tbuckley/cabot-search huggingface dataset:
The Accuracy of PillCam ESO Capsule Endoscopy Versus Conventional Upper Endoscopy for the Diagnosis of Esophageal Varices: A Prospective Three-Center Pilot Study
Authors: G. M. Eisen, R. Eliakim, A. Zaman, J. Schwartz, D. Faigel, E. Rondonotti, F. Villa, E. Weizman, K. Yassin, R. deFranchis
Journal: Endoscopy (2006)

Background and Study Aims: Variceal bleeding is a major complication of cirrhosis, and is associated with a 20 % mortality at 6 weeks. Current international guidelines recommend that patients with cirrhosis are screened by conventional upper endoscopy (esophagogastroduodenoscopy, EGD) in order to detect esophageal varices. The recently developed PillCam ESO esophageal capsule endoscope has been shown to be an accurate diagnostic tool in the investigation of patients with gastroesophageal reflux and Barrett's esophagus. We compared the PillCam ESO capsule endoscope with EGD for the detection of esophagogastric varices and portal hypertensive gastropathy in patients with cirrhosis. Patients and Methods: A pilot trial was conducted at three sites. Patients with cirrhosis who were undergoing clinically indicated EGD for screening or surveillance for esophageal varices underwent a PillCam ESO study followed by an EGD within 48 hours. Capsule videos were assessed by an investigator who was blinded to the patient's medical history and EGD findings. Results: A total of 23 of the 32 enrolled patients were found to have esophageal varices at both EGD and PillCam ESO endoscopy. In one patient PillCam ESO detected small varices that were not seen at EGD. The overall concordance between PillCam ESO and EGD was 96.9 % for the diagnosis of esophageal varices and 90.6 % for the diagnosis of portal hypertensive gastropathy. There were no adverse events related to PillCam ESO endoscopy. Conclusions: In a high-prevalence population, PillCam ESO may represent an accurate noninvasive alternative to EGD for the detection of esophageal varices and portal hypertensive gastropathy. A large-scale trial is underway to validate and expand these findings.
Thrombolytic Treatment and Balloon Angioplasty in Chronic Occlusion of the Aortic Bifurcation
Authors: Ernst Pilger
Journal: Annals of Internal Medicine (1994)

Objective: To evaluate nonsurgical alternatives in reopening chronically occluded aortic bifurcation. Design: Uncontrolled randomized study. Setting: University-affiliated referral center for vascular diseases. Patients: Twenty-five of 39 consecutive patients with chronic aortoiliac disease including a totally occluded aortic bifurcation were found to be acceptable candidates for an aortobifemoral prosthetic graft. Intervention: Patients were randomly assigned to receive either streptokinase or urokinase or recombinant tissue-type plasminogen activator (rt-PA). In cases of successful thrombolysis and residual obstructions, subsequent balloon angioplasty was attempted. Prosthetic bypass grafting was done if thrombolytic treatment and balloon angioplasty failed. Results: Complete lysis was achieved in 5 of 25 patients (20%). In 10 (40%) patients, lysis showed residual obstructions, which were reopened mechanically in 8 patients; 2 patients had extra-anatomical bypass grafts. Ten patients (40%) without thrombolysis had surgical aortobifemoral bypass grafts. Overall, recanalization and clinical improvement were achieved in 13 of 25 patients (52%) by thrombolytic therapy and subsequent balloon angioplasty. The recanalization rate did not differ among the different thrombolytic drugs. However, rt-PA therapy resulted in reopening after 4 days of treatment; streptokinase, after 6 days; and urokinase, after 9 days (P < 0.005). No major complications or deaths occurred. Conclusion: Thrombolytic treatment followed by balloon angioplasty may help avoid the need for aortobifemoral prosthetic bypass grafting in more than 50% of patients with chronic aortoiliac disease.
A new mechanism preventing proarrhythmia in chronic heart failure: rapid phase‐III repolarization explains the low proarrhythmic potential of amiodarone in contrast to sotalol in a model of pacing‐induced heart failure
Authors: Gerrit Frommeyer, Peter Milberg, Patricia Witte, Jörg Stypmann, Matthias Koopmann, Martin Lücke, Nani Osada, Günter Breithardt, Michael Fehr, Lars Eckardt
Journal: European Journal of Heart Failure (2011)
Intravascularly Administered RGD-Displaying Measles Viruses Bind to and Infect Neovessel Endothelial Cells In Vivo
Authors: Hooi Tin Ong, Theodore R Trejo, Linh D Pham, Ann L Oberg, Stephen J Russell, Kah-Whye Peng
Journal: Molecular Therapy (2009)

