bluuebunny/crossref_metadata_2025_split huggingface dataset:
The short‐term effect of flavonoid‐rich dark chocolate on retinal vessel diameter in glaucoma patients and age‐matched controls
Authors: Terai Naim , Gedenk Alexandra , Spoerl Eberhard , Pillunat Lutz E , Stodtmeister Richard 
Published: March 2014

AbstractPurposeTo investigate the effect of flavonoid‐rich dark chocolate and non‐flavonoid‐rich white chocolate on retinal vessel diameter in glaucoma patients and age‐matched controls.MethodsThirty glaucoma patients and 30 age‐matched subjects were assigned to dark or white chocolate by randomization with forced equal distribution. The number in each of the four groups was 15. Measured parameters included systemic blood pressure (BP), blood glucose levels, static retinal vessel analysis, as measured by central retinal artery equivalent (CRAE) (which relates to the diameter of the central retinal artery), central retinal vein equivalent (CRVE) (which relates to the diameter of central retinal vein) and the arterio‐venous ratio (AVR), which represents the CRAE/CRVE ratio, dynamic retinal vessel analysis as measured by the change in vessel diameter in response to flicker light stimulation. Three recording cycles from each were averaged.ResultsBlood pressure parameters (systolic BP, diastolic BP and pulse), IOP and blood glucose levels did not differ significantly between both groups before and after consumption of white or dark chocolate. Static vessel analysis did not show any significant changes in CRAE, CRVE or AVR before and after dark or white chocolate in both groups (p > 0.05).Mean dilatation of the venules in the control group was 3.2 ± 0.9 % before dark chocolate and 4.2 ± 1.4 % after dark chocolate intake, which was statistically significantly different (p = 0.01). Mean dilatation of the arterioles in the control group was 2.8 ± 1.8 % before dark chocolate and 3.5 ± 1.8 % after dark chocolate intake with a trend to statistical significance (p = 0.14), but not reaching the significance level. Mean diameter changes in the glaucoma group did not show any significant differences after dark chocolate consumption.ConclusionThe present study showed a significant improvement of venous vasodilatation 2 hr after dark chocolate intake in the control group, but not in the glaucoma group. This effect might be indicative of an increased bioavailability of nitric oxide (NO) after dark chocolate consumption. The lack of finding a significant venous response after dark chocolate in the glaucoma group might be related to the already impaired endothelial function in these patients.
Segregation analysis suggests that keratoconus is a complex non‐mendelian disease
Authors: Kriszt Ágnes , Losonczy Gergely , Berta András , Vereb György , Takács Lili 
Published: March 2014

AbstractPurposeComplex segregation analysis of 60 unrelated sporadic keratoconus (KC) families was performed to reveal the presumed mode of inheritance in our dataset.MethodsSixty probands, 212 family members and 212 age and gender matched healthy controls underwent clinical and videokeratographic examination. Family aggregation and distribution of videokeratography parameters were examined. Segregation of KSI, KISA and 6mm Fourier asymmetry alone or in covariate analysis with gender or the presence of Fleischer ring, exploring mendelian and non‐mendelian models of inheritance was tested using complex segregation analysis with the S.A.G.E. program package.ResultsIn 145 relatives of probands, the estimated prevalence of manifest KC was 7.6% (95% CI: 3.3–11.9) based on KISA index, indicating strong familial aggregation. All examined videokeratography indices were able to differentiate between KC and non‐KC family members as well as normal controls (anova p < 0.001). Hypotheses accepted as most parsimonius models of inheritance (p > 0.1) for all indices indicated the presence of a non‐mendelian major gene effect (MG). Inclusion of Fleischer ring as covariate improved the fit of MG models. Mendelian, Sporadic and polygenic models were consistently rejected.ConclusionsComplex segregation analysis indicates a strong genetic contribution to the transmission of keratoconus. Inheritance is most probably due to a non‐mendelian major gene effect. Low genotype‐phenotype correlation in sporadic KC families can make linkage studies difficult, thus genome wide association studies, epigenetic and pathway analyses may provide more information on disease pathogenesis in non‐familial keratoconus.
Melatonin attenuates antipsychotic metabolic effects: an eight‐week randomized, double‐blind, parallel‐group, placebo‐controlled clinical trial
Authors: Romo‐Nava Francisco , Alvarez‐Icaza González Dení , Fresán‐Orellana Ana , Saracco Alvarez Ricardo , Becerra‐Palars Claudia , Moreno Julia , Ontiveros Uribe Martha P , Berlanga Carlos , Heinze Gerhard , Buijs Ruud M 
Published: March 2014

