bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genetic population structure in the boky‐boky (Carnivora: Eupleridae), a conservation flagship species in the dry deciduous forests of central western Madagascar
Authors: van Vuuren B. Jansen , Woolaver L. , Goodman S. M. 
Published: October 2011

AbstractThe boky‐boky, Mungotictis decemlineata, is an endemic and presumed forest‐dependent carnivoran species restricted to lowland central western Madagascar. It inhabits dry deciduous forests, which have been severely reduced in surface area with ∼60% destroyed or degraded by humans during the past 60 years. M. decemlineata is limited to the remnant forests of the central and southern Menabe, and using samples collected from sites across this zone, a phylogeographic study was conducted based on two mitochondrial (1140 base pairs [bp] of cytochrome b and 563 bp of the control region) and one nuclear fragment (591 bp of the seventh intron of the fibrinogen gene). Forty‐seven individuals were included from the central Menabe from four principal localities and two animals from the southern Menabe from a single locality. Low sequence divergence (1.65% for the combined fragment, 4.26% for the control region and 0.78% for cytochrome b) characterized specimens across a zone of 130 km delimited by the Tsiribihina River to the north and the Mangoky River to the south; this area includes most of the geographical range of M. decemlineata. Phylogenetic trees, haplotype networks and exact test of population differentiation did not reveal any meaningful geographic partitioning of genetic variation. However, shallow yet significant genetic structure was revealed by ΦST calculations for the combined as well as separate DNA fragments, which we ascribe to isolation‐by‐distance. We proposed two different scenarios to explain the lack of meaningful phylogeographical structure in Mungotictis: (1) for this forest‐dependent species, dispersal during periods of more continuous forest cover gave rise to a genetic meta‐population or (2) that it is able to cross non‐forested zones and broadly disperses, leading to high levels of genetic homogeneity. Current inferences favour the first hypothesis. The short‐ and medium‐term future of this taxon is in jeopardy associated with habitat destruction across its geographical range.
An analysis of the interrelationship between maternal age, body mass index and racial origin in the development of gestational diabetes mellitus
Authors: Makgoba M , Savvidou MD , Steer PJ 
Published: October 2011

Please cite this paper as: Makgoba M, Savvidou M, Steer P. An analysis of the interrelationship between maternal age, body mass index and racial origin in the development of gestational diabetes mellitus. BJOG 2011; DOI: 10.1111/j.1471‐0528.2011.03156.x.Objective  To examine the individual association between advancing maternal age, body mass index (BMI) and racial origin with the development of gestational diabetes mellitus (GDM) and the interaction between these factors.Design  Retrospective study.Setting  Fifteen maternity units in northwest London between 1988 and 2000.Population  The study included 1688 women who developed GDM and 172 632 who did not. All women were nulliparous. BMI was calculated at first antenatal visit and maternal age and racial origin (White European, Black African, Black Caribbean or South Asian) were self‐reported.Methods  Binary logistic regression analysis.Main outcome measures  Development of GDM within each racial group.Results  There was a strong positive association between advancing maternal age and increasing BMI, individually, and the development of GDM (P < 0.01 for both). Compared with White Europeans aged 20–24 years, the odds ratios for GDM development were significantly higher in women older than 30 years if they were White Europeans (P < 0.001), older than 25 years if they were Black Africans (P < 0.001) and older than 20 years if they were South Asians (P < 0.001). The odds ratios for GDM development were significantly higher in Black Africans and South Asians (P < 0.001 for both) irrespective of BMI, compared with White Europeans with normal BMI.Conclusion  Maternal age and BMI interact with racial group in relation to the prevalence of GDM. Both factors are important in the development of GDM, particularly so in Black African and South Asian women.
Brain‐derived neurotrophic factor uses CREB and Egr3 to regulate NMDA receptor levels in cortical neurons
Authors: Kim Julia H. , Roberts Daniel S. , Hu Yinghui , Lau Garrick C. , Brooks‐Kayal Amy R. , Farb David H. , Russek Shelley J. 
Published: October 2011

