tbuckley/cabot-search huggingface dataset:
Comparison of Low and Moderate Dosages of Extended-Release Quetiapine in Borderline Personality Disorder: A Randomized, Double-Blind, Placebo-Controlled Trial
Authors: Donald W. Black, Mary C. Zanarini, Ann Romine, Martha Shaw, Jeff Allen, S. Charles Schulz
Journal: American Journal of Psychiatry (2014)

The authors compared the efficacy and tolerability of low and moderate dosages of extended-release quetiapine in adults with borderline personality disorder.Ninety-five participants with DSM-IV borderline personality disorder were randomly assigned to receive 150 mg/day of quetiapine (the low-dosage group; N=33), 300 mg/day of quetiapine (the moderate-dosage group; N=33), or placebo (N=29). Total score over time on the clinician-rated Zanarini Rating Scale for Borderline Personality Disorder ("Zanarini scale") was analyzed in a mixed-effects model accounting for informative dropout.Participants in the low-dosage quetiapine group had significant improvement on the Zanarini scale compared with those in the placebo group. Time to response (defined as a reduction of 50% or more on the Zanarini scale total score) was significantly shorter for both the low-dosage quetiapine group (hazard ratio=2.54, p=0.007) and the moderate-dosage quetiapine group (hazard ratio=2.37, p=0.011) than for the placebo group. Among participants who completed the study, 82% in the low-dosage quetiapine group were rated as "responders," compared with 74% in the moderate-dosage group and 48% in the placebo group. Treatment-emergent adverse events included sedation, change in appetite, and dry mouth. The overall completion rate for the 8-week double-blind treatment phase was 67% (67% for the low-dosage quetiapine group, 58% for the moderate-dosage quetiapine group, and 79% for the placebo group). Participants who experienced sedation were more likely to drop out.Participants treated with 150 mg/day of quetiapine had a significant reduction in the severity of borderline personality disorder symptoms compared with those who received placebo. Adverse events were more likely in participants taking 300 mg/day of quetiapine.
Developmental pathways to amygdala-prefrontal function and internalizing symptoms in adolescence
Authors: Cory A Burghy, Diane E Stodola, Paula L Ruttle, Erin K Molloy, Jeffrey M Armstrong, Jonathan A Oler, Michelle E Fox, Andrea S Hayes, Ned H Kalin, Marilyn J Essex, Richard J Davidson, Rasmus M Birn
Journal: Nature Neuroscience (2012)
Effect of interval training on the BODE index, SF-36, EuroQol and St-George's Respiratory Questionnaires scores in COPD patients across GOLD stages I-IV
Authors: Vasileios Andrianopoulos, Stavroula Spetsioti, Alexandra Chatzi, Nikolaos Chinkiamis, Ioannis Nasis, Theodora Vasilogiannakopoulou, Anastasia Panagopoulou, Emmanouela Kostaki, Georgia Koutsoflini, Nikolaos Koulouris, Ioannis Vogiatzis
Journal: European Respiratory Journal (2012)