ObjectiveSecond‐generation antipsychotics (SGAs) are among the first‐line treatments for bipolar disorder and schizophrenia, but have a tendency to generate metabolic disturbances. These features resemble a metabolic syndrome for which a central autonomic imbalance has been proposed that may originate from the hypothalamic suprachiasmatic nuclei. In a clinical trial, we hypothesized that melatonin, a hormone that regulates the suprachiasmatic nucleus, could attenuate SGA‐induced adverse metabolic effects.MethodsIn an eight‐week, double‐blind, randomized, placebo‐controlled, parallel‐group clinical trial, we evaluated the metabolic effect of melatonin in SGA‐treated patients in terms of weight, blood pressure, lipid, glucose, body composition, and anthropometric measures. A total of 44 patients treated with SGAs, 20 with bipolar disorder and 24 with schizophrenia, randomly received placebo (n = 24) or melatonin 5 mg (n = 20).ResultsThe melatonin group showed a decrease in diastolic blood pressure (5.1 versus 1.1 mmHg for placebo, p = 0.003) and attenuated weight gain (1.5 versus 2.2 kg for placebo, F = 4.512, p = 0.040) compared to the placebo group. The strong beneficial metabolic effects of melatonin in comparison to placebo on fat mass (0.2 versus 2.7 kg, respectively, p = 0.032) and diastolic blood pressure (5.7 versus 5.5 mmHg, respectively, p = 0.001) were observed in the bipolar disorder and not in the schizophrenia group. No adverse events were reported.ConclusionsOur results show that melatonin is effective in attenuating SGAs' adverse metabolic effects, particularly in bipolar disorder. The clinical findings allow us to propose that SGAs may disturb a centrally mediated metabolic balance that causes adverse metabolic effects and that nightly administration of melatonin helps to restore. Melatonin could become a safe and cost‐effective therapeutic option to attenuate or prevent SGA metabolic effects.
Brain electrical source imaging in manic and depressive episodes of bipolar disorder
Authors: Painold Annamaria , Faber Pascal L , Milz Patricia , Reininghaus Eva Z , Holl Anna K , Letmaier Martin , Pascual‐Marqui Roberto D , Reininghaus Bernd , Kapfhammer Hans‐Peter , Lehmann Dietrich 
Published: March 2014

ObjectiveBipolar disorder (BD) electroencephalographic (EEG) studies have reported varying results. The present study compared EEG in BD during manic and depressive episodes, using brain electrical source imaging [standardized low‐resolution electromagnetic tomography (sLORETA)] to assess the cortical spatial distribution of the sources of EEG oscillation frequencies.MethodsTwo independent datasets (a total of 95 patients with bipolar I disorder, of whom 59 were female) were analyzed. Dataset #1 comprised 14 patients in a manic as well as a depressive episode. Dataset #2 comprised 26 patients in a manic episode and 55 patients in a depressive episode. From the head surface‐recorded EEG, sLORETA cortical activity was computed in eight EEG frequency bands, and compared between mood states in both datasets. The results from the two datasets were combined using conjunction analysis.ResultsConjunction analysis yielded significant differences between mood states: In manic compared to depressive states, patients had lesser theta frequency band activity (right‐hemispheric lateral lower prefrontal and anterior temporal, mainly Brodmann areas 13, 38, and 47), and greater beta‐2 and beta‐3 frequency band activity (extended bilateral prefrontal‐to‐parietal, mainly Brodmann area 6, and the cingulate).ConclusionsThe spatial organization of the brain's electrical oscillations differed in patients with BD between manic and depressive mood states. The brain areas implementing the main functions that show opposing abnormalities during manic and depressive episodes were affected by unduly increased or decreased activity (beta or theta). The discussion considers that facilitating (beta) or inhibiting (theta) electrical activity can in either case result in behavioral facilitation or inhibition, depending on the function of the brain area.
Determinants of Weight Changes During the First 96 Hours of Life in Full‐Term Newborns
Authors: Fonseca Maria João , Severo Milton , Barros Henrique , Santos Ana Cristina 
Published: March 2014

