bluuebunny/crossref_metadata_2025_split huggingface dataset:
Predictors of antidepressant adherence: Results of a Japanese Internet‐based survey
Authors: Shigemura Jun , Ogawa Tetsuo , Yoshino Aihide , Sato Yutaka , Nomura Soichiro 
Published: February 2010

Aim:  The purpose of the present study was to identify the psychosocial/pharmacological predictors of antidepressant (AD) adherence.Methods:  An Internet‐based survey was conducted among 1151 Japanese individuals with major depressive disorder. Subjects were asked to report their degree of non‐adherence for each AD taken using a 5‐point Likert scale: 0, never forget; 1, rarely forget; 2, occasionally forget; 3, sometimes forget; and 4, often forget. The highest number reported among each subject was assigned as their low adherence index (LAI). Individuals with an LAI ≥ 3 were defined as members of the low adherence (LA) group. Predictors of LA was analyzed using bivariate and multivariate models, both among the total number of subjects and single AD subgroup (n = 657).Results:  Nearly one‐third of subjects (n = 381, 33.1%) reported LA. On bivariate analysis, LA was associated with lower age, worker or student status (vs unemployed or housewife), higher daily dosing frequency (DDF), low drug satisfaction, and a neutral/negative doctor–patient relationship (DPR; P < 0.001). In a multivariate model, LA was predicted by age (≤34 years: odds ratio [OR], 1.64), worker or student status (OR, 1.87), higher DDF (≥twice daily: OR, 1.61), and neutral/negative DPR (OR, 1.54; P < 0.01). Among the single‐AD subgroup, adherence was similar between those on selective serotonin reuptake inhibitors/serotonin‐noradrenaline reuptake inhibitors and tricyclics. Use of neither medication was associated with adherence in a multivariate model.Conclusion:  LA was predicted by lower age, worker or student status, higher DDF, and neutral/negative DPR. Adherence was not significantly different between subjects on newer agents and tricyclics.
RECLAIMING THE PATIENT'S VOICE AND SPIRIT IN DYING: AN INSIGHT FROM ISRAEL
Authors: SHALEV CARMEL 
Published: February 2010

ABSTRACTIn the latter half of the 20th century, Western medicine moved death from the home to the hospital. As a result, the process of dying seems to have lost its spiritual dimension, and become a matter of prolonging material life by means of medical technology. The novel quandaries that arose led in turn to medico‐legal regulation. This paper describes the recent regulation of dying in Israel under its Dying Patient Law, 2005. The Law recognizes advance directives in principle, but limits their effect and form through complex medico‐legal artifices. It reflects a culture that places high value on both scientific medicine and the sanctity of life as such, and illustrates a medical culture that pitches battle against death. At the same time, the Law constructs the will of the individual in a medico‐legal language that is alien to the lay person. The paper suggests an alternative approach to advance care planning that is patient‐centred and addresses the psycho‐social needs of the individual in terms of her relational autonomy. From this perspective, advance care planning becomes an opportunity to extract the patient from the medical context and allow her to speak about her approaching death with close ones in her own terms of reference. To this end, there is a need for facilitation of an intimate encounter where patients can speak about their concerns with their loved ones. The paper also presents a methodological approach of attentive listening, which can be applied across diverse cultures and circumstances.
END‐OF‐LIFE CARE IN THE 21st CENTURY: ADVANCE DIRECTIVES IN UNIVERSAL RIGHTS DISCOURSE
Authors: BEŠIREVIĆ VIOLETA 
Published: February 2010

ABSTRACTThis article explores universal normative bases that could help to shape a workable legal construct that would facilitate a global use of advance directives. Although I believe that advance directives are of universal character, my primary aim in approaching this issue is to remain realistic. I will make three claims. First, I will argue that the principles of autonomy, dignity and informed consent, embodied in the Oviedo Convention and the UNESCO Declaration on Bioethics and Human Rights, could arguably be regarded as universal bases for the global use of advance directives. Second, I will demonstrate that, despite the apparent consensus of ethical authorities in support of their global use, it is unlikely, for the time being, that such consensus could lead to unqualified legal recognition of advance directives, because of different understandings of the nature of the international rules, meanings of autonomy and dignity which are context‐specific and culture‐specific, and existing imperfections that make advance directives either unworkable or hardly applicable in practice. The third claim suggests that the fact that the concept of the advance directive is not universally shared does not mean that it should not become so, but never as the only option in managing incompetent patients. A way to proceed is to prioritize work on developing higher standards in managing incompetent patients and on progressing towards the realization of universal human rights in the sphere of bioethics, by advocating a universal, legally binding international convention that would outlaw human rights violations in end‐of‐life decision‐making.
Supporting parents: development of a tool to measure self‐efficacy of parents with learning disabilities
Authors: Bloomfield Linda , Kendall Sally , Fortuna Sandra 
Published: February 2010

