bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differences in subjective response to alcohol in heavy‐ and light‐drinking Chinese men versus Caucasian American men
Authors: Rueger Sandra Y. , Hu Hongxing , McNamara Patrick , Cao Dingcai , Hao Wei , King Andrea C. 
Published: September 2014

AbstractAimsTo compare subjective responses to alcohol among Han Chinese and Caucasian American males.DesignDouble‐blinded, placebo‐controlled human laboratory design. Participants completed three randomized experimental sessions with high and low alcohol and placebo beverages.SettingChinese participants were examined at Xinjiang Medical University, China. Caucasian participants were examined at the University of Chicago, USA.Participants Seventy Han Chinese (35 heavy/35 light drinkers) and 75 Caucasian Americans (43 heavy/32 light drinkers).MeasurementsBreath alcohol concentration (BrAC) and the ‘stimulation’ and ‘sedation’ subscales of the Biphasic Alcohol Effects Scale were assessed at pre‐drink baseline and four time‐points after beverage consumption. The ‘like’ and ‘want’ subscales of the Drug Effects Questionnaire were also assessed at the post‐drink assessments.FindingsComparisons with light drinkers showed that high‐ and low‐dose alcohol produced decreases in stimulation, liking and wanting in Chinese versus Caucasians (P < 0.05), and dose‐dependent increases in sedation in both groups (P < 0.001). Among heavy drinkers, high‐dose alcohol produced higher stimulation (P < 0.001) but with concomitant higher sedation for both doses (P < 0.05) for Chinese versus Caucasians. Alcohol also demonstrated significantly lower liking (P < 0.001) in Chinese versus Caucasian heavy drinkers for both doses. Interestingly, both groups showed dose‐dependent increases in wanting relative to placebo (P < 0.05), but the magnitude of the increase was lower in Chinese drinkers.ConclusionsStimulating effects of alcohol are predominant in Chinese male binge drinkers, as has been found in Caucasians, but with less hedonic and motivational reward, potentially explaining some of the lower risk for alcohol disorders in Asian subgroups.
A 19‐Mb de novo deletion on BTA 22 including MITF leads to microphthalmia and the absence of pigmentation in a Holstein calf
Authors: Wiedemar Natalie , Drögemüller Cord 
Published: September 2014

SummaryMutations in MITF lead to a large variety of phenotypes in human, mice and other species. They mostly affect pigmentation and hearing, whereas in mice, they may additionally cause microphthalmia and osteopetrosis. In this study, we report a single case of a Holstein calf with lack of pigmentation and microphthalmia born to healthy parents. Mendelian analysis of high‐density SNP genotypes reveals a large number of parentage errors showing missing paternal alleles in the offspring, indicating a deletion encompassing 19 Mb on BTA 22. The genomic deletion affects the paternal allele and includes MITF and 131 other annotated genes. As the calf shows only one copy of the BTA 22 segment, the observed phenotype is probably caused by haploinsufficiency of the genes in that genomic region. Both the observed lack of skin pigmentation and reduced eye size can most likely be explained by a lack of MITF function.
Genome‐scan analysis for genetic mapping of quantitative trait loci underlying birth weight and onset of puberty in doe kids (Capra hircus)
Authors: Esmailizadeh A. K. 
Published: September 2014

