tbuckley/cabot-search huggingface dataset:
Circulating Pregnancy-Associated Plasma Protein A Predicts Outcome in Patients With Acute Coronary Syndrome but No Troponin I Elevation
Authors: Juha Lund, Qiu-Ping Qin, Tuomo Ilva, Kim Pettersson, Liisa-Maria Voipio-Pulkki, Pekka Porela, Kari Pulkki
Journal: Circulation (2003)

Risk stratification in troponin (cTn)-negative acute coronary syndrome (ACS) remains a clinical challenge. We investigated the predictive value of circulating pregnancy-associated plasma protein A (PAPP-A), a novel marker of atherosclerotic plaque activity, in these patients.Two hundred consecutive hospitalized ACS patients were included, of whom 136 (69 men and 67 women; mean+/-SD age, 66+/-16 years) remained cTnI-negative for up to 24 hours. PAPP-A was measured at admission, 6 to 12 hours, and 24 hours. During 6-month follow-up, 26 (19.1%) of the cTnI-negative patients reached a primary end point (cardiovascular death, myocardial infarction, or revascularization). At a cutoff level of 2.9 mIU/L, elevated PAPP-A was an independent predictor of adverse outcome (adjusted risk ratio [RR], 4.6; 95% confidence interval, 1.8 to 11.8; P=0.002). Another independent predictor was admission CRP >2.0 mg/L (RR, 2.6; P=0.03).Measurement of plasma PAPP-A, a zinc-binding matrix metalloproteinase, is a strong independent predictor of ischemic cardiac events and need of revascularization in patients who present with suspected myocardial infarction but remain troponin negative.
Esophageal capsule endoscopy in patients with suspected esophageal disease: double blinded comparison with esophagogastroduodenoscopy and assessment of interobserver variability
Authors: M. Delvaux, I. Papanikolaou, I. Fassler, H. Pohl, W. Voderholzer, T. Rösch, G. Gay
Journal: Endoscopy (2007)

See also: Commentaire de travail de M. Delvaux et al., pp. 16Endoscopy 2008; 40(01): 89-89DOI: 10.1055/s-0032-1306801
Herpes simplex virus reactivation as a trigger of mucous lesions in pemphigus vulgaris
Authors: M. Kurata, Y. Mizukawa, Y. Aoyama, T. Shiohara
Journal: British Journal of Dermatology (2014)

Journal Article Herpes simplex virus reactivation as a trigger of mucous lesions in pemphigus vulgaris Get access M. Kurata, M. Kurata Department of Dermatology Kyorin University School of Medicine Shinkawa, 6‐20‐2 Mitaka Tokyo 181‐8611 Japan Search for other works by this author on: Oxford Academic Google Scholar Y. Mizukawa, Y. Mizukawa Department of Dermatology Kyorin University School of Medicine Shinkawa, 6‐20‐2 Mitaka Tokyo 181‐8611 Japan Correspondence Yoshiko Mizukawa. E‐mail: ymizu@ks.kyorin-u.ac.jp Search for other works by this author on: Oxford Academic Google Scholar Y. Aoyama, Y. Aoyama Department of Dermatology Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences Okayama 700‐8558 Japan Search for other works by this author on: Oxford Academic Google Scholar T. Shiohara T. Shiohara Department of Dermatology Kyorin University School of Medicine Shinkawa, 6‐20‐2 Mitaka Tokyo 181‐8611 Japan Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 171, Issue 3, 1 September 2014, Pages 554–560, https://doi.org/10.1111/bjd.12961 Published: 01 September 2014
Hepatitis delta virus infects the cells of hepadnavirus-induced hepatocellular carcinoma in woodchucks
Authors: Natalia Freitas, Jessica Salisse, Celso Cunha, Ilia Toshkov, Stephan Menne, Severin O. Gudima
Journal: Hepatology (2012)