AbstractBackgroundNewborn weight loss (NWL) in the first 3 days of life is around 6 percent of birthweight (BW). We aim to describe the determinants of an excessive and insufficient NWL in the first 96 hours of life.MethodsA sample of 1,288 full‐term singletons without congenital abnormality belonging to Generation XXI birth cohort was selected. Newborns were recruited in 2005–2006 at all public units providing obstetrical and neonatal care in Porto, Portugal. Information was collected by face‐to‐face interview and additionally abstracted from clinical records. Anthropometrics were obtained by trained examiners and newborn weight change (NWC) was estimated as (weight–BW)/BW × 100. We categorized NWL as excessive (below 10th percentile of the sample distribution of NWC: ≤−9.4% of BW), normal (between 10th and 90th percentiles: −9.3 to −4.2%) and insufficient (above 90th percentile: ≥ −4.1%). Adjusted odds ratios (OR) and 95 percent confidence intervals (CI) were calculated using multinomial regression models.ResultsExcessive NWL was positively associated with maternal age ≥40 years (OR = 3.32, 95%CI 1.19–9.25), maternal education (OR = 1.04, 95% CI 1.00–1.09), cesarean delivery (OR = 2.42, 95% CI 1.12–5.23), and phototherapy‐treated jaundice (OR = 1.69, 95% CI 1.00–2.87). Insufficient NWL was positively associated with low BW (OR = 2.68, 95% CI 1.13–6.33), and formula/mixed feeding (OR = 1.74, 95% CI 1.13–2.66).ConclusionExcessive NWL was positively associated with maternal age and education, cesarean delivery, and phototherapy‐treated jaundice. Insufficient NWL reflected child's feeding. As breastfed newborns did not lose weight excessively, but newborns with formula/mixed feeding had insufficient NWL, our study supports that breastfeeding provides excellent nutrition during this period.
Monocyte-derived dendritic cells from Crohn's disease patients exhibit decreased ability to activate T helper type 17 responses in memory cells
Authors: Nieminen J K , Sipponen T , Färkkilä M , Vaarala O 
Published: March 2014

Summary
An increased activation of interleukin (IL)-17A-producing immune cells is a well-established feature of Crohn's disease (CD). Mechanisms that contribute to this aberrant immune activation are, however, less clear. Given that an enhanced induction of innate-immunity associated cytokines IL-6 and IL-23, which promote IL-17 immunity, is also clearly implicated in CD, we hypothesized that monocyte-derived dendritic cells (moDCs) of CD patient origin would mount exaggerated IL-17A responses in T cells. However, we found a significantly attenuated up-regulation of the IL-17A response in allogeneic T helper memory cells in the presence of culture media from lipopolysaccharide (LPS)-stimulated moDCs of CD patients when compared with moDCs of control subjects (median fold-increase in IL-17A mRNA expression 1·09 versus 1·44, P = 0·038). This was accompanied by a lower expression of IL-1β and IL-6 transcripts in the LPS-treated moDCs (median 9·55 versus 13·9 relative units, P = 0·042, and 2·66 versus 9·06 relative units, P = 0·049, respectively). In addition, the up-regulation of autophagy-related LC3 transcripts was decreased in moDCs of CD patients (median fold-increase in mRNA expression 1·22 versus 1·52, P = 0·029). Our findings reveal similar immunological aberrancies in CD in the general population as reported in CD patients with mutated intracellular bacterial sensor NOD2, namely attenuated activation of innate cytokines and impaired autophagy, combined with a reduced capacity to up-regulate the T helper type 17 (Th17) response. The results presented here emphasize a defective anti-microbial response in the pathogenesis of CD. The increased mucosal Th1 and Th17 responses, which may contribute to the pathogenesis, could be the consequences of primary defects in the innate immunity.
Astrocytic JWA Expression is Essential to Dopaminergic Neuron Survival in the Pathogenesis of Parkinson's Disease
Authors: Miao Shu‐Han , Sun Hong‐Bin , Ye Yang , Yang Jing‐Jing , Shi Yao‐Wei , Lu Ming , Hu Gang , Zhou Jian‐Wei 
Published: March 2014

