bluuebunny/crossref_metadata_2025_split huggingface dataset:
Rate of X chromosome aneuploidy in young fertile women: Comparison of cultured and uncultured cell preparations using fluorescencein situhybridisation
Authors: PATTON Kirralee , MURCH Ashleigh , GOLDBLATT Jack , WETHERALL John , DOHERTY Dorota , HADLOW Narelle 
Published: June 2010

Background: X chromosome aneuploidy <10% in female patients is a routinely used reporting limit in diagnostic cytogenetics. X aneuploidy (<10%) is commonly detected in women investigated for infertility or recurrent miscarriages. It is unclear if this aneuploidy is causally relevant or related to the culture process. Information about the background rate of X aneuploidy in young fertile women would be helpful in resolving this issue.Aim: This study aimed to investigate the rate of X aneuploidy in young fertile women in cultured and uncultured samples to determine if the commonly used <10% limit is relevant.Method: Volunteers (aged 22–40 years) with proven fertility (n = 78) participated. The number of X chromosome signals in 500 cultured and 500 uncultured preparations were enumerated using FISH.Results: Significantly, all participants had <5% X aneuploidy in both preparations, X chromosome loss occurred (2.4%) more frequently than gain (0.7%). Cultured preparations had a mean of 2.1% cells with X chromosome aneuploidy (95% CI 1.9–2.3%) compared with a mean rate of 0.9% aneuploidy in uncultured preparations (95% CI 0.7–1.1%). The relative risk for cultured preparations having X aneuploidy compared with uncultured cells was 2.33 (P < 0.001) (95% CI 2.1–2.6).Conclusion: Young fertile women had <5% X aneuploidy. The rate of X aneuploidy was higher in cultured (2.1%) compared with uncultured (0.9%) preparations (P < 0.001). This data may provide useful background information when considering low level X aneuploidy in other groups of women with clinical indications for karyotype.
Relationship between the serum CA‐125 level and bone mineral density in healthy pre‐ and post‐menopausal women
Authors: AHN Ki Hoon , PARK Hyun Tae , KIM Tak , HUR Jun Young , KIM Young Tae , LEE Kyu Wan , KIM Sun Haeng 
Published: June 2010

Background:  Osteoporosis and tumour‐associated antigen (TAA) levels are associated with inflammatory processes, but little remains known about TAA levels and bone mineral density (BMD).Aims:  We determined whether or not high‐normal TAA levels are associated with a lower BMD in healthy women.Methods:  A total of 3769 healthy women were enrolled from the health screening programme over 5 years. Each participant had undergone a basic health examination. Serum carbohydrate antigen (CA)‐125, CA‐19‐9, carcinoembryonic antigen (CEA) and alpha‐fetoprotein levels were evaluated as tumour markers. The correlations between serum TAA levels and BMD were analysed.Results:  Carbohydrate antigen 125 and CEA levels were positively associated with a higher BMD in the pre‐menopause. In the post‐menopause, the CA‐125 level was positively associated with BMD. In the pre‐menopause, CA‐125 (r = 0.102; P < 0.001) and CEA levels (r = 0.134; P < 0.001) had a significant correlation with BMD. In the post‐menopause, CA‐125 was negatively associated with alkaline phosphatase (r = −0.298; P < 0.001).Conclusions:  There was a significant positive association between CA‐125 and BMD in healthy women. Additional basic and clinical studies on the relationship between CA‐125 and bone are needed.
Prenatal family support, postnatal family support and postpartum depression
Authors: XIE Ri‐Hua , YANG Jianzhou , LIAO Shunping , XIE Haiyan , WALKER Mark , WEN Shi Wu 
Published: June 2010

Background:  Inadequate social support is an important determinant of postpartum depression (PPD). Social support for pregnant women consists of supports from various sources and can be measured at different gestation periods. Differentiating the effects of social support from different sources and measured at different gestation periods may have important implications in the prevention of PPD. In the family centred Chinese culture, family support is likely to be one of the most important components in social support.Aims:  The aim of this study was to assess the association of prenatal family support and postnatal family support with PPD.Methods:  A prospective cohort study was conducted between February and September 2007 in Hunan, China. Family support was measured with social support rating scale at 30–32 weeks of gestation (prenatal support) and again at 2 weeks of postpartum visit (postnatal support). PPD was defined as Edinburgh Postnatal Depression Scale (EPDS) score ≥13.Results:  A total of 534 pregnant women were included, and among them, 103 (19.3%) scored 13 or more on the EPDS. PPD was 19.4% in the lowest tertile versus 18.4% in the highest quartile (adjusted odds ratio: 1.04, 95% confidence interval 0.60, 1.80) for prenatal support from all family members, and PPD was 39.8% in the lowest tertile versus 9.6% in the highest tertile (adjusted odds ratio: 4.4, 95% confidence interval 2.3, 8.4) for postnatal support from all family members. Among family members, support from husband had the largest impact on the risk of developing PPD.Conclusions:  Lack of postnatal family support, especially the support from husband, is an important risk factor of PPD.
Taxonomic status of Amebachia Uchida in the genus Netelia Gray (Hymenoptera; Ichneumonidae; Tryphoninae) with descriptions of four new species from Japan
Authors: KONISHI Kazuhiko 
Published: June 2010