In COPD patients, functional capacity, health-related quality of life and health status are respectively assessed by the clinical tools of BODE index, SF-36, EuroQol and St-George9s Respiratory Questionnaires. Interval training as a therapeutic modality elicits substantial physiological effects; however, the impact of interval training to those tools across the whole spectrum of COPD severity still remains unknown.  Objective:  To investigate whether beneficial effect of interval training is reflected to BODE and the 3 Questionnaires in GOLD stages(I-IV).  Methods:  In a large cohort of 106 COPD patients, rehabilitative intervention and control groups consisted of 71 and 35 patients, respectively. Exercise training involved 30min cycling by alternating 30-s exercise intervals at 100%Wpeak with 30-s rest and large-muscle group resistance training for a period of 10 weeks, 3-times/week.  Results:  Interval training improved significantly the clinical condition of patients across GOLD stages:II .(BODE:1.9 vs 1.1, SF-36pcs:39.6 vs 44.9, SF-36mcs:43.7 vs 49.3, EuroQol-VAS:54.1 vs 70.8, St-George9s:50.5 vs 38.9),  III. (BODE:3.8 vs 2.3, SF-36psc:38.5 vs 43.0, SF-36mcs:40.1 vs 47.4, EuroQol-VAS:48.6 vs 65.5, St-George9s:52.6 vs 40.4) , IV .(BODE:5.7 vs 4.1, SF-36psc:33.1 vs 40.9, SF-36mcs:33.2 vs 46.3, EuroQol-VAS:40.4 vs 58.2, St-George9s:60.1 vs 46.2) (P . Non significant changes were shown for patients in GOLD stage I and the control group.  Conclusions:  Beneficial effects of interval training in functional capacity, health-related quality of life and physical status are reflected by improved clinical condition of patients in GOLD stages II-IV.
Fluid Retention with Minoxidil
Authors: C. VENKATA S. RAM
Journal: Annals of Internal Medicine (1978)

Letters and Corrections1 August 1978Fluid Retention with MinoxidilC. VENKATA S. RAM, M.D., MICHAEL J. REICHGOTT, M.D., PH.D.C. VENKATA S. RAM, M.D.Search for more papers by this author, MICHAEL J. REICHGOTT, M.D., PH.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-89-2-288_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: In their discussion of resistant hypertension in a recent issue (1), Drs. Gifford and Tarazi state that fluid retention accompanying minoxidil treatment is "barely controllable" by diuretics in "high doses." This point may be somewhat overstated. While minoxidil undoubtedly causes a severe degree of fluid retention, this side effect can in most instances be controlled with appropriate doses of a loop-diuretic alone or by the addition of metolazone (2, 3) in conjunction with dietary restriction of sodium intake....References1. GIFFORDTARAZI RR: Resistant hypertension: diagnosis and management. Ann Intern Med 88:661-665, 1978 LinkGoogle Scholar2. REICHGOTTRAM MC: Synergism between metolazone and loop-diuretics (abstract). Clin Res 25:275A, 1977 Google Scholar3. RAMREICHGOTT CM: Treatment of loop-diuretic resistant edema by the addition of metolazone. Curr Ther Res 22:686, 1977 Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: C. VENKATA S. RAM, M.D.; MICHAEL J. REICHGOTT, M.D., PH.D.Affiliations: University of Texas Health Science Center Hospital of The University of Pennsylvania Dallas, TX 75235 and Philadelphia, PA 19104 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byThe Effects of the Potassium Channel Opener Minoxidil on Renal Electrolytes Transport in the Loop of HenlePruritic Rash with Actinic Keratosis and Impending Exfoliation in a Patient with Hypertension Managed with MinoxidilMinoxidil in Severe and Moderately Severe Hypertension, in Association with Methyldopa and Chlortalidone 1 August 1978Volume 89, Issue 2Page: 288-289KeywordsDiureticsResistant hypertensionSodium ePublished: 1 December 2008 Issue Published: 1 August 1978 PDF downloadLoading ...
Inhibition of amiloride-sensitive apical Na+ conductance by acetylcholine in rabbit cortical collecting duct perfused in vitro.
Authors: M Takeda, K Yoshitomi, J Taniguchi, M Imai
Journal: Journal of Clinical Investigation (1994)