J. Neurochem. (2012) 120, 210–219.AbstractRegulation of gene expression via brain‐derived neurotrophic factor (BDNF) is critical to the development of the nervous system and may well underlie cognitive performance throughout life. We now describe a mechanism by which BDNF can exert its effects on postsynaptic receptor populations that may have relevance to both the normal and diseased brain where BDNF levels either rise or fall in association with changes in excitatory neurotransmission. Increased levels of NMDA receptors (NMDARs) occur in rat cortical neurons via synthesis of new NMDA receptor 1 (NR1) subunits. The majority of synthesis is controlled by binding of cAMP response element binding protein (CREB) and early growth response factor 3 (Egr3) to the core NR1 promoter (NR1‐p) region. BDNF‐mediated NR1 transcription depends upon induction of the mitogen‐activated protein kinase (MAPK) pathway through activation of the TrK‐B receptor. Taken together with the fact that NMDAR activation stimulates BDNF synthesis, our results uncover a feed‐forward gene regulatory network that may enhance excitatory neurotransmission to change neuronal behavior over time.
Acute administration of fluoxetine normalizes rapid eye movement sleep abnormality, but not depressive behaviors in olfactory bulbectomized rats
Authors: Wang Yi‐Qun , Tu Zhi‐Cai , Xu Xing‐Yuan , Li Rui , Qu Wei‐Min , Urade Yoshihiro , Huang Zhi‐Li 
Published: October 2011

J. Neurochem. (2012) 120, 314–324.AbstractIn humans, depression is associated with altered rapid eye movement (REM) sleep. However, the exact nature of the relationship between depressive behaviors and sleep abnormalities is debated. In this study, bilateral olfactory bulbectomy (OBX) was carried out to create a model of depression in rats. The sleep–wake profiles were assayed using a cutting‐edge sleep bioassay system, and depressive behaviors were evaluated by open field and forced swimming tests. The monoamine content and monoamine metabolite levels in the brain were determined by a HPLC‐electrochemical detection system. OBX rats exhibited a significant increase in REM sleep, especially between 15:00 and 18:00 hours during the light period. Acute treatment with fluoxetine (10 mg/kg, i.p.) immediately abolished the OBX‐induced increase in REM sleep, but hyperactivity in the open field test and the time spent immobile in the forced swimming test remained unchanged. Neurochemistry studies revealed that acute administration of fluoxetine increased serotonin (5‐HT) levels in the hippocampus, thalamus, and midbrain and decreased levels of the 5‐HT metabolite 5‐hydroxyindoleacetic acid (5‐HIAA). The ratio of 5‐HIAA to 5‐HT decreased in almost all regions of the brain. These results indicate that acute administration of fluoxetine can reduce the increase in REM sleep but does not change the depressive behaviors in OBX rats, suggesting that there was no causality between REM sleep abnormalities and depressive behaviors in OBX rats.
D2‐Dopamine receptors target regulator of G protein signaling 9‐2 to detergent‐resistant membrane fractions
Authors: Celver Jeremy , Sharma Meenakshi , Kovoor Abraham 
Published: October 2011