Hepatitis delta virus (HDV) is a natural subviral agent of human hepatitis B virus (HBV). HDV enhances liver damage during concomitant infection with HBV. The molecular pathogenesis of HDV infection remains poorly understood. To advance our understanding of the relationship between HDV infection and liver cancer, it was determined whether HDV could infect in vivo the cells of hepadnavirus-induced hepatocellular carcinoma (HCC). Woodchucks ( Marmota monax ) that were chronically infected with HBV-related woodchuck hepatitis virus (WHV) and already developed HCCs were used as an experimental model. The locations of HCCs within the livers were determined using ultrasound imaging followed by open surgery. One week after surgery the WHV carrier woodchucks were superinfected with WHV-enveloped HDV (wHDV). Six weeks later the animals were sacrificed and HDV replication in normal liver tissues and in center masses of HCCs was evidenced by Northern analysis, real-time polymerase chain reaction assay, and immunohistochemistry. Based on accumulation levels of HDV RNAs and numbers of infected cells, the efficiency of wHDV infection appears to be comparable in most HCCs and normal liver tissues. Conclusion : Cells of WHV-induced HCCs are susceptible to HDV infection in vivo , and therefore express functional putative WHV receptors and support the steps of the attachment/entry governed by the hepadnavirus envelope proteins. Because others previously hypothesized that hepadnavirus-induced HCCs are resistant to reinfection with a hepadnavirus in vivo , our data suggest that if such a resistance exists it likely occurs via a block at the post-entry step. The demonstrated ability of HDV to infect already formed HCCs may facilitate development of novel strategies further dissecting the mechanism of liver pathogenesis associated with HDV infection. (HEPATOLOGY 2012;56:76–85)
VACCINES IN THE TREATMENT OF GONORRHOEA
Authors: E. D. McCrea
Journal: BMJ (1928)

TREATMENT OF GONORRHOEA BY VACCINES.[TMEDCA BJOISNAL 765Dvke4 hias noted that Groutip 3 serums are sometimes deficienit in.agglutinins, whereas others are of high titre.. Pr'ofessor Fr euchleii of Copenhagen informns mne that, in a series of 400 tranisftusions, he has miiet the same phenomenon oil four e occasions, and thle soluitioln of the difficultv is the in ariable mar(tI.efiny of I1tih titre Group 3 stock serumis- an observation recommniended to comm-lereial firmus for attention.Meanwhile, we lhave the cross-test.Dyke4 quotes the technique of the American Society of immiulnologists, wlich con-siders that tlirty miniutes at room temperature is suffi- cient Preventioni of unitoward results; the present case affords eviden ce that this time may be insufficienit.Mv own rule is s1ow1f to incubate the bloods at 370 C. for onle to on1e and a quiarter houirs in a damttp chanmber; the hollow-gr-ouind slide is placed in a Petri dish lined with dampl) filter-p)aper.To save time, if all is well at the end of twenty minultes the donor is bled, and when seventy-five nmintutes has elapsed from the time of mixin-g the bloods, anid not before, unless the case is so desperate that the extra risk miiust be taken, the actual transfusion is com- mlenlced.Hitlherto all trouible has beeni obviated, and this J. believe to be the only-safe m-lethod of pirocedure iunitil suich timl-e as reliable hiigh titre Giioi) 3 sei,unis are mariaiketed.
Availability of endogenous peptides limits expression of an M3a-Ld major histocompatibility complex class I chimera.
Authors: J M Vyas, R R Rich, D D Howell, S M Shawar, J R Rodgers
Journal: The Journal of Experimental Medicine (1994)

Taking advantage of our understanding of the peptide specificity of the major histocompatibility complex class I-b molecule M3a, we sought to determine why these molecules are poorly represented on the cell surface. To this end we constructed a chimeric molecule with the alpha 1 and alpha 2 domains of M3a and alpha 3 of Ld thereby allowing use of available monoclonal antibodies to quantify surface expression. Transfected, but not control, B10.CAS2 (H-2M3b) cells were lysed readily by M3a-restricted monoclonal cytotoxic T lymphocytes. Thus, the chimera bound, trafficked, and presented endogenous mitochondrial peptides. However, despite high levels of M3a-Ld mRNA, transfectants were negative by surface staining. This finding was consistent with inefficient trafficking to the cell surface. Incubation at 26 degrees C, thought to permit trafficking of unoccupied heavy (H) chains, resulted in detectable cell surface expression of chimeric molecules. Incubation with exogenous peptide at 26 degrees C (but not at 37 degrees C) greatly enhanced expression of M3a-Ld molecules in a dose-dependent manner, suggesting stabilization of unoccupied molecules. Stable association of beta 2-microglobulin with the chimeric H chain was observed in labeled cell lysates only in the presence of exogenous specific peptide, indicating that peptide is required for the formation of a ternary complex. These results indicate that surface expression of M3a-Ld is limited largely by the steady-state availability of endogenous peptides. Since most known M3a-binding peptides are N-formylated, native M3a may normally be expressed at high levels only during infection by intracellular bacteria.
Immunosuppressive factor(s) extracted from lymphoid cells of nonresponder mice primed with L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT) III. Immunochemical properties of the GAT-specific suppressive factor.
Authors: J Theze, J A Kapp, B Benacerraf
Journal: The Journal of Experimental Medicine (1977)