AbstractThe lectotype of Amebachia baibarana Uchida, 1928, which is the type species of Amebachia Uchida, was re‐examined. Though this species was synonymized with Netelia (Netelia) laevis (= Paniscus laevis Cameron, 1905) and Amebachia has been synonymized under the subgenus Netelia of the genus Netelia, it is concluded that A. baibarana is a distinct species from N. laevis and Amebachia should be a subgenus of the genus Netelia. Netelia laevis is transferred from the subgenus Netelia to Apatagium. Four new species of Netelia (Amebachia), N. (A.) yoshimatsui sp. nov., N. (A.) rasilella sp. nov., N. (A.) fulvistigma sp. nov., and N. (A.) vicinalis sp. nov. are described from Japan, and a key to the species of this subgenus is provided.
Quercetin and Ethanol Attenuate the Progression of Atherosclerotic Plaques With Concomitant Up Regulation of Paraoxonase1 (PON1) Gene Expression and PON1 Activity in LDLR−/− Mice
Authors: Leckey Leslie C. , Garige Mamatha , Varatharajalu Ravi , Gong Maokai , Nagata Takako , Spurney Christopher F. , Lakshman Raj M. 
Published: June 2010

Background:  As moderate wine drinking is atheroprotective, it is clinically relevant to elucidate its possible mechanism/s of action/s. Our objective is to demonstrate the potential benefits of the wine components, quercetin and ethanol, on the development of aortic plaques with parallel changes in antiatherogenic factors.Methods and Results:  The effects of quercetin and ethanol on the development of aortic atherosclerotic lesions, liver PON1 gene expression, and serum PON1 activity were measured in LDLR−/− mice on an atherogenic diet for 4 and 8 weeks. Depending on the duration and dosage of these modulators, 12.5 to 25 mg/dl quercetin (12.5Q to 25Q) and 18 to 25% ethanol, the magnitude of decreases in aortic lesions caused by moderate ethanol and quercetin ranged from 20 to 70% (p < 0.05 to p < 0.001) based on ultrasound biomicroscopy (UBM) analyses, and from 18 to 61% (p < 0.05 to p < 0.001) based on morphometric analyses. The composite plot of all the UBM and morphometric data showed significant correlation between these 2 methods (p = 0.0001, Pearson r = 0.79 for 4‐week treatment; p = 0.000004, Pearson r = 0.84 for 8‐week treatment). Concomitantly, 4‐week treatments with 12.5Q and 18% ethanol up regulated liver PON1 mRNA by 41% (p < 0.05) and 37% (p < 0.05), respectively, accompanied by 92% (p < 0.001) and 61% (p < 0.001) increases in serum PON1 activity, respectively. The corresponding values after 8‐week treatment with 12.5Q and 18% ethanol were 23% (p < 0.05) and 40% (p < 0.02) with respect to the up regulation of liver PON1 mRNA expression, while the stimulations of serum PON1 activity were 75% (p < 0.001) and 90% (p < 0.001), respectively.Conclusions:  Based on these findings, we conclude that quercetin and moderate ethanol significantly inhibit the progression of atherosclerosis by up regulating the hepatic expression of the antiatherogenic gene, PON1, with concomitant increased serum PON1 activity.
Differential Changes in MAP Kinases, Histone Modifications, and Liver Injury in Rats Acutely Treated With Ethanol
Authors: Aroor Annayya R. , James Taryn T. , Jackson Daniel E. , Shukla Shivendra D. 
Published: June 2010