J. Neurochem. (2012) 120, 56–69.AbstractDetergent‐resistant membranes (DRM) are thought to contain structures such as lipid rafts that are involved in compartmentalizing cell membranes. We report that the majority of D2‐dopamine receptors (D2R) expressed endogenously in mouse striatum or expressed in immortalized cell‐lines is found in DRM. In addition, exogenous co‐expression of D2R in a cell line shifted the expression of regulator of G protein signaling 9‐2 (RGS9‐2) into DRM. RGS9‐2 is a protein that is highly enriched in the striatum and specifically regulates striatal D2R. In the striatum, RGS9‐2 is mostly associated with DRMs but when expressed in cell lines, RGS9‐2 is present in the soluble cytoplasmic fraction. In contrast, the majority of mu opioid receptors and delta opioid receptors are found in detergent‐soluble membrane and there was no shift of RGS9‐2 into DRM after co‐expression of mu opioid receptor. These data suggest that the targeting of RGS9‐2 to DRM in the striatum is mediated by D2R and that DRM is involved in the formation of a D2R signaling complex. D2R‐mediated targeting of RGS9‐2 to DRM was blocked by the deletion of the RGS9‐2 DEP domain or by a point mutation that abolishes the GTPase accelerating protein function of RGS9‐2.
Intraportal administration of DPP‐IV inhibitor regulates insulin secretion and food intake mediated by the hepatic vagal afferent nerve in rats
Authors: Fujiwara Kansuke , Gotoh Koro , Chiba Seiichi , Masaki Takayuki , Katsuragi Isao , Kakuma Tetsuya , Yoshimatsu Hironobu 
Published: October 2011

J. Neurochem. (2012) 121, 66–76.AbstractGlucagon‐like peptide‐1 (GLP‐1) stimulates insulin secretion and suppresses food intake. Recent studies indicate that the hepatic vagal afferent nerve is involved in this response. Dipeptidyl peptidase‐IV (DPP‐IV) inhibitor extends the half‐life of endogenous GLP‐1 by preventing its degradation. This study aimed to determine whether DPP‐IV inhibitor‐induced elevation of portal GLP‐1 levels affect insulin secretion and feeding behavior via the vagal afferent nerve and hypothalamus. The effect of DPP‐IV inhibitor infusion into the portal vein or peritoneum on portal and peripheral GLP‐1 levels, food intake, and plasma insulin and glucose was examined in sham‐operated and vagotomized male Sprague–Dawley rats. Analyses of neuronal histamine turnover and immunohistochemistry were used to identify the CNS pathway that mediated the response. Intraportal administration of the DPP‐IV inhibitor significantly increased portal (but not peripheral) GLP‐1 levels, increased insulin levels, and decreased glucose levels. The DPP‐IV inhibitor suppressed 1‐ and 12‐ but not 24‐h cumulative food intake. Intraportal infusion of the DPP‐IV inhibitor increased hypothalamic neuronal histamine turnover and increased c‐fos expression in several areas of the brain. These responses were blocked by vagotomy. Our results indicate that DPP‐IV inhibitor‐induced changes in portal but not systemic GLP‐1 levels affect insulin secretion and food intake. Furthermore, our findings suggest that a neuronal pathway that includes the hepatic vagal afferent nerve and hypothalamic neuronal histamine plays an important role in the pharmacological actions of DPP‐IV inhibitor.
Control of neurite outgrowth by RhoA inactivation
Authors: Jeon Chan‐Young , Moon Mi‐Young , Kim Jong‐Hyun , Kim Hee‐Jun , Kim Jae‐Gyu , Li Yi , Jin Jae‐Kwang , Kim Pyeung‐Hyeun , Kim Hyoung‐Chun , Meier Kathryn E. , Kim Yong‐Sun , Park Jae‐Bong 
Published: October 2011