The GAT-specific suppressor T-cell factor (GAT-TsF) extracted from lymphoid cells from GAT-primed, nonresponder DBA/1 mice has been partially characterized. It is a protein that has affinity for GAT and determinants encoded by the I region of the H-2 complex. On the basis of specificity and avidity, GAT-TsF resembles anti-GAT-MBSA antibodies produced by DBA/1 mice in spite of the fact that it is too small to be classical antibody and has no constant-region determinants of heavy or light chains. Further, GAT or a fragment of GAT is associated with the GAT-TsF. GAT-TsF has been partially purified from the crude extract by absorption to GAT-Sepharose and elution with 0.4 to 0.6 KCl. GAT-TsF purified on the basis of its affinity for GAT bears I-region determinants but not detectable GAT or GAT fragment.
How should women be advised on weight management in pregnancy?
Authors: L. Poston, L. C. Chappell
Journal: BMJ (2012)

There is not yet sufficient evidence to support any particular intervention 

Obesity in pregnant women has considerable resource implications, with increased odds of caesarean or instrumental delivery, haemorrhage, infection, longer duration of hospital stay, and need for neonatal intensive care.1 At a time when more than half the women of reproductive age in the United Kingdom are overweight or obese,2 any analysis of weight management interventions in pregnancy is timely and welcome. In the linked paper (doi:10.1136/bmj.e2088), Thangaratinam and colleagues present a comprehensive and well conducted meta-analysis of studies that have tried to improve maternal weight and obstetric outcomes through dietary and lifestyle interventions across the body mass index (BMI) range.3 However, many of the included studies are of small size and limited quality. The authors conclude that interventions can improve some outcomes for the mother and baby and that dietary advice, rather than advice on physical activity, is most effective. Importantly, there was no evidence of harm.

Internationally, the guidelines for weight management in pregnancy vary. Because the US Institute of Medicine (IOM) recommends limits for gestational weight gain (table⇓),4 most published intervention studies focus mainly on this parameter. In the UK, however, the National Institute for Health and Clinical Excellence (NICE) guidelines for weight management in pregnancy do not advise regular weighing of pregnant women beyond their first visit because evidence for an effective intervention to improve clinical outcomes in a UK population has been lacking.5

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Ventricular coupling via the pericardium: normal versus tamponade
Authors: H. Harasawa, K. S Li, T. Nakamoto, L. Coghlan, H R. Singleton, L. J Dell'Italia, W. P Santamore
Journal: Cardiovascular Research (1993)

Objective: The aim was to examine how regional variations in pericardial pressure affect the mechanical coupling between the ventricles. Methods: Canine hearts from 14 dogs (14.5-18 kg) were removed and placed in cold cardioplegia solution. Balloons were inserted into the left and right ventricles and the atria. Pericardial pressure over the left ventricle (Pclv) and the right ventricle (Pcrv) was measured with thin balloon catheters. Ventricular and pericardial pressures were measured, and ventricular and pericardial coupling was calculated, under control conditions and with increases in pericardial tension and fluid. Results: At baseline, regional differences in pericardial pressure occurred [Pclv>Pcrv, 4.0(SD 0.9) v 2.9(0.6) mm Hg, p < 0.05]. Ventricular coupling via the pericardium was defined as ΔPclv/ΔPcrv for right ventricular volume increases and ΔPcrv/ΔPclv for left ventricular volume increases. This ratio increased more after increasing right ventricular volume than after increasing left ventricular volume [ΔPclv/ΔPcrv>ΔPcrv/ΔPclv, 1.14(0.33) v 0.51(0.15), p < 0.05]. Increasing the pericardial tension by clamping the pericardium increased pericardial pressures, yet did not alter the regional variations in pressure [Pclv>Pcrv, 8.4(2.2) v 6.4(2.5) mm Hg, p < 0.05] or pericardial coupling [ΔPclv/ ΔPcrv>ΔPclv/ΔPcrv, 1.18(0.46) v 0.54(0.16), p < 0.05]. In contrast, creating a mild tamponade increased pericardial pressures, eliminated regional differences in pressure, and altered the coupling between ventricles [ΔPclv/ΔPcrv≈ΔPclv/ΔPcrv, 0.95(0.11) v 1.05(0.08), p=NS]. These regional differences in pericardial pressure might have a geometrical basis. In four in vivo canine experiments using cine magnetic resonance, the short axis radius of curvature for the right ventricle was greater than for the left ventricle [38.3(4.4) mm v 29.2(3.8) mm, p < 0.05]. Conclusions: The pericardium partially protects right ventricular filling: regional differences in pericardial pressure normally occurred with lower pericardial pressure over the right ventricle, and left to right ventricular coupling was less. This protection of right ventricular filling was lost with even a small pericardial effusion. Cardiovascular Research 1993; 27:1470-1476
Macrophage-Stimulating Protein Is Produced by Tubular Cells and Activates Mesangial Cells
Authors: Teresa Rampino, Chiara Collesi, Marilena Gregorini, Milena Maggio, Grazia Soccio, Paola Guallini, Antonio Dal Canton
Journal: Journal of the American Society of Nephrology (2002)

