bluuebunny/crossref_metadata_2025_split huggingface dataset:
ETHICAL ISSUES IN FORENSIC PSYCHIATRIC RESEARCH ON MENTALLY DISORDERED OFFENDERS
Authors: MUNTHE CHRISTIAN , RADOVIC SUSANNA , ANCKARSÄTER HENRIK 
Published: December 2009

ABSTRACTThis paper analyses ethical issues in forensic psychiatric research on mentally disordered offenders, especially those detained in the psychiatric treatment system. The idea of a ‘dual role’ dilemma afflicting forensic psychiatry is more complicated than acknowledged. Our suggestion acknowledges the good of criminal law and crime prevention as a part that should be balanced against familiar research ethical considerations. Research aiming at improvements of criminal justice and treatment is a societal priority, and the total benefit of studies has to be balanced against the risks for research subjects inferred by almost all systematic studies. Direct substantial risks must be balanced by health benefits, and normal informed consent requirements apply. When direct risks are slight, as in register‐based epidemiology, lack of consent may be counter‐balanced by special measures to protect integrity and the general benefit of better understanding of susceptibility, treatment and prevention. Special requirements on consent procedures in the forensic psychiatric context are suggested, and the issue of the relation between decision competence and legal accountability is found to be in need of further study. The major ethical hazard in forensic psychiatric research connects to the role of researchers as assessors and consultants in a society entertaining strong prejudices against mentally disordered offenders.
AGAINST RISK‐BENEFIT REVIEW OF PRISONER RESEARCH
Authors: CHWANG ERIC 
Published: December 2009

ABSTRACTThe 2006 Institute of Medicine (IOM) report, ‘Ethical Considerations for Research Involving Prisoners’, recommended five main changes to current US Common Rule regulations on prisoner research. Their third recommendation was to shift from a category‐based to a risk‐benefit approach to research review, similar to current guidelines on pediatric research. However, prisoners are not children, so risk‐benefit constraints on prisoner research must be justified in a different way from those on pediatric research. In this paper I argue that additional risk‐benefit constraints on prisoner research are unnecessary: the current Common Rule regulations, omitting category‐based restrictions but conjoined with the IOM report's other four main recommendations, ensure that prisoner research is as ethical as non‐prisoner research is. I explain why four problems which which may be more prevalent in prisons and which risk‐benefit constraints may seem to address – coercion, undue inducements, exploitation, and protection from harm – are in fact not solved by adding further risk‐benefit constraints on prisoner research.
PRISONER RESEARCH – LOOKING BACK OR LOOKING FORWARD?
Authors: THOMAS DAVID L. 
Published: December 2009

ABSTRACTMuch has been written about prisoner research and the controversies surrounding prisoners as human subjects. The Institute of Medicine recently released a report addressing some of these issues. This report, which generated further controversy, needs to be fully discussed in the literature and certain aspects are examined in this work. Further, in the body of literature there has been little acknowledgement of the concept of the right of prisoners to be involved in research. This needs to be pursued from an ethical perspective and eventually a legal one. This paper explores that concept and documents some facilities in which a prisoner's right to research has occurred.
C‐reactive protein and leucocyte activation in psoriasis vulgaris according to severity and therapy
Authors: Coimbra S , Oliveira H , Reis F , Belo L , Rocha S , Quintanilha A , Figueiredo A , Teixeira F , Castro E , Rocha‐Pereira P , Santos‐Silva A 
Published: December 2009

AbstractBackground  Psoriasis vulgaris is a chronic recurrent inflammatory skin disease and psoriatic lesions have shown leucocyte infiltration.Objectives  We aimed to study C‐reactive protein (CRP) and leucocyte activation markers/inhibitors as potential monitors of psoriasis vulgaris.Methods  A cross‐sectional (n = 73) and a longitudinal study (before, at 3, 6 and 12 weeks of therapy; n = 47) was performed; 10 patients started topical treatment, 17 narrow‐band ultraviolet light B (NBUVB) and 20 psolaren associated to UVA (PUVA); psoriasis severity was defined by Psoriasis Area and Severity Index (PASI).Results  Compared with control (n = 38), we found higher CRP levels, total leukocyte/neutrophil count, elastase, lactoferrin and α1‐antitrypsin. Increasing PASI was linked to increasing CRP and a trend to higher elastase and lactoferrin, suggesting that worsening enhances inflammatory response with neutrophil activation. CRP correlated with PASI, total leucocytes, neutrophils, elastase, lactoferrin and α1‐antitrypsin. NBUVB and PUVA presented similar effects.Conclusion  We propose CRP as a useful marker of psoriasis severity that could be used to monitor psoriasis and its treatment, and, together with PASI and elastase, could also be used as a global index of severity.
Candida balanitis: risk factors
Authors: Lisboa C , Santos A , Dias C , Azevedo F , Pina‐Vaz C , Rodrigues A 
Published: December 2009

