bluuebunny/crossref_metadata_2025_split huggingface dataset:
Widespread decoupling of mtDNA variation and species integrity in Grammia tiger moths (Lepidoptera: Noctuidae)
Authors: SCHMIDT B. CHRISTIAN , SPERLING FELIX A. H. 
Published: October 2008

Abstract.
We investigate the diversity of the North American tiger moth genus Grammia Rambur (Lepidoptera: Noctuidae) by comparing mitochondrial DNA (mtDNA) ‘barcode’ fragments of cytochrome oxidase I with non‐molecular characters such as morphology, ecology, behaviour and distribution. Mitochondrial DNA genealogy is strikingly at odds with morpho‐species taxonomy for most of the 28 sampled species, as haplotypic polyphyly not only is taxonomically widespread, but involves multiple shared haplotypes among two to four species. Morpho‐ecological traits show that those species sharing haplotypes are often not closely related. Furthermore, high mtDNA divergences occur within species. Haplotypic variation is highly discordant with species taxonomy, but variation at a continental scale reveals significant geographic structuring of haplogroups, transcending morpho‐species boundaries. A nested clade analysis and comparison of non‐molecular with mtDNA data indicate that most discordance between mtDNA and taxonomy in Grammia is explained best by taxonomically and geographically widespread ongoing hybridization events resulting in mtDNA introgression. We hypothesize that broad areas of sympatry, interspecifically compatible genitalic structure, and species overlap in pheromone components facilitate hybridization, with disparate interspecies abundances promoting mitochondrial introgression. The molecular evolution of Grammia challenges the view that interspecific gene exchange occurs rarely and is restricted to recently diverged species. These results show the value of mtDNA in detecting cryptic hybridization, while highlighting the inherent dangers of drawing taxonomic conclusions based solely on mtDNA.
Increased rates of white matter hyperintensities in late‐onset bipolar disorder
Authors: Tamashiro Jaqueline Hatsuko , Zung Stevin , Zanetti Marcus Vinicius , De Castro Cláudio Campi , Vallada Homero , Busatto Geraldo F , De Toledo Ferraz Alves Tânia Correa 
Published: October 2008

Objectives:  Magnetic resonance imaging (MRI) studies have reported an increased frequency of white matter hyperintensities (WMH) in association with late‐onset (LO) depression, and this has supported the notion that vascular‐related mechanisms may be implicated in the pathophysiology of LO mood disorders. Recent clinical studies have also suggested a link between LO bipolar disorder (LO‐BD) and cerebrovascular risk factors, but this has been little investigated with neuroimaging techniques. In order to ascertain whether there could be a specific association between WMH and LO‐BD, we directly compared WMH rates between LO‐BD subjects (illness onset ≥ 60 years), early‐onset BD subjects (EO‐BD, illness onset <60 years), and elderly healthy volunteers.Methods:  T2‐weighted MRI data were acquired in LO‐BD subjects (n = 10, age = 73.60 ± 4.09), EO‐BD patients (n = 49, age = 67.78 ± 4.44), and healthy subjects (n = 24, age = 69.00 ± 7.22). WMH rates were assessed using the Scheltens scale.Results:  There was a greater prevalence of WMH in LO‐BD patients relative to the two other groups in the deep parietal region (p = 0.018) and basal ganglia (p < 0.045). When between‐group comparisons of mean WMH scores were conducted taking account of age differences (ANCOVA), there were more severe scores in LO‐BD patients relative to the two other groups in deep frontal and parietal regions, as well as in the putamen (p < 0.05).Conclusions:  Our results provide empirical support to the proposed link between vascular risk factors and LO‐BD. If extended in future studies with larger samples, these findings may help to clarify the pathophysiological distinctions between bipolar disorder emerging at early and late stages of life.
Preventing recurrence of bipolar I mood episodes and hospitalizations: family psychotherapy plus pharmacotherapy versus pharmacotherapy alone
Authors: Solomon David A , Keitner Gabor I , Ryan Christine E , Kelley Joan , Miller Ivan W 
Published: October 2008