We examined effects of acetylcholine (ACh) on the electrical parameters and intracellular Ca2+ concentration ([Ca2+]i) in the isolated rabbit cortical collecting duct (CCD) perfused in vitro using the conventional microelectrode technique and microscopic fluorescence spectrophotometry. ACh (10(-8) to 10(-5) M) in the bath caused a positive deflection of the transepithelial voltage (VT) and an increase in [Ca2+]i. Carbachol also showed similar but smaller effects. The effects of ACh were antagonized by muscarinic receptor antagonists. ACh at 10(-6) M hyperpolarized the apical membrane voltage and increased the fractional resistance of the apical membrane of the collecting duct cells accompanied by a positive deflection of VT and an increase in transepithelial resistance, whereas it did not affect these parameters in the beta-intercalated cells. In the presence of 10(-5) M amiloride in the lumen, the effects of ACh were almost completely abolished. The ACh-induced increase in [Ca2+]i is accounted for by the release of Ca2+ from intracellular store and Ca2+ entry from the bath. In the absence of Ca2+ in the bath, the ACh-induced changes in electrophysiological parameters were significantly smaller than those observed in the presence of Ca2+. Both phorbol-12-myristate-13-acetate (PMA) and phorbol-12,13-dibutylate (PDBu), activators of protein kinase C (PKC), also inhibited the apical Na+ conductance. In the presence of PMA or PDBu in the bath, ACh did not show further inhibitory effect. 1-(5-Isoquinolinylsulfonyl)-2-methylpiperazine, an inhibitor of PKC, partially attenuated the effect of ACh. These observations indicate that ACh inhibits the apical Na+ conductance partly by both increasing [Ca2+]i and activating PKC. Such an action of ACh may partially explain its natriuretic effect.
Coronary diastolic pressure-flow relation and zero flow pressure explained on the basis of intramyocardial compliance.
Authors: J A Spaan
Journal: Circulation Research (1985)

In the controversy about the mechanisms determining the high zero flow pressures and the further interpretation of coronary diastolic pressure flow relations, this paper takes a stand in favor of intramyocardial compliance as the primary cause of the high zero flow pressures. An attempt has been made to estimate the compliance distribution within the coronary circulation and to show the specific effect of intramyocardial compliance on arterial and venous pressure-flow relations. Since no data are available on the distensibility of coronary arterioles and capillaries, these data were taken from studies on mesenteric vessels. Based on these data, it is shown that, depending on the transmural pressure, smooth muscle tone may either increase or decrease arteriolar compliance. A compliance distribution has been proposed based on assumed pressure, volume, and distensibility distributions. For all but the venous division of the circulation, experimental data on volume could be found in the literature. Based on this compartmental analysis, it is predicted that overall intramyocardial compliance may exceed epicardial arterial compliance by a factor 45. The literature presenting functional evidence for intramyocardial compliance effects has been reviewed. Experimental results on venous outflow during long diastoles have been analyzed. Pf = 0 coronary pressure at zero flow, is higher when measured later in diastole. It is shown that this may be explained by charging of intramyocardial compliance in the period before flow ceases. The discrepancy between results on pressure-flow relations in the fully dilated bed and autoregulated bed are related to the differences in pressure, resistance, and compliance distributions.
Effect of L-ornithine-L-aspartate on patients with and without TIPS undergoing glutamine challenge: a double blind, placebo controlled trial
Authors: C J Rees
Journal: Gut (2000)

