over the next five years. It recently set out ambitious plans to form larger multi-provider organisations comprising …
Persistent liver lesions in rats after a single oral dose of polybrominated biphenyls (firemaster FF-1) and concomitant PBB tissue levels.
Authors: R D Kimbrough, V W Burse, J A Liddle
Journal: Environmental Health Perspectives (1978)

In a preliminary study, 12 male and 12 female weanling Sherman strain rats were given a single dose of 1000 mg polybrominated biphenyls (PBBs) FireMaster FF1 Lot 7042 kg/body weight as a 5% solution in corn oil. Three male and three female weanling rats were given corn oil. One day after dosing PBB blood levels ranged from 78 to 162 ppm and 42 days later they ranged from 1.1 to 2.99 ppm. The liver was the only organ with pathological changes. In a long-term recovery study groups of 20 male and female rats, 2 months old, were given 0 or 1000 mg PBBs/kg body weight as a single dose in peanut oil. Five rats per group killed 2, 6, 10, and 14 months after dosing had pronounced liver pathology, including hepatic porphyria in the female rats and neoplastic nodules also mainly in female rats. Chemical analyses of blood, liver, and adipose tissue for PPBs 10 and 14 months after dosing gave the following mean results. Blood levels in females were 2.9 and 2.92 ppm, respectively, and males 0.94 and 1.34 ppm, respectively. Adipose tissue levels in females were 1202 and 783 ppm and in males 713 and 866 ppm, respectively. The liver levels in females were 37 and 22 ppm and in males 60 and 63 ppm, respectively.
Defective Extracellular Pyrophosphate Metabolism Promotes Vascular Calcification in a Mouse Model of Hutchinson-Gilford Progeria Syndrome That Is Ameliorated on Pyrophosphate Treatment
Authors: Ricardo Villa-Bellosta, José Rivera-Torres, Fernando G. Osorio, Rebeca Acín-Pérez, José A. Enriquez, Carlos López-Otín, Vicente Andrés
Journal: Circulation (2013)

Progerin is a mutant form of lamin A responsible for Hutchinson-Gilford progeria syndrome (HGPS), a premature aging disorder characterized by excessive atherosclerosis and vascular calcification that leads to premature death, predominantly of myocardial infarction or stroke. The goal of this study was to investigate mechanisms that cause excessive vascular calcification in HGPS.We performed expression and functional studies in wild-type mice and knock-in Lmna(G609G/+) mice expressing progerin, which mimic the main clinical manifestations of HGPS. Lmna(G609G/+) mice showed excessive aortic calcification, and primary aortic vascular smooth muscle cells from these progeroid animals had an impaired capacity to inhibit vascular calcification. This defect in progerin-expressing vascular smooth muscle cells is associated with increased expression and activity of tissue-nonspecific alkaline phosphatase and mitochondrial dysfunction, which leads to reduced ATP synthesis. Accordingly, Lmna(G609G/+) vascular smooth muscle cells are defective for the production and extracellular accumulation of pyrophosphate, a major inhibitor of vascular calcification. We also found increased alkaline phosphatase activity and reduced ATP and pyrophosphate levels in plasma of Lmna(G609G/+) mice without changes in phosphorus and calcium. Treatment with pyrophosphate inhibited vascular calcification in progeroid mice.Excessive vascular calcification in Lmna(G609G) mice is caused by reduced extracellular accumulation of pyrophosphate that results from increased tissue-nonspecific alkaline phosphatase activity and diminished ATP availability caused by mitochondrial dysfunction in vascular smooth muscle cells. Excessive calcification is ameliorated on pyrophosphate treatment. These findings reveal a previously undefined pathogenic process in HGPS that may also contribute to vascular calcification in normal aging, because progerin progressively accumulates in the vascular tissue of individuals without HGPS.
Acute Coronary Care in the Thrombolytic Era
Authors: Peter T. Kuo
Journal: JAMA (1988)

In the early 1970s, the approach to acute coronary artery occlusion and its complications included, primarily, measures to reduce myocardial oxygen demand and to block catecholamine release. The recent advent of thrombolytic therapy has opened a new vista of acute coronary care. Aggressive intervention in the acute coronary event with early thrombolytic therapy, followed by balloon angioplasty and bypass surgery when needed, can lead to preservation or revival of viable stunned myocardium and improvement of cardiac function. Drs Califf, Mark, and Wagner and 66 other contributors to this book have provided readers with the latest information on this vitally important, rapidly evolving area of health care. Among the diverse mechanisms involved in the acute interruption of coronary blood flow, plaque fissuring is considered to be a predominating factor. Minor plaque fissuring can promote atheromatous growth, while a major fissure would result in thrombotic occlusion. Thus, study of the molecular physiological
Hedgehog-responsive progenitors: Predictors of liver outcomes?
Authors: Jason Coombes, Wing-Kin Syn
Journal: Hepatology (2012)

Sancho-Bru et al. reported that progenitor-cell expansion occurs during alcoholic hepatitis (AH).1 Critically, they observed that K7 and prominin-1 progenitors were independent predictors of 90-day mortality. Their findings are consistent with a previous study documenting the accumulation of Hedgehog (Hh)-responsive progenitors in humans and mice with alcoholic liver disease,2 and where the greatest number of Hh-responsive progenitors were detected in livers of patients with a high discriminant function (DF; >32). Studies suggest that proinflammatory cytokines, growth factors, and morphogens such as Hh3 modulate the progenitor response. Hh ligands secreted by dying hepatocytes directly trigger proliferation of progenitor cells. It is likely that the worse the injury or death, the greater the amount of Hh ligand secreted. In turn, this leads to a more pronounced progenitor response. Hh also induces reprogramming of progenitors to fibroblasts and promotes the transition of quiescent hepatic stellate cells to activated myofibroblasts. Thus, resurrection of Hh signaling could explain the observed correlation of K7 with MELD and DF.1 Given the importance of Hh in the repair-inflammatory response, it is surprising that the degree of inflammation did not correlate with progenitor response or outcome. It is possible that immunohistochemistry could have underestimated the size of the inflammatory response, and flow cytometry of total liver tissues would have been more accurate if available. As Hh modulates sinusoidal endothelial function, it would be critical to ascertain if Hh pathway activation regulates leukocyte subset recruitment and therefore dictates liver outcomes. The observation that K7+ cells are found in patients with the highest mortality questions the role of the progenitor response. Is it simply a bystander effect of injury (marker of injury), an ineffectual attempt at liver repair, or both? Inhibition of the Hh pathway in a mouse model of chronic injury led to an attenuated progenitor response and reduced fibrosis,4 whereas blockade during acute liver injury resulted in a blunted progenitor response, impaired liver regeneration, and reduced survival,5 suggesting that progenitors play a pivotal role in liver repair. Indeed, authors in this study noted that high levels of EpCAM-expressing progenitors may lead to improved outcomes after AH. Future studies will need to address the functional capacity of liver progenitor subsets. Jason Coombes M.D.*, Wing-Kin Syn M.D.*, * Queen Elizabeth Hospital, University Hospital Birmingham NHS Trust, Birmingham, United Kingdom.
Data Mining Approach Shows Promise in Detecting Unexpected Drug Interactions
Authors: Tracy Hampton
Journal: JAMA (2011)

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