Background:  Acute ethanol is known to affect cells and organs but the underlying molecular mechanisms are poorly explored. Recent developments highlight the potential importance of mitogen‐activated protein kinases, MAPKs (i.e., ERK1/2, p38, and JNK1/2) signaling, and histone modifications (i.e., acetylation, methylation, and phosphorylation) in the actions of ethanol in hepatocytes. We have therefore investigated significance of these molecular steps in vivo using a model in which rats were acutely administered ethanol intraperitoneally (IP).Methods:  Ethanol was administered IP (3.5 gm/kg body weight) to 12‐week‐old male Sprague–Dawley rats. Liver was subsequently removed at 1 and 4 hours. Serum was used for alcohol and ALT assays. At the time of the removal of liver, small portions of each liver were formalin‐fixed and stained with hematoxylin and eosin (H&E) and used for light microscopy. Western blot analysis was carried out with specific primary antibodies for various parameters.Results:  There were clear differences at 1 and 4 hours in blood ethanol, ALT, steatosis, and cleaved caspase 3. Apoptosis at 1 hour was followed by necrosis at 4 hours. Acute alcohol elicited a marked increase in the phosphorylation of ERK1/2 and moderate increases in the phosphorylation of p38 MAPK and JNK. Temporally different phosphorylation of histone H3 at ser‐10 and ser‐28 occurred and acetylation of histone H3 at lys 9 increased progressively.Conclusions:  There were distinct differences in the behavior of the activation of the 3 MAP kinases and histone modifications after acute short exposure of liver to ethanol in vivo. Although all 3 MAPKs were rapidly activated at 1 hour, the necrosis, occurring at 4 hours, correlated to sustained activation of ERK1/2. Transient activation of p38 is associated with rapid phosphorylation of histone H3, whereas prolonged activation of ERK1/2 is correlated to persistent histone H3 acetylation.
Withdrawal Severity After Chronic Intermittent Ethanol in Inbred Mouse Strains
Authors: Metten Pamela , Sorensen Michelle L. , Cameron Andy J. , Yu Chia‐Hua , Crabbe John C. 
Published: June 2010

Background: To study withdrawal, ethanol is usually administered chronically without interruption. However, interest has recurred in models of episodic exposure. Increasing evidence suggests that chronic intermittent exposure to ethanol leads to a sensitization effect in both withdrawal severity and ethanol consumption. The goal of the present study was to examine mouse inbred strain differences in withdrawal severity following chronic intermittent exposure using the handling‐induced convulsion as the behavioral endpoint. We also sought to compare the withdrawal responses of inbred strains across acute, chronic continuous, and chronic intermittent exposure regimens.Methods: Male mice from 15 standard inbred strains were exposed to ethanol vapor for 16 hours each day for 3 days and removed to an air chamber during the intervening 8 hours. Mice in the control groups were handled the same, except that they were exposed only to air. Daily blood ethanol concentrations were averaged for each mouse to estimate total dose of ethanol experienced.Results: Across strains, mice had an average daily blood ethanol concentration (BEC) of 1.45 ± 0.02 mg/ml and we restricted the range of this value to 1.00–2.00 mg/ml. To evaluate strain differences, we divided data into two dose groups based on BEC, low dose (1.29 ± 0.1 mg/ml) and high dose (1.71 ± 0.02 mg/ml). After the third inhalation exposure, ethanol‐exposed and air‐exposed groups were tested hourly for handling‐induced convulsions for 10 hour and at hour 24 and 25. Strains differed markedly in the severity of withdrawal (after subtraction of air control values) in both dose groups.Conclusion: The chronic intermittent exposure paradigm is sufficient to elicit differential withdrawal responses across nearly all strains. Data from the high‐dose groups correlated well with withdrawal data derived from prior acute (single high dose) and chronic continuous (for 72 hours) ethanol withdrawal studies, supporting the influence of common genes on all three responses.
Motivation for Alcohol Becomes Resistant to Quinine Adulteration After 3 to 4 Months of Intermittent Alcohol Self‐Administration
Authors: Hopf Frederic W. , Chang Shao‐Ju , Sparta Dennis R. , Bowers Michael S. , Bonci Antonello 
Published: June 2010

