Miracle-dz/UniFAR-FTUs huggingface dataset:
The Effects of Simulation on Nursing Students' Critical Thinking Scores: A Quantitative Study

Simulation has become the innovative method of incorporating clinical and theoretical knowledge and experiences for nursing students. It is essential for educators to offer strategies that develop students' critical-thinking abilities. This experiment used the Health Sciences Reasoning Test to determine if critical-thinking scores improved in the associate degree in nursing student after exposure to multiple clinical simulation scenarios (Facione & Facione. Health Sciences Reasoning Test (HSRT): a test for critical thinking skills for health care professionals. Test manual. Millbrae, CA: The California Academic Press LLC; 2006). Participants were 53 students from the medical-surgical course of an associate degree in nursing program of a college of nursing in the Midwest. Control participants received two simulation scenarios, and experimental participants received five scenarios. As predicted, experimental participants showed a greater increase in critical-thinking scores, demonstrating that simulation can enhance the quality of nursing education providing guaranteed clinical experiences that increase critical-thinking skills, as well as providing high-tech training for nursing students. Implications for nursing education and further research are discussed.
Associations Between Psychosocial Factors and Incidence of Sexually Transmitted Disease Among South African Adolescents

Background Adolescents living in South Africa are at high risk for HIV and other sexually transmitted diseases (STDs). The present study sought to identify correlates of curable STD incidence among a cohort of adolescents in Eastern Cape Province, South Africa. Methods Data were collected in conjunction with an HIV/STD prevention intervention randomized controlled trial.1 At 54 months postintervention, curable STD incidence (gonorrhea, chlamydial infection, and trichomoniasis) was assayed and self-report measures of potential correlates of STD incidence were collected. Results Participants were adolescents reporting at least 1 sexual partner in the past 3 months (n = 659). As expected, univariate analyses revealed that girls were more likely than boys to have an STD. In addition, intimate partner violence, unprotected sex, and having older partners were associated with incident STD. In Poisson multiple regression analyses, sex (risk ratio [RR], 4.00; 95% confidence interval [CI], 2.51–6.39), intimate partner violence (RR, 1.23; 95% CI, 1.12–1.35), unprotected sex (RR, 1.42; 95% CI, 1.09–2.01), and multiple partners (RR, 1.70; 95% CI, 1.11–2.61), but not partner’s age (RR, 1.00; 95% CI, 0.94–1.07) were associated with incident STD, adjusting for 42-month STD prevalence. Binge drinking, forced sex, and age were unrelated to STD incidence in both analyses. Interactions between sex and the hypothesized correlates were nonsignificant, suggesting that sex did not modify these relationships. Conclusions Interventions to reduce HIV/STD incidence among adolescents in South Africa should address the risk associated with sex, unprotected sex, intimate partner violence, and multiple partnerships.
Hepatitis B e antigen and its precursors promote the progress of hepatocellular carcinoma by interacting with NUMB and decreasing p53 activity

Hepatitis B viral infection is one of the leading causes of hepatocellular carcinoma (HCC) worldwide. Although several viral factors have been identified that may increase the risk for HCC development, the molecular mechanisms leading to the transformation of normal hepatocytes into cancer cells remain elusive. In this study, we demonstrated that the intracellular hepatitis B e antigen (HBeAg) and its precore precursors, but not their homologous core protein, could associate with NUMB and thereby impair the stability and transcriptional activity of tumor suppressor p53. HBeAg and its precursors could disrupt p53‐NUMB and HDM2‐NUMB interactions and tricomplex p53‐HDM2‐NUMB formation, inhibit the acetylation and translocation of p53 from cytosol to the nucleus, promote HDM2‐mediated ubiquitination and degradation of p53, and suppress p53‐dependent apoptosis. A xenograft tumorigenicity assay showed that expression of HBeAg and its precursors promoted carcinogenesis in a mouse model. Immunohistochemical analysis of the bioptic liver samples of HCC patients revealed that HBeAg positivity was associated with reduced transcriptional activity of p53. Taken together, the results suggest a role of intracellular HBeAg and its precursors in HCC development. Conclusion: HBeAg and its precursors promote HDM2‐mediated degradation and impair transcriptional activity of p53 by interacting with NUMB, consequently contributing to HCC development. (Hepatology 2016;64:390‐404)
Nonabsorbable disaccharides for hepatic encephalopathy: A systematic review and meta‐analysis

