bluuebunny/crossref_metadata_2025_split huggingface dataset:
Psychotic features in bipolar and unipolar depression
Authors: Goes Fernando S , Sadler Bradley , Toolan Jennifer , Zamoiski Rachel D , Mondimore Francis M , MacKinnon Dean F , Schweizer Barbara ,   The Bipolar Disorder Phenome Group, Raymond DePaulo J , Potash James B 
Published: September 2010

Background:  While some prior studies have found higher rates of psychotic depression in those with bipolar disorder or a bipolar relative, others have failed to confirm these observations. We examined the relationship of psychotic depression to polarity in several large familial samples of mood disorder.Methods:  A total of 4,724 subjects with major mood disorder in three family studies on the genetics of bipolar I disorder (BPI) or recurrent major depressive disorder (MDDR) were administered semi‐structured interviews by clinicians. Determination of psychotic features was based on a report of hallucinations and/or delusions during the most severe depressive episode in the Schedule for Affective Disorders and Schizophrenia‐Lifetime Version or the Diagnostic Interview for Genetic Studies interview. Rates of psychotic depression were calculated by diagnostic category and comparisons were made between diagnoses within and across studies using the generalized estimating equation.Results:  A diagnosis of BPI disorder was strongly predictive of psychotic features during depression compared to MDDR [odds ratio (OR) = 4.61, p < 0.0005]. Having bipolar II compared to MDDR was not predictive of psychosis (OR = 1.05, p = 0.260), nor was having a family history of BPI in MDDR subjects (OR = 1.20, p = 0.840).Conclusions:  Psychotic features during a depressive episode increased the likelihood of a BPI diagnosis. Prospective studies are needed to confirm these findings. The potential genetic underpinnings of psychotic depression warrant further study.
Phenomenology of mixed states: a principal component analysis study
Authors: Bertschy G , Gervasoni N , Favre S , Liberek C , Ragama‐Pardos E , Aubry J‐M , Gex‐Fabry M , Dayer A 
Published: September 2010

Objectives:  To contribute to the definition of external and internal limits of mixed states and study the place of dysphoric symptoms in the psychopathology of mixed states.Methods:  One hundred and sixty‐five inpatients with major mood episodes were diagnosed as presenting with either pure depression, mixed depression (depression plus at least three manic symptoms), full mixed state (full depression and full mania), mixed mania (mania plus at least three depressive symptoms) or pure mania, using an adapted version of the Mini International Neuropsychiatric Interview (DSM‐IV version). They were evaluated using a 33‐item inventory of depressive, manic and mixed affective signs and symptoms.Results:  Principal component analysis without rotation yielded three components that together explained 43.6% of the variance. The first component (24.3% of the variance) contrasted typical depressive symptoms with typical euphoric, manic symptoms. The second component, labeled ‘dysphoria’, (13.8%) had strong positive loadings for irritability, distressing sensitivity to light and noise, impulsivity and inner tension. The third component (5.5%) included symptoms of insomnia. Median scores for the first component significantly decreased from the pure depression group to the pure mania group. For the dysphoria component, scores were highest among patients with full mixed states and decreased towards both patients with pure depression and those with pure mania.Conclusions:  Principal component analysis revealed that dysphoria represents an important dimension of mixed states.
A near‐infrared spectroscopy study of prefrontal cortex activation during a verbal fluency task and carbon dioxide inhalation in individuals with bipolar disorder
Authors: Matsuo Koji , Kouno Toshiaki , Hatch John P , Seino Kai , Ohtani Toshiyuki , Kato Nobumasa , Kato Tadafumi 
Published: September 2010

