bluuebunny/crossref_metadata_2025_split huggingface dataset:
Parenting stress and its association with perceived agreement about the disclosure decision in parents following donor conception
Authors: Gebhardt Anja J. , Sydsjö Gunilla , Skoog Svanberg Agneta , Indekeu Astrid , Lampic Claudia 
Published: April 2017

AbstractIntroductionFor many donor‐conceiving heterosexual parents, the process of deciding whether and what to tell children about their genetic origin is challenging. We hypothesized that incomplete couple agreement about disclosure could be associated with parenting stress. The aim of the study was to investigate: (1) parenting stress levels among heterosexual parents of young children following gamete donation and (2) whether parenting stress is related to perceived agreement about disclosure of the donor conception to the children.Material and methodsThis study is part of the longitudinal multicenter Swedish Study on Gamete Donation and included a total of 213 heterosexual parents with children aged 1–4 years following oocyte donation (n = 103) and sperm donation (n = 110). Parents individually completed a questionnaire that included validated instruments on parenting stress (SPSQ) and relationship quality (ENRICH), as well as a study‐specific measure on disclosure agreement. Multiple regression analysis was applied.ResultsIncomplete couple agreement on disclosure to the children was not statistically significantly associated with increased levels of parenting stress. Relationship satisfaction consistently and significantly accounted for variation in parenting stress levels, indicating that relationship satisfaction had a buffering impact on parenting stress.ConclusionsParental stress does not appear to be negatively influenced by incomplete couple agreement about disclosure to children. As children grow up, reaching agreement about what to tell the child about the donor conception might become more relevant for couples' stress related to parenthood.
Inhibitory action of oxytocin on spontaneous contraction of rat distal colon by nitrergic mechanism: involvement of cyclic GMP and apamin‐sensitive K+ channels
Authors: Wang R. , Han M. T. , Lv X. L. , Yu Y. A. , Chai S. Q. , Qu C. M. , Liu C. Y. 
Published: April 2017

AbstractAimThe mechanisms underlying the inhibitory effects of oxytocin (OT) on colon tone are not totally understood. We explore the mechanisms of OT on spontaneous contractility in rat distal colon and identify the mediators involved in this action.MethodsIn rat distal colon strips, mechanical activity was analysed and the production of nitric oxide (NO) in tissue loaded with the fluorochrome DAF‐FM was visualized by confocal microscopy. OT receptor (OTR) expression was determined by Western blotting and immunofluorescence.ResultsIn rat distal colon, OT produced a concentration‐dependent reduction in the spontaneous contraction, which was abolished by the OTR antagonist atosiban, the neural blocker tetrodotoxin and the inhibitor of neuronal nitric oxide synthase (nNOS) NPLA. The inhibitory effects of OT were not affected by propranolol, atropine, the nicotinic cholinoceptor blocker hexamethonium, the vasoactive intestinal peptide receptor antagonist VIPHyb, the P2 purinoceptor antagonist PPADS, the adenosine A1 receptors antagonist DPCPX and the prostacyclin receptor antagonist Ro1138452. The soluble guanylyl cyclase (sGC) inhibitor ODQ and the small conductance Ca2+‐activated K+ (CaK+) channels blocker apamin significantly reduced the relaxation induced by OT, nicotine, sodium nitroprusside and the sGC activator BAY 41‐2272. The neural release of NO elicited by OT was prevented by NPLA, tetrodotoxin and atosiban. The presence of the OTR and its co‐localization with nNOS was detected by immunohistochemistry and Western blotting experiments.ConclusionThese results demonstrate the NO release from enteric neurones induced by activation of OTR mediates distal colon relaxation. sGC and small conductance CaK+ channels are involved in this relaxation.
Protein S‐sulfhydration by hydrogen sulfide in cardiovascular system
Authors: Meng Guoliang , Zhao Shuang , Xie Liping , Han Yi , Ji Yong 
Published: April 2017

