tbuckley/cabot-search huggingface dataset:
Hypertensive disorders of pregnancy and the recent increase in obstetric acute renal failure in Canada: population based retrospective cohort study
Authors: A. Mehrabadi, S. Liu, S. Bartholomew, J. A. Hutcheon, L. A. Magee, M. S. Kramer, R. M. Liston, K. S. Joseph
Journal: BMJ (2014)

<b>Objective</b> To examine whether changes in postpartum haemorrhage, hypertensive disorders of pregnancy, or other risk factors explain the increase in obstetric acute renal failure in Canada. <b>Design</b> Retrospective cohort study. <b>Setting</b> Canada (excluding the province of Quebec). <b>Participants</b> All hospital deliveries from 2003 to 2010 (n=2 193 425). <b>Main outcome measures</b> Obstetric acute renal failure identified by ICD-10 diagnostic codes. <b>Methods</b> Information on all hospital deliveries in Canada (excluding Quebec) between 2003 and 2010 (n=2 193 425) was obtained from the Canadian Institute for Health Information. Temporal trends in obstetric acute renal failure were assessed among women with and without postpartum haemorrhage, hypertensive disorders of pregnancy, or other risk factors. Logistic regression was used to determine if changes in risk factors explained the temporal increase in obstetric acute renal failure. <b>Results</b> Rates of obstetric acute renal failure rose from 1.66 to 2.68 per 10 000 deliveries between 2003-04 and 2009-10 (61% increase, 95% confidence interval 24% to 110%). Adjustment for postpartum haemorrhage, hypertensive disorders, and other factors did not attenuate the increase. The temporal increase in acute renal failure was restricted to deliveries with hypertensive disorders (adjusted increase 95%, 95% confidence interval 38% to 176%), and was especially pronounced among women with gestational hypertension with significant proteinuria (adjusted increase 171%, 71% to 329%). No significant increase occurred among women without hypertensive disorders (adjusted increase 12%, −28 to 72%). <b>Conclusions</b> The increase in obstetric acute renal failure in Canada between 2003 and 2010 was restricted to women with hypertensive disorders and was especially pronounced among women with pre-eclampsia. Further study is required to determine the cause of the increase among women with pre-eclampsia.
Anabolic Deficiency in Men With Chronic Heart Failure
Authors: Ewa A. Jankowska, Bartosz Biel, Jacek Majda, Alicja Szklarska, Monika Lopuszanska, Marek Medras, Stefan D. Anker, Waldemar Banasiak, Philip A. Poole-Wilson, Piotr Ponikowski
Journal: Circulation (2006)

Background— The age-related decline of circulating anabolic hormones in men is associated with increased morbidity and mortality. We studied the prevalence and prognostic consequences of deficiencies in circulating total testosterone (TT) and free testosterone, dehydroepiandrosterone sulfate (DHEAS), and insulin-like growth factor-1 (IGF-1) in men with chronic heart failure (CHF). Methods and Results— Serum levels of TT, DHEAS, and IGF-1 were measured with immunoassays in 208 men with CHF (median age 63 years; median left ventricular ejection fraction 33%; New York Heart Association class I/II/III/IV, 19/102/70/17) and in 366 healthy men. Serum levels of free testosterone were estimated (eFT) from levels of TT and sex hormone binding globulin. Deficiencies in DHEAS, TT, eFT, and IGF-1, defined as serum levels at or below the 10th percentile of healthy peers, were seen across all age categories in men with CHF. DHEAS, TT, and eFT were inversely related to New York Heart Association class irrespective of cause (all P &lt;0.01). DHEAS correlated positively with left ventricular ejection fraction and inversely with N-terminal pro-brain natriuretic peptide (both P &lt;0.01). Circulating TT, eFT, DHEAS, and IGF-1 levels were prognostic markers in multivariable models when adjusted for established prognostic factors (all P &lt;0.05). Men with CHF and normal levels of all anabolic hormones had the best 3-year survival rate (83%, 95% CI 67% to 98%) compared with those with deficiencies in 1 (74% survival rate, 95% CI 65% to 84%), 2 (55% survival rate, 95% CI 45% to 66%), or all 3 (27% survival rate, 95% CI 5% to 49%) anabolic endocrine axes ( P &lt;0.0001). Conclusions— In male CHF patients, anabolic hormone depletion is common, and a deficiency of each anabolic hormone is an independent marker of poor prognosis. Deficiency of &gt;1 anabolic hormone identifies groups with a higher mortality.
Topical NSAIDs have unknown effectiveness
Authors: Peter C Gøtzsche
Journal: BMJ (2008)