SummaryThe objective of this study was to locate quantitative trait loci (QTL) causing variation in birth weight and age of puberty of doe kids in a population of Rayini cashmere goats. Four hundred and thirty kids from five half‐sib families were genotyped for 116 microsatellite markers located on the caprine autosomes. The traits recorded were birth weight of the male and female kids, body weight at puberty, average daily gain from birth to age of puberty and age at puberty of the doe kids. QTL analysis was conducted using the least squares interval mapping approach. Linkage analysis indicated significant QTL for birth weight on Capra hircus chromosomes (CHI) 4, 5, 6, 18 and 21. Five QTL located on CHI 5, 14 and 29 were associated with age at puberty. Across‐family analysis revealed evidence for overlapping QTL affecting birth weight (78 cM), body weight at puberty (72 cM), average daily gain from birth to age of puberty (72 cM) and age at puberty (76 cM) on CHI 5 and overlapping QTL controlling body weight at puberty and age at puberty on CHI 14 at 18–19 cM. The proportion of the phenotypic variance explained by the detected QTL ranged between 7.9% and 14.4%. Confirming some of the previously reported results for birth weight and growth QTL in goats, this study identified more QTL for these traits and is the first report of QTL for onset of puberty in doe kids.
P‐Wave Duration in Lead aVR and the Risk of Atrial Fibrillation in Hypertension
Authors: Francia Pietro , Ricotta Agnese , Balla Cristina , Adduci Carmen , Semprini Lorenzo , Frattari Alessandra , Modestino Anna , Mercanti Federico , Sensini Isabella , Caprinozzi Massimo , Tocci Giuliano , Volpe Massimo 
Published: September 2014

BackgroundHypertension entails atrial remodeling that affect P‐wave (PW) duration on electrocardiogram (ECG). PW indices (e.g., variance, dispersion, and terminal force) are associated with a higher risk for atrial fibrillation (AF), but their calculation requires multiple measurements of PW duration, limiting their use in clinical practice. We evaluated whether PW duration in specific ECG leads may identify patients with increased susceptibility to AF in a population of hypertensive patients.MethodsIn a case–control study, AF and control subjects were matched for age, sex, and left atrial (LA) dimensions. PW duration was measured from digitally stored ECGs. Logistic regression was used to assess the association of PW duration and indices with AF.ResultsWe enrolled 44 hypertensive AF patients (16 paroxysmal and 28 persistent) and 44 hypertensive controls. AF and control subjects were matched for sex (males, n = 27), age (67 ± 8 years), LA diameter (40 ± 5 mm), and were comparable for left ventricular mass (45 ± 11 g/m2.7 vs 48 ± 12 g/m2.7, P = 0.19), ejection fraction (58 ± 7% in both groups), and prevalence of mild valvular heart disease (7% vs 5%; P = 0.64). PW duration in lead aVR was significantly higher in AF patients as compared with controls (115 ± 18 ms vs 101 ± 14 ms; P < 0.0001) and was the best independent predictor of AF in multivariable logistic regression (PW ≥ 100 ms: RR = 3.7; 95% CI: 1.3–10.3; P = 0.02).ConclusionsSimple measurement of PW duration in lead aVR allows effective identification of AF patients in a population of hypertensives. Confirmation of this finding in a larger population would provide a simple and effective risk marker of AF in hypertensive patients.
Correlation of Electrocardiogram and Regional Cardiac Magnetic Resonance Imaging Findings in ST‐Elevation Myocardial Infarction: A Literature Review
Authors: Rinta‐Kiikka Irina , Tuohinen Suvi , Ryymin Pertti , Kosonen Petteri , Huhtala Heini , Gorgels Anton , Bayés de Luna Antonio , Nikus Kjell 
Published: September 2014

BackgroundPatients with acute ST‐elevation myocardial infarction (STEMI) benefit substantially from emergent coronary reperfusion. The principal mechanism is to open the occluded coronary artery to minimize myocardial injury. Thus the size of the area at risk is a critical determinant of the patient outcome, although other factors, such as reperfusion injury, have major impact on the final infarct size. Acute coronary occlusion almost immediately induces metabolic changes within the myocardium, which can be assessed with both the electrocardiogram (ECG) and cardiac magnetic resonance (CMR) imaging.MethodsThe 12‐lead ECG is the principal diagnostic method to detect and risk‐stratify acute STEMI. However, to achieve a correct diagnosis, it is paramount to compare different ECG parameters with golden standards in imaging, such as CMR. In this review, we discuss aspects of ECG and CMR in the assessment of acute regional ischemic changes in the myocardium using the 17 segment model of the left ventricle presented by American Heart Association (AHA), and their relation to coronary artery anatomy.ResultsUsing the 17 segment model of AHA, the segments 12 and 16 remain controversial. There is an important overlap in myocardial blood supply at the antero‐lateral region between LAD and LCx territories concerning these two segments.ConclusionNo all‐encompassing correlation can be found between ECG and CMR findings in acute ischemia with respect to coronary anatomy.
Cardioprotective and Cardiotoxic Effects of Quercetin and Two of Its In Vivo Metabolites on Differentiated H9c2 Cardiomyocytes
Authors: Daubney James , Bonner Philip L. , Hargreaves Alan J. , Dickenson John M. 
Published: September 2014