Objectives:  This study compared the efficacy of three treatment conditions in preventing recurrence of bipolar I mood episodes and hospitalization for such episodes: individual family therapy plus pharmacotherapy, multifamily group therapy plus pharmacotherapy, and pharmacotherapy alone.Methods:  Patients with bipolar I disorder were enrolled if they met criteria for an active mood episode and were living with or in regular contact with relatives or significant others. Subjects were randomly assigned to individual family therapy plus pharmacotherapy, multifamily group therapy plus pharmacotherapy, or pharmacotherapy alone, which were provided on an outpatient basis. Individual family therapy involved one therapist meeting with a single patient and the patient’s family members, with the content of each session and number of sessions determined by the therapist and family. Multifamily group psychotherapy involved two therapists meeting together for six sessions with multiple patients and their respective family members, with the content of each session preset. All subjects were prescribed a mood stabilizer, and other medications were used as needed. Subjects were assessed monthly for up to 28 months. Following recovery from the index mood episode, subjects were assessed for recurrence of a mood episode and for hospitalization for such episodes.Results:  Of a total of 92 subjects that were enrolled in the study, 53 (58%) recovered from their intake mood episode. The analyses in this report focus upon these 53 subjects, 42 (79%) of whom entered the study during an episode of mania. Of the 53 subjects who recovered from their intake mood episode, the proportion of subjects within each treatment group who suffered a recurrence by month 28 did not differ significantly between the three treatment conditions. However, only 5% of the subjects receiving adjunctive multifamily group therapy required hospitalization, compared to 31% of the subjects receiving adjunctive individual family therapy and 38% of those receiving pharmacotherapy alone, a significant difference. Time to recurrence and time to hospitalization did not differ significantly between the three treatment groups.Conclusion:  For patients with bipolar I disorder, adjunctive multifamily group therapy may confer significant advantages in preventing hospitalization for a mood episode.
Equally increased risk for metabolic syndrome in patients with bipolar disorder and schizophrenia treated with second‐generation antipsychotics
Authors: Correll Christoph U , Frederickson Anne M , Kane John M , Manu Peter 
Published: October 2008

Objective:  Although second‐generation antipsychotics (SGAs) are widely used in treating schizophrenia and bipolar disorder, their effects on dyslipidemia, glucose intolerance, metabolic syndrome (MetS), and coronary heart disease (CHD) risk are less well documented for bipolar disorder. We compared bipolar disorder and schizophrenia patients receiving SGAs to determine whether MetS prevalence is influenced by the primary psychiatric diagnosis or concomitant mood stabilizer treatment.Methods:  Admission assessment of MetS criteria (abdominal obesity, fasting hypertriglyceridemia, low high‐density lipoprotein cholesterol, hyperglycemia, arterial hypertension) and the calculated 10‐year CHD risk in bipolar disorder and schizophrenia patients treated with SGAs and closely matched for age, sex, and race.Results:  Compared to schizophrenia patients (n = 111), those with bipolar disorder (n = 74) had lower body mass index (27.1 ± 5.3 versus 29.9 ± 8.1, p = 0.0053), were more likely treated with mood stabilizers (60.8 versus 36.0, p = 0.0009), and less likely treated with clozapine (1.3% versus 15.3%, p = 0.0017) or two antipsychotics (10.8% versus 34.2%, p = 0.0003). Despite these differences, bipolar disorder and schizophrenia patients had comparable rates of MetS (43.2% versus 45.9%, p = 0.71) and predicted CHD events (10‐year risk >10%: 18.9% versus 23.4%, p = 0.47). Using ≥100 mg/dL as the adapted glucose criterion, MetS rates were 54.0% in both diagnostic groups (p = 1.0). Mood stabilizer co‐treatment was not associated with MetS or its individual criteria.Conclusions:  Patients with bipolar disorder and schizophrenia who are treated with SGAs have similarly high rates of MetS. These findings suggest a shared susceptibility to antipsychotic‐related metabolic dysregulations that is not primarily related to psychiatric diagnosis or concomitant mood stabilizer treatment.
Relationship of cerebrospinal fluid glucose metabolites to MRI deep white matter hyperintensities and treatment resistance in bipolar disorder patients
Authors: Regenold William T , Hisley K Calvin , Phatak Pornima , Marano Christopher M , Obuchowski Abraham , Lefkowitz David M , Sassan Amritpal , Ohri Sameer , Phillips Tony L , Dosanjh Narveen , Conley Robert R , Gullapalli Rao 
Published: October 2008