Dieppe claimed in an editorial about osteoarthritis that topical non-steroidal anti-inflammatory drugs (NSAIDs) are as effective as oral NSAIDs.1 He refers to a report from the National Institute for Health and Clinical Excellence (NICE), which describes two meta-analyses. He notes that the authors assessed the trials for quality, but the 424 page report says nothing about that quality. The …
Thallium reinjection after stress-redistribution imaging. Does 24-hour delayed imaging after reinjection enhance detection of viable myocardium?
Authors: V Dilsizian, W R Smeltzer, N M Freedman, R Dextras, R O Bonow
Journal: Circulation (1991)

Thallium reinjection immediately after conventional stress-redistribution imaging improves the detection of viable myocardium, as many myocardial regions with apparently "irreversible" thallium defects on standard 3-4-hour redistribution images manifest enhanced thallium uptake after reinjection. Because the 10-minute period between reinjection and imaging may be too short, the present study was designed to determine whether 24-hour imaging after thallium reinjection provides additional information regarding myocardial viability beyond that obtained by imaging shortly after reinjection.We studied 50 patients with chronic stable coronary artery disease undergoing exercise thallium tomography, radionuclide angiography, and coronary arteriography. Immediately after the 3-4-hour redistribution images were obtained, 1 mCi thallium was injected at rest, and images were reacquired at 10 minutes and 24 hours after reinjection. The stress, redistribution, reinjection, and 24-hour images were then analyzed qualitatively and quantitatively. Of the 127 abnormal myocardial regions on the stress images, 55 had persistent defects on redistribution images by qualitative analysis, of which 25 (45%) demonstrated improved thallium uptake after reinjection. At the 24-hour study, 23 of the 25 regions (92%) with previously improved thallium uptake by reinjection showed no further improvement. Similarly, of the 30 regions determined to have irreversible defects after reinjection, 29 (97%) remained irreversible on 24-hour images. These findings were confirmed by the quantitative analysis. The mean normalized thallium activity in regions with enhanced thallium activity after reinjection increased from 57 +/- 13% on redistribution studies to 70 +/- 14% after reinjection but did not change at 24 hours (71 +/- 14%). In regions with irreversible defects that were unaltered by reinjection, mean regional thallium activity did not differ from the reinjection to the 24-hour studies (57 +/- 17% and 58 +/- 17%, respectively). Twenty-four-hour imaging after reinjection showed improvement in only four of 35 irreversible regions (involving three of the 50 patients).These data indicate that thallium reinjection at rest after 3-4 hours of redistribution provides most of the clinically relevant information pertaining to myocardial viability in regions with apparently irreversible thallium defects. Hence, thallium reinjection may be used instead of 24-hour imaging in most patients in whom a persistent thallium defect is observed on conventional redistribution images.
Measles, mumps, and rubella vaccination and bowel problems or developmental regression in children with autism: population study
Authors: B. Taylor
Journal: BMJ (2002)

<h3>Abstract</h3> <b>Objectives:</b> To investigate whether measles, mumps, and rubella (MMR) vaccination is associated with bowel problems and developmental regression in children with autism, looking for evidence of a "new variant" form of autism. <b>Design:</b> Population study with case note review linked to independently recorded vaccine data. <b>Setting:</b> Five health districts in north east London. <b>Participants:</b> 278 children with core autism and 195 with atypical autism, mainly identified from computerised disability registers and born between 1979 and 1998. <b>Main outcome measures:</b> Recorded bowel problems lasting at least three months, age of reported regression of the child9s development where it was a feature, and relation of these to MMR vaccination. <b>Results:</b> The proportion of children with developmental regression (25% overall) or bowel symptoms (17%) did not change significantly (P value for trend 0.50 and 0.47, respectively) during the 20 years from 1979, a period which included the introduction of MMR vaccination in October 1988. No significant difference was found in rates of bowel problems or regression in children who received the MMR vaccine before their parents became concerned about their development (where MMR might have caused or triggered the autism with regression or bowel problem), compared with those who received it only after such concern and those who had not received the MMR vaccine. A possible association between non-specific bowel problems and regression in children with autism was seen but this was unrelated to MMR vaccination. <b>Conclusions:</b> These findings provide no support for an MMR associated "new variant" form of autism with developmental regression and bowel problems, and further evidence against involvement of MMR vaccine in the initiation of autism. <h3>What is already known on this topic</h3> A "new variant" form of autism has been hypothesised, associated with developmental regression and bowel problems and caused or triggered by the MMR vaccination This postulated association along with media attention has had a major adverse effect on public confidence in the vaccine Although population studies have shown no association between autism and MMR vaccine it has been further postulated that various environmental or genetic cofactors are required for the effect <h3>What this study adds</h3> The proportion of children with autism who had developmental regression or bowel problems has not changed over the 20 years from 1979 Neither developmental regression nor bowel problems in children with autism was associated with MMR vaccination No evidence was found for a "new variant" form of autism
Heroin Use as an Attempt To Cope: Clinical Observations
Authors: EDWARD J. KHANTZIAN, JOHN E. MACK, ALAN F. SCHATZBERG
Journal: American Journal of Psychiatry (1974)