AbstractWhilst mitotic rat embryonic cardiomyoblast‐derived H9c2 cells have been widely used as a model system to study the protective mechanisms associated with flavonoids, they are not fully differentiated cardiac cells. Hence, the aim of this study was to investigate the cardioprotective and cardiotoxic actions of quercetin and two of its major in vivo metabolites, quercetin 3‐glucuronide and 3′‐O‐methyl quercetin, using differentiated H9c2 cells. The differentiated cardiomyocyte‐like phenotype was confirmed by monitoring expression of cardiac troponin 1 after 7 days of culture in reduced serum medium containing 10 nM all‐trans retinoic acid. Quercetin‐induced cardiotoxicity was assessed by monitoring MTT reduction, lactate dehydrogenase (LDH) release, caspase 3 activity and reactive oxygen species production after prolonged flavonoid exposure (72 hr). Cardiotoxicity was observed with quercetin and 3′‐O‐methyl quercetin, but not quercetin 3‐glucuronide. Cardioprotection was assessed by pre‐treating differentiated H9c2 cells with quercetin or its metabolites for 24 hr prior to 2‐hr exposure to 600 μM H2O2, after which oxidative stress‐induced cell damage was assessed by measuring MTT reduction and LDH release. Cardioprotection was observed with quercetin and 3′‐O‐methyl quercetin, but not with quercetin 3‐glucuronide. Quercetin attenuated H2O2‐induced activation of ERK1/2, PKB, p38 MAPK and JNK, but inhibitors of these kinases did not modulate quercetin‐induced protection or H2O2‐induced cell death. In summary, quercetin triggers cardioprotection against oxidative stress‐induced cell death and cardiotoxicity after prolonged exposure. Further studies are required to investigate the complex interplay between the numerous signalling pathways that are modulated by quercetin and which may contribute to the cardioprotective and cardiotoxic effects of this important flavonoid.
Effect of urban vs. rural residence on the association between atopy and wheeze in Latin America: findings from a case–control analysis
Authors: Endara P. , Vaca M. , Platts‐Mills T. A. E. , Workman L. , Chico M. E. , Barreto M. L. , Rodrigues L. C. , Cooper P. J. 
Published: September 2014

SummaryBackgroundThe association between atopy and asthma is attenuated in non‐affluent populations, an effect that may be explained by childhood infections such as geohelminths.ObjectiveTo investigate the association between atopy and wheeze in schoolchildren living in urban and rural areas of Ecuador and examine the effects of geohelminths on this association.MethodsWe performed nested case–control studies among comparable populations of schoolchildren living in rural communities and urban neighbourhoods in the Province of Esmeraldas, Ecuador. We detected geohelminths in stool samples, measured recent wheeze and environmental exposures by parental questionnaire, and atopy by specific IgE (sIgE) and skin prick test (SPT) reactivity to aeroallergens.ResultsAtopy, particularly sIgE to house dust mite (HDM), was more strongly associated with recent wheeze in urban than rural schoolchildren: (urban, adj. OR 5.19, 95% CI 3.37–8.00, P < 0.0001; rural, adj. OR 1.81, 95%CI 1.09–2.99, P = 0.02; interaction, P < 0.001). The population fractions of wheeze attributable to atopy were approximately two‐fold greater in urban schoolchildren: SPT to any allergen (urban 23.5% vs. rural 10.1%), SPT to HDM (urban 18.5% vs. rural 9.6%), and anti‐HDM IgE (urban 26.5% vs. rural 10.5%), while anti‐Ascaris IgE was related to wheeze in a high proportion of rural (49.7%) and urban (35.4%) children. The association between atopy and recent wheeze was attenuated by markers of geohelminth infections.ConclusionsOur data suggest that urban residence modifies the association between HDM atopy and recent wheeze, and this effect is explained partly by geohelminth infections.
Optimal management of hypothyroidism, hypothyroxinaemia and euthyroid TPO antibody positivity preconception and in pregnancy
Authors: Chan Shiao , Boelaert Kristien 
Published: September 2014