Hydrogen sulfide (H2S), independently of any specific transporters, has a number of biological effects on the cardiovascular system. However, until now, the detailed mechanism of H2S was not clear. Recently, a novel post‐translational modification induced by H2S, named S‐sulfhydration, has been proposed. S‐sulfhydration is the chemical modification of specific cysteine residues of target proteins by H2S. There are several methods for detecting S‐sulfhydration, such as the modified biotin switch assay, maleimide assay with fluorescent thiol modifying regents, tag‐switch method and mass spectrometry. H2S induces S‐sulfhydration on enzymes or receptors (such as p66Shc, phospholamban, protein tyrosine phosphatase 1B, mitogen‐activated extracellular signal‐regulated kinase 1 and ATP synthase subunit α), transcription factors (such as specific protein‐1, kelch‐like ECH‐associating protein 1, NF‐κB and interferon regulatory factor‐1), and ion channels (such as voltage‐activated Ca2+ channels, transient receptor potential channels and ATP‐sensitive K+ channels) in the cardiovascular system. Although significant progress has been achieved in delineating the role of protein S‐sulfhydration by H2S in the cardiovascular system, more proteins with detailed cysteine sites of S‐sulfhydration as well as physiological function need to be investigated in further studies. This review mainly summarizes the role and possible mechanism of S‐sulfhydration in the cardiovascular system. The S‐sulfhydrated proteins may be potential novel targets for therapeutic intervention and drug design in the cardiovascular system, which may accelerate the development and application of H2S‐related drugs in the future.Linked ArticlesThis article is part of a themed section on Spotlight on Small Molecules in Cardiovascular Diseases. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v175.8/issuetoc
Cross‐species studies of cognition relevant to drug discovery: a translational approach
Authors: Robbins T W 
Published: April 2017

This review advances the case that bidirectional, cross‐species translation of findings from experimental animals to and from humans is an important strategy for drug discovery. Animal models of mental disorders require appropriate behavioural or cognitive outcome variables that can be generalized cross‐species. One example is the treatment of impulsive behaviour in attention deficit hyperactivity disorder (ADHD) with stimulant drugs. Performance on the stop signal reaction task as an index of impulsivity is improved both in healthy human volunteers and in patients with adult ADHD by stimulant drugs and also by the selective noradrenaline reuptake blocker atomoxetine. Functional neuroimaging evidence suggests a modulation of circuitry including the inferior prefrontal cortex by this drug. Parallel work in rats had shown that atomoxetine improves stop signal performance by affecting possibly homologous regions of the rodent prefrontal cortex. This parallel effect of atomoxetine in rodents and humans could potentially be exploited in other disorders in which impulsivity plays a role, such as stimulant abuse and Parkinson's disease. A contrasting relative lack of involvement of 5‐HT mechanisms in the stop signal reaction time task will also be described. Research in humans and experimental animals that demonstrate effects of serotoninergic agents such as the selective serotonin (5‐HT) reuptake inhibitor citalopram on probabilistic learning and reversal (upon which atomoxetine has little effect) will also be reviewed, possibly relevant to the treatment of clinical depression, Finally, other promising examples of parallel studies of behavioural effects of CNS‐active drugs in animals and humans will also be described.Linked ArticlesThis article is part of a themed section on Pharmacology of Cognition: a Panacea for Neuropsychiatric Disease? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.19/issuetoc
Targeting on poly(ADP‐ribose) polymerase activity with DNA‐damaging hybrid lactam‐steroid alkylators in wild‐type and BRCA1‐mutated ovarian cancer cells
Authors: Trafalis Dimitrios T. , Polonifi Aikaterini , Dalezis Panayiotis , Nikoleousakos Nikolaos , Katsamakas Sotirios , Sarli Vasiliki 
Published: April 2017

Conjugated lactam‐steroid alkylators (LSA) have been shown to exhibit superior activity at controlling cancer models and overlap drug resistance to conventional chemjournalapy. Hybrid LSA combine two active compounds in a single molecule and incorporate modified steroids bearing lactam moiety in one or more steroid rings functioning as vectors for cytotoxic agents. We first describe a novel class of LSA that generate excellent anticancer activity against UWB1.289 and UWB1.289 + BRCA1 human ovarian cancer cell lines. Both UWB1.289 and UWB1.289 + BRCA1 cells carry mutations in the tumor suppressor gene TP53 while UWB1.289 cell line carries a germline BRCA1 mutation. In vitro, in vivo, and in silico, experimental methods were utilized to determine the poly(ADP‐ribose) polymerases (PARPs) activity and mRNA transcription, DNA damage, cytostatic and cytotoxic effects, and virtual molecular interactions, in order to study the molecular mechanisms of activity of the tested LSA. LSA produce anticancer activity through dual action by combining the direct induction of cellular DNA damage with the inhibition of PARP activity and consecutive DNA repair activity. BRCA1‐mutated UWB1.289 ovarian cancer cells with defective PARP‐oriented repair mechanism show significantly higher sensitivity to these agents. Combined drug effect on DNA damage and repair is a novel approach in cancer therapeutics.
Weight loss in obese girls with polycystic ovarian syndrome is associated with a decrease in Anti‐Muellerian Hormone concentrations
Authors: Reinehr Thomas , Kulle Alexandra , Rothermel Juliane , Knop Caroline , Lass Nina , Bosse Christina , Holterhus Paul‐Martin 
Published: April 2017