The authors suggest that addicts' use of opiates represents a unique and characteristic way of dealing with ordinary human problems and the real world around them. Through five case reports they illustrate how addicts resort to drugs because they have failed to develop symptomatic, characterologic, or other adaptive solutions to stress. In addition, they describe how the pseudoculture of the addict also plays a part infilling his social vacuum and providing an alternative to the establishment of meaningful attachments to other people. The implications for treatment are considered.
Should liver metastases of breast cancer be biopsied to improve treatment choice?
Authors: G. Curigliano, V. Bagnardi, G. Viale, L. Fumagalli, N. Rotmensz, G. Aurilio, M. Locatelli, G. Pruneri, S. Giudici, M. Bellomi, P. Della Vigna, L. Monfardini, F. Orsi, F. Nolè, E. Munzone, A. Goldhirsch
Journal: Annals of Oncology (2011)
Inhibition of lactate removal by ketone bodies in rat liver. Evidence for a quantitatively important role of the plasma membrane lactate transporter in lactate metabolism.
Authors: H K Metcalfe, J P Monson, S G Welch, R D Cohen
Journal: Journal of Clinical Investigation (1986)

We studied the effect of DL-3-hydroxybutyrate and acetoacetate on lactate transport into isolated hepatocytes and on lactate removal in the isolated perfused rat liver. Ketone bodies inhibited lactate transport into isolated hepatocytes (maximum, 35% at concentrations of 10-20 mM). Lactate removal and glucose production by perfused livers were examined before and after the introduction of a constant infusion of hydroxybutyrate, acetoacetate, or appropriate control into the portal venous limb. Lactate removal was significantly inhibited within 10 s of the appearance of increasing concentrations of ketone bodies in the effluent. Corresponding decreases in glucose production were observed. The dependence of inhibition on D-3-hydroxybutyrate concentration was documented in isolated perfused livers (maximum inhibition of lactate removal, 58% at 14 mM). This phenomenon could be a factor in the development of lactic acidosis accompanying ketoacidosis, and indicates that plasma membrane lactate transport may determine the rate of hepatic lactate removal.
Early effects of gliadin on enterocyte intracellular signalling involved in intestinal barrier function
Authors: M G Clemente
Journal: Gut (2003)

<b>Background and aims:</b> Despite the progress made in understanding the immunological aspects of the pathogenesis of coeliac disease (CD), the early steps that allow gliadin to cross the intestinal barrier are still largely unknown. The aim of this study was to establish whether gliadin activates a zonulin dependent enterocyte intracellular signalling pathway(s) leading to increased intestinal permeability. <b>Methods:</b> The effect of gliadin on the enterocyte actin cytoskeleton was studied on rat intestinal epithelial (IEC-6) cell cultures by fluorescence microscopy and spectrofluorimetry. Zonulin concentration was measured on cell culture supernatants by enzyme linked immunosorbent assay. Transepithelial intestinal resistance (Rt) was measured on ex vivo intestinal tissues mounted in Ussing chambers. <b>Results:</b> Incubation of cells with gliadin led to a reversible protein kinase C (PKC) mediated actin polymerisation temporarily coincident with zonulin release. A significant reduction in Rt was observed after gliadin addition on rabbit intestinal mucosa mounted in Ussing chambers. Pretreatment with the zonulin inhibitor FZI/0 abolished the gliadin induced actin polymerisation and Rt reduction but not zonulin release. <b>Conclusions:</b> Gliadin induces zonulin release in intestinal epithelial cells in vitro. Activation of the zonulin pathway by PKC mediated cytoskeleton reorganisation and tight junction opening leads to a rapid increase in intestinal permeability.
Inhibition of Gastric Cancer Invasion and Metastasis by <i>PLA2G2A</i>, a Novel β-Catenin/TCF Target Gene
Authors: Kumaresan Ganesan, Tatiana Ivanova, Yonghui Wu, Vikneswari Rajasegaran, Jeanie Wu, Ming Hui Lee, Kun Yu, Sun Young Rha, Hyun Cheol Chung, Bauke Ylstra, Gerrit Meijer, Kon Oi Lian, Heike Grabsch, Patrick Tan
Journal: Cancer Research (2008)