SummaryNormal physiological changes of pregnancy warrant the need to employ gestation specific reference ranges for the interpretation of thyroid function tests. Thyroid hormones play crucial roles in foetal growth and neurodevelopment which are dependent on adequate supply of maternal thyroid hormones from early gestation onwards. The prevention of significant adverse obstetric and neurodevelopmental outcomes from hypothyroidism requires a strategy of empirical levothyroxine dose increases and predictive dose adjustments in pregnancy combined with regular thyroid function testing, starting before pregnancy and until the postpartum period. Subclinical hypothyroidism has been associated with an increased risk of pregnancy loss and neurocognitive deficits in children, especially when diagnosed before or during early pregnancy. Whilst trials of levothyroxine replacement for mild hypothyroidism in pregnancy have not indicated definite evidence of improvements in these outcomes, professional guidelines recommend treatment, especially if evidence of underlying thyroid autoimmunity is present. Studies of isolated hypothyroxinaemia in pregnancy have shown conflicting evidence with regards to adverse obstetric and neurodevelopmental outcomes and no causative relationships have been determined. Treatment of this condition in pregnancy may be considered in those with underlying thyroid autoimmunity. Whilst the evidence for a link between the presence of anti‐TPO antibodies and increased risks of pregnancy loss and infertility is compelling, the results of ongoing randomized trials of levothyroxine in euthyroid women with underlying autoimmunity are currently awaited. Further studies to define the selection of women who require levothyroxine replacement and to determine the benefits of a predictive dose adjustment strategy are required.
Insulin ameliorating endotoxaemia‐induced muscle wasting is associated with the alteration of hypothalamic neuropeptides and inflammation in rats
Authors: Duan Kaipeng , Yu Wenkui , Lin Zhiliang , Tan Shanjun , Bai Xiaowu , Gao Tao , Xi Fengchan , Li Ning 
Published: September 2014

SummaryObjectivesSeptic patients always develop muscle wasting, which delays the rehabilitation and contributes to the increased complications and mortality. Previous studies have implied the crucial role of central inflammation and neuropeptides in the energy balance and muscle metabolism. Insulin has been confirmed to attenuate muscle degradation and inhibit inflammation. We tested the hypothesis whether insulin ameliorating muscle wasting was associated with modulating hypothalamic inflammation and neuropeptides.Design and subjectsThirty‐two adult male Sprague–Dawley rats were in intraperitoneally injected with lipopolysaccharide (LPS) (5 mg/kg) or saline, followed by subcutaneous injection of insulin (5 IU/kg) or saline. Twenty‐four hours after injection, skeletal muscle and hypothalamus tissues were harvested. Muscle wasting was measured by the mRNA expression of two E3 ubiquitin ligases, muscle ring finger 1 (MuRF‐1) and muscle atrophy F‐box (MAFbx), as well as 3‐methylhistidine (3‐MH) and tyrosine release. Hypothalamic inflammatory markers and neuropeptides expression were also measured in four groups.ResultsLPS injection led to significant increase in hypothalamic inflammation as well as muscle wasting. Also, increased hypothalamic neuropeptides, proopiomelanocortin (POMC), cocaine and amphetamine‐related transcript (CART) and neuropeptides Y (NPY) and decreased agouti‐related protein (AgRP) were observed. Insulin treatment ameliorated endotoxaemia‐induced muscle wasting and hypothalamic inflammation, and attenuated the alteration of neuropeptides, POMC, CART and AgRP.ConclusionHypothalamic inflammation and neuropeptides are involved in the endotoxaemia‐induced muscle wasting. Insulin treatment can reduce muscle wasting, which is associated with reduced hypothalamic inflammation and alteration of hypothalamic neuropeptides.
Two cases of steroid‐responsive encephalomyelitis with reversible diffuse cerebral arterial stenosis: A case report and review of the literature
Authors: Tomizawa Yuji , Kanou Masayoshi , Koinuma Takashi , Misawa Shihoko , Shiotsuki Hiromi , Noda Kazuyuki , Hattori Nobutaka , Okuma Yasuyuki 
Published: September 2014