AbstractBackground  The amount of available information on the prevalence and incidence of candida balanitis is still surprisingly scarce.Objectives  To determine the prevalence of candida colonization and candida balanitis in men attending a Sexually Transmitted Diseases (STD) clinic. To identify risk factors associated with candida balanitis.Methods  During a 36‐month period, a cross‐sectional study was carried out on consecutive men attendees of the STD clinic in Hospital S. João, Porto. Clinical and epidemiological data were recorded. Specimen collection from the glans penis and the coronal sulcus followed two procedures: a cotton tipped swab and the direct impression on the surface of CHROMagar Candida medium. Risk factors were considered singly and in combination through logistic regression models.Results  Among 478 men enrolled, the prevalence of candida colonization was 26.2% and the prevalence of candida balanitis was 18%. Candida colonization was strongly associated with an age above 60 years (OR = 3.375; 95% CI: 1.547–7.362) and with the presence of other cause of balanitis apart from Candida organisms (OR: 2.466; 95% CI: 1.491–4.078). An age above 40 years (OR: 2.27; 95% CI: 1.005–4.500), diabetes mellitus (OR: 19.390; 95% CI: 7.789–48.273) and more than ten candida colonies recovered by culture (OR: 9.586; 95% CI: 2.682–34.263) were risk factors for candida balanitis.Conclusions  This study highlights the impact of factors other than sexual behaviours upon the epidemiology of this infection. For both candida colonization and infection, age was an important risk factor. Diabetes mellitus was an independent risk factor for candida balanitis. More than ten colonies recovered from culture are associated with clinical signs and symptoms.
Intermittent hypoxia during sleep induces reactive gliosis and limited neuronal death in rats: implications for sleep apnea
Authors: Aviles‐Reyes Rolando Xavier , Angelo Maria Florencia , Villarreal Alejandro , Rios Hugo , Lazarowski Alberto , Ramos Alberto Javier 
Published: December 2009

J. Neurochem. (2010) 112, 854–869.AbstractSleep apnea (SA) can be effectively managed in humans but it is recognized that when left untreated, SA causes long‐lasting changes in neuronal circuitry in the brain. Recent neuroimaging studies gave suggested that these neuronal changes are also present even in patients successfully treated for the acute effects of SA. The cellular mechanisms that account for these changes are not certain but animal models of intermittent hypoxia (IH) during sleep have shown neuronal death and impairment in learning and memory. Reactive gliosis has a drastic effect on neuronal survival and circuitry and in this study we examined the neuro‐glial response in brain areas affected by SA. Glial and neuronal alterations were analyzed after 1, 3, 5 and 10 days of exposure to IH (8 h/day during the sleep phase, cycles of 6 min each, 10–21% O2) and observed significant astroglial hyperplasia and hypertrophy in parietal brain cortex and hippocampus by studying gliofibrillary acidic protein, Vimentin, S100B and proliferating cell nuclear antigen expression. In addition, altered morphology, reduced dendrite branching and caspase activation were observed in the CA‐1 hippocampal and cortical (layers IV–V) pyramidal neurons at short exposure times (1–3 days). Surprisingly, longer exposure to IH reduced the neuronal death rate and increased neuronal branching in the presence of persistent reactive gliosis. Up‐regulation of hypoxia inducible factor 1 alpha (HIF‐1α) and mdr‐1, a HIF‐1α target gene, were observed and increased expression of receptor for advanced end glycated products and its binding partner S100B were also noted. Our results show that a low number of hypoxic cycles induce reactive gliosis and neuronal death whereas continuous exposure to IH cycles reduced the rate of neuronal death and induced neuronal branching on surviving neurons. We hypothesize that HIF‐1α and S100B glial factor may improve neuronal survival under hypoxic conditions and propose that the death/survival/re‐growth process observed here may underlie brain circuitry changes in humans with SA.
Aging‐dependent changes of microglial cells and their relevance for neurodegenerative disorders
Authors: Von Bernhardi Rommy , Tichauer Juan E. , Eugenín Jaime 
Published: December 2009