Objectives:  Both diabetes mellitus and magnetic resonance image (MRI) deep white matter hyperintensities (WMHs) are more common in bipolar disorder (BD) patients than in matched controls. Deep—as opposed to periventricular—WMHs and diabetes are associated with treatment resistance and poorer outcome. This study investigated whether brain glucose metabolism by the polyol pathway—a pathway linked to nervous tissue disease in diabetes—is related to deep WMH volume and treatment resistance in BD patients.Methods:  Volumes of fluid‐attenuated inversion recovery WMHs were quantified and correlated with cerebrospinal fluid (CSF) concentrations of glucose metabolites in 20 nondiabetic patients with BD and nondiabetic comparison subjects with schizophrenia (n = 15) or transient neurologic symptoms (neurologic controls, n = 15).Results:  BD patients, but not schizophrenic patients, had significantly greater volumes of deep but not periventricular WMHs compared to neurologic controls. BD subjects also had significantly greater CSF concentrations of sorbitol and fructose (the polyol pathway metabolites of glucose) compared to controls. Significant positive correlations between CSF metabolites and WMH volumes were found only in the BD group and were between deep WMH volumes and CSF sorbitol (ρ = 0.487, p = 0.029) and fructose (ρ = 0.474, p = 0.035). An index of treatment resistance correlated significantly with deep WMH volume (ρ = 0.578, p = 0.008), sorbitol (ρ = 0.542, p = 0.013), and fructose (ρ = 0.692, p = 0.001) in BD subjects but not in other subjects.Conclusions:  This is the first reported evidence of relationships between abnormal brain glucose metabolism and both deep WMHs and treatment resistance in a group of BD patients. Further studies are necessary to determine the significance of these findings to BD pathophysiology.
Cigarette smoking in the early course of bipolar disorder: association with ages‐at‐onset of alcohol and marijuana use
Authors: Heffner Jaimee L , DelBello Melissa P , Fleck David E , Anthenelli Robert M , Strakowski Stephen M 
Published: October 2008

Objectives:  Despite the high prevalence of smoking among individuals with bipolar disorder, few studies have attempted to identify correlates of smoking status in this group. We examined illness characteristics of bipolar disorder as well as co‐occurring alcohol and marijuana use as correlates of cigarette smoking, including the developmental timing of the onset of regular alcohol and cannabis use (i.e., three or more times per week for a month or more).Methods:  Demographic and clinical characteristics of 134 patients with bipolar I disorder, the majority of whom were adolescents, who were hospitalized for their first manic episode were analyzed to identify correlates of smoking status.Results:  A total of 61 (45.5%) of the patients were smokers at the time of their first hospitalization. Smokers were significantly more likely than nonsmokers to report recent use of marijuana (55.7% versus 18.1%) and alcohol (67.2% versus 25.4%). Among those who had ever used marijuana (48.5%) or alcohol (45.5%) regularly, current cigarette smokers reported a significantly earlier age‐at‐onset of regular use of both substances than reported by nonsmokers. Earlier age‐at‐onset of marijuana use was the only significant predictor of current smoking in a multivariate analysis. None of the bipolar disorder characteristics examined (i.e., symptom severity, age‐at‐onset of illness, rapid cycling, and psychosis) were correlated with smoking status.Conclusions:  Smoking status in the early course of bipolar disorder is related to both current and past alcohol and marijuana use, but not to characteristics of bipolar illness. Earlier initiation of regular marijuana use is associated with an increased risk of smoking cigarettes.
Brief daily suckling shifts locomotor behavior and induces PER1 protein in paraventricular and supraoptic nuclei, but not in the suprachiasmatic nucleus, of rabbit does
Authors: Meza Enrique , Juárez Claudia , Morgado Elvira , Zavaleta Yael , Caba Mario 
Published: October 2008

AbstractNursing in the rabbit is a circadian event during which mother and pups interact for a period of < 5 min every day. Here we explored behavioral and neuronal changes in the mother by analyzing the suprachiasmatic nucleus (SCN), and oxytocinergic (OT) neurons in the paraventricular nucleus (PVN) and the supraoptic nucleus (SON). We maintained lactating does in a light–dark cycle (lights on at 07 : 00 hours; ZT0); they were scheduled to nurse during either the day (ZT03) or the night (ZT19). Groups of intact and nursing females was perfused, one at each 4‐h point through a 24‐h cycle. We explored, by immunohistochemistry, the PER1 expression and double‐labeling, with OT antibody, of neurons in the PVN and SON at lactation on day 7. In the SCN, intact and lactating groups had peak PER1 expression at ZT11; however, there was a reduction in PER1 at peak time in the nursing groups. There was a locomotor activity rhythm with increased activity around the time of lights‐on in intact subjects and around the time of suckling in lactating does. There was an induction of PER1 in OT cells in the PVN and SON that shifted in phase with timing of nursing. We further explored the maintenance of the PER1 expression in OT cells in nursing‐deprived does and found a significant decrease at 24 and 48 h after the last nursing. We conclude that suckling induced PER1 in the PVN and SON, but not in the SCN, in nursing does, and also shifted their locomotor behavior.
Down‐regulation of protocadherin‐α A isoforms in mice changes contextual fear conditioning and spatial working memory
Authors: Fukuda Emi , Hamada Shun , Hasegawa Sonoko , Katori Shota , Sanbo Makoto , Miyakawa Tsuyoshi , Yamamoto Toshifumi , Yamamoto Hideko , Hirabayashi Takahiro , Yagi Takeshi 
Published: October 2008

