Miracle-dz/UniFAR-FTUs huggingface dataset:
Benchmarking Treatment Adherence and Therapist Competence in Individual Cognitive-Behavioral Treatment for Youth Anxiety Disorders

Evidence-based treatments (EBTs) for youth are typically developed and established through studies in research settings designed to ensure treatment integrity, that is, protocol adherence and competence by therapists. An important question for implementation science is how well integrity is maintained when these EBTs are delivered in community settings. The present study investigated whether the integrity achieved by therapists in community settings achieved a benchmark set by therapists in a research setting when they delivered the same EBT—an individual cognitive-behavioral treatment (ICBT) for youth anxiety. Therapists (N = 29; 68.97% White; 13.79% male) provided ICBT to 68 youths (M age = 10.60 years, SD = 2.03; 82.35% White; 52.94% male) diagnosed with a principal anxiety disorder in research or community settings. Training and supervision protocols were the same across settings. Two independent teams of trained coders rated 744 sessions using observational instruments designed to assess ICBT adherence and competence. Both adherence and competence were higher in the research setting. Group differences in competence were consistent across treatment, but differences in adherence were most pronounced when treatment shifted to exposure, widely viewed as the most critical component of ICBT. When using the benchmarks from the research setting, therapists from the community settings fell short for indices of adherence and competence. However, given differences between therapists and clients, as well as the fact that treatment outcomes were similar across settings, our findings raise questions about whether it is appropriate to use treatment integrity benchmarks from research settings for community.
The Development of Mood Repair Response Repertories: I. Age-Related Changes Among 7- to 14-Year-Old Depressed and Control Children and Adolescents

The purpose of this study was to test developmentally informed hypotheses about regulatory responses to sadness that attenuate versus exacerbate it (adaptive versus maladaptive mood repair responses, respectively) across late childhood, early adolescence, and mid-adolescence. In a multi-site study in Hungary, clinic-based, 7- to 14-year-olds with Diagnostic and Statistical Manual of Mental Disorders’ (4th ed., text rev.) depressive disorders (N = 697; 55% male) and age/sex matched (at 1:2) nondepressed, school-based controls (N = 1,394) reported on their usual responses to sadness/dysphoria; parental reports were obtained separately. Adaptive and maladaptive response repertoire scores were compared across ages within and across subject groups, and by informant, controlling for confounds. Contrary to Hypothesis 1, older (vs. younger) youths in both groups reported fewer adaptive regulatory responses. Maladaptive response repertoires were unrelated to age among controls but significantly increased with age among depressed youths, particularly the girls. Partially supporting Hypothesis 2, subject groups differed in age-related trajectories of mood repair repertories, but not as expected (e.g., younger depressed children reported larger adaptive response repertoires than did controls). Parental reports revealed no developmental changes in offspring’s mood repair repertories. Parent-offspring reports were most discordant for younger (vs. older) offspring, tended to converge around age 11, and were consistently and significantly larger in the depressed sample. Self-reported adaptive mood repair repertories appear to have been laid down by late childhood and then undergo “trimming” across ages 7–14 years. The extensive maladaptive mood repair response repertoires of depressed youths, which increased with age, distinguish them primarily from controls. Therefore, reducing maladaptive regulatory responses to sadness should be a priority when treating depressed youths.
Liver‐specific deletion of prohibitin 1 results in spontaneous liver injury, fibrosis, and hepatocellular carcinoma in mice