SummaryObjectiveThe Anti‐Muellerian Hormone (AMH) has been reported as surrogate marker of antral follicles, which are the origins of hyperandrogenism in polycystic ovarian syndrome (PCOS). Therefore, AMH may be useful for the diagnosis of PCOS. The objective was to study the longitudinal changes in AMH concentrations in girls with and without PCOS.DesignThis is a longitudinal study of obese girls participating in a 1‐year lifestyle intervention.PatientsForty obese girls aged 13‐16 years (50% with PCOS) were included in the study. Girls with and without PCOS were matched to age, BMI and change in weight status.MeasurementsAMH, gonadotropins, androstenedione, testosterone, oestradiol and sex hormone‐binding globulin (SHBG) were determined.ResultsObese girls with PCOS demonstrated significantly (P<.001) higher AMH concentrations (5.8±3.1 ng/mL) compared to obese girls without PCOS (2.4±1.4 ng/mL). None of the girls without PCOS had AMH concentrations ≥6 ng/mL and none of the PCOS girls showed AMH concentrations ≤3 ng/mL. Weight loss in girls with PCOS was associated with a significant drop in AMH concentrations (−1.4±1.8 ng/mL, P=.045). AMH was significantly related to testosterone (cross‐sectional: b‐coefficient 3.7±1.7, P=.001, longitudinal: b‐coefficient 0.54±0.47, P=.026) and luteinizing hormone (LH) (cross‐sectional: b‐coefficient 0.05±0.04, P=.039, longitudinal: b‐coefficient 0.005±0.004, P=.039), but not to any other analysed parameter in multiple linear regression analyses adjusted to multiple confounders.ConclusionsAMH was increased in adolescent girls with PCOS and normalized with weight loss. AMH was cross‐sectionally and longitudinally related to hyperandrogenism.
Quantitative evaluation of metal artifacts using different CBCT devices, high‐density materials and field of views
Authors: Codari Marina , de Faria Vasconcelos Karla , Ferreira Pinheiro Nicolielo Laura , Haiter Neto Francisco , Jacobs Reinhilde 
Published: April 2017

AbstractObjectiveTo objectively compare the influence of different cone‐beam computed tomography (CBCT) devices, high‐density materials and field of views (FOVs) on metal artifact expression.Material and methodsFor this in vitro study, three customized acrylic resin phantoms containing high‐density materials cylinders: titanium, copper–aluminum alloy and amalgam were scanned on three CBCT devices using high‐resolution protocols, same voxel size (0.2 mm) and different FOVs. After fully automatic segmentation and image registration, the same region of interest was defined for the small and medium FOVs. The difference between the segmented and the real volume of the metal cylinders was assessed. Moreover for each segmented slice, the area difference between the segmented and the real axial section was determined. The artifacts on the background were measured as normalizing standard deviation of voxel values in the vicinity of the cylinder, in three different distances.ResultsConsiderable differences were observed in volume measurements for all CBCTs devices and materials for both FOV sizes (up to 67%). The slice per slice area analysis indicated higher artifacts at the edges of the metal cylinder. Within the materials, amalgam and titanium had, respectively, the worst and best artifact expression in all the CBCT devices. Standard deviation values varied differently between the three distances in each device.ConclusionOur in vitro study showed that different CBCT devices, high‐density materials and FOV should be considered while evaluating CBCT images. More carefully, diagnosis conclusions should be drawn in images containing amalgam and copper–aluminum alloy.
Subsequent malignancies after allogeneic hematopoietic stem cell transplantation
Authors: Gündüz Mehmet , Özen Mehmet , Şahin Uğur , Toprak Selami Koçak , Civriz Bozdağ Sinem , Kurt Yüksel Meltem , Arslan Önder , Özcan Muhit , Demirer Taner , Beksaç Meral , İlhan Osman , Gürman Günhan , Topçuoğlu Pervin 
Published: April 2017