J. Neurochem.(2012)120, 684–698.AbstractcAMP induces neurite outgrowth in the rat pheochromocytoma cell line 12 (PC12). In particular, di‐butyric cAMP (db‐cAMP) induces a greater number of primary processes with shorter length than the number induced by nerve growth factor (NGF). db‐cAMP up‐ and down‐regulates GTP‐RhoA levels in PC12 cells in a time‐dependent manner. Tat‐C3 toxin stimulates neurite outgrowth, whereas lysophosphatidic acid (LPA) and constitutively active (CA)‐RhoA reduce neurite outgrowth, suggesting that RhoA inactivation is essential for the neurite outgrowth from PC12 cells stimulated by cAMP. In this study, the mechanism by which RhoA is inactivated in response to cAMP was examined. db‐cAMP induces phosphorylation of RhoA and augments the binding of RhoA with Rho guanine nucleotide dissociation inhibitor (GDI). Moreover, RhoA (S188D) mimicking phosphorylated RhoA induces greater neurite outgrowth than RhoA (S188A) mimicking dephosphorylated form does. Additionally, db‐cAMP increases GTP‐Rap1 levels, and dominant negative (DN)‐Rap1 and DN‐Rap‐dependent RhoGAP (ARAP3) block neurite outgrowth induced by db‐cAMP. DN‐p190RhoGAP and the Src inhibitor PP2 suppress neurite outgrowth, whereas transfection of c‐Src and p190RhoGAP cDNAs synergistically stimulate neurite outgrowth. Taken together, RhoA is inactivated by phosphorylation of itself, by p190RhoGAP which is activated by Src, and by ARAP3 which is activated by Rap1 during neurite outgrowth from PC12 cells in response to db‐cAMP.
Visual guidance of recovery from lens‐induced myopia in tree shrews (Tupaia glis belangeri)
Authors: Amedo Angela O , Norton Thomas T 
Published: October 2011

Citation information: Amedo AO & Norton TT. Visual guidance of recovery from lens‐induced myopia in tree shrews (Tupaia glis belangeri). Ophthalmic Physiol Opt 2012, 32, 89–99. doi: 10.1111/j.1475‐1313.2011.00875.xAbstractPurpose:  To examine, in tree shrews, the visual guidance of recovery from negative lens‐induced myopia by measuring the effect of wearing low‐power negative or positive lenses during recovery. To learn if removing a negative lens for 2 h per day, after compensation has occurred, is sufficient to produce recovery.Methods:  Starting 16 days after natural eye opening (days of visual experience), juvenile tree shrews wore a monocular −5 D lens for 11 days to produce compensation (age‐appropriate refraction while wearing the lens). Recovery in four groups was started by discontinuing −5 D lens wear, which caused the treated eyes to be refractively myopic, and substituting: no lens (n = 7), a plano lens (n = 8), a −2 D lens (n = 6) or a +2 D lens (n = 10). In a fifth group (n = 6), the −5 D lens was removed for 2 h each day but worn the remainder of the time. Non‐cycloplegic refractive measurements were made daily for the first 10 days and then less frequently. After 31–35 days, the lens‐guided recovery period was ended for most animals; periodic measures were continued to assess post‐lens recovery changes.Results:  All the eyes responded to the −5 D lens and were myopic (−4.8 ± 0.1 D, mean ± S.E.M.) compared to the untreated fellow control eye. In all groups except the −2 D lens group, some animals exhibited slow or incomplete recovery. During recovery, the treated eye of most animals recovered until its refraction, measured with the recovery‐lens in place, was near to that of the control eye. Measured without the lens, the −2 D group was myopic and the +2 D group was hyperopic. With the lens in place, the plano‐lens, −2 D lens, and +2 D lens groups remained slightly myopic (−1.0 ± 0.3 D, −0.6 ± 0.2 D and −1.3 ± 0.1 D, respectively). The rate of recovery during the first four days was unrelated to the amount of myopia initially experienced by the recovering eyes. Removal of the −5 D lens for 2 h each day produced recovery.Conclusions:  During recovery, the emmetropization mechanism uses the presence of myopia, but perhaps not the magnitude, to guide eyes toward a refractive state similar to the control eye, regardless of whether the optically‐recovered eye is longer or shorter than the fellow control eye. Wearing a goggle frame containing a lens of any power limits the recovery. The recovery signal can be intermittent, present for only 2 h per day, and still mediate recovery in competition with increasing amounts of hyperopia as recovery progresses.
Mechanism of action of the insecticides, lindane and fipronil, on glycine receptor chloride channels
Authors: Islam Robiul , Lynch Joseph W 
Published: October 2011