Nonabsorbable disaccharides (NADs) have been used to treat hepatic encephalopathy (HE) since 1966. However, a Cochrane Review, published in 2004, found insufficient evidence to recommend their use in this context. This updated systematic review evaluates the effects of the NADs, lactulose and lactitol, for the treatment and prevention of HE in patients with cirrhosis. Thirty‐eight randomized controlled trials, involving 1,828 patients, were identified through electronic and manual searches; 31 randomized controlled trials looked at the treatment of HE, while seven looked at its primary/secondary prevention. Random‐effects meta‐analyses showed that, compared to placebo/no intervention, NADs had a beneficial effect on HE (relative risk [RR] = 0.63, 95% confidence interval [CI] 0.53‐0.74, number needed to treat [NNT] = 4) and serious liver‐related adverse events such as liver failure, variceal bleeding, serious infections, spontaneous bacterial peritonitis, and hepatorenal syndrome (RR = 0.42, 95% CI 0.26‐0.69, NNT = 50). Treatment was also associated with a reduction in mortality in patients with overt HE (RR = 0.36, 95% CI 0.14‐0.94, NNT = 20), although not in patients with minimal HE. Meta‐analyses of the prevention randomized controlled trials showed that NADs prevented the development of HE (RR = 0.47, 95% CI 0.33‐0.68, NNT = 6), the risk of developing serious liver‐related adverse events (RR = 0.48, 95% CI 0.33‐0.70, NNT = 6), and reduced mortality (RR = 0.63, 95% CI 0.40‐0.98, NNT = 20). Use of NADs was associated with nonserious gastrointestinal adverse events. There were no differences in the efficacy or safety of lactulose and lactitol. Conclusions: NADs have beneficial effects in the treatment and prevention of HE; their use, in this context, confers additional benefits including a reduction in serious liver‐related morbidities and all‐cause mortality. (Hepatology 2016;64:908‐922)
A review of vilazodone exposures with focus on serotonin syndrome effects

Abstract Background: Vilazodone is an antidepressant with selective serotonin reuptake inhibition and partial 5HT1A agonism. Serotonin syndrome is believed to be due to excessive stimulation of 5-HT2A and 5-HT1A receptors, resulting in the clinical triad of altered mentation, autonomic instability and neuromuscular abnormalities. The goal of this study is to define serotonergic effects after vilazodone exposure. Methods: A retrospective review of two databases: the American Association of Poison Controls Centers’ National Poison Data System (NPDS) and the American College of Medical Toxicology’s Toxicology Investigators Consortium (ToxIC Registry). A case series of four patients from one medical toxicology service is also presented. Results: During the 52-month study period, a total of 3192 vilazodone human exposures were reported to NPDS. Of these, 1734 (54%) were isolated vilazodone cases. The clinical effects of vilazodone toxicity included drowsiness (20%), vomiting (14%), tachycardia (11%) and agitation (10%). Most patients (71%) had symptoms for between 2 and 24 h, though some (14%) remained symptomatic for more than 24 h. The most common treatment was intravenous fluids (15%) and the most serious intubation (2%). From the ToxIC Registry, a total of 23 cases of vilazodone exposures were identified. Of these, 17 (74%) had vilazodone listed as the first (primary) agent and 10 (43%) involved vilazodone-only ingestions. Nine (39%) cases documented serotonin syndrome; and most (8/9; 89%) listed vilazodone as the primary agent. All (n = 4) subjects in the case series with acute vilazodone toxicity had serotonin syndrome. Conclusions: Vilazodone overdose, including vilazodone-only ingestions, are associated with serotonin syndrome. Serotonergic toxicity and appropriate treatments should be considered when caring for patients with vilazodone ingestions.
Evaluation of technology to identify and assess overweight children and adolescents.