AbstractWe evaluated 979 patients for the development of post‐transplant lymphoproliferative disease (PTLD) and solid malignancies after allogeneic hematopoietic stem cell transplantations (allo‐HSCT) as a late complication. We found 15 (1.5%) subsequent malignancies; three of these malignancies were PTLD, and twelve were solid tumors. The median time from allo‐HSCT to the development of PTLD was 9 (3‐20) months and that from allo‐HSCT to the development of solid tumors was 93 (6‐316) months. The cumulative incidence of evolving subsequent malignancy in patients was 1.3% (±0.5 SE) at 5 years and 3.9% (±1.2 SE) at 10 years. The cumulative incidence of developing subsequent malignancy in patients with benign hematological diseases as the transplant indication was 7.4%±4.2 SE at 5 years. More subsequent malignancy developed in patients having ≥1 year chronic graft‐vs‐host disease (GVHD; 3.7% in ≥1 year chronic GVHD and 0.7% in <1 year chronic GVHD patient groups, P=.002). Subsequent epithelial tumor risk was higher in ≥1 year chronic GVHD patients than <1 year (3.7% vs 0.1%, P<.001). In multivariate analysis, benign hematological diseases as transplant indication (RR: 5.6, CI 95%: 1.4‐22.3, P=.015) and ≥1 year chronic GVHD (RR: 7.1, 95% CI: 2.3‐22.5, P=.001) were associated with the development of subsequent malignancy.
Impact of caring for patients with severe and complex disabilities on health care workers’ quality of life: determinants and specificities
Authors: Rousseau Marie‐Christine , Baumstarck Karine , Leroy Tanguy , Khaldi‐Cherif Cherazad , Brisse Catherine , Boyer Laurent , Resseguier Noémie , Morando Claire , Billette De Villemeur Thierry , Auquier Pascal 
Published: April 2017

AimIndividuals with severe and complex disabilities, defined by a combination of profound intellectual impairment and serious motor deficit resulting in extreme dependence, often remain in hospital or at residential facilities. The aim of this study was to identify the determinants of quality of life (QoL) of 238 health care workers (HCWs) caring for individuals with severe and complex disabilities.MethodWe conducted a cross‐sectional study. The recruitment of the HCWs was performed in five French centres specializing in patients with severe and complex disabilities. The selection criteria were age above 18 years, being an institutional referent HCW (a resource person coordinating various issues for or about the patient), and agreeing to participate. Sociodemographic, health, professional variables, and psycho‐behavioural (QoL, burn‐out, and coping strategies) data were collected.ResultsOf the 362 eligible HCWs, 65.7% returned the questionnaires. The scores of the physical and social dimensions of QoL were significantly lower, and the score of the psychological dimension significantly higher, than those of a comparison group. The main factors modulating QoL were age, financial difficulties, nature of coping strategy, and burn‐out.InterpretationThis research provides preliminary evidence that caring for patients with severe and complex disabilities affects the QoL of HCWs. These results support the need for optimization of the work environments for HCWs.
Multimodal neurophysiological monitoring in healthy infants born at term: normative continuous somatosensory evoked potentials data
Authors: Lori Silvia , Gabbanini Simonetta , Bastianelli Maria , Bertini Giovanna , Corsini Iuri , Dani Carlo 
Published: April 2017

AimTo describe accurate, standardized 1h‐multimodal neurophysiological monitoring (1h‐MNM), while simultaneously recording VEEG, aEEG, and SEP‐C bilaterally from median nerves, and to collect neonatal normative SEP‐C data related to behavioural states.MethodTwenty healthy, term newborn infants (13 males, 7 females; gestational age 37–42wks; mean 39.6wks, standard deviation [SD] 1.3wks) underwent 1h‐MNM within 2 days of life, with focus on recording of the SEP‐C (band‐pass setting 1–100 Hz, rate of stimulation 1.1 Hz, 50 alternate stimuli).Results1h‐MNM was easily obtained with identification of cervical (N13) and cortical (N1, P1) SEP‐C responses in all infants. SEP‐C minimal and maximum N1 latencies/N1–P1 amplitudes were identified, bilaterally, during periods of spontaneous sleep active‐quiet‐active (AS‐QS‐AS) and quiet‐wakefulness. Minimal latencies and amplitudes occurred in 60% of active sleep/quiet‐wakefulness, with the maximums in 70% of quiet sleep. The SEP‐C mean values were latencies of N13=13.6ms (SD 1.4ms) and N1=33.6ms (SD 3.9ms) to 34.2ms (SD 4.8ms) in left and right hemisphere respectively; central‐conduction‐time (CCT) (N13–N1), 20.0ms (SD 4.3ms) to 20.6ms (SD 4.8ms); N1–P1 amplitude=4.6ms (SD 2.7ms) to 3.8μV (SD 2.2μV).Interpretation1h‐MNM can record simultaneously VEEG/aEEG/SEP‐C in newborn infants, showing the modulation of SEP cortical responses in relation to behavioural states in all infants studied using an appropriate neonatal method. We emphasize the importance of obtaining neonatal SEP‐C normative data to better identify pathological findings in neonatal brain injury.
Acute kidney injury, plasma lactate concentrations and lactic acidosis in metformin users: A GoDarts study
Authors: Connelly Paul J. , Lonergan Mike , Soto‐Pedre Enrique , Donnelly Louise , Zhou Kaixin , Pearson Ewan R. 
Published: April 2017