Systemically administered vectors must cross the endothelial lining of tumor blood vessels to access cancer cells. Vectors that interact with markers on the lumenal surface of these endothelial cells might have enhanced tumor localization. Here, we generated oncolytic measles viruses (MVs) displaying αvβ3 integrin-binding peptides, cyclic arginine-glycine-aspartate (RGD) or echistatin, on the measles hemagglutinin protein. Both viruses had expanded tropisms, and efficiently entered target cells via binding to integrins, but also retained their native tropisms for CD46 and signaling lymphocyte activation molecule (SLAM). When fluorescently labeled and injected intravascularly into chick chorioallantoic membranes (CAMs), in contrast to unmodified viruses, the integrin-binding viral particles bound to the lumenal surface of the developing chick neovessels and infected the CAM vascular endothelial cells. In a mouse model of VEGF-induced angiogenesis in the ear pinna, the integrin-binding viruses, but not the parental virus, infected cells at sites of new blood vessel formation. When given intravenously to mice bearing tumor xenografts, the integrin-binding virus infected endothelial cells of tumor neovessels in addition to tumor parenchyma. To our knowledge, this is the first report demonstrating that oncolytic MVs can be engineered to target the lumenal endothelial surface of newly formed blood vessels when administered intravenously in living animals. Systemically administered vectors must cross the endothelial lining of tumor blood vessels to access cancer cells. Vectors that interact with markers on the lumenal surface of these endothelial cells might have enhanced tumor localization. Here, we generated oncolytic measles viruses (MVs) displaying αvβ3 integrin-binding peptides, cyclic arginine-glycine-aspartate (RGD) or echistatin, on the measles hemagglutinin protein. Both viruses had expanded tropisms, and efficiently entered target cells via binding to integrins, but also retained their native tropisms for CD46 and signaling lymphocyte activation molecule (SLAM). When fluorescently labeled and injected intravascularly into chick chorioallantoic membranes (CAMs), in contrast to unmodified viruses, the integrin-binding viral particles bound to the lumenal surface of the developing chick neovessels and infected the CAM vascular endothelial cells. In a mouse model of VEGF-induced angiogenesis in the ear pinna, the integrin-binding viruses, but not the parental virus, infected cells at sites of new blood vessel formation. When given intravenously to mice bearing tumor xenografts, the integrin-binding virus infected endothelial cells of tumor neovessels in addition to tumor parenchyma. To our knowledge, this is the first report demonstrating that oncolytic MVs can be engineered to target the lumenal endothelial surface of newly formed blood vessels when administered intravenously in living animals.
Waiting list scandal prompts calls for shake-up at US Veterans Affairs
Authors: M. McCarthy
Journal: BMJ (2014)

Allegations that staff at the US Department of Veterans Affairs (VA) falsified waiting lists to hide how long veterans had to wait for care has led to the resignation of the department’s under secretary for health, Robert A Petzel, and to calls for the agency’s secretary to step down.

The uproar was sparked by reports that Phoenix VA Health Care System in Arizona had kept two sets of records: one showing that the facility was getting appointments for veterans in a timely manner, within 14 to 30 days, and …
Heart rate variation analysis may not effectively detect sleep apnoeas in heart failure
Authors: S. Teramoto, H. Kume, Y. Yamaguchi, H. Yamamoto, M. Ishii, T. Ishii, Y. Ouchi
Journal: European Respiratory Journal (2006)