Accessible summary

Many parents with learning disabilities have their children removed and put into care.
Parents with learning disabilities often need support to manage their children and to be good parents.
This article is about how we worked with parents to find a way of seeing whether the support given to them is helpful.
If parenting support is seen to be helpful, more funding may be available for future support.

SummaryThere has been a steady increase over the last 20 years in the number of parents with learning disabilities who are referred to social workers and community health practitioners. It is a common experience for parents with learning disabilities to have their child removed from the home and placed permanently in care, and although they are often judged as inadequate parents, it is known that they can be good enough parents when provided with parenting support. This article reports the development of a tool to measure the self‐efficacy of parents with learning disabilities, which will help to evaluate parenting initiatives specifically aimed at this parent group. A tool to measure parenting self‐efficacy (TOPSE) has been adapted to be accessible to parents with learning disabilities. Eighteen parents took part in the study to complete and comment on the tool with the help of a researcher from the community learning disabilities team. This tool, which consists of 45 self‐efficacy statements, now needs to be tested on a larger sample of parents with learning disabilities.
Re‐engineering Legal Opportunity Structures in the European Union? The Starting Line Group and the Politics of the Racial Equality Directive
Authors: EVANS CASE RHONDA , GIVENS TERRI E. 
Published: February 2010

AbstractUsing the Racial Equality Directive to test competing explanations concerning the types of actors who seek to liberalize legal opportunity structures, we find that it was pursued by a coalition of societal interests working through European Union institutions that sought reforms intended to facilitate strategic litigation.
Effect of l‐Dopa on metabotropic glutamate receptor 5 in the brain of parkinsonian monkeys
Authors: Ouattara Bazoumana , Gasparini Fabrizio , Morissette Marc , Grégoire Laurent , Samadi Pershia , Gomez‐Mancilla Baltazar , Di Paolo Thérèse 
Published: February 2010

J. Neurochem. (2010) 113, 715–724.AbstractBehavioral investigations of selective and potent metabotropic glutamate receptor type 5 (mGluR5) antagonists in animal models suggest involvement of mGluR5 in compensatory mechanisms of the basal ganglia circuitry in Parkinson’s disease and levodopa (l‐Dopa) induced motor complications. This study investigated mGluR5 changes in MPTP lesioned monkeys. The effect of a chronic 1 month treatment with l‐Dopa on mGluR5‐specific binding and mRNA levels was investigated in MPTP monkeys killed 4 or 24 h after their last l‐Dopa administration. [3H]ABP688 specific binding in the putamen was elevated in l‐Dopa‐treated MPTP monkeys killed 24 h but not 4 h after their last l‐Dopa dose compared with vehicle‐treated MPTP monkeys. Caudate nucleus [3H]ABP688‐specific binding was elevated in both groups of l‐Dopa treated compared with vehicle–treated MPTP monkeys. In contrast, caudate nucleus and putamen mGluR5 mRNA levels were elevated only in l‐Dopa‐treated MPTP monkeys killed 4 h after their last l‐Dopa administration. MPTP monkeys killed 4 h after their last l‐Dopa treatment showed higher caudate nucleus and putamen l‐Dopa concentrations compared with those killed after 24 h. Hence, mGluR5 in the putamen are sensitive to presence of l‐Dopa leading to a rapid decrease of [3H]ABP688‐specific binding possibly involving a direct mGluR5/dopamine receptors interaction.
Longterm quiescent cells in the aged human subventricular neurogenic system specifically express GFAP‐δ
Authors: Van Den Berge Simone A. , Middeldorp Jinte , Zhang C. Eleana , Curtis Maurice A. , Leonard Brian W. , Mastroeni Diego , Voorn Pieter , Van De Berg Wilma D. J. , Huitinga Inge , Hol Elly M. 
Published: January 2010