PURPOSE The current obesity epidemic has produced a generation of children that may be the first to have a life expectancy shorter than their parents. To address the obesity epidemic, experts have published recommendations for providers. Research suggests the publication of guidelines may not change provider behavior. DESIGN AND METHODS This study evaluates computer assistance for implementing obesity guidelines in school-based health centers. RESULTS Significant improvements in identification and assessment of obesity in children with technology support were noted. PRACTICE IMPLICATIONS Computer decision support shows promise for promoting the implementation of current recommendations by supporting providers in identifying, assessing, and providing tailored recommendations for children at risk of obesity.
Differential Regulation of Myocardial NF κ B Following Acute or Chronic TNF- α Exposure

Abstract Tumor necrosis factor α (TNF- α ) is a critical mediator of myocardial dysfunction during acute inflammatory states. TNF- α is also present in the serum of patients with chronic cardiac diseases. In monocytes, TNF- α stimulates cells by activating distinct signaling pathways that involve nuclear translocation of NF κ B. Since NF κ B may also regulate the expression of genes that could contribute to myocardial dysfunction, the cardiomyocyte NF κ B activation following acute or chronic TNF- α challenges was investigated. To accomplish this, the authors either acutely administered TNF- α to healthy mice, or used transgenic mice which chronically overexpress TNF- α exclusively in cardiac myocytes. Following acute administration of TNF- α , cardiac NF κ B translocation was detected from 15 min to 2 h post-challenge. The time course of I κ B α degradation was consistent with the kinetics of NF κ B translocation. I κ B β degradation was slower and less dramatic. In transgenic mice chronically overexpressing TNF- α , myocardial NF κ B activation was detected at all ages tested (21, 40, and 75 days). In contrast to acutely challenged animals, two distinct NF κ B proteins were activated in chronically challenged animals, p50–p65 heterodimers as well as p50 homodimers. Activation of both could be transiently blocked by administration of a recombinant chimeric TNF- α receptor antagonist (rhTNFR:Fc). I κ B α , but not I κ B β , levels were elevated in transgenics when compared to wild-type animals. These data indicate that following acute TNF- α administration, which simulates bacterial sepsis, myocardial p50–p65 translocates within minutes. Chronic TNF- α exposure, which is thought to occur in long-standing congestive heart failure, results in translocation of transcriptionally inactive p50 homodimers in addition to transcriptionally active p50–p65 heterodimers. It is speculated that activation of p50 homodimers constitutes an adaptive response to minimize the inflammatory consequences of chronic cardiac TNF- α exposure.
Evaluation of vascular effects after photodynamic and photothermal therapies using benzoporphyrin derivative monoacid ring A on a rodent dorsal skinfold model

Background and Objectives: Pulsed dye laser (PDL) irradiation is the standard clinical treatment for vascular lesions. However, PDL treatment of port wine stain birthmarks (PWS) is variable and unpredictable. Photodynamic therapy (PDT) using benzoporphyrin derivative monoacid ring A (BPD) and yellow light may induce substantial vascular effects and potentially offer a more effective treatment. In this study, we utilize a rodent dorsal skinfold model to evaluate the vascular effects of BPD-PDT at 576 nm as compared to PDL. Study Design/Materials and Methods: A dorsal skinfold window was created on the backs of female Sprague-Dawley rats, allowing epidermal and subdermal irradiation and subdermal imaging. One mg/kg BPD was administered intravenously via a jugular venous catheter. Study groups were: control (no BPD, no light), PDL (585 nm, τp 1.5 ms, 10 J/cm2), and PDT (BPD + continuous wave irradiation (CW) at 576nm, τp 16 min, 96 J/cm2). Vessels were imaged and assessed for damage using laser speckle imaging (LSI) before, immediately after, and 18 hours post-intervention. Results: Epidermal irradiation was accomplished without blistering, scabbing or ulceration. PDL and PDT resulted in similar reductions in vascular perfusion 18 hours post-intervention (34.6% and 33.4%, respectively). Conclusions: BPD-PDT can achieve safe and selective vascular effects and may offer an alternative therapeutic option for treatment of hypervascular skin lesions including PWS birthmarks.
Relations Between Quality of Life, Family Factors, Adherence, and Glycemic Control in Pediatric Patients With Type 1 Diabetes Mellitus

This study examined relations among diabetes-specific family factors, adherence to medical regimen, quality of life (QOL), and glycemic control in youth and adolescents with type 1 diabetes. During an endocrinologist visit, patient and parent–caregiver dyads (n = 70) completed family factors and QOL measures and participated in a structured interview to assess medical regimen compliance, and the patient's glycemic control was assessed by a medical professional. Combined measures accounted for 42% of the variance in glycemic control. QOL partially mediated adherence and glycemic control. Ethnic minority status was associated with poorer glycemic control.
Cibenzoline intoxication: Effect of combined hemoperfusion-hemodialysis on plasma clearance