Prohibitin 1 (PHB1) is a highly conserved, ubiquitously expressed protein that participates in diverse processes including mitochondrial chaperone, growth and apoptosis. The role of PHB1 in vivo is unclear and whether it is a tumor suppressor is controversial. Mice lacking methionine adenosyltransferase 1A (MAT1A) have reduced PHB1 expression, impaired mitochondrial function, and spontaneously develop hepatocellular carcinoma (HCC). To see if reduced PHB1 expression contributes to the Mat1a knockout (KO) phenotype, we generated liver‐specific Phb1 KO mice. Expression was determined at the messenger RNA and protein levels. PHB1 expression in cells was varied by small interfering RNA or overexpression. At 3 weeks, KO mice exhibit biochemical and histologic liver injury. Immunohistochemistry revealed apoptosis, proliferation, oxidative stress, fibrosis, bile duct epithelial metaplasia, hepatocyte dysplasia, and increased staining for stem cell and preneoplastic markers. Mitochondria are swollen and many have no discernible cristae. Differential gene expression revealed that genes associated with proliferation, malignant transformation, and liver fibrosis are highly up‐regulated. From 20 weeks on, KO mice have multiple liver nodules and from 35 to 46 weeks, 38% have multifocal HCC. PHB1 protein levels were higher in normal human hepatocytes compared to human HCC cell lines Huh‐7 and HepG2. Knockdown of PHB1 in murine nontransformed AML12 cells (normal mouse hepatocyte cell line) raised cyclin D1 expression, increased E2F transcription factor binding to cyclin D1 promoter, and proliferation. The opposite occurred with PHB1 overexpression. Knockdown or overexpression of PHB1 in Huh‐7 cells did not affect proliferation significantly or sensitize cells to sorafenib‐induced apoptosis. Conclusion: Hepatocyte‐specific PHB1 deficiency results in marked liver injury, oxidative stress, and fibrosis with development of HCC by 8 months. These results support PHB1 as a tumor suppressor in hepatocytes. (HEPATOLOGY 2010.)
Gastrointestinal Side Effects Associated With Clindamycin: 1,000 Consecutive Patients

The incidence and parameters associated with diarrhea related to clindamycin usage were studied in a population of both inpatients and outpatients. Diarrhea occurred in 66 (6.6%) of the 1,000 patients. In three of them, substantial morbidity was associated with the diarrhea. Of the multiple parameters that were evaluated, a significant association with diarrhea was found only for age (patients over the age of 20 years) (P .05). (Arch Intern Med136:876-879, 1976)
Digital clubbing in association with hepatopulmonary syndrome

A 49-year-old woman with known alcohol related liver disease (Model for End-Stage Liver Disease score of 6) was referred to our center for consideration for liver transplantation (LT). She had successfully undergone variceal band ligation 5 years previously following her index bleed. Past medical history was unremarkable but she was smoking two cigarettes per day with a past history of 30 pack-years. On examination, she was noted to have digital clubbing (Fig. 1), peripheral cyanosis, and spider nevi. Clinical examination was unremarkable. Arterial blood gas analysis on room air demonstrated type 1 respiratory failure (partial pressure of oxygen in arterial blood [PaO2] 1⁄4 7.44 kPa, PaCO2 1⁄4 4.34 kPa) with an increased alveolar-arterial gradient (P[A-a]O2) of 7.1 kPa (normal range 1⁄4 2-3 kPa). Orthodeoxia was also evident (supine PaO2 1⁄4 7.44 kPa; standing PaO2 1⁄4 6.18 kPa). A chest radiograph was normal. Pulmonary function tests (PFTs) demonstrated a mild obstructive pattern (1-second forced exFig. 1. Digital clubbing.
E‐cadherin antagonizes transforming growth factor β1 gene induction in hepatic stellate cells by inhibiting RhoA–dependent Smad3 phosphorylation