SummaryA main neurogenic niche in the adult human brain is the subventricular zone (SVZ). Recent data suggest that the progenitors that are born in the human SVZ migrate via the rostral migratory stream (RMS) towards the olfactory bulb (OB), similar to what has been observed in other mammals. A subpopulation of astrocytes in the SVZ specifically expresses an assembly‐compromised isoform of the intermediate filament protein glial fibrillary acidic protein (GFAP‐δ). To further define the phenotype of these GFAP‐δ expressing cells and to determine whether these cells are present throughout the human subventricular neurogenic system, we analysed SVZ, RMS and OB sections of 14 aged brain donors (ages 74‐93). GFAP‐δ was expressed in the SVZ along the ventricle, in the RMS and in the OB. The GFAP‐δ cells in the SVZ co‐expressed the neural stem cell (NSC) marker nestin and the cell proliferation markers proliferating cell nuclear antigen (PCNA) and Mcm2. Furthermore, BrdU retention was found in GFAP‐δ positive cells in the SVZ. In the RMS, GFAP‐δ was expressed in the glial net surrounding the neuroblasts. In the OB, GFAP‐δ positive cells co‐expressed PCNA. We also showed that GFAP‐δ cells are present in neurosphere cultures that were derived from SVZ precursors, isolated postmortem from four brain donors (ages 63‐91). Taken together, our findings show that GFAP‐δ is expressed in an astrocytic subpopulation in the SVZ, the RMS and the OB. Importantly, we provide the first evidence that GFAP‐δ is specifically expressed in longterm quiescent cells in the human SVZ, which are reminiscent of NSCs.
Short‐term calorie restriction reverses vascular endothelial dysfunction in old mice by increasing nitric oxide and reducing oxidative stress
Authors: Rippe Catarina , Lesniewski Lisa , Connell Melanie , LaRocca Thomas , Donato Anthony , Seals Douglas 
Published: January 2010

SummaryTo determine if short‐term calorie restriction reverses vascular endothelial dysfunction in old mice, old (O, n = 30) and young (Y, n = 10) male B6D2F1 mice were fed ad libitum (AL) or calorie restricted (CR, approximately 30%) for 8 weeks. Ex vivo carotid artery endothelium‐dependent dilation (EDD) was impaired in old ad libitum (OAL) vs. young ad libitum (YAL) (74 ± 5 vs. 95 ± 2% of maximum dilation, P < 0.05), whereas old calorie‐restricted (OCR) and YCR did not differ (96 ± 1 vs. 94 ± 3%). Impaired EDD in OAL was mediated by reduced nitric oxide (NO) bioavailability associated with decreased endothelial NO synthase expression (aorta) (P < 0.05), both of which were restored in OCR. Nitrotyrosine, a cellular marker of oxidant modification, was markedly elevated in OAL (P < 0.05), whereas OCR was similar to Y. Aortic superoxide production was 150% greater in OAL vs. YAL (P < 0.05), but normalized in OCR, and TEMPOL, a superoxide dismutase (SOD) mimetic that restored EDD in OAL (to 97 ± 2%), had no effect in Y or OCR. OAL had increased expression and activity of the oxidant enzyme, NADPH oxidase, and its inhibition (apocynin) improved EDD, whereas NADPH oxidase in OCR was similar to Y. Manganese SOD activity and sirtuin1 expression were reduced in OAL (P < 0.05), but restored to Y in OCR. Inflammatory cytokines were greater in OAL vs. YAL (P < 0.05), but unaffected by CR. Carotid artery endothelium‐independent dilation did not differ among groups. Short‐term CR initiated in old age reverses age‐associated vascular endothelial dysfunction by restoring NO bioavailability, reducing oxidative stress (via reduced NADPH oxidase–mediated superoxide production and stimulation of anti‐oxidant enzyme activity), and upregulation of sirtuin‐1.
Long‐Term Outcome Following Successful Catheter Ablation of Atrial Tachycardia Originating From the Pulmonary Veins: Absence of Late Atrial Fibrillation
Authors: TEH ANDREW W. , KALMAN JONATHAN M. , MEDI CAROLINE , ROSSO RAPHAEL , BALASUBRAMANIAM RICHARD , LEE GEOFFREY , HALLORAN KAREN , SPARKS PAUL B. , MORTON JOSEPH B. , VOHRA JITENDRA K. , KISTLER PETER M. 
Published: February 2010