AimsMetformin is renally excreted and has been associated with the development of lactic acidosis. Although current advice is to omit metformin during illnesses that may increase the risk of acute kidney injury (AKI), the evidence supporting this is lacking. We investigated the relationship between AKI, lactate concentrations and the risk of lactic acidosis in those exposed to metformin.Materials and MethodsWe undertook a population‐based case‐control study of lactic acidosis in 1746 participants with Type 2 diabetes and 846 individuals without diabetes with clinically measured lactates with and without AKI between 1994 and 2014. AKI was stratified by severity according to “Kidney Disease: Improving Global Outcomes” guidelines. Mixed‐effects logistic and linear regression were used to analyse lactic acidosis risk and lactate concentrations, respectively.ResultsEighty‐two cases of lactic acidosis were identified. In Type 2 diabetes, those treated with metformin had a greater incidence of lactic acidosis [45.7 per 100 000 patient years; 95% confidence interval (CI) 35.9‐58.3] compared to those not exposed to this drug (11.8 per 100 000 patient years; 95% CI 4.9‐28.5). Lactate concentrations were 0.34 mmol/L higher in the metformin‐exposed cohort (P < .001). The risk of lactic acidosis was higher in metformin users [odds ratio (OR) 2.3; P = .002] and increased with AKI severity (stage 1: OR 3.0, P = .002; stage 2: OR 9.4, P < .001; stage 3: OR 16.1, P < .001).ConclusionsA clear association was found between metformin, lactate accumulation and the development of lactic acidosis. This relationship is strongest in those with AKI. These results provide robust evidence to support current recommendations to omit metformin in any illness that may precipitate AKI.
Intraclass differences in the risk of hospitalization for heart failure among patients with type 2 diabetes initiating a dipeptidyl peptidase‐4 inhibitor or a sulphonylurea: Results from the OsMed Health‐DB registry
Authors: Fadini Gian Paolo , Saragoni Stefania , Russo Pierluigi , Degli Esposti Luca , Vigili de Kreutzenberg Saula , Melazzini Mario , Avogaro Angelo ,   on behalf of the OsMed Health DB Network
Published: April 2017

AimsTo re‐analyse data from a previous retrospective study on 127 555 patients, in which we showed that dipeptidyl peptidase‐4 (DPP‐4) inhibitor therapy was associated with a lower risk of hospitalization for HF (HHF) than sulphonylurea (SU) therapy, in order to evaluate intraclass differences among DPP‐4 inhibitors and SUs.MethodsWe included patients with type 2 diabetes (T2D) initiating DPP‐4 inhibitor or SU therapy, alone or in combination with metformin. Patients undergoing intraclass switch, those with a previous HHF, those receiving insulin treatment, and those with <6 months observation were excluded. We calculated the incidence of first and total HHF events/1000 person‐years. Cox proportional hazard and Poisson multiple regression models, as well as propensity‐score matching, were used to account for baseline confounders.ResultsThe analysis included 17 615 DPP‐4 inhibitor users (60.1% sitagliptin; 27.0% vildagliptin; 12.9% saxagliptin) and 86 734 SU users (37.5% glibenclamide; 34.6% glimepiride; 27.9% gliclazide). No intraclass difference in the incidence rate of first and total HHF events was noted among the 3 DPP‐4 inhibitors or among the 3 SUs. Multivariable adjustments for baseline confounders or propensity‐score matching did not change the results. In addition, no intraclass difference in HHF risk was observed in patients at high compared with low cardiovascular risk.ConclusionsIn a cohort of patients with T2D taken from approximately one‐third of the Italian population, no intraclass difference was noted for DPP‐4 inhibitor and SU therapy with regard to HHF risk.