Cadherins mediate cell‐cell adhesion and catenin (ctn)‐related signaling pathways. Liver fibrosis is accompanied by the loss of E‐cadherin (ECAD), which promotes the process of epithelial‐mesenchymal transition. Currently, no information is available about the inhibitory role of ECAD in hepatic stellate cell activation. Because of ECAD's potential for inhibiting the induction of transforming growth factor β1 (TGFβ1), we investigated whether ECAD overexpression prevents TGFβ1 gene induction; we also examined what the molecular basis could be. Forced expression of ECAD decreased α‐smooth muscle actin and vimentin levels and caused decreases in the constitutive and inducible expression of the TGFβ1 gene and its downstream genes. ECAD overexpression decreased Smad3 phosphorylation, weakly decreased Smad2 phosphorylation, and thus inhibited Smad reporter activity induced by either treatment with TGFβ1 or Smad3 overexpression. Overexpression of a dominant negative mutant of ras homolog gene family A (RhoA) diminished the ability of TGFβ1 to elicit its own gene induction. Consistently, transfection with a constitutively active mutant of RhoA reversed the inhibition of TGFβ1‐inducible or Smad3‐inducible reporter activity by ECAD. Studies using the mutant constructs of ECAD revealed that the p120‐ctn binding domain of ECAD was responsible for TGFβ1 repression. Consistently, ECAD was capable of binding p120‐ctn, which recruited RhoA; this prevented TGFβ1 from increasing RhoA‐mediated Smad3 phosphorylation. In the liver samples of patients with mild or severe fibrosis, ECAD expression reciprocally correlated with the severity of fibrosis. Conclusion: Our results demonstrate that ECAD inhibits Smad3/2 phosphorylation by recruiting RhoA to p120‐ctn at the p120‐ctn binding domain, whereas the loss of ECAD due to cadherin switching promotes the up‐regulation of TGFβ1 and its target genes, and facilitates liver fibrosis. (HEPATOLOGY 2010.)
Treatment of children with chronic hepatitis B virus infection in the United States: Patient selection and therapeutic options

Chronic hepatitis B virus (HBV) infection in children presents a therapeutic challenge for the practitioner. Decisions regarding selection of patients who may benefit from treatment, appropriate timing of treatment, and the choice of antiviral therapy are complex and are compounded by the limited number of drugs that have been studied in children. An expert panel of nationally recognized pediatric liver specialists was convened by the Hepatitis B Foundation on August 11, 2009, to consider clinical practice relative to the therapeutic options available for children. A detailed account of these discussions is provided, and the opinions expressed are based on consensus of the experts, as well as on published evidence when available. The panel concludes that, at this time, there is no established benefit of treatment of children in the immune tolerant phase, and there is a very high risk of development of drug resistance. In addition, there is no indication for treatment of children in the inactive carrier state. For children in the immune active or reactivation phases, liver histology can help guide treatment decisions, and family history of liver disease, especially hepatocellular carcinoma, may argue for early treatment in some cases. Outside of clinical trials, interferon is the agent of choice in most cases. Nucleos(t)ide analogues are secondary therapies, and children who receive these agents require careful monitoring for development of resistance. There are a few situations when treatment is indicated regardless of HBV DNA or alanine aminotransferase levels. There is still much to be elucidated about the appropriate use of HBV therapy in children. Until more clinical data and therapeutic options are available, a conservative approach is warranted. (HEPATOLOGY 2010.)
Erectile dysfunction and coronary artery disease prediction: evidence‐based guidance and consensus

• A significant proportion of men with erectile dysfunction (ED) exhibit early signs of coronary artery disease (CAD), and this group may develop more severe CAD than men without ED (Level 1, Grade A). • The time interval among the onset of ED symptoms and the occurrence of CAD symptoms and cardiovascular events is estimated at 2–3 years and 3–5 years respectively; this interval allows for risk factor reduction (Level 2, Grade B). • ED is associated with increased all‐cause mortality primarily due to increased cardiovascular mortality (Level 1, Grade A). • All men with ED should undergo a thorough medical assessment, including testosterone, fasting lipids, fasting glucose and blood pressure measurement. Following assessment, patients should be stratified according to the risk of future cardiovascular events. Those at high risk of cardiovascular disease should be evaluated by stress testing with selective use of computed tomography (CT) or coronary angiography (Level 1, Grade A). • Improvement in cardiovascular risk factors such as weight loss and increased physical activity has been reported to improve erectile function (Level 1, Grade A). • In men with ED, hypertension, diabetes and hyperlipidaemia should be treated aggressively, bearing in mind the potential side effects (Level 1, Grade A). • Management of ED is secondary to stabilising cardiovascular function, and controlling cardiovascular symptoms and exercise tolerance should be established prior to initiation of ED therapy (Level 1, Grade A). • Clinical evidence supports the use of phosphodiesterase 5 (PDE5) inhibitors as first‐line therapy in men with CAD and comorbid ED and those with diabetes and ED (Level 1, Grade A). • Total testosterone and selectively free testosterone levels should be measured in all men with ED in accordance with contemporary guidelines and particularly in those who fail to respond to PDE5 inhibitors or have a chronic illness associated with low testosterone (Level 1, Grade A). • Testosterone replacement therapy may lead to symptomatic improvement (improved wellbeing) and enhance the effectiveness of PDE5 inhibitors (Level 1, Grade A). • Review of cardiovascular status and response to ED therapy should be performed at regular intervals (Level 1, Grade A).
Mechanisms of action of LCPUFA effects on infant growth and neurodevelopment: perinatal biochemistry and physiology of LCPUFA discussion