Atrial Fibrillation and Pulmonary Vein Tachycardia. Objectives: This study aimed to characterize the long‐term outcome and incidence of atrial fibrillation (AF) in patients following catheter ablation of focal atrial tachycardia (AT) from the pulmonary veins (PV).
Background:
Although both AT and AF may originate from ectopic foci within PVs, it is unknown whether PV AT patients subsequently develop AF.
Methods:
Twenty‐eight patients with 29 PV ATs (14%) from a consecutive series of 194 patients who underwent RFA for focal AT were included. Patients with concomitant AF prior to the index procedure were excluded.
Results:
The minimum follow‐up duration was 4 years; mean age 38 ± 18 years with symptoms for 6.5 ± 10 years, having tried 1.5 ± 0.9 antiarrhythmic drugs. The distribution of foci was: left superior 12 (41%), right superior 10 (34%), left inferior 5 (17%), and right inferior 2 (7%). The focus was ostial in 93% and 2–4 cm distally within the vein in 7%. Mean tachycardia cycle length was 364 ± 90 ms. Focal ablation was performed in 25 of 28 patients. There were 6 recurrences with 5 from the original site. Twenty‐six patients were available for long‐term clinical follow‐up. At a mean of 7.2 ± 2.1 years, 25 of 26 (96%) were free from recurrence off antiarrhythmic drugs. No patients developed AF.
Conclusions:
Focal ablation for tachycardia originating from the PVs is associated with long‐term freedom from both AT and AF. Therefore, although PV AT and PV AF share a common anatomic distribution, PV AT is a distinct clinical entity successfully treated with focal RFA and not associated with AF in the long term. (J Cardiovasc Electrophysiol, Vol. pp. 747‐750, July 2010)
Epigenetics in atherosclerosis and inflammation
Authors: Wierda Rutger J. , Geutskens Sacha B. , Jukema J. Wouter , Quax Paul H.A. , van den Elsen Peter J. 
Published: January 2010

Abstract
Introduction
Epigenetics explained
Atherosclerosis
Epigenetics and association with atherosclerosis
Epigenetic regulation of cell activity
Chemokines, their receptors and other genes involved in inflammation
Epigenetics in (vascular) inflammation
MicroRNAs
Conclusions
Atherosclerosis is a multifactorial disease with a severe burden on western society. Recent insights into the pathogenesis of atherosclerosis underscore the importance of chronic inflammation in both the initiation and progression of vascular remodelling. Expression of immunoregulatory molecules by vascular wall components within the atherosclerotic lesions is accordingly thought to contribute to the ongoing inflammatory process. Besides gene regulatory proteins (transcription factors), epigenetic mechanisms also play an essential and fundamental role in the transcriptional control of gene expression. These epigenetic mechanisms change the accessibility of chromatin by DNA methylation and histone modifications. Epigenetic modulators are thus critically involved in the regulation of vascular, immune and tissue‐specific gene expression within the atherosclerotic lesion. Importantly, epigenetic processes are reversible and may provide an excellent therapeutic target. The concept of epigenetic regulation is gradually being recognized as an important factor in the pathogenesis of atherosclerosis. Recent research provides an essential link between inflammation and reprogramming of the epigenome. In this review we therefore discuss the basis of epigenetic regulation – and the contribution thereof in the regulation of inflammatory processes in general and during atherosclerosis in particular. Moreover we highlight potential therapeutic interventions based on epigenetic mechanisms.
Interstitial cells of Cajal, macrophages and mast cells in the gut musculature: morphology, distribution, spatial and possible functional interactions
Authors: Mikkelsen Hanne B. 
Published: January 2010

Abstract

Introduction
Identification of the cells
Cell distribution
Inflammation
Diabetes mellitus
Conclusions

Interstitial cells of Cajal (ICC) are recognized as pacemaker cells for gastrointestinal movement and are suggested to be mediators of neuromuscular transmission. Intestinal motility disturbances are often associated with a reduced number of ICC and/or ultrastructural damage, sometimes associated with immune cells. Macrophages and mast cells in the intestinal muscularis externa of rodents can be found in close spatial contact with ICC. Macrophages are a constant and regularly distributed cell population in the serosa and at the level of Auerbach’s plexus (AP). In human colon, ICC are in close contact with macrophages at the level of AP, suggesting functional interaction. It has therefore been proposed that ICC and macrophages interact. Macrophages and mast cells are considered to play important roles in the innate immune defence by producing pro‐inflammatory mediators during classical activation, which may in itself result in damage to the tissue. They also take part in alternative activation which is associated with anti‐inflammatory mediators, tissue remodelling and homeostasis, cancer, helminth infections and immunophenotype switch. ICC become damaged under various circumstances – surgical resection, possibly post‐operative ileus in rodents – where innate activation takes place, and in helminth infections – where alternative activation takes place. During alternative activation the muscularis macrophage can switch phenotype resulting in up‐regulation of F4/80 and the mannose receptor. In more chronic conditions such as Crohn’s disease and achalasia, ICC and mast cells develop close spatial contacts and piecemeal degranulation is possibly triggered.
Mechanisms in the loss of capillaries in systemic sclerosis: angiogenesis versus vasculogenesis
Authors: Manetti Mirko , Guiducci Serena , Ibba‐Manneschi Lidia , Matucci‐Cerinic Marco 
Published: January 2010