<h3>BACKGROUND AND AIM</h3> An oral glutamine load in cirrhotic patients awaiting liver transplantation was shown to cause a rise in blood ammonia and psychometric abnormalities which were reversed by hepatic transplantation. l-Ornithine-l-aspartate (LOLA) has been shown to reduce ammonia and improve psychometric function in patients with hepatic encephalopathy. The aim of the present study was to assess the effect of LOLA in healthy patients with cirrhosis and no evidence of clinical encephalopathy after challenging the central nervous system by administration of oral glutamine. <h3>PATIENTS AND METHODS</h3> Eight cirrhotics (Child9s B or C) without transjugular intrahepatic portosystemic shunts (TIPS) and seven with TIPS underwent two oral glutamine (20 g) challenges, receiving LOLA (5 g intravenously) on one occasion and placebo on the other in random order. Psychometric tests, including choice reaction time (CRT) and number connection test, were performed before and after glutamine, together with electroencephalography and blood ammonia. <h3>RESULTS</h3> Mean basal ammonia was 27 (SEM 5) μmol/l in non-TIPS and 76 (10) μmol/l in TIPS patients (p&lt;0.05). Basal CRT 2 was 0.643 (0.033) s in non-TIPS and 0.825 (0.076) s in TIPS patients (p&lt;0.02). In non-TIPS patients, ammonia increased to 36 (10) μmol/l when LOLA was administered and to 62 (13) μmol/l with placebo (p&lt;0.02). There was no alteration in psychometric function in non-TIPS patients after glutamine when LOLA was given but when placebo was given, glutamine caused prolongation of CRT (p=0.02). Glutamine did not affect psychometric function in TIPS patients with or without LOLA. <h3>CONCLUSION</h3> This study showed that LOLA ameliorated the deleterious psychometric effects of glutamine in Child9s grade B and C patients with cirrhosis without TIPS and supports its use in clinical practice in hepatic encephalopathy.
Increased Survival in Pancreatic Cancer with nab-Paclitaxel plus Gemcitabine
Authors: Daniel D. Von Hoff, Thomas Ervin, Francis P. Arena, E. Gabriela Chiorean, Jeffrey Infante, Malcolm Moore, Thomas Seay, Sergei A. Tjulandin, Wen Wee Ma, Mansoor N. Saleh, Marion Harris, Michele Reni, Scot Dowden, Daniel Laheru, Nathan Bahary, Ramesh K. Ramanathan, Josep Tabernero, Manuel Hidalgo, David Goldstein, Eric Van Cutsem, Xinyu Wei, Jose Iglesias, Markus F. Renschler
Journal: New England Journal of Medicine (2013)

In a phase 1-2 trial of albumin-bound paclitaxel (nab-paclitaxel) plus gemcitabine, substantial clinical activity was noted in patients with advanced pancreatic cancer. We conducted a phase 3 study of the efficacy and safety of the combination versus gemcitabine monotherapy in patients with metastatic pancreatic cancer.We randomly assigned patients with a Karnofsky performance-status score of 70 or more (on a scale from 0 to 100, with higher scores indicating better performance status) to nab-paclitaxel (125 mg per square meter of body-surface area) followed by gemcitabine (1000 mg per square meter) on days 1, 8, and 15 every 4 weeks or gemcitabine monotherapy (1000 mg per square meter) weekly for 7 of 8 weeks (cycle 1) and then on days 1, 8, and 15 every 4 weeks (cycle 2 and subsequent cycles). Patients received the study treatment until disease progression. The primary end point was overall survival; secondary end points were progression-free survival and overall response rate.A total of 861 patients were randomly assigned to nab-paclitaxel plus gemcitabine (431 patients) or gemcitabine (430). The median overall survival was 8.5 months in the nab-paclitaxel-gemcitabine group as compared with 6.7 months in the gemcitabine group (hazard ratio for death, 0.72; 95% confidence interval [CI], 0.62 to 0.83; P<0.001). The survival rate was 35% in the nab-paclitaxel-gemcitabine group versus 22% in the gemcitabine group at 1 year, and 9% versus 4% at 2 years. The median progression-free survival was 5.5 months in the nab-paclitaxel-gemcitabine group, as compared with 3.7 months in the gemcitabine group (hazard ratio for disease progression or death, 0.69; 95% CI, 0.58 to 0.82; P<0.001); the response rate according to independent review was 23% versus 7% in the two groups (P<0.001). The most common adverse events of grade 3 or higher were neutropenia (38% in the nab-paclitaxel-gemcitabine group vs. 27% in the gemcitabine group), fatigue (17% vs. 7%), and neuropathy (17% vs. 1%). Febrile neutropenia occurred in 3% versus 1% of the patients in the two groups. In the nab-paclitaxel-gemcitabine group, neuropathy of grade 3 or higher improved to grade 1 or lower in a median of 29 days.In patients with metastatic pancreatic adenocarcinoma, nab-paclitaxel plus gemcitabine significantly improved overall survival, progression-free survival, and response rate, but rates of peripheral neuropathy and myelosuppression were increased. (Funded by Celgene; ClinicalTrials.gov number, NCT00844649.).
The impact of anti-HLA antibodies on unrelated cord blood transplantations
Authors: Minoko Takanashi, Yoshiko Atsuta, Koki Fujiwara, Hideki Kodo, Shunro Kai, Hiroyuki Sato, Masatoshi Kohsaki, Hiroshi Azuma, Hidenori Tanaka, Atsuko Ogawa, Kazunori Nakajima, Shunichi Kato
Journal: Blood (2010)
Randomised clinical trial comparing sequential and concomitant therapies for<i>Helicobacter pylori</i>eradication in routine clinical practice
Authors: Adrian G McNicholl, Alicia C Marin, Javier Molina-Infante, Manuel Castro, Jesús Barrio, Julio Ducons, Xavier Calvet, Cristobal de la Coba, Miguel Montoro, Felipe Bory, Angeles Perez-Aisa, Montserrat Forné, Javier P Gisbert
Journal: Gut (2013)