AbstractWe present two cases of steroid‐responsive encephalomyelitis that showed reversible diffuse cerebral arterial stenosis by magnetic resonance imaging. A 22‐year‐old Asian man and a 37‐year‐old Asian man initially presented with fever and headache. There were no other specific neurological deficits on admission. Cerebrospinal fluid examination showed mononuclear‐dominant pleocytosis; both cases were diagnosed as aseptic meningitis. Cerebrospinal fluid protein levels were relatively high in both cases. Several days after admission, disturbance of consciousness, external ophthalmoplegia and respiratory failure requiring mechanical ventilation occurred. Although there were no specific abnormal findings in the brain parenchyma, magnetic resonance angiography showed diffuse arterial stenosis. Spinal magnetic resonance imaging showed a longitudinally extensive spinal cord lesion. There was no evidence of infectious disease; intravenous methylprednisolone (1 g/day) was given. Both cases responded well to steroid therapy. The diffuse cerebral arterial stenosis in magnetic resonance angiography improved after treatment. Diffuse cerebral arterial stenosis in magnetic resonance angiography combined with high cerebral spinal fluid protein level could be clues to early diagnosis of steroid‐responsive encephalomyelitis. Interestingly, these findings could be interpreted as blood–brain barrier disruption, which is thought to be a main pathophysiology of steroid‐responsive encephalomyelitis.
Does increasing immunoglobulin levels impact survival in solid organ transplant recipients with hypogammaglobulinemia?
Authors: Florescu Diana F. , Kalil Andre C. , Qiu Fang , Grant Wendy , Morris Michael C. , Schmidt Cynthia M. , Florescu Marius C. , Poole Jill A. 
Published: September 2014

AbstractBackgroundSevere hypogammaglobulinemia (IgG < 400 mg/dL) has adverse impact on mortality during the first year post‐transplantation. The aim of the study was to determine whether increasing IgG levels to ≥400 mg/dL improved outcomes.MethodsKaplan–Meier analyses were performed to estimate survival, log‐rank test to compare survival distributions between groups, and Fisher's exact test to determine the association between hypogammaglobulinemia and rejection or graft loss.ResultsThirty‐seven solid organ transplant (SOT) recipients were included. Hypogammaglobulinemia was diagnosed at median of 5.6 months (range: 0–291.8 months) post‐transplantation. Types of transplants: liver–small bowel (17); liver–small bowel–kidney (2); liver (5); small bowel (4); liver–kidney (1); kidney/kidney–pancreas (3); heart (3); heart–kidney (1); and heart–lung (1). The three‐yr survival after the diagnosis of hypogammaglobulinemia was 49.5% (95% CI: 32.2–64.6%). Patients were dichotomized based upon IgG level at last follow‐up: IgG ≥ 400 mg/dL (23 patients) and IgG < 400 mg/dL (14 patients). There was no evidence of a difference in survival (p = 0.44), rejection rate (p = 0.44), and graft loss censored for death (p = 0.99) at one yr between these two groups. There was no difference in survival between patients receiving or not immunoglobulin (p = 0.99) or cytomegalovirus hyperimmunoglobulin (p = 0.14).ConclusionSevere hypogammaglobulinemia after SOT is associated with high mortality rates, but increasing IgG levels to ≥400 mg/dL did not seem to translate in better patient or graft survival in this cohort.
HER2‐Positive Endometrial Cancer Subtype Carries Poor Prognosis
Authors: Łapińska‐Szumczyk Sylwia , Supernat Anna , Majewska Hanna , Gulczyński Jacek , Łuczak Agata , Biernat Wojciech , Wydra Dariusz , Żaczek Anna J. 
Published: September 2014