Abstract Elevated expression of the PLA2G2A phospholipase in gastric cancer (GC) is associated with improved patient survival. To elucidate function and regulation of PLA2G2A in GC, we analyzed a panel of GC cell lines. PLA2G2A was specifically expressed in lines with constitutive Wnt activity, implicating β-catenin–dependent Wnt signaling as a major upstream regulator of PLA2G2A expression. The invasive ability of PLA2G2A-expressing AGS cells was enhanced by PLA2G2A silencing, whereas cellular migration in non–PLA2G2A-expressing N87 cells was inhibited by enforced PLA2G2A expression, indicating that PLA2G2A is both necessary and sufficient to function as an inhibitor of GC invasion in vitro. We provide evidence that antiinvasive effect of PLA2G2A occurs, at least in part, through its ability to inhibit the S100A4 metastasis mediator gene. Consistent with its invasion inhibitor role, PLA2G2A expression was elevated in primary gastric, colon, and prostrate early-stage tumors, but was decreased in metastatic and late-stage tumors. There was a strong association between PLA2G2A promoter methylation status and PLA2G2A expression, suggesting that the loss of PLA2G2A expression in late-stage cancers may be due to epigenetic silencing. Supporting this, among the non–PLA2G2A-expressing lines, pharmacologic inhibition of epigenetic silencing reactivated PLA2G2A in Wnt-active lines, but in non–Wnt-active lines, a combination of Wnt hyperactivation and inhibition of epigenetic silencing were both required for PLA2G2A reactivation. Our results highlight the complexity of PLA2G2A regulation and provide functional evidence for PLA2G2A as an important regulator of invasion and metastasis in GC. [Cancer Res 2008;68(11):4277–86]
Combined Lysophosphatidic Acid/Platelet-Derived Growth Factor Signaling Triggers Glioma Cell Migration in a Tenascin-C Microenvironment
Authors: Katrin Lange, Martial Kammerer, Falk Saupe, Monika E. Hegi, Stefan Grotegut, Erika Fluri, Gertraud Orend
Journal: Cancer Research (2008)

The antiadhesive extracellular matrix molecule tenascin-C abrogates cell spreading on fibronectin through competitive inhibition of syndecan-4, thereby preventing focal adhesion kinase (FAK) activation and triggering enhanced proteolytic degradation of both RhoA and tropomyosin 1 (TM1). Here, we show that simultaneous signaling by lysophosphatidic acid (LPA) and platelet-derived growth factor (PDGF) initiates glioma cell spreading and migration through syndecan-4-independent activation of paxillin and FAK and by stabilizing expression of RhoA, TM1, TM2, and TM3. By using gene silencing methods, we show that paxillin, TM1, TM2, and TM3 are essential for LPA/PDGF-induced cell spreading on a fibronectin/tenascin-C (FN/TN) substratum. LPA/PDGF-induced cell spreading and migration on FN/TN depends on phosphatidylinositol 3-kinase, RhoKinase, and mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1/2 but is independent of phospholipase C and Jun kinase. RNA microarray data reveal expression of tenascin-C, PDGFs, LPA, and the respective receptors in several types of cancer, suggesting that the TN/LPA/PDGF axis exists in malignant tumors. These findings may in turn be relevant for diagnostic or therapeutic applications targeting cancer.
Efficacy, safety, and immunology of an inactivated alum-adjuvant enterovirus 71 vaccine in children in China: a multicentre, randomised, double-blind, placebo-controlled, phase 3 trial
Authors: Feng-Cai Zhu, Fan-Yue Meng, Jing-Xin Li, Xiu-Ling Li, Qun-Ying Mao, Hong Tao, Yun-Tao Zhang, Xin Yao, Kai Chu, Qing-Hua Chen, Yue-Mei Hu, Xing Wu, Pei Liu, Lin-Yang Zhu, Fan Gao, Hui Jin, Yi-Juan Chen, Yu-Ying Dong, Yong-Chun Liang, Nian-Min Shi, Heng-Ming Ge, Lin Liu, Sheng-Gen Chen, Xing Ai, Zhen-Yu Zhang, Yu-Guo Ji, Feng-Ji Luo, Xiao-Qin Chen, Ya Zhang, Li-Wen Zhu, Zheng-Lun Liang, Xin-Liang Shen
Journal: The Lancet (2013)
Role of human basophils and mast cells in the pathogenesis of allergic diseases
Authors: R.P. Schleimer, C.C. Fox, R.M. Naclerio, M. Plaut, P.S. Creticos, A.G. Togias, J.A. Warner, A. Kagey-Sobotka, L.M. Lichtenstein
Journal: Journal of Allergy and Clinical Immunology (1985)
Trastuzumab before breast surgery: is concurrent administration with anthracycline-containing chemotherapy necessary?
Authors: L. Del Mastro, C. Bighin, G. Bini, S. Giraudi, P. Taveggia, A. Levaggi, G. Canavese, G. Rescinito, P. Pronzato
Journal: Annals of Oncology (2010)
PLASMA ESTERASE ACTIVITY IN PATIENTS WITH LIVER DISEASE AND THE NEPHROTIC SYNDROME
Authors: Henry G. Kunkel, Sylvia M. Ward
Journal: The Journal of Experimental Medicine (1947)