J. Neurochem. (2010) 112, 1099–1114.AbstractAmong multiple structural and functional brain changes, aging is accompanied by an increase of inflammatory signaling in the nervous system as well as a dysfunction of the immune system elsewhere. Although the long‐held view that aging involves neurocognitive impairment is now dismissed, aging is a major risk factor for neurodegenerative diseases such as Alzheimer`s disease, Parkinson`s disease and Huntington’s disease, among others. There are many age‐related changes affecting the brain, contributing both to certain declining in function and increased frailty, which could singly and collectively affect neuronal viability and vulnerability. Among those changes, both inflammatory responses in aged brains and the altered regulation of toll like receptors, which appears to be relevant for understanding susceptibility to neurodegenerative processes, are linked to pathogenic mechanisms of several diseases. Here, we review how aging and pro‐inflammatory environment could modulate microglial phenotype and its reactivity and contribute to the genesis of neurodegenerative processes. Data support our idea that age‐related microglial cell changes, by inducing cytotoxicity in contrast to neuroprotection, could contribute to the onset of neurodegenerative changes. This view can have important implications for the development of new therapeutic approaches.
DNA methylation regulates adenosine A2A receptor cell surface expression levels
Authors: Buira Sandra P. , Albasanz José Luis , Dentesano Guido , Moreno Jesús , Martín Mairena , Ferrer Isidre , Barrachina Marta 
Published: December 2009

J. Neurochem. (2010) 112, 1273–1285.AbstractAdenosine A2A receptors (A2ARs) appear to play important roles in inflammation and in certain diseases of the nervous system. Pharmacological modulation of A2ARs is particularly useful in Parkinson’s disease and has been tested in schizophrenia. However, little is known about the regulation of A2AR gene (ADORA2A). A bioinformatic analysis revealed the presence of three CpG islands in the 5′ UTR region of human ADORA2A. Next, HeLa, SH‐SY5Y and U87‐MG cells were treated for 48 h with 5 μM 5‐azacytidine (Aza). Increased A2AR levels were demonstrated in HeLa and SH‐SY5Y cells when compared with non‐treated cells. No modifications were seen in U87‐MG cells. The increased A2AR mRNA and protein levels were accompanied by a loss of DNA methylation pattern in HeLa and SH‐SY5Y cells, as measured with the SEQUENOM MassArray platform. The Aza treatment also reduced the affinity of a methyl‐CpG‐binding protein for ADORA2A by quantitative chromatin immunoprecipitation in HeLa cells. Interestingly, A2AR levels were reduced by S‐adenosyl‐l‐methionine treatment in U87‐MG and methyl‐CpG‐binding protein affinity was increased for ADORA2A by quantitative chromatin immunoprecipitation. Therefore, these results show for the first time that DNA methylation plays a role in ADORA2A transcription and, subsequently, in constitutive A2AR cell surface levels.
Stress and GABAAreceptors
Authors: Skilbeck Kelly J. , Johnston Graham A. R. , Hinton Tina 
Published: December 2009

J. Neurochem.(2010)112, 1115–1130.AbstractGABAAreceptors are sensitive to subtle changes in the environment in both early‐life and adulthood. These neurochemical responses to stress in adulthood are sex‐dependent. Acute stress induces rapid changes in GABAAreceptors in experimental animals, with the direction of the changes varying according to the sex of the animals and the stress‐paradigm studied. These rapid alterations are of particular interest as they provide an example of fast neurotransmitter system plasticity that may be mediated by stress‐induced increases in neurosteroids, perhaps via effects on phosphorylation and/or receptor trafficking. Interestingly, some studies have also provided evidence for long‐lasting changes in GABAAreceptors as a result of exposure to stressors in early‐life. The short‐ and long‐term stress sensitivity of the GABAergic system implicates GABAAreceptors in the non‐genetic etiology of psychiatric illnesses such as depression and schizophrenia in which stress may be an important factor.
Inhibition of Aβ aggregation and neurotoxicity by the 39‐kDa receptor‐associated protein
Authors: Kerr Megan L. , Gasperini Robert , Gibbs Marie E. , Hou Xu , Shepherd Claire E. , Strickland Dudley K. , Foa Lisa , Lawen Alfons , Small David H. 
Published: December 2009