ABSTRACT. Until now, hepatocytes have been the only known cell source of macrophage-stimulating protein (MSP), and tissue macrophages have been the cells on which the biologic effects of MSP have been proved. To extend the understanding of the biologic meaning of MSP, it was investigated whether MSP operates in the kidney. MSP protein was evaluated by Western blot in supernatant of cultured human tubular cells (HK2) and human mesangial cells (HMC). MSP mRNA was investigated in HK2 by reverse transcription–polymerase chain reaction (RT-PCR). The expression of the MSP receptor, RON, was evaluated in HMC and HK2 by Western blot. RON mRNA was investigated in HMC by RT-PCR. The expression of MSP and RON in normal human renal tissue was studied by immunohistochemistry. HMC were stimulated with recombinant MSP (rMSP) and HK2 supernatant to study cell growth, migration, and the capacity to invade an artificial collagen matrix and synthesize interleukin-6 (IL-6). HK2 produced MSP and expressed RON in a form that was phosphorylated by rMSP. HMC expressed RON but did not produce MSP. MSP in HK2 supernatant and rMSP induced in HMC phosphorylation of RON, growth, migration, invasion, and IL-6 synthesis. In normal human kidney, tubules expressed MSP and RON. These results indicate a novel field of operation for MSP and suggest a pathogenic role of the MSP/RON system in renal disease. In fact, MSP released by tubular cells may recruit monocytes/macrophages in inflammatory tubulointerstitial disorders. In addition, MSP either circulating or as paracrine product may sustain glomerular mesangioproliferative disease.
Symptoms and Patient-Reported Well-Being: Do They Predict Survival in Malignant Pleural Mesothelioma? A Prognostic Factor Analysis of EORTC-NCIC 08983: Randomized Phase III Study of Cisplatin With or Without Raltitrexed in Patients With Malignant Pleural Mesothelioma
Authors: Andrew Bottomley, Corneel Coens, Fabio Efficace, Rabab Gaafar, Christian Manegold, Sjaak Burgers, Mark Vincent, Catherine Legrand, Jan P. van Meerbeeck
Journal: Journal of Clinical Oncology (2007)

Malignant pleural mesothelioma (MPM) is a rare disease. Unlike other advanced cancer types, little is known about patient-reported symptoms or health-related quality of life (HRQOL) and their possible prognostic value. This study reports an evaluation of the prognostic value of these factors using data gathered from a recent randomized controlled trial.Patients were entered onto this trial if they had a histologically proven unresectable MPM, not pretreated with chemotherapy, WHO performance status < or = 2, and adequate hematologic, renal, and hepatic function. Patients were randomly assigned to receive cisplatin 80 mg/m2 intravenously on day 1, without or with preceding infusion of raltitrexed 3 mg/m2. HRQOL was assessed using the European Organisation for Research and Treatment of Cancer (EORTC) QLQ-C30/Lung Cancer 13 tool. The Cox proportional hazards regression model was used for the univariate and multivariate analyses of survival, along with a bootstrap validation technique. Included were the EORTC prognostic index (PI) composed of stage of disease, histology type, time since diagnosis, and WBC, and, in addition, 10 selected key symptoms and HRQOL scales.Two hundred fifty patients were randomly assigned (80% male; median age, 58 years; WHO performance status 0, 1, 2 in 25%, 62%, and 13% of cases, respectively). Two hundred twenty-nine patients (91.6%) had a valid HRQOL assessment. The final multivariate model retained the PI, pain (P < .0001), and appetite loss (P = .0100) as independent prognostic indicators of survival.Results suggest that the PI, pain, and appetite loss may be independent prognostic factors in patients with advanced MPM.
When Should a Trial of Fluoxetine for Major Depression Be Declared Failed?
Authors: Frederic M Quitkin, Eva Petkova, Patrick J McGrath, Bonnie Taylor, Charles Beasley, Jonathan Stewart, Jay Amsterdam, Maurizio Fava, Jerrold Rosenbaum, Frederick Reimherr, Jan Fawcett, Ying Chen, Donald Klein
Journal: American Journal of Psychiatry (2003)