Heart rate variation analysis may not effectively detect sleep apnoeas in heart failureTo the Editors:In a recent issue of the European Respiratory Journal, VAZIR et al.[1] demonstrated that spectral analysis of heart rate variations (HRV) may be useful as a ''rule-out test'' for sleep-disordered breathing (SDB) in patients with mild-to-moderate congestive heart failure (CHF).This is an interesting approach to the diagnosis of SDB in CHF patients without sleepiness.As CHF patients with Cheyne-Stokes respiration (CSR)/central sleep apnoea (CSA) are often asymptomatic, this noninvasive approach may be effective to rule out SDB in patients.However, we feel that there are a number of problems with the article by VAZIR et al. [1].
A novel interaction of nucleophosmin with BCL2-associated X protein regulating death evasion and drug sensitivity in human hepatoma cells
Authors: Shao-Jung Lo, Li-Ching Fan, Yow-Fu Tsai, Kuo-Yang Lin, Hsiao-Ling Huang, Tong-Hong Wang, Hsuan Liu, Tse-Chin Chen, Shiu-Fen Huang, Chee-Jen Chang, Yu-Jr Lin, Benjamin Yat-Ming Yung, Sen-Yung Hsieh
Journal: Hepatology (2012)

Death evasion is crucial for both carcinogenesis and resistance to anticancer therapies. Recently, we identified nucleophosmin (NPM) as a key factor counteracting death stimuli in human hepatocellular carcinoma (HCC) cells. Here we report the identification of a novel NPM-BCL2-associated X protein (BAX) pathway orchestrating death evasion in human HCC cells. Silencing of NPM expression significantly sensitized HCC cells-particularly those bearing inactivated p53 gene (Huh7, Hep3B, and Mahlavu)-to ultraviolet irradiation, mitomycin C, doxorubicin, cisplatin, sorafenib, and lapatinib. This sensitizing effect was not changed further, as p53 expression had been simultaneously silenced. Following cell stress, NPM and BAX were induced and exported out of the nucleoli and nucleus, respectively. BAX was translocated to cytoplasm in cells with relatively high NPM level, or accumulated in the mitochondria in cells with relatively low NPM level and undergoing apoptosis. Subcellular fractionation revealed that silencing of NPM expression greatly enhanced mitochondrial translocation and oligomerization of BAX in Huh7 and Mahlavu cells. In situ proximity ligation assays and reciprocal co-immunoprecipitation revealed a direct interaction between NPM and BAX in the cytoplasm. Silencing of BAX expression abolished the sensitization effect exerted by silencing of NPM in HCC cells. Clinically, up-regulation of NPM was significantly associated with advanced tumor stage and poor prognosis.By directly blockading BAX mitochondrial translocation and activation, NPM helps human HCC cells evade death induction independently of p53-mediated cell death. Silencing of NPM significantly sensitized HCC cells to anticancer therapies. NPM is a potential cotarget in combination with other therapies for HCC, particularly those that harbor inactivated p53 gene. Our findings are of clinical significance because NPM up-regulation and p53 mutations are usually found in advanced human cancers, including HCC.
Response to Davidson
Authors: Curt L. Rohlfing, Randie R. Little, Hsiao-Mei Wiedmeyer, Jack D. England, David E. Goldstein
Journal: Diabetes Care (2001)

We appreciate the interest of M.B. Davidson (1) in our study on the use of GHb as a screening test for diabetes (2). We agree with the author's contention that “diagnosis of diabetes is untenable in a person with a normal HbAlc level,” because these individuals are …
New Rashes for Old
Authors: A. Smith, D. Bell, D. F. Smith, M. Bell
Journal: BMJ (1960)

<h3>ABSTRACT</h3> Parasites in aquatic systems are highly diverse and ubiquitous. In marine environments, parasite-host interactions contribute substantially to shaping microbial communities, but their nature and complexity remain poorly understood. In this study, we examined the relationship between Perkinsea parasitoids and bloom-forming dinoflagellate species. Our aim was to determine whether parasite-host species interactions are specific and whether the diversity and distribution of parasitoids are shaped by their dinoflagellate hosts. Several locations along the Catalan coast (NW Mediterranean Sea) were sampled during the blooms of five dinoflagellate species and the diversity of Perkinsea was determined by combining cultivation-based methods with metabarcoding of the V4 region of 18S rDNA. Most known species of Parviluciferaceae, and others not yet described, were detected, some of them coexisting in the same coastal location, and with a wide distribution. The specific parasite-host interactions determined for each of the studied blooms demonstrated the host preferences exhibited by parasitoids in nature. The dominance of a species within the parasitoid community is driven by the presence and abundances of its preferred host(s).The absence of parasitoid species, often associated with a low abundance of their preferred hosts, suggested that high infection rates are reached only under conditions that favour parasitoid propagation, especially dinoflagellate blooms.
Characteristics and regulation of bile salt synthesis and secretion by human hepatoma HepG2 cells
Authors: Allen D. Cooper, Wendy Y. Craig, Takahiro Taniguchi, Gregory T. Everson
Journal: Hepatology (1994)