Dr Pat Levitt: Was there some correlation between levels of DHA and visual acuity when the differences in DHA in human milk were rather modest? Dr Sheila Innis: There was a significant difference in visual acuity between infants in the highest tertile of DHA, who received milk with a mean of 0.31% DHA, and infants in the lowest tertile of DHA, who received milk with 0.17% DHA. There was no difference between infants in the lowest or highest tertile and infants in the middle tertile, who received milk with 0.22% DHA. So, differences were not present in the functional test when differences in DHA were small.
Congenital eye diseases in Abuja, Nigeria

Aim: To look at the incidence of congenital eye disease in Rachel Eye Center, Abuja, in the hope that some of the more common problems may be highlighted and strategies for a more effective service may evolve. Materials and Methods: The case notes of all new patients aged one year or less who presented at the Rachel Eye Center, Abuja, where between 150-250 new cases are seen every month, over a ten-year period (1990 and 2000) were reviewed. Results: One hundred and thirty seven patients with a definitive diagnosis were selected for the study, of which 30.5% had congenital eye disease. The commonest causes were nasolacrimal duct obstruction (12.4%), cataract with or without microphthalmos (5.1%), strabismus (2.9%), and buphthalmos (2.9%). Conclusion: Further research is needed to determine what proportion of congenital cataracts is associated with rubella in Nigeria, even though the association is well established elsewhere, so that the MMR (measles, mumps, and rubella) vaccine may be included in the Expanded Programme on Immunization, if it is found to be a problem of public health significance. There is also a need to strengthen the institution of social welfare in the country so that those born incurably blind can be better assisted. Key words: congenital blindness, cataract, rubella, mumps, measles Nigerian Journal of Ophthalmology Vol 12(2) 2004: 46-49
Problems with complaint handling: expectations and outcomes

Purpose – The purpose of this paper is to contribute to the current debate about problems with the NHS complaints system.Design/methodology/approach – The paper examines, in light of a recent audit of NHS complaint handling by the Healthcare Commission, the underlying reasons for complaints and for dissatisfaction with the way a complaint is handled. It discusses the implications of various recommendations and research findings for enhancing and improving complaints handling.Findings – More emphasis is needed on the quality of interpersonal interaction with complainants for successful resolution of complaints. Attending to the process alone will not reduce dissatisfaction among complainants.Practical implications – Learning from complaints to improve services is important to complainants as well as to healthcare providers and communicating this should be an integral part of the process.Originality/value – The value of the paper is that it re‐emphasises the important role that complaints can play in the co.
Effect of sorafenib on murine liver regeneration