Although the newer antidepressants are widely used, little is known about how long it takes to see their full effect. The authors sought to determine how many weeks a fluoxetine trial with no improvement should continue before treatment is changed.The data involved 840 patients in a 12-week open trial of fluoxetine, 20 mg/day, followed by a blinded, placebo-controlled discontinuation study. Outcomes at 4, 6, 8, 10, and 12 weeks were classified as nonresponse, partial response, response, and remission and were based on Hamilton Depression Rating Scale scores. The rate of remission at week 12 was calculated for each group of patients without remission at the earlier time points. The time to relapse during weeks 13-26 of the discontinuation study was examined in patients taking placebo and fluoxetine in relation to status at week 6.Patients unimproved at week 6 had a remission rate at week 12 of 31%-41%. For patients with remission at week 12, level of improvement at week 6 did not affect prognosis in weeks 13-26. Of the unimproved patients at week 8, 23% had remissions by week 12. The week 12 remission rate for unimproved patients at week 4 was clearly high enough to justify continued treatment; the rate for unimproved patients at week 10 was too low.These data suggest that nonresponse to fluoxetine should not be declared until 8 weeks of treatment have elapsed. Practitioners should discuss trial length with patients at the beginning of treatment.
Ketotifen effectively prevents mucosal damage in experimental colitis.
Authors: R Eliakim, F Karmeli, E Okon, D Rachmilewitz
Journal: Gut (1992)

The effects of ketotifen, a 9mast cell stabiliser,9 on two models of experimental colitis were examined. The inflammatory response elicited by either trinitrobenzene sulphonic acid or acetic acid resulted in increased colonic synthesis of platelet activating factor, prostaglandin E2, thromboxane B2, leukotrienes B4 and C4, and myeloperoxidase activity. Intragastric administration of ketotifen 100 micrograms/100 grams twice daily significantly decreased mucosal damage when given prophylactically 48 hours before the induction of colitis and then throughout the experiment. This effect was consistent in both models and was accompanied by a significant reduction in mucosal generation of platelet activating factor, prostaglandin E2, thromboxane B2, and leukotrienes C4 and B4. Myeloperoxidase activity was reduced as well, reaching significance only in the acetic acid model. This study shows that both trinitrobenzene sulphonic acid and acetic acid colitis can be pharmacologically manipulated by ketotifen. The mechanism of action of ketotifen has not yet been determined. Ketotifen9s potential in the treatment of active inflammatory bowel disease or in the prevention of exacertations, or both, remains to be elucidated.
Transfer of the <i>sFLT-1</i> Gene in Morris Hepatoma Results in Decreased Growth and Perfusion and Induction of Genes Associated with Stress Response
Authors: Kerstin Schmidt, Johannes Hoffend, Annette Altmann, Ludwig G. Strauss, Antonia Dimitrakopoulou-Strauss, Britta Engelhardt, Dirk Koczan, Jörg Peter, Silke Vorwald, Helmut Eskerski, Michael Eisenhut, Jürgen Metz, Ralf Kinscherf, Uwe Haberkorn
Journal: Clinical Cancer Research (2005)

Abstract Purpose: Inhibition of tumor angiogenesis is emerging as a promising target in the treatment of malignancies. Therefore, monitoring of antiangiogenic approaches with functional imaging and histomorphometrical analyses are desirable to evaluate the biological effects caused by this treatment modality. Experimental Design: Using a bicistronic retroviral vector for transfer of the soluble receptor for the vascular endothelial growth factor (sFLT) hepatoma (MH3924A) cell lines with sFLT expression were generated. In human umbilical vein endothelial cells cultured with conditioned medium of sFLT-expressing hepatoma cells, the inhibitory action of secreted sFLT was determined using a Coulter counter and a thymidine incorporation assay. Furthermore, in vivo experiments were done to measure the effects on tumor growth and perfusion. Finally, the tumors were examined by immunohistochemistry (including computer-assisted morphometry) and DNA chip analysis. Results: Stable sFLT-expressing hepatoma cells inhibited endothelial cell proliferation in vitro. In vivo, growth and perfusion, as measured by H215O positron emission tomography, were reduced in genetically modified tumors. However, the immunohistochemically quantified microvascularization and macrovascularization, as indicated by CD31- and α-actin-positive area, revealed no significant changes, whereas the number of apoptotic cells was increased in sFLT-expressing tumors, although not significantly. DNA chip analysis of tumors with gene transfer showed an increase of genes related to apoptosis, signal transduction, and oxidative stress. Conclusion: Our results suggest that sFLT expression inhibits tumor growth and perfusion and enhances expression of apoptosis-related genes in this model. Enhanced expression of genes for signal transduction, stress, and metabolism indicates tumor defense reactions.