AbstractEndometrial cancer (EC) is a hormone‐dependent, most frequent malignancy of the female genital tract, yet no molecular subtype classification based receptor status (estrogen receptor [ER], progesterone receptor [PR], human epidermal growth factor receptor 2 [HER2]) has been established so far. Assuming that molecular subtypes might differ fundamentally in EC, we analyzed expression levels of ER, PR, and HER2 with immunohistochemistry and aimed to determine clinical significance of four molecular subtypes: ER+/PR+/HER2+; ER+/PR+/HER2−, ER−/PR−/HER2+, and ER−/PR−/HER2−. The study included 400 formalin‐fixed paraffin‐embedded primary tumor EC samples which covered all stages of endometrial carcinoma, from IA to IVB. ER−/PR−/HER2+ subtype correlated with the poorest outcome, ER+/PR+/HER2− subtype was associated with the most favorable prognosis (p = 0.002). Molecular subtype division remained an independent prognostic factor in multivariate analysis, accompanying parameters such as diabetes, hypertension, stage, myometrial infiltration, and metastases, all of which yielded hazard ratios between 1.39 and 2.23. ER+/PR+/HER2+ and ER+/PR+/HER2− subtypes had low average TP53 and TOP2A expression levels when compared with ER−/PR−/HER2+ and ER−/PR−/HER2− (both p < 0.00001). Molecular subtypes in EC do show diversity in terms of prognosis, clinicopathological, and molecular characteristics. ER−/PR−/HER2+ subtype exhibit is exceptionally aggressive tumor characteristics. Subtype differentiation might aid prediction of treatment response in EC.
Physiological and pathophysiological implications of lipid sensing in the brain
Authors: Picard A. , Moullé V. S. , Le Foll C. , Cansell C. , Véret J. , Coant N. , Le Stunff H. , Migrenne S. , Luquet S. , Cruciani‐Guglielmacci C. , Levin B. E. , Magnan C. 
Published: September 2014

AbstractFatty acid (FA)‐sensitive neurons are present in the brain, especially the hypothalamus, and play a key role in the neural control of energy homeostasis. Through neuronal output, FA may modulate feeding behaviour as well as insulin secretion and action. Subpopulations of neurons in the ventromedial and arcuate hypothalamic nuclei are selectively either inhibited or activated by FA. Molecular effectors of these FA effects probably include chloride or potassium ion channels. While intracellular metabolism and activation of the ATP‐sensitive K+ channel appear to be necessary for some of the signalling effects of FA, at least half of the FA responses in ventromedial hypothalamic neurons are mediated by interaction with FAT/CD36, an FA transporter/receptor that does not require intracellular metabolism to activate downstream signalling. Thus, FA or their metabolites can modulate neuronal activity as a means of directly monitoring ongoing fuel availability by brain nutrient‐sensing neurons involved in the regulation of energy and glucose homeostasis. Recently, the role of lipoprotein lipase in FA sensing has also been shown in animal models not only in hypothalamus, but also in hippocampus and striatum. Finally, FA overload might impair neural control of energy homeostasis through enhanced ceramide synthesis and may contribute to obesity and/or type 2 diabetes pathogenesis in predisposed subjects.