Abstract
Introduction
Mechanisms and biomarkers of endothelial damage in SSc
Mechanisms of defective angiogenesis in SSc
Mechanisms of defective vasculogenesis in SSc
Conclusions and perspectives on vascular treatment strategies
Systemic sclerosis (SSc, scleroderma) is a chronic, multisystem connective tissue disorder affecting the skin and various internal organs. Although the disease is characterized by a triad of widespread microangiopathy, fibrosis and autoimmunity, increasing evidence indicates that vascular damage is a primary event in the pathogenesis of SSc. The progressive vascular injury includes persistent endothelial cell activation/damage and apoptosis, intimal thickening, delamination, vessel narrowing and obliteration. These profound vascular changes lead to vascular tone dysfunction and reduced capillary blood flow, with consequent tissue ischemia and severe clinical manifestations, such as digital ulceration or amputation, pulmonary arterial hypertension and scleroderma renal crisis. The resulting tissue hypoxia induces complex cellular and molecular mechanisms in the attempt to recover endothelial cell function and tissue perfusion. Nevertheless, in SSc patients there is no evidence of significant angiogenesis and the disease evolves towards chronic tissue ischemia, with progressive and irreversible structural changes in multiple vascular beds culminating in the loss of capillaries. A severe imbalance between pro‐angiogenic and angiostatic factors may also lead to impaired angiogenic response during SSc. Besides insufficient angiogenesis, defective vasculogenesis with altered numbers and functional defects of bone marrow‐derived endothelial progenitor cells may contribute to the vascular pathogenesis of SSc. The purpose of this article is to review the contribution of recent studies to the understanding of the complex mechanisms of impaired vascular repair in SSc. Indeed, understanding the pathophysiology of SSc‐associated vascular disease may be the key in dissecting the disease pathogenesis and developing novel therapies. Either angiogenic or vasculogenic mechanisms may potentially become in the future the target of therapeutic strategies to promote capillary regeneration in SSc.
Sub‐lethal heat shock induces plasma membrane translocation of 70‐kDa heat shock protein in viable, but not in apoptotic, U‐937 leukaemia cells
Authors: LASUNSKAIA ELENA B. , FRIDLIANSKAIA IRINA , ARNHOLDT ANDREA V. , KANASHIRO MILTON , GUZHOVA IRINA , MARGULIS BORIS 
Published: February 2010

Lasunskaia EB, Fridlianskaia I, Arnholdt AV, Kanashiro M, Guzhova I, Margulis B. Sub‐lethal heat shock induces plasma membrane translocation of 70‐kDa heat shock protein in viable, but not in apoptotic, U‐937 leukaemia cells. APMIS 2010; 118: 179–87.Heat shock protein 70 kDa, Hsp70, is an important intracellular factor that protects cells from stress. Unusual plasma membrane expression of Hsp70, observed in some cancer cells, contributes to the cell’s recognition and elimination by the immune system. Induction of apoptosis in cancer cells was demonstrated to increase Hsp70 translocation to the surface membrane, enhancing immunogenic effects through the stimulation of dendritic cells. As hyperthermia is proposed as a method of choice for anti‐cancer therapy, we examined whether apoptosis induction by heat shock enhances Hsp70 membrane translocation in U‐937 leukaemia cells. Cells were exposed to sub‐lethal heat shock, and intracellular and membrane‐bound Hsp70 expression was evaluated in apoptotic and viable cell sub‐populations, employing flow cytometry and immunofluorescence. Heat shock induced Hsp70 membrane translocation in the viable cells that were able to enhance Hsp70 production upon heating, but not in the cells undergoing apoptosis that continued to express low basal levels of the intracellular protein. Data suggest that the protein translocation was associated with the increasing Hsp70 content rather than the apoptotic process. Apoptosis does not contribute to externalization of Hsp70, at least in the cells with low levels of this protein.