Introduction. Cibenzoline is an antiarrhythmic drug used to treat patients with supraventricular or ventricular arrhythmias. Cibenzoline overdose is associated with proarrhythmic and hemodynamic effects such as hypotension and congestive heart failure. Case Report. We report a case of cardiogenic shock due to cibenzoline overdose in a patient with progressive renal insufficiency. Discussion. The standard treatment of a cibenzoline intoxication is symptomatic, but we used combined hemoperfusion-hemodialysis to treat our patient. Conclusions. This was associated with a rapid decline in plasma cibenzoline concentration and improvement of the clinical condition. However, only 28.98 mg of an estimated body pool of cibenzoline (447.2 to 806.6 mg) was removed during the 8 hours of treatment.
Validity of self-reported psychiatric diagnoses among patients seeking treatment for a substance use disorder

Patients seeking treatment for substance use disorders (SUDs) frequently report a history of psychiatric diagnoses, but the validity of these diagnoses is not well established. The study aimed to validate self-reported historical mental diagnoses in patients with an SUD using psychometric tests and structured interviews. This cross-sectional study of participants (n = 30) with an SUD compared their self-reported prior psychiatric diagnoses with current clinical diagnoses based on psychometric tests and structured psychosocial interviews. Of the 11 participants reporting a prior diagnosis of bipolar disorder (BD), only one received a current clinical diagnosis of BD. The historical diagnosis of a personality disorder was confirmed in the two participants reporting this diagnosis, and 15 new diagnoses were made. Bipolar disorder was over-diagnosed in participants with an SUD who instead might have personality disorders. Self-reported psychiatric diagnoses presented by patients for treatment of an SUD should.
Liver protects metastatic prostate cancer from induced death by activating E‐cadherin signaling

Liver is one of the most common sites of cancer metastasis. Once disseminated, the prognosis is poor as these tumors often display generalized chemoresistance, particularly for carcinomas that derive not from the aerodigestive tract. When these cancers seed the liver, the aggressive cells usually undergo a mesenchymal to epithelial reverting transition that both aids colonization and renders the tumor cells chemoresistant. In vitro studies demonstrate that hepatocytes drive this phenotypic shift. However, the in vivo evidence and the molecular signals that protect these cells from induced death are yet to be defined. Herein, we report that membrane surface E‐cadherin‐expressing prostate cancer cells were resistant to cell death by chemotherapeutic drugs but E‐cadherin null cells or those expressing E‐cadherin only in the cytoplasm were sensitive to death signals and chemotherapies both in vitro and in vivo. While cell‐cell E‐cadherin ligandation reduced mitogenesis, this chemoprotection was proliferation‐independent as killing of both 5‐ethynyl‐2′‐deoxyuridine‐positive (or Ki67+) and 5‐ethynyl‐2′‐deoxyuridine‐negative (Ki67‐) cells was inversely related to membrane‐bound E‐cadherin. Inhibiting the canonical survival kinases extracellular signal‐regulated protein kinases, protein kinase B, and Janus kinase, which are activated by chemotherapeutics in epithelial cell‐transitioned prostate cancer, abrogated the chemoresistance both in cell culture and in animal models of metastatic cancer. For disseminated tumors, protein kinase B disruption in itself had no effect on tumor survival but was synergistic with chemotherapy, leading to increased killing. Conclusion: Liver microenvironment‐driven phenotypic switching of carcinoma cells and subsequent survival signaling results in activation of canonical survival pathways that protect the disseminated prostate cancer liver micrometastases in a proliferation‐independent manner, and these pathways can be targeted as an adjuvant treatment to improve the efficacy of traditional chemotherapeutics (Hepatology 2016;64:1725‐1742)
Catch-Up Growth and Endocrine Changes in Childhood Celiac Disease

Childhood celiac disease may lead to a failure of statural growth. After institution of a gluten-free diet most patients exhibit catch-up growth. Catch-up growth is a remarkable phenomenon characterized by a supranormal height velocity. One of the hypothetical mechanisms of catch-up growth is that an increased activity of the somatotrophic axis is involved. In order to provide further insight in the physiology of catch-up growth, auxological and endocrine changes were prospectively studied in 28 children with newly diagnosed celiac disease. The results demonstrate a malnutrition-like state of the somatotrophic axis at the time of diagnosis and a rapid recovery of this axis towards normal functioning after institution of the gluten-free diet. Although several correlations between these endocrine alterations and auxological parameters were detected, it is questionable whether the endocrine changes are the driving force behind catch-up growth.
Nanosilver Application in Dental Cements