Bile salt uptake, synthesis and secretion by the human hepatoma-derived cell line HepG2 were studied. The cells transported and secreted bile salts largely by means of passive mechanisms. The cells synthesized and secreted the normal human primary bile salts. The ratio of cholate to chenodeoxycholate was 1.5:1. The degree of conjugation, about 35%, was lower than normal, and the glycine-to-taurine ratio was abnormal (4.5:1). This was not due to amino acid deficiency in the medium. Contrary to the report of others, little 3 alpha,7 alpha,12 alpha-trihydroxy-5 beta-cholestan-26-oic acid was secreted. This was confirmed by gas chromatography-mass spectrometry. The total rate of synthesis was about 33% that of normal liver. The specific activity of bile salts synthesized from [3H]mevalonate was about 20 times higher than that of the cellular cholesterol derived from the same precursor. The regulation of bile salt synthesis by two compounds that could alter the precursor pool of cholesterol was studied. After a 24-hr incubation in serum-free medium, the compound 25(OH)cholesterol inhibited the rate of bile salt synthesis compared with control values, possibly by depleting the intracellular free cholesterol pool. Surprisingly, however, progesterone, which inhibits cholesterol esterification and should have expanded this pool, also inhibited bile salt synthesis under those conditions. The effect of these compounds on the level of mRNA for cholesterol 7 alpha-hydroxylase was also determined by Northern-blot analysis. The cholesterol 7 alpha-hydroxylase mRNA was 3.7 kb, similar to that in the rat. The incubation of cells in 25(OH)cholesterol or progesterone, as above, resulted in a decreased level of mRNA. The reduction was proportional to the reduction in bile salt synthesis, suggesting that these compounds act at a pretranslational level. Taken together, these results suggest that our particular subclone of HepG2 cells will be useful for studies of the regulation of bile salt synthesis, but not of transport, by human liver-derived tissue.
Early and Delayed Brain SPECT Images With 1–123 IMP in a Patient With Heterotopic Gray Matter
Authors: S. KOSUDA, K. TSUCHIYA, S. KUSANO, J. HATADA, K. SHIMA, H. CHIGASAKI, S. NAKAJIMA
Journal: Clinical Nuclear Medicine (1994)

A 63-year-old woman with numbness of the fingers bilaterally underwent 1–123 IMP SPECT and magnetic resonance imaging. On both early and delayed SPECT images with 1–123 IMP, increased accumulation of 1–123 IMP was noted in the posterior horn of the left lateral ventricle and in the white matter of the left parietc–occipital lobe. These areas were consistent with lesions of which the signal intensity approximates that of the normal gray matter on all pulse sequences. Thus, a focally increased accumulation in the white matter on both early and delayed SPECT images with I–123 IMP may reflect heterotopic gray matter.
Evidence for hyperplasia in mesenteric resistance vessels of spontaneously hypertensive rats using a three-dimensional disector.
Authors: M J Mulvany, U Baandrup, H J Gundersen
Journal: Circulation Research (1985)