J. Neurochem. (2010) 112, 1199–1209.AbstractAggregation of β‐amyloid protein (Aβ) to form oligomers is considered to be a key step in generating neurotoxicity in the Alzheimer’s disease brain. Agents that bind to Aβ and inhibit oligomerization have been proposed as Alzheimer’s disease therapeutics. In this study, we investigated the binding of fluorescein‐labeled Aβ1–42 (FluoAβ1–42) to SH‐SY5Y neuroblastoma cells and examined the effect of the 39‐kDa receptor‐associated protein (RAP), on the Aβ cell interaction. FluoAβ1–42 bound to the cells in a punctate pattern. Surprisingly, when RAP was added to the incubations, FluoAβ1–42 and RAP were found to be co‐localized on the cell surface, suggesting that RAP and Aβ may bind to each other. Experiments using the purified proteins confirmed that a RAP–Aβ complex was stable and resistant to sodium dodecyl sulfate. RAP also inhibited Aβ oligomerization. We next examined whether RAP could inhibit the neurotoxic effects of Aβ. Addition of Aβ1–42 to SH‐SY5Y cells caused an increase in intracellular Ca2+ that was inhibited by treatment of the Aβ peptide with RAP. RAP also blocked an Aβ‐induced inhibition of long‐term memory consolidation in 1‐day‐old chicks. This study demonstrates that RAP binds to Aβ and is an inhibitor of the neurotoxic effects of Aβ.
Endogenous purinergic signaling is required for osmotic volume regulation of retinal glial cells
Authors: Wurm Antje , Lipp Stephan , Pannicke Thomas , Linnertz Regina , Krügel Ute , Schulz Angela , Färber Katrin , Zahn Dirk , Grosse Johannes , Wiedemann Peter , Chen Ju , Schöneberg Torsten , Illes Peter , Reichenbach Andreas , Bringmann Andreas 
Published: December 2009

J. Neurochem.(2010)112, 1261–1272.AbstractIntense neuronal activity in the sensory retina is associated with a volume increase of neuronal cells (Uckermannet al.,J. Neurosci. 2004,24:10149) and a decrease in the osmolarity of the extracellular space fluid (Dmitrievet al.,Vis. Neurosci.1999, 16:1157). Here, we show the existence of an endogenous purinergic mechanism that prevents hypoosmotic swelling of retinal glial (Müller) cells in mice. In contrast to the cells from wild‐type mice, hypoosmotic stress induced rapid swelling of glial cell somata in retinal slices from mice deficient in P2Y1, adenosine A1receptors, or ecto‐5′‐nucleotidase (CD73). Consistently, glial cell bodies in retinal slices from wild‐type mice displayed osmotic swelling when P2Y1or A1receptors, or CD73, were pharmacologically blocked. Exogenous ATP, UTP, and UDP inhibited glial swelling in retinal slices, while the swelling of isolated glial cells was prevented by ATP but not by UTP or UDP, suggesting that uracil nucleotides indirectly regulate the glial cell volume via activation of neuronal P2Y4/6and neuron‐to‐glia signaling. It is suggested that autocrine/paracrine activation of purinergic receptors and enzymes is crucially involved in the regulation of the glial cell volume.
Global change in four semi‐arid transnational river basins: Analysis of institutional water sharing preparedness
Authors: Falkenmark Malin , Fraiture Charlotte de , Vick Margaret J. 
Published: December 2009

AbstractClimate change has exacerbated concerns about water security. The authors stress the need for countries in basins where populations are growing to anticipate the water shortage implications for food production. The paper analyses the future status of the interdependence among riparian states in four semi‐arid transnational basins under the climate change SRES A2 scenario and projected population growth with a focus on the potential for rainfed agriculture on current croplands and the requirements for irrigation water. Increasing water interdependence among basin states requires institutional preparedness and water sharing arrangements. We conclude that the inclusion of long‐term trends in the design of water sharing agreements will improve their robustness to cope with change and mitigate the potential risk of conflict.
Prevalence and predictors of recurrence of major depressive disorder in the adult population
Authors: Hardeveld F. , Spijker J. , De Graaf R. , Nolen W. A. , Beekman A. T. F. 
Published: December 2009