SummaryAimsTo investigate the role of astrocytic JWA expression in dopaminergic (DA) neuron degeneration and in the pathogenesis of Parkinson's disease (PD).MethodsConditional astrocytic JWA null (JWA∆2/∆2/GFAP‐Cre) mice and U251 glioma cells were used to evaluate the effects of JWA gene on DA neuron degeneration. The oxidative stress‐driven molecular events were determined in both in vivo and in vitro models.ResultsConditional astrocytic JWA knockout resulted in significant activation of astrocytes measured by increase in glial fibrillary acidic protein‐positive cells (1.34 × 103 ± 74.5 vs. 8.44 × 103 ± 1.35 × 103, P < 0.01) in mouse substantia nigra, accompanied by loss of DA neurons (1.03 × 104 ± 238 vs. 6.17 × 103 ± 392, P < 0.001). Deficiency of JWA significantly aggravated reactive oxygen species (ROS) accumulation in substantia nigra compared with the wild‐type mice. Increasing JWA expression in U251 glioma cells inhibited ROS with a concomitant increase in intracellular glutathione. Furthermore, suppression of IKKβ‐nuclear factor (NF)‐κB signaling pathway was shown to regulate JWA in a PD model.ConclusionsThe JWA gene exerts neuroprotective roles against DA neuronal degeneration via modulating intracellular redox status and NF‐κB signaling pathway and is a potential treatment target for PD.
Abnormally Altered Patterns of Whole Brain Functional Connectivity Network of Posterior Cingulate Cortex in Remitted Geriatric Depression: A Longitudinal Study
Authors: Jiang Wen‐Hao , Yuan Yong‐Gui , Zhou Hong , Bai Feng , You Jia‐Yong , Zhang Zhi‐Jun 
Published: March 2014

SummaryAimsA longitudinal study investigated the remitted geriatric depression (RGD) patients' persistent cognitive impairment and potential correlation with their PCC functional connectivity network.MethodsA total of 14 RGD patients and 18 matched controls were recruited. All subjects finished the neuropsychological tests and functional magnetic resonance imaging scan at baseline and follow‐up. A spherical region of interest was placed in PCC to calculate the functional connectivity, and further analysis was employed to detect correlations between longitudinal changes in the brain regions and neuropsychological data.ResultsThere were significant cognitive declines in RGD patients at baseline and follow‐up. Altered patterns of functional connectivity were detected within the RGD group showing correlations with neuropsychological tests. The longitudinal change in functional connectivity between PCC and cerebellum posterior lobe was correlated with longitudinal changes in auditory verbal memory test‐recall (r = 0.550, P = 0.042). The longitudinal change in functional connectivity between PCC and right parahippocampal gyrus was correlated with Trail Making Test‐A (r = 0.631, P = 0.015). The longitudinal change in functional connectivity between PCC and supramarginal_R was correlated with Mini‐Mental State Examination (r = −0.630, P = 0.016).ConclusionsRGD patients performed worse cognitive function, and altered PCC functional connectivity network might have a role in these cognitive declines.
Mineral trioxide aggregate upregulates odonto/osteogenic capacity of bone marrow stromal cells from craniofacial bones via JNK and ERK MAPK signalling pathways
Authors: Wang Y. , Li J. , Song W. , Yu J. 
Published: March 2014

AbstractObjectivesThe aim of this study was to investigate effects of mineral trioxide aggregate (MTA) on odonto/osteogenic differentiation of bone marrow stromal cells (BMSCs) from craniofacial bones.Materials and methodsCraniofacial BMSCs were isolated from rat mandible and effects of MTA on their proliferation, differentiation and MAPK pathway involvement were subsequently investigated, in vitro. MTT (3‐(4,5‐dimethylthiazol‐2‐yl)‐2,5‐diphenyl‐2,5‐tetrazoliumbromide) assay was performed to evaluate proliferation of the MTA‐treated cells. Alkaline phosphatase (ALP) activity, alizarin red staining, real‐time reverse transcription polymerase chain reaction and western blot assays were used to assess differentiation capacity as well as MAPK pathway involvement.Results0.02 mg/ml MTA‐treated BMSCs had significantly higher ALP activity and formed more mineralized nodules than the untreated group. Odonto/osteoblastic marker genes/proteins (Alp, Runx2/RUNX2, Osx/OSX, Ocn/OCN and Dspp/DSP respectively) in MTA‐treated cells were remarkably upregulated compared to untreated ones. Mechanistically, phosphorylated Jun N‐terminal kinase (P‐JNK) and phosphorylated extracellular regulated protein kinases (P‐ERK) in MTA‐treated BMSCs increased significantly in a time‐dependent manner, while inhibition of JNK and ERK MAPK pathways dramatically blocked MTA‐induced odonto/osteoblastic differentiation, as indicated by reduced ALP levels, weakened mineralization capacity and downregulated levels of odonto/osteoblastic marker genes (Alp, Runx2, Osx, Ocn and Dspp).ConclusionMineral trioxide aggregate promoted odonto/osteogenic capacity of craniofacial BMSCs via JNK and ERK MAPK signalling pathways.
EUS‐guided FNA cytology of pancreatic neuroendocrine tumour (PanNET): a retrospective study of 132 cases over an 18‐year period in a single institution
Authors: Chen S. , Lin J. , Wang X. , Wu H. H. , Cramer H. 
Published: March 2014