<h3>Objectives</h3> No trial has compared non-bismuth quadruple 'sequential' and 'concomitant' regimens in settings with increasing clarithromycin rates. The study aims to compare the effectiveness and safety of these therapies for <i>Helicobacter pylori</i> treatment. <h3>Design</h3> Prospective randomised clinical trial in 11 Spanish hospitals. Patients naïve to eradication therapy with non-investigated/functional dyspepsia or peptic ulcer disease were included. Randomised (1:1) to sequential (omeprazole (20 mg/12 h) and amoxicillin (1 g/12 h) for 5 days, followed by 5 days of omeprazole (20 mg/12 h), clarithromycin (500 mg/12 h) and metronidazole (500 mg/12 h)), or concomitant treatment (same drugs taken concomitantly for 10 days). Eradication was confirmed with <sup>13</sup>C-urea breath test or histology 4 weeks after treatment. Adverse events (AEs) and compliance were evaluated with questionnaires and residual medication count. <h3>Results</h3> 338 consecutive patients were randomised. Mean age was 47 years, 60% were women, 22% smokers and 20% had peptic ulcer. Concomitant and sequential eradication rates were, respectively, 87% vs 81% by intention-to-treat (p=0.15) and 91% vs 86% (p=0.131) per protocol. Respective compliances were 83% vs 82%. Treatment-emergent AEs were reported in 59% of patients (no differences found between treatments). AEs were mostly mild (60%), and average length was 6.1 days, causing discontinuation only in 12 patients. Multivariate analysis: 'concomitant' treatment showed an OR of 1.5 towards better eradication rate in a borderline significance CI (95% CI 0.9 to 2.8). <h3>Conclusions</h3> Concomitant therapy led to a non-statistically significant advantage (5%) over sequential therapy, coming closer to 90% cure rates. Both therapies showed an acceptable safety profile. <b>ClincialTrials.gov:</b>NCT01273441.
Associations of Recreational Physical Activity and Leisure Time Spent Sitting With Colorectal Cancer Survival
Authors: Peter T. Campbell, Alpa V. Patel, Christina C. Newton, Eric J. Jacobs, Susan M. Gapstur
Journal: Journal of Clinical Oncology (2013)