AbstractDiverse protocadherins (Pcdhs), which are encoded as a large cluster (composed of α, β and γ clusters) in the genome, are localized to axons and synapses. The Pcdhs have been proposed to contribute to the generation of sophisticated neural networks and to regulate brain function. To address the molecular roles of Pcdhs in regulating individual behavior, here we generated knockdown mice of Pcdh‐α proteins and examined their behavioral abnormalities. There are two alternative splicing variants of the Pcdh‐α constant region, Pcdh‐α A and B isoforms, with different cytoplasmic tails. Pcdh‐αΔBneo/ΔBneo mice, in which the Pcdh‐α B splicing variant was absent and the Pcdh‐α A isoforms were down‐regulated to approximately 20% of the wild‐type level, exhibited enhanced contextual fear conditioning and disparities in an eight‐arm radial maze. Similar abnormalities were found in Pcdh‐αΔAneo/ΔAneo mice, which lacked 57 amino acids of the Pcdh‐α A cytoplasmic tail. These learning abnormalities were, however, not seen in Pcdh‐αΔB/ΔB mice [in which the neomycin‐resistance (neo) gene cassette was removed from the Pcdh‐αΔBneo/ΔBneo alleles], in which the expression level of the Pcdh‐α A isoforms was recovered, although the Pcdh‐α B isoforms were still completely missing in the brain. In addition, the amount of 5‐hydroxytryptamine increased in the hippocampus of the hypomorphic Pcdh‐α A mutant mice but not in recovery Pcdh‐αΔB/ΔB. These results suggested that the level of Pcdh‐α A isoforms in the brain has an important role in regulating learning and memory functions and the amount of 5‐hydroxytryptamine in the hippocampus.
Medial temporal lobe structures participate differentially in consolidation of safe and aversive taste memories
Authors: De la Cruz Vanesa , Rodriguez‐Ortiz Carlos J. , Balderas Israela , Bermudez‐Rattoni Federico 
Published: October 2008

AbstractTaste memories are amongst the most important kinds of memories, as adequate identification of safe and toxic edibles will determine the subject’s survival. Despite the well‐established role that the medial temporal lobe plays in consolidation of memory, specific contributions of the different regions of the temporal lobe to taste memory consolidation remain unknown. In the present report, we assessed the participation of perirhinal cortex (Ph), dorsal hippocampus (Hipp), basolateral (BLA) and central nuclei of the amygdala (CeA) in safe and aversive taste memories by means of local infusions of the protein synthesis inhibitor anisomycin in the rat. The results showed that protein synthesis in the CeA, but not BLA, is required to stabilize taste aversion memory. Surprisingly, the Ph and Hipp seem to be essential to consolidate safe taste memory. These data suggest that different networks within the temporal lobe are recruited to consolidate memory depending on the consequences associated with tastes.
Rescue of hippocampal LTP and learning deficits in a rat model of psychosis by inhibition of glycine transporter‐1 (GlyT1)
Authors: Manahan‐Vaughan Denise , Wildförster Verena , Thomsen Christian 
Published: October 2008