BACKGROUND AND PURPOSE Docking studies predict that the insecticides, lindane and fipronil, block GABAA receptors by binding to 6′ pore‐lining residues. However, this has never been tested at any Cys‐loop receptor. The neurotoxic effects of these insecticides are also thought to be mediated by GABAA receptors, although a recent morphological study suggested glycine receptors mediated fipronil toxicity in zebrafish. Here we investigated whether human α1, α1β, α2 and α3 glycine receptors were sufficiently sensitive to block by either compound as to represent possible neurotoxicity targets. We also investigated the mechanisms by which lindane and fipronil inhibit α1 glycine receptors.EXPERIMENTAL APPROACH Glycine receptors were recombinantly expressed in HEK293 cells and insecticide effects were studied using patch‐clamp electrophysiology.KEY RESULTS Both compounds completely inhibited all tested glycine receptor subtypes with IC50 values ranging from 0.2–2 µM, similar to their potencies at vertebrate GABAA receptors. Consistent with molecular docking predictions, both lindane and fipronil interacted with 6′ threonine residues via hydrophobic interactions and hydrogen bonds. In contrast with predictions, we found no evidence for lindane interacting at the 2′ level. We present evidence for fipronil binding in a non‐blocking mode in the anaesthetic binding pocket, and for lindane as an excellent pharmacological tool for identifying the presence of β subunits in αβ heteromeric glycine receptors.CONCLUSIONS AND IMPLICATIONS This study implicates glycine receptors as novel vertebrate toxicity targets for fipronil and lindane. Furthermore, lindane interacted with pore‐lining 6′ threonine residues, whereas fipronil may have both pore and non‐pore binding sites.
Intrathecal neurotensin is hypotensive, sympathoinhibitory and enhances the baroreflex in anaesthetized rat
Authors: Zogovic B , Pilowsky PM 
Published: October 2011

BACKGROUND AND PURPOSE The neuromodulatory effects of the gut‐neuropeptide neurotensin on sympathetic vasomotor tone, central respiratory drive and adaptive reflexes in the spinal cord, are not known.EXPERIMENTAL APPROACH Neurotensin (0.5 µM–3 mM) was administered into the intrathecal (i.t.) space at the sixth thoracic spinal cord segment in urethane‐anaesthetized, paralysed, vagotomized male Sprague–Dawley rats. Pulsatile arterial pressure, splanchnic sympathetic nerve activity (sSNA), phrenic nerve activity, ECG and end‐tidal CO2 were recorded.KEY RESULTS Neurotensin caused a dose‐related hypotension, sympathoinhibition and bradycardia. The maximum effects were observed at 3000 µM, where the decreases in mean arterial pressure (MAP), heart rate (HR) and sSNA reached −25 mmHg, −26 beats min−1 and −26% from baseline, respectively. The sympathetic baroreflex was enhanced. Changes in central respiratory drive were characterized by a fall in the amplitude of the phrenic nerve activity. Finally, administration of SR 142948A (5 mM), a potent, selective antagonist at neurotensin receptors, caused a potent hypotension (−35 mmHg), bradycardia (−54 beats min−1) and sympathoinhibition (−44%). A reduction in the amplitude and frequency of the phrenic nerve activity was also observed.CONCLUSIONS AND IMPLICATIONS The data demonstrate that neurotensin plays an important role in the regulation of spinal cardiovascular function, affecting both tone and adaptive reflexes.
Ionic and Cellular Mechanisms Underlying the Development of Acquired Brugada Syndrome in Patients Treated with Antidepressants
Authors: MINOURA YOSHINO , DI DIEGO JOSÉ M. , BARAJAS‐MARTÍNEZ HECTOR , ZYGMUNT ANDREW C. , HU DAN , SICOURI SERGE , ANTZELEVITCH CHARLES 
Published: October 2011