Streptococcus mutans is the microorganism mostly responsible for initiation of tooth decay and also for the progression of an established lesion. Silver has been used for its antibacterial properties for many years, in different forms: ionised and elementary forms, as silver zeolites or as nanoparticles. The purpose of this study was to evaluate the antibacterial activity of three dental cements modified by nanosilver. Three cements were used: Sealapex, RelyX ARC, and Vitrebond. The cements were incorporated with 0.05 mL of silver nanoparticles solution. Control groups were prepared without silver. Six Petri plates with BHI were inoculated with S. mutans using sterile swabs. Three cavities were made in each agar plate (total = 18) and filled with the manipulated cements. They were incubated at 37∘C for 48 h, and the inhibition halos were measured. The paired t-Test was used for statistical analysis (𝑃<0.05). No inhibition halos were obtained for Sealapex and Rely X, but Vitrebond showed bactericidal activity without silver and enhanced effect with silver incorporation.
Hepatitis C virus double‐stranded RNA is the predominant form in human liver and in interferon‐treated cells

Hepatitis C virus (HCV) is unique among RNA viruses in its ability to establish chronic infection in the majority of exposed adults. HCV persists in the liver despite interferon (IFN)‐stimulated gene (ISG) induction; robust induction actually predicts treatment failure and viral persistence. It is unclear which forms of HCV RNA are associated with ISG induction and IFN resistance during natural infections. To thoroughly delineate HCV RNA populations, we developed conditions that fully separate the strands of long double‐stranded RNA (dsRNA) and allow the released RNAs to be quantified in reverse transcription/polymerase chain reaction assays. These methods revealed that dsRNA, a pathogen‐associated molecular pattern (PAMP), comprised 52% (standard deviation, 28%) of the HCV RNA in the livers of patients with chronic infection. HCV dsRNA was proportionally higher in patients with the unfavorable IL28B TT (rs12979860) genotype. Higher ratios of HCV double‐stranded to single‐stranded RNA (ssRNA) correlated positively with ISG induction. In Huh‐7.5 cells, IFN treatment increased the total amount of HCV dsRNA through a process that required de novo viral RNA synthesis and shifted the ratio of viral dsRNA/ssRNA in favor of dsRNA. This shift was blocked by ribavirin (RBV), an antiviral drug that reduces relapse in HCV patients. Northern blotting established that HCV dsRNA contained genome‐length minus strands. Conclusion: HCV dsRNA is the predominant form in the HCV‐infected liver and has features of both a PAMP and a genomic reservoir. Interferon treatment increased rather than decreased HCV dsRNA. This unexpected finding suggests that HCV produces dsRNA in response to IFN, potentially to antagonize antiviral defenses. (Hepatology 2017;66:357–370).
New tubulin targeting agents currently in clinical development

Background: The first tubulin targeting agents were approved as cancer chemotherapeutics over 40 years ago and tubulin as an antitumor target continues to attract significant drug discovery and development attention. Mechanism of action as defined by tubulin binding sites and effect on microtubules distinguishes these agents, but the end result is equivalent in that microtubule disruption leads to cell cycle arrest at G2/M phase of the cell cycle and subsequent apoptotic cell death. Objectives: The goal of this review is to describe the state of clinical development of tubulin targeting agents as of early 2008, with descriptions of clinical experience slanted toward the most advanced trials for each agent. Method: Objective information in this review was obtained exclusively from public sources that included journals, scientific meeting abstracts, posters and oral presentations, websites and public presentations from companies. Opinions expressed in this review are exclusively from the author. Results/conclusions: A large number of tubulin targeting agents are currently in clinical development, including microtubule stabilizing and destabilizing compounds acting through all three of the characterized tubulin binding sites. With the approval of ixabepilone for refractory breast cancer, the epothilones appear best positioned to make an impact among the new microtubule stabilizing compounds. There are 17 microtubule destabilizing agents under clinical assessment, with many only in Phase I and results to date include at best modest efficacy signals with no obvious indication trend.