ObjectiveTo determine the diagnostic accuracy and pitfalls of endoscopic ultrasound (EUS)‐guided fine needle aspiration (FNA) cytology of pancreatic neuroendocrine tumour (PanNET).MethodsA search of our laboratory information system was performed from July 1992 to June 2010 to identify all FNA cytology and corresponding surgical specimens in which the diagnosis of PanNET was rendered or considered.ResultsOne hundred and thirty‐two cases diagnosed by EUS‐guided FNA were collected. Histological correlation was available for 77 (58%) of FNAs; 55 patients may have been treated elsewhere or had no surgery because of advanced disease or co‐morbidity. Among 56 cases diagnosed as PanNET on FNA, 54 (96%) were confirmed histologically; the remaining two were poorly differentiated adenocarcinoma with focal neuroendocrine features in one case and no tumour was found in the other. Follow‐up histology of nine patients diagnosed as suspicious for PanNET on FNA showed four PanNETs, two pancreatic ductal adenocarcinomas (PDA), one solid pseudopapillary tumour (SPT) and two cases of chronic pancreatitis. Nine cases rendered by FNA as atypical (n = 3), no atypical cells identified (n = 4) or unsatisfactory (n = 2) were PanNETs on histology. Lastly, three cases of oncocytic variant of PanNET were misdiagnosed on FNA as either adenocarcinoma (n = 2) or as suspicious for carcinoma (n = 1).ConclusionsOverall, 54 of the 70 histologically confirmed PanNET cases (77%) were correctly diagnosed by preoperative FNA as PanNET. FNA cases designated as no atypical cells identified and unsatisfactory (7/132, 5%) were attributable to sampling error. Diagnostic pitfalls in our study mainly included PDA, SPT and chronic pancreatitis.
Follow the liar: the effects of adult lies on children's honesty
Authors: Hays Chelsea , Carver Leslie J. 
Published: March 2014

AbstractRecent research shows that most adults admit they lie to children. We also know that children learn through modeling and imitation. To date there are no published studies that examine whether lying to children has an effect on children's honesty. We aimed to bridge the gap in this literature by examining the effects of adults' lies on elementary and preschool‐aged children's behavior using a modified temptation resistance paradigm, in which children are tempted to peek at a toy they have been told not to look at, and later given a chance to either admit peeking, or try to conceal their transgression by lying. Prior to being tested, half of the children were told a lie and half were not. We then measured both cheating (peeking) and lie‐telling behaviors. We hypothesized that lying to a child would increase the likelihood that they would both peek at the toy and lie about having done so. Results showed that school‐age children were more likely to peek if they had been lied to, and were also more likely to lie about peeking. In contrast with the school‐age children, there was no difference in peeking or lying for preschoolers who were and were not lied to. These results have important implications for parenting and educational settings.
A meta‐analysis of the hypoglycaemic risk in randomized controlled trials with sulphonylureas in patients with type 2 diabetes
Authors: Monami M. , Dicembrini I. , Kundisova L. , Zannoni S. , Nreu B. , Mannucci E. 
Published: March 2014

AimTo assess hypoglycaemic risk with sulphonylureas in comparison with other drugs in randomized controlled trials.MethodsRandomized trials with a duration ≥24 weeks, enrolling patients with type 2 diabetes, comparing sulphonylureas with placebo or active drugs different from other sulphonylureas. The principal outcome was the effect of sulphonylureas on the incidence of any or severe hypoglycaemia. Cumulative incidence of hypoglycaemia was estimated combining sulphonylurea groups of different trials with a random effect model and used for meta‐regression analyses.ResultsThe incidence of severe hypoglycaemia in patients treated with sulphonylureas was 1.2 [1.0–1.6]%. The overall risk of severe hypoglycaemia was increased more than threefold with sulphonylureas than with comparators. The proportion of patients with at least one hypoglycaemia while on sulphonylureas was 17.4 [14.5–20.8]%. The overall risk (Mantel–Haenszel Odds Ratio) of any hypoglycaemia with sulphonylureas versus comparators was 3.69 [3.47–3.93] (p < 0.001). Meta‐regression analysis suggested that the incidence of any hypoglycaemia was higher in trials enrolling patients with higher body mass index (BMI) and lower haemoglobin A1c (HbA1c).ConclusionsIn conclusion, hypoglycaemia, including severe hypoglycaemia, is frequent in patients treated with sulphonylureas, particularly when baseline HbA1c levels are lower and BMI levels higher. Further studies are needed to characterize predictors for the identification of patients at higher risk.