Antidepressant‐Induced Brugada Syndrome.
Introduction:
Tricyclic antidepressants are known to induce cardiac arrhythmias at therapeutic or supratherapeutic doses. The tricyclic antidepressant, amitriptyline, is reported to induce ST segment elevation in the right precordial electrocardiogram (ECG) leads, thus unmasking Brugada syndrome (BrS). The mechanism by which antidepressants induce the BrS phenotype and associated sudden death is not well established.
Methods and Results:
Action potentials (AP) were simultaneously recorded from epicardial and endocardial sites of isolated coronary‐perfused canine right ventricular wedge preparations, together with a transmural pseudo‐ECG. Amitriptyline alone (0.2 μM–1 mM) failed to induce a BrS phenotype. NS5806 (8 μM), a transient outward potassium channel current (Ito) agonist, was used to produce an outward shift of current mimicking a genetic predisposition to BrS. In the presence of NS5806, a therapeutic concentration of amitriptyline (0.2 μM) accentuated the epicardial AP notch leading to ST‐segment elevation of the ECG. All‐or‐none repolarization at some epicardial sites but not others gave rise to phase‐2‐reentry and polymorphic ventricular tachycardia (VT) in 6 of 9 preparations. Isoproterenol (100 nM) or quinidine (10 μM) reversed the effects of amitriptyline aborting phase 2 reentry and VT (4/4). Using voltage‐clamp techniques applied to isolated canine ventricular myocytes, 0.2 μM amitriptyline was shown to produce use‐dependent inhibition of sodium channel current (INa), without significantly affecting Ito (n = 5).
Conclusions:
Our data suggest that amitriptyline‐induced inhibition of INa unmasks the Brugada ECG phenotype and facilitates development of an arrhythmogenic substrate only in the setting of a genetic predisposition by creating repolarization heterogeneities that give rise to phase 2 reentry and VT.
FGF‐23 is associated with cardiac troponin T and mortality in hemodialysis patients
Authors: Holden Rachel M. , Beseau David , Booth Sarah L. , Adams Michael A. , Garland Jocelyn S. , Morton Ross A. , Collier Christine P. , Foley Robert N. 
Published: October 2011

AbstractFibroblast growth factor 23 (FGF‐23) is elevated in patients with end‐stage kidney disease and has been linked with mortality, vascular calcification, markers of bone turnover, and left ventricular hypertrophy. In this cohort study, we determined the correlates of FGF‐23 (including cardiac troponin T [cTNT]) and determined its association with mortality over 3.5 years of follow‐up in 103 prevalent hemodialysis patients. Mean age was 61.2 (15.5) and the mean dialysis vintage was 4.19 years (4.6). The median (interquartile range) FGF‐23 was 1259 (491, 2885) RU/mL. Independent predictors (estimate standard error) of log‐transformed FGF‐23 concentrations included phosphorus (0.75 [0.237], P = 0.002) and cardiac troponin T (1.04 [0.41], P = 0.01). There were 57 deaths. In the fully adjusted model, the significant predictors of mortality included age and albumin. The independent association between FGF‐23 and cTNT is a novel finding. Whether this relationship supports the possibility that a downstream effect of dysregulated phosphorous homeostasis may be enhanced cardiac remodeling requires further study.
Large Electric‐Field Induced Strain in BiFeO3 Ceramics
Authors: Rojac Tadej , Kosec Marija , Damjanovic Dragan 
Published: October 2011

Large bipolar strain of up to 0.36% (peak‐to‐peak value) was measured in BiFeO3 ceramics at low frequency (0.1 Hz) and large amplitude (140 kV/cm) of the driving field. This strain is comparable to that achievable in highly efficient morphotropic phase boundary (MPB) Pb‐based perovskite ceramics, such as Pb(Zr,Ti)O3 and Pb(Mg,Nb)O3–PbTiO3. The strain showed a strong dependence on the field frequency, and is probably largely associated with domain switching involving predominantly non‐180° domain walls. In addition, application of an electric field of low frequency rearranges the defects, which act as pinning centers for the domain walls. The resulting depinning of the domain walls leads to a more efficient switching and, consequently, to an increased response. The large strain reported here suggests that the domain‐wall motion in BiFeO3 may be as large as in classical lead‐based ferroelectrics. We hope that this finding might further stimulate the search of new lead‐free MPB compositions based on BiFeO3.