Cellular dimensions in mesenteric resistance vessels from 10 spontaneously hypertensive rats and 10 Wistar-Kyoto rats have been determined using a random volume with an unbiased counting rule as the counting unit (the disector). With this method, vessels first were mounted on a myograph. Media thickness (spontaneously hypertensive rats, 11.3 micron; Wistar-Kyoto rats, 8.6 micron; P less than 0.01), lumen diameter (spontaneously hypertensive rats, 178 micron; Wistar-Kyoto rats, 194 micron; P greater than 0.1), and maximum active wall tension response (spontaneously hypertensive rats, 3.2 N/m; Wistar-Kyoto rats, 2.5 N/m; P less than 0.05) were determined. After fixation, serial sections normal to the long axis of the smooth muscle cells were made. In each vessel, the disector was a defined volume of the vessel wall (volume ca. 25 X 10(3) micron3) which was contained in about eight of these sections. The number of nuclei within the disector was counted using an unbiased, three-dimensional counting rule. On the basis that cells were mononuclear (an assumption that was tested), the ratio of this number divided by disector volume equaled the numerical cellular density. Measurement of the fraction of media taken up by smooth muscle cells then gave mean cell volume (spontaneously hypertensive rats, 563 micron3; Wistar-Kyoto rats, 615 micron3; P greater than 0.1). From the myograph measurements, the number of cells per unit length (spontaneously hypertensive rats, 10.4/micron; Wistar-Kyoto rats, 7.4/micron; P less than 0.05) and maximum force production per cell (spontaneously hypertensive rats, 5.1 microN; Wistar-Kyoto rats, 5.7 microN; P greater than 0.1) could then be calculated.(ABSTRACT TRUNCATED AT 250 WORDS)
Preliminary Findings from the New York City Neighborhood Asthma and Allergy Study
Authors: L.M. Acosta, I.F. Goldstein, A.G. Rundle, O.E. Olmedo, G.L. Chew, R.B. Mellins, J. Quinn, A. Divjan, L. Hoepner, H. Andrews
Journal: Journal of Allergy and Clinical Immunology (2009)
Prognosis after first myocardial infarction. Comparison of Q-wave and non-Q-wave myocardial infarction in the Framingham Heart Study
Authors: C. J. Berger
Journal: JAMA (1992)

To compare the short- and long-term prognosis following a first Q-wave or non-Q-wave myocardial infarction.Cohort study with a mean follow-up period of 5.1 +/- 4.9 years.Population-based.Framingham (Mass) Heart Study subjects with an initial recognized myocardial infarction during a 17-year period were studied, including 227 men and 136 women with a mean age of 67.2 years. Seventy-seven percent of first infarctions were Q-wave infarctions and 23% were non-Q-wave infarctions.Reinfarction and death from coronary heart disease.During the follow-up period, subjects with non-Q-wave infarctions had a significantly higher rate of reinfarction than subjects in the Q-wave group (P = .02 for the entire follow-up). The 10-year reinfarction rates were 44.8% vs 27.4%. When analyzed separately by age and sex, differences in reinfarction rates were only noted in men and in those under the age of 65 years. There were no differences in coronary heart disease death rates based on Q-wave status, even when examined separately by age and sex. Multivariate analysis revealed a 1.8-fold higher risk of reinfarction in the non-Q-wave group (95% confidence interval, 1.1 to 3.1), and also demonstrated that baseline hypertension was an independent risk factor for predicting reinfarction (relative risk, 1.8; 95% confidence interval, 1.1 to 3.2). There were no differences in the rates of sudden death or all-cause mortality following the two types of myocardial infarction. Additionally, subjects with a first Q-wave infarction had a higher rate of subsequent congestive heart failure, while those with non-Q-wave infarctions had a significantly higher rate of coronary insufficiency (unstable angina with transient ST-T wave abnormalities).These results confirm and extend findings from prior studies that have identified patients with first non-Q-wave myocardial infarctions as potentially unstable, with greater subsequent morbidity and similar mortality to their counterparts with Q-wave infarctions.
Posttraumatic Stress Disorder and Exposure to Violence in Adolescents
Authors: Jill Rathus, Scott Wetzler, Gregory Asnis
Journal: JAMA (1995)

<h3>To the Editor.</h3> —In the article by Dr Singer and colleagues,<sup>1</sup>we applaud the demonstration of a link between adolescents' exposure to violence and trauma symptoms, calling much-needed attention to a neglected public health problem. Using a self-report symptom checklist, the study by Singer et al identifies a range of trauma symptoms, but does not evaluate whether or not adolescents exposed to violence meet diagnostic criteria for posttraumatic stress disorder (PTSD) or other psychiatric conditions. In our Adolescent Depression and Suicide Program, we have preliminary data on the rates of mood disorders and PTSD due to violence exposure based on structured interviews (the<i>Structured Diagnostic Interview for DSM-III-R</i><sup>2</sup>and the PTSD Symptom Scale—Interview Version<sup>3</sup>). Our population consists of inner-city youths, predominantly of Hispanic and African-American ethnicity, 12 to 19 years of age, presenting to an outpatient psychiatric clinic. We report herein data from 34 adolescent subjects. Consistent