Hepatocellular carcinoma (HCC) is a common cause of cancer‐related death. Sorafenib prolongs survival of patients with advanced disease and is approved for the systemic treatment of unresectable HCC. It possesses antiangiogenic and antiproliferative properties by way of inhibition of the receptor tyrosine kinases vascular endothelial growth factor receptor 2 (VEGFR‐2) and platelet‐derived growth factor receptor‐beta 1/2 (PDGFR‐β) and the kinase RAF. Sorafenib represents a candidate compound for adjuvant therapy in HCC patients. The aim of our study was to investigate whether sorafenib affects liver regeneration. C57BL6 mice received sorafenib orally at 30 mg/kg/day or its vehicle either for 14 days until the day before hepatectomy or starting the day after surgery or both. Animals were sacrificed 24, 72, and 120 hours after hepatectomy. Liver regeneration was calculated as a percent of initial liver weight. Bromodeoxyuridine (BrdU) incorporation and phospho‐extracellular signal‐regulated kinase (pERK1/2) were determined by immunohistochemistry on liver sections. VEGF‐A, PDGF‐BB, and hepatocyte growth factor (HGF) levels were measured in liver tissue homogenates. Histological analysis of scar tissue was performed. Treatment stopped 1 day before surgery had no impact on liver regeneration. Continuous sorafenib treatment and treatment started 1 day after surgery had statistically significant effects on liver regeneration at 120 hours compared to vehicle‐treated control animals (72% ± 12 versus control 88% ± 15 and 70% ± 13 versus control 86% ± 5 at 120 hours, both P ≤ 0.02). BrdU incorporation showed decreased numbers of positive nuclei in both groups receiving sorafenib after surgery. Phospho‐ERK levels were reduced in sorafenib‐treated animals. An increase of VEGF‐A levels was observed in mice receiving sorafenib. Wound‐healing complications were observed in animals receiving sorafenib after surgery and confirmed on histological sections. Conclusion: This preclinical study shows that sorafenib did not impact on liver regeneration when ceased before surgery; however, administration after hepatectomy affected late liver regeneration. (HEPATOLOGY 2011;53:577‐586)
Why are antenatal HIV testing policies in London failing

The prevalence of human immunodeficiency virus (HIV) infection in women who have had live births has increased since 1988, particularly in London (Unlinked Anonymous HIV Surveys Steering Group, 1995). In 1994,1 in every 580 women delivering in London was infected with HIV and in some London maternity units this figure was as high as 1 in every 200 women. As HIV infection can be transmitted from mother to child during pregnancy, labour or breastfeeding (vertical transmission), this rising prevalence has particular relevance to the care of these women during pregnancy, labour and the puerperium.
The use of whole organ decellularization for the generation of a vascularized liver organoid

A major roadblock to successful organ bioengineering is the need for a functional vascular network within the engineered tissue. Here, we describe the fabrication of three‐dimensional, naturally derived scaffolds with an intact vascular tree. Livers from different species were perfused with detergent to selectively remove the cellular components of the tissue while preserving the extracellular matrix components and the intact vascular network. The decellularized vascular network was able to withstand fluid flow that entered through a central inlet vessel, branched into an extensive capillary bed, and coalesced into a single outlet vessel. The vascular network was used to reseed the scaffolds with human fetal liver and endothelial cells. These cells engrafted in their putative native locations within the decellularized organ and displayed typical endothelial, hepatic, and biliary epithelial markers, thus creating a liver‐like tissue in vitro. Conclusion: These results represent a significant advancement in the bioengineering of whole organs. This technology may provide the necessary tools to produce the first fully functional bioengineered livers for organ transplantation and drug discovery. (HEPATOLOGY 2011;53:604‐617)
Do Community and Caregiver Factors Influence Hospice Use at the End of Life Among Older Adults With Alzheimer Disease?

Hospice is an underused service among people with Alzheimer disease. This study used the Hospice Use Model to examine community, care recipient, and caregiver characteristics associated with hospice use before death among 145 community-dwelling care recipients with Alzheimer disease and their caregivers. Secondary analysis using logistic regression modeling indicated that older age, male gender, black race, and better functional health of care recipients with Alzheimer disease were associated with a decreased likelihood of using hospice (model &khgr;25 = 23.5, P = .0003). Moreover, care recipients recruited from an Alzheimer clinic were more likely to use hospice than those recruited from adult day-care centers. Caregiver factors were not independent predictors of hospice use. However, there was a significant interaction between hours of care provided each week and recruitment site. Among care recipients from the Alzheimer clinic, the probability of hospice use increased as caregiving intensity increased. This relationship was reversed in care recipients from day-care centers. Results suggest that adult day-care centers need to partner with hospice programs in the community. In conclusion, care recipient and community service factors influence hospice use in individuals with Alzheimer disease.