Purpose Little is known about the association of recreational physical activity or leisure time spent sitting with survival after colorectal cancer diagnosis. This study examined the associations of prediagnosis and postdiagnosis recreational physical activity and leisure time spent sitting with mortality among patients with colorectal cancer. Patients and Methods From a cohort of adults without colorectal cancer at baseline in 1992-1993, we identified 2,293 participants who were diagnosed with invasive, nonmetastatic colorectal cancer up to mid-2007. At baseline, before their cancer diagnosis, and again after their cancer diagnosis, participants completed detailed questionnaires that included information concerning recreational physical activity and leisure time spent sitting. Results During a maximum follow-up of 16.1 years after colorectal cancer diagnosis, 846 patients with colorectal cancer died, 379 of them from colorectal cancer. Engaging in 8.75 or more metabolic equivalent (MET) hours per week of recreational physical activity (equivalent to approximately 150 minutes per week of walking) compared with fewer than 3.5 MET hours per week was associated with lower all-cause mortality (prediagnosis physical activity: relative risk [RR], 0.72; 95% CI, 0.58 to 0.89; postdiagnosis physical activity: RR, 0.58; 95% CI, 0.47 to 0.71). Spending 6 or more hours per day of leisure time sitting compared with fewer than 3 hours per day was associated with higher all-cause mortality (prediagnosis sitting time: RR, 1.36; 95% CI, 1.10 to 1.68; postdiagnosis sitting time: RR, 1.27; 95% CI, 0.99 to 1.64). Conclusion More recreational physical activity before and after colorectal cancer diagnosis was associated with lower mortality, whereas longer leisure time spent sitting was associated with higher risk of death.
Fitness of the US Workforce
Authors: Nicolaas P. Pronk
Journal: Annual Review of Public Health (2015)

Fitness matters for the prevention of premature death, chronic diseases, productivity loss, excess medical care costs, loss of income or family earnings, and other social and economic concerns. The workforce may be viewed as a corporate strategic asset, yet its fitness level appears to be relatively low and declining. Over the past half-century, obesity rates have doubled, physical activity levels are below par, and cardiorespiratory fitness often does not meet minimum acceptable job standards. During this time, daily occupational energy expenditure has decreased by more than 100 calories. Employers should consider best practices and design workplace wellness programs accordingly. Particular attention should be paid to human-centered cultures. Research should address ongoing surveillance needs regarding fitness of the US workforce and close gaps in the evidence base for fitness and business-relevant outcomes. Policy priorities should consider the impact of both state and federal regulations, adherence to current regulations that protect and promote worker health, and the introduction of incentives that allow employers to optimize the fitness of their workforce through supportive legislation and organizational policies.
Evidence that Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand Induction by 5-Aza-2′-Deoxycytidine Sensitizes Human Breast Cancer Cells to Adriamycin
Authors: Jing Xu, Jun-Ying Zhou, Michael A. Tainsky, Gen Sheng Wu
Journal: Cancer Research (2007)

Abstract The DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine (5-aza-CdR) inhibits DNA methyltransferase activity and sensitizes cancer cells to chemotherapy, but the mechanisms of its sensitization are not fully understood. Here, we show that 5-aza-CdR induces tumor necrosis factor–related apoptosis-inducing ligand (TRAIL) in the human breast cancer MDA-231 cells. Induction of TRAIL by 5-aza-CdR correlated with inactivation of Akt. Furthermore, we show that overexpression of the active form of Akt by adenovirus infection or inhibition of the Akt downstream target glycogen synthase kinase 3 by its pharmacologic inhibitors abolishes TRAIL induction by 5-aza-CdR. Importantly, we show that the combined treatment of breast cancer cells with 5-aza-CdR and Adriamycin significantly increases apoptotic cell death compared with the treatment with either agent alone. Moreover, the combined treatment activated both death receptor and mitochondrial apoptotic pathways, whereas Adriamycin alone activated only the mitochondrial pathway while 5-aza-CdR failed to activate either. More importantly, down-regulation of TRAIL by small interference RNA silencing decreased 5-aza-CdR–mediated Adriamycin-induced caspase activation and apoptosis, thus conferring Adriamycin resistance. Taken together, our results suggest that induction of TRAIL by 5-aza-CdR is critical for enhancing chemosensitivity of breast cancer cells to Adriamycin. [Cancer Res 2007;67(3):1203–11]