Background:  Continued consumption of alcohol despite deleterious consequences is a hallmark of alcoholism and represents a critical challenge to therapeutic intervention. Previous rat studies showed that enduring alcohol self‐administration despite pairing alcohol with normally aversive stimuli was only observed after very long‐term intake (>8 months). Aversion‐resistant alcohol intake has been previously interpreted to indicate pathological or compulsive motivation to consume alcohol. However, given the time required to model compulsive alcohol seeking in previous studies, there is considerable interest in developing more efficient and quantitative rodent models of aversion‐resistant alcohol self‐administration.Methods:  Outbred Wistar rats underwent 3 to 4 months or approximately 1.5 months of intermittent, home‐cage, two‐bottle access (IAA) to 20% alcohol (v/v) or water. Then, after brief operant training, the effect of the bitter‐tasting quinine (0.1 g/l) on the motivation to seek alcohol was quantified via progressive ratio (PR). Motivation for quinine‐adulterated 2% sucrose under PR was assayed in a separate cohort of 3 to 4 months IAA rats. The effects of quinine on home‐cage alcohol consumption in IAA rats and rats with continuous access to alcohol were also examined. Finally, a dose–response for quinine taste preference in IAA and continuous‐access animals was determined.Results:  Motivation for alcohol after 3 to 4 months IAA, measured using an operant PR procedure, was not altered by adulteration of alcohol with 0.1 g/l quinine. In contrast, after 3 to 4 months of IAA, motivation for sucrose under PR was significantly reduced by adulteration of sucrose with 0.1 g/l quinine. In addition, motivation for alcohol after only approximately 1.5 months IAA was significantly reduced by adulteration of alcohol with 0.1 g/l quinine. Furthermore, home‐cage alcohol intake by IAA rats was insensitive to quinine at concentrations (0.01, 0.03 g/l) that significantly reduced alcohol drinking in animals with continuous access to alcohol. Finally, no changes in quinine taste preference after 3 to 4 months IAA or continuous access to alcohol were observed.Conclusions:  We have developed a novel and technically simple hybrid operant/IAA model in which quinine‐resistant motivation for alcohol is evident after an experimentally tractable period of time (3 to 4 months vs. 8 months). Quinine dramatically reduced sucrose and water intake by IAA rats, indicating that continued responding for alcohol in IAA rats despite adulteration with the normally aversive quinine might reflect maladaptive or compulsive motivation for alcohol. This model could facilitate identification of novel therapeutic interventions for pathological alcohol seeking in humans.
Delay Discounting Behavior and White Matter Microstructure Abnormalities in Youth With a Family History of Alcoholism
Authors: Herting Megan M. , Schwartz Daniel , Mitchell Suzanne H. , Nagel Bonnie J. 
Published: June 2010

Background:  Youth with family history of alcohol abuse have a greater risk of developing an alcohol use disorder (AUD). Brain and behavior differences may underlie this increased vulnerability. The current study examined delay discounting behavior and white matter microstructure in youth at high risk for alcohol abuse, as determined by a family history of alcoholism (FH+), and youth without such family history (FH−).Methods:  Thirty‐three healthy youth (FH+ = 15, FH− = 18), ages 11 to 15 years, completed a delay discounting task and underwent diffusion tensor imaging. Tract‐based spatial statistics (Smith et al., 2006), as well as follow‐up region‐of‐interest analyses, were performed to compare fractional anisotropy (FA) between FH+ and FH− youth.Results:  FH+ youth showed a trend toward increased discounting behavior and had significantly slower reaction times (RTs) on the delay discounting paradigm compared to FH− youth. Group differences in FA were seen in several white matter tracts. Furthermore, lower FA in the left inferior longitudinal fasciculus and the right optic radiation statistically mediated the relationship between FH status and slower RTs on the delay discounting task.Conclusions:  Youth with a family history of substance abuse have disrupted white matter microstructure, which likely contributes to less efficient cortical processing and may act as an intrinsic risk factor contributing to an increased susceptibility of developing AUD. In addition, FHP youth showed a trend toward greater impulsive decision making, possibly representing an inherent personal characteristic that may facilitate substance use onset and abuse in high‐risk youth.
Period 2 Gene Deletion Abolishes β‐Endorphin Neuronal Response to Ethanol
Authors: Agapito Maria , Mian Nadia , Boyadjieva Nadka I. , Sarkar Dipak K. 
Published: June 2010