By a study of plasma esterase in various hypoproteinemic states information was gained concerning the synthesis of a protein by the liver, which may be applicable to the problem of albumin synthesis. Patients with infectious hepatitis and cirrhosis showed defective formation of plasma esterase that paralleled the defect in albumin formation. The defect could only be altered in patients with cirrhosis by very prolonged therapy indicating that liver function itself had to improve before the proteins could be formed in a normal manner. Patients with the nephrotic syndrome showed a normal or hypernormal formation of plasma esterase. Following spontaneous remissions or the administration of albumin the esterase level showed a marked rise which was in direct contrast to the difficult alterability of the enzyme level in patients with severe liver involvement. It is suggested that the defect in protein synthesis by patients with the nephrotic syndrome may be due to the lack of certain essential materials, one of which may be albumin itself, rather than to any abnormality in the liver.
MCP-1 contributes to macrophage infiltration into adipose tissue, insulin resistance, and hepatic steatosis in obesity
Authors: H. Kanda
Journal: Journal of Clinical Investigation (2006)

Adipocytes secrete a variety of bioactive molecules that affect the insulin sensitivity of other tissues. We now show that the abundance of monocyte chemoattractant protein-1 (MCP-1) mRNA in adipose tissue and the plasma concentration of MCP-1 were increased both in genetically obese diabetic (db/db) mice and in WT mice with obesity induced by a high-fat diet. Mice engineered to express an MCP-1 transgene in adipose tissue under the control of the aP2 gene promoter exhibited insulin resistance, macrophage infiltration into adipose tissue, and increased hepatic triglyceride content. Furthermore, insulin resistance, hepatic steatosis, and macrophage accumulation in adipose tissue induced by a high-fat diet were reduced extensively in MCP-1 homozygous KO mice compared with WT animals. Finally, acute expression of a dominant-negative mutant of MCP-1 ameliorated insulin resistance in db/db mice and in WT mice fed a high-fat diet. These findings suggest that an increase in MCP-1 expression in adipose tissue contributes to the macrophage infiltration into this tissue, insulin resistance, and hepatic steatosis associated with obesity in mice.
No evidence for a role of human herpesvirus type 8 in sarcoidosis: molecular and serological analysis
Authors: None Lebbé, None Agbalika, None Flageul, None Pellet, None Rybojad, None Cordoliani, None Farge, None Vignon-Pennamen, None Sheldon, None Morel, None Calvo, None Schulz
Journal: British Journal of Dermatology (1999)

The aim of this study was to analyse the association between human herpesvirus type 8 (HHV8) and sarcoidosis. Using nested polymerase chain reaction (PCR), we tested the presence of HHV8 DNA sequences in 13 skin specimens and peripheral blood mononuclear cells from eight patients suffering from sarcoidosis. We also looked for the presence of HHV8 antibodies in the sera of 28 patients with sarcoidosis using three techniques: two indirect immunofluorescence assays and an enzyme-linked immunosorbent assay with recombinant capsid protein fragment encoded by open-reading frame 65. HHV8 PCR analysis was negative while HHV8 serological studies showed an overall prevalence of 18% among patients suffering from sarcoidosis: 43% in patients from sub-Saharan Africa, 17% in patients from Northern Africa, 12.5% in patients from the French West Indies and 0% in French patients. In conclusion, our results do not indicate an association between HHV8 and sarcoidosis but reflect the seroepidemiology of this virus in different geographical regions.