Abstract N‐methyl‐d‐aspartate (NMDA) receptor hypofunction is believed to comprise a central factor in the cognitive symptoms of psychotic illnesses such as schizophrenia. In the MK801 model of psychosis in rats, NMDA hypofunction also occurs, and animals display a profound impairment of both hippocampus‐dependent learning and synaptic plasticity. The NMDA receptor may thus comprise a useful target for therapeutic amelioration of the symptoms of psychosis. However, direct activation of the receptor could lead to disturbed synaptic information storage. One possibility, however, is to enhance NMDA receptor function indirectly through elevation of glycine levels. We investigated the effects of inhibition of the glycine transporter‐1, GlyT1, on long‐term potentiation (LTP) and long‐term depression (LTD) in the dentate gyrus of freely behaving rats that had been treated previously with MK801. LTP, but not LTD, was impaired in MK801‐treated animals. Systemic application of the GlyT1‐inhibitor N[3‐(4’‐flurophenyl)‐3‐(4’‐phenylphenoxy) propyl]sarcosine (NFPS) rescued LTP but had no effect on LTD in MK801‐treated animals. Application of the antagonist to vehicle‐treated controls resulted in a disruption of LTP but not LTD. NFPS significantly ameliorated reference memory deficits in a radial maze that occurred following MK801 treatment. NFPS‐treated controls performed less well, however, than vehicle‐injected controls. These data support that treatment with a glycine transporter inhibitor can ameliorate deficits in both LTP and learning that occur in a rat model of psychosis, and may therefore prove a useful strategy to address cognitive disruption in psychotic illnesses. Use of the inhibitor in healthy subjects is neither beneficial to synaptic plasticity nor hippocampus‐dependent learning.
GABAA receptors present higher affinity and modified subunit composition in spinal motor neurons from a genetic model of amyotrophic lateral sclerosis
Authors: Carunchio Irene , Mollinari Cristiana , Pieri Massimo , Merlo Daniela , Zona Cristina 
Published: October 2008

AbstractAmyotrophic lateral sclerosis is a neurodegenerative disease characterized by the selective degeneration of motor neurons in the spinal cord, brainstem and cerebral cortex. In this study we have analysed the electrophysiological properties of GABAA receptors and GABAA alpha1 and alpha2 subunits expression in spinal motor neurons in culture obtained from a genetic model of ALS (G93A) and compared with transgenic wild type SOD1 (SOD1) and their corresponding non transgenic litter mates (Control). Although excitotoxic motor neuron death has been extensively studied in relation to Ca2+‐dependent processes, strong evidence indicates that excitotoxic cell death is also remarkably dependent on Cl− ions and on GABAA receptor activation. In this study we have analysed the electrophysiological properties of GABAA receptors and the expression of GABAAα1 and α2 subunits in cultured motor neurons obtained from a genetic model of amyotrophic lateral sclerosis (G93A) and compared them with transgenic wild‐type Cu,Zn superoxide dismutase and their corresponding non‐transgenic littermates (Control). In all tested motor neurons, the application of γ‐aminobutyric acid (GABA) (0.5–100 μm) evoked an inward current that was reversibly blocked by bicuculline (100 μm), thus indicating that it was mediated by the activation of GABAA receptors. Our results indicate that the current density at high GABA concentrations is similar in control, Cu,Zn superoxide dismutase and G93A motor neurons. However, the dose‐response curve significantly shifted toward lower concentration values in G93A motor neurons and the extent of desensitization also increased in these neurons. Finally, multiplex single‐cell real‐time polymerase chain reaction and immunofluorescence revealed that the amount of GABAAα1 subunit was significantly increased in G93A motor neurons, whereas the levels of α2 subunit were unchanged. These data show that the functionality and expression of GABAA receptors are altered in G93A motor neurons inducing a higher Cl− influx into the cell with a possible consequent neuronal excitotoxicity acceleration.
Glial responses, neuron death and lesion resolution after intracerebral hemorrhage in young vs. aged rats
Authors: Wasserman Jason K. , Yang Helen , Schlichter Lyanne C. 
Published: October 2008

AbstractIntracerebral hemorrhage (ICH) usually affects older humans but almost no experimental studies have assessed aged animals. We address how aging alters inflammation, neuron death and lesion resolution after a hemorrhage in the rat striatum. In the normal aged brain, microglia displayed a ‘dystrophic’ phenotype, with shorter cellular processes and large gaps between adjacent cells, and there was more astrocyte reactivity. The ICH injury was monitored as hematoma volume and number of dying neurons at 1 and 3 days, and the volume of the residual lesion, ventricles and lost tissue at 28 days. Inflammation at 1 and 3 days was assessed from densities of microglia with resting vs. activated morphologies, or expressing the lysosomal marker ED1. Despite an initial delay in neuron death in aged animals, by 28 days, there was no difference in neuron density or volume of tissue lost. However, lesion resolution was impaired in aged animals and there was less compensatory ventricular expansion. At 1 day after ICH, there were fewer activated microglia/macrophages in the aged brain, but by 3 days there were more of these cells at the edge of the hematoma and in the surrounding parenchyma. In both age groups a glial limitans had developed by 3 days, but astrocyte reactivity and the spread of activated microglia/macrophages into the surrounding parenchyma was greater in the aged. These findings have important implications for efforts to reduce secondary injury after ICH and to develop anti‐inflammatory therapies to treat ICH in aged humans.