Background:  Ethanol exposure during early life has been shown to permanently alter the circadian expression of clock regulatory genes and the β‐endorphin precursor proopiomelanocortin (POMC) gene in the hypothalamus. Ethanol also alters the stress‐ and immune‐regulatory functions of β‐endorphin neurons in laboratory rodents. Our aim was to determine whether the circadian clock regulatory Per2 gene modulates the action of ethanol on β‐endorphin neurons in mice.Methods:  Per2 mutant (mPer2Brdml) and wild type (C57BL/6J) mice were used to determine the effect of Per2 mutation on ethanol‐regulated β‐endorphin neuronal activity during neonatal period using an in vitro mediobasal hypothalamic (MBH) cell culture model and an in vivo milk formula feeding animal model. The β‐endorphin neuronal activity following acute and chronic ethanol treatments was evaluated by measuring the peptide released from cultured cells or peptide levels in the MBH tissues, using enzyme‐linked immunosorbent assay (ELISA).Results:  Per2 mutant mice showed a higher basal level of β‐endorphin release from cultured MBH cells and a moderate increase in the peptide content in the MBH in comparison with control mice. However, unlike wild type mice, Per2 mutant mice showed no stimulatory or inhibitory β‐endorphin‐secretory responses to acute and chronic ethanol challenges in vitro. Furthermore, Per2 mutant mice, but not wild type mice, failed to show the stimulatory and inhibitory responses of MBH β‐endorphin levels to acute and chronic ethanol challenges in vivo.Conclusions:  These results suggest for the first time that the Per2 gene may be critically involved in regulating β‐endorphin neuronal function. Furthermore, the data revealed an involvement of the Per2 gene in regulating β‐endorphin neuronal responses to ethanol.
Ethanol Enhances Taurine‐Activated Glycine Receptor Function
Authors: Welsh Brian T. , Kirson Dean , Allen Hunter M. , Mihic S. John 
Published: June 2010

Background: Emerging evidence suggests that taurine acts as a partial agonist on glycine receptors (GlyR) in vitro and in vivo. Ethanol acts as an allosteric modulator on the GlyR producing a leftward shift of the glycine concentration–response curve, with no enhancing effects observed at saturating glycine concentrations. However, to date, no electrophysiological studies have been performed on ethanol modulation of taurine‐activated GlyR.Methods: Wild‐type α1 GlyR, or those bearing a serine‐267 to isoleucine replacement (S267I), were homomerically expressed inXenopusoocytes and voltage clamped at −70 mV. Ethanol was co‐applied with varying concentrations of glycine or taurine and the enhancing effects of ethanol compared.Results: Ethanol potentiated glycine‐ and taurine‐activated GlyR responses in a concentration‐dependent manner. It shifted taurine and glycine concentration–response curves to the left, having no effects at saturating agonist concentrations. Chelation of zinc by tricine decreased ethanol enhancement of taurine‐gated GlyR function. The S267I mutation prevented ethanol enhancement of taurine‐mediated responses as previously also reported for glycine.Conclusion: Ethanol modulates taurine activation of GlyR function by a mechanism similar to that of the full agonist glycine. The lack of effect of ethanol at saturating taurine concentrations provides mechanistic information on alcohol actions at the GlyR.
Clinical Significance of Early Recurrences of Atrial Tachycardia After Atrial Fibrillation Ablation
Authors: CHOI JONG‐IL , PAK HUI‐NAM , PARK JAE SEOK , KWAK JAE JIN , NAGAMOTO YASUTSUGU , LIM HONG EUY , PARK SANG WEON , HWANG CHUN , KIM YOUNG‐HOON 
Published: June 2010

Early Recurrence After AF Ablation. Background: Atrial tachycardia (AT) commonly recurs within 3 months after radiofrequency catheter ablation for atrial fibrillation (AF). However, it remains unclear whether early recurrence of atrial tachycardia (ERAT) predicts late recurrence of AF or AT. Methods: Of 352 consecutive patients who underwent circumferential pulmonary vein isolation with or without linear ablation(s) for AF, 56 patients (15.9%) with ERAT were identified by retrospective analysis. ERAT was defined as early relapse of AT within a 3‐month blanking period after ablation. Results: During 21.7 ± 12.5 months, the rate of late recurrence was higher in patients with ERAT (41.1%) compared with those without ERAT (11.8%, P < 0.001). In a multivariable model, positive inducibility of AF or AT immediately after ablation (65.2% vs 36.4%, P = 0.046; odd ratio, 3.9; 95% confidence interval, 1.0–14.6) and the number of patients who underwent cavotricuspid isthmus (CTI) ablation (73.9% vs 42.4%, P = 0.042; odd ratio, 4.5; 95% confidence interval, 1.1–19.5) were significantly related to late recurrence in the ERAT group. The duration of ablation (174.3 ± 62.3 vs 114.7 ± 39.5 minutes, P = 0.046) and the procedure time (329.3 ± 83.4 vs 279.2 ± 79.7 minutes, P = 0.027) were significantly longer in patients with late recurrence than in those without late recurrence following ERAT. Conclusions: The late recurrence rate is higher in the patients with ERAT compared with those without ERAT following AF ablation, and is more often noted in the patients who underwent CTI ablation and had a prolonged procedure time. Furthermore, inducibility of AF or AT immediately after ablation independently predicts late recurrence in patients with ERAT. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1331‐1337, December 2010)