Hardeveld F, Spijker J, De Graaf R, Nolen WA, Beekman ATF. Prevalence and predictors of recurrence of major depressive disorder in the adult population.Objective:  Knowledge of the risk of recurrence after recovery of a major depressive disorder (MDD) is of clinical and scientific importance. The purpose of this paper was to provide a systematic review of the prevalence and predictors of recurrence of MDD.Method:  Studies were searched in Medline en PsychINFO using the search terms ‘recur*’, ‘relaps*’, ‘depress*’, ‘predict*’ and course.Results:  Recurrence of MDD in specialised mental healthcare settings is high (60% after 5 years, 67% after 10 years and 85% after 15 years) and seems lower in the general population (35% after 15 years). Number of previous episodes and subclinical residual symptoms appear to be the most important predictors. Gender, civil status and socioeconomic status seem not related to the recurrence of MDD.Conclusion:  Clinical factors seem the most important predictors of recurrence. Data from studies performed in the general population and primary care on the recurrent course of MDD are scarce.
Activity and safety of combination chemotherapy with methotrexate, ifosfamide, l‐asparaginase and dexamethasone (MILD) for refractory lymphoid malignancies: a pilot study
Authors: Tsukune Yutaka , Isobe Yasushi , Yasuda Hajime , Shimizu Seiichi , Katsuoka Yuna , Hosone Masaru , Oshimi Kazuo , Komatsu Norio , Sugimoto Koichi 
Published: December 2009

AbstractOptimal salvage chemotherapy has not been established for lymphoid malignancy, which is refractory to the conventional cyclophosphamide, doxorubicin, vincristine, and prednisone regimen. To explore an effective regimen, we conducted a phase I pilot study of combination chemotherapy with methotrexate, ifosfamide, l‐asparaginase and dexamethasone (MILD), which are unaffected by MDR1‐encoded P‐glycoprotein. A total of 18 patients with lethal lymphoid malignancy were enrolled over a 2‐yr period. The median age was 63 yr. Eleven patients had T/NK‐cell malignancies, six had B‐cell malignancies, and one was diagnosed with a blastic plasmacytoid dendritic cell neoplasm. Patients aged ≥60 and <60 yr were planned to receive a set of starting doses of methotrexate and ifosfamide, which should induce myelosuppression. Eleven patients completed two courses of MILD therapy. Treatment‐related death because of systemic mucormycosis was observed in one patient. Major treatment‐related adverse events were grade 3 or more hematologic toxicities, which included lymphopenia corresponding to dose‐limiting toxicity. The most common grade 3 non‐hematologic toxicity was febrile neutropenia. Of the 14 evaluated patients, three achieved a complete response, and four showed a partial response. The overall response rate was 57%. It was very interesting that all of seven responders had T/NK‐cell malignancies. MILD therapy was feasible and presented acceptable toxicity in patients with refractory or lethal lymphoid malignancies. The efficacy for T/NK‐cell malignancies should be further evaluated.
Treatment response to bortezomib in multiple myeloma correlates with plasma hepatocyte growth factor concentration and bone marrow thrombospondin concentration
Authors: Ludek Pour , Hana Svachova , Zdenek Adam , Martina Almasi , Dana Kralova , Tomas Buchler , Lucie Kovarova , Marta Krejci , Jaroslav Michalek , Miroslav Penka , Jiri Vorlicek , Roman Hajek 
Published: December 2009

AbstractMultiple myeloma (MM) is associated with increased rate of bone marrow angiogenesis. Increased concentration of hepatocyte growth factor (HGF) is associated with poor prognosis in patients treated with conventional chemotherapy or thalidomide. We have shown previously that decreased level of thrombospondin, an angiogenesis inhibitor, correlates with poor response to high‐dose chemotherapy. The aim of our current study was to evaluate association between therapeutic response to bortezomib and thrombospondin and HGF levels. Peripheral blood plasma concentration of HGF and bone marrow plasma concentration of thrombospondin were measured in patients with MM prior to the initiation of bortezomib therapy. Overall, 58 patients were enrolled, 44/58 (76%) of them with relapsed disease. Treatment outcomes were analyzed for possible associations with pretreatment HGF and thrombospondin levels. Patients who achieved complete response had significantly higher pretreatment HGF levels and lower pretreatment thrombospondin levels than others. More than 70% of patients with low pretreatment HGF and high pretreatment thrombospondin concentrations achieved very good partial response or complete response, in contrast to only 20% of patients with high HGF and low thrombospondin levels. High pretreatment thrombospondin and low pretreatment HGF concentrations are associated with therapeutic response to bortezomib in patients with MM.