Objectives:  There is evidence of prefrontal cortex (PFC) dysfunction in patients with bipolar disorder (BP). Magnetic resonance and neuropathological studies show abnormalities of the brain microvasculature in patients with BP. However, the underlying biological mechanisms are not well understood. We investigated the relationship between activation of the PFC during a cognitive task and the vascular function in response to a physiological task in patients with BP.Methods:  Fourteen euthymic patients with BP and 14 control subjects matched for age, sex, and education were recruited. We examined the response of the PFC during a verbal fluency task and during 5% CO2 inhalation using a 24‐channel near‐infrared spectroscopy imaging system to measure alteration of oxygenated and deoxygenated hemoglobin.Results:  The BP patients showed a significantly lower level of PFC activation during the cognitive task compared to the healthy controls, but the task‐performance of the BP patients was not significantly different from that of the controls. The vascular response of the BP patients to CO2 was not significantly different from that of controls.Conclusions:  This study suggests functional hypoactivation of the PFC during a cognitive load in patients with BP while they are in a euthymic state. The mechanism of this hypoactivation is different from that of vascular regulation in response to a physiological stimulus.
White matter abnormalities in children with and at risk for bipolar disorder
Authors: Frazier Jean A , Breeze Janis L , Papadimitriou George , Kennedy David N , Hodge Steven M , Moore Constance M , Howard James D , Rohan Michael P , Caviness Verne S , Makris Nikos 
Published: September 2010

Objectives:  Diffusion tensor magnetic resonance imaging (DT‐MRI) assesses the integrity of white matter (WM) tracts in the brain. Children with bipolar disorder (BPD) may have WM abnormalities that precede illness onset. To more fully examine this possibility, we scanned children with DSM‐IV BPD and compared them to healthy peers and children at risk for BPD (AR‐BPD), defined as having a first‐degree relative with the disorder.Methods:  Ten children with BPD, eight healthy controls (HC), and seven AR‐BPD, similar in age, had MRI scans on a 1.5 Tesla GE scanner, including a standard DT‐MRI sequence (T2‐EPI) with 25 axial slices. Fractional anisotropy (FA) values were compared between groups to determine regions of significant difference (p < 0.05).Results:  Compared to HC, children with BPD had decreased FA in right and left superior frontal tracts, including the superior longitudinal fasciculus I (SLF I) and the cingulate‐paracingulate WM (CG‐PACWM). In addition, the BPD group had reduced FA in left orbital frontal WM and the right corpus callosum body. Compared to AR‐BPD, children with BPD showed reduced FA in the right and left CG‐PACWM. Both the BPD and AR‐BPD groups showed reduced FA relative to HC in bilateral SLF I.Conclusions:  The bilateral SLF I finding in both the BPD and AR‐BPD groups may represent a trait‐based marker or endophenotype of the disorder. The finding of decreased FA in the right and left CG‐PACWM in children with BPD compared to the other two groups may represent a disease‐state related finding.
Familial aggregation of postpartum mood symptoms in bipolar disorder pedigrees
Authors: Payne Jennifer L , MacKinnon Dean F , Mondimore Francis M , McInnis Melvin G , Schweizer Barbara , Zamoiski Rachel B , McMahon Francis J , Nurnberger John I , Rice John P , Scheftner William , Coryell William , Berrettini Wade H , Kelsoe John R , Byerley William , Gershon Elliot S , Raymond DePaulo J , Potash James B 
Published: September 2010

Objectives:  We sought to determine if postpartum mood symptoms and depressive episodes exhibit familial aggregation in bipolar I pedigrees.Methods:  A total of 1,130 women were interviewed with the Diagnostic Interview for Genetic Studies as part of the National Institute of Mental Health (NIMH) Genetics Initiative Bipolar Disorder Collaborative Study and were asked whether they had ever experienced mood symptoms within four weeks postpartum. Women were also asked whether either of two major depressive episodes described in detail occurred postpartum. We examined the odds of postpartum mood symptoms in female siblings, who had previously been pregnant and had a diagnosis of bipolar I, bipolar II, or schizoaffective (bipolar type) disorders (n = 303), given one or more relatives with postpartum mood symptoms.Results:  The odds ratio for familial aggregation of postpartum mood symptoms was 2.31 (p = 0.011) in an Any Mood Symptoms analysis (n = 304) and increased to 2.71 (p = 0.005) when manic symptoms were excluded, though this was not significantly different from the Any Mood Symptoms analysis. We also examined familial aggregation of postpartum major depressive episodes; however, the number of subjects was small.Conclusions:  Limitations of the study include the retrospective interview, the fact that the data were collected for other purposes and the inability to control for such factors as medication use. Taken together with previous studies, these data provide support for the hypothesis that there may be a genetic basis for the trait of postpartum mood symptoms generally and postpartum depressive symptoms in particular in women with bipolar disorder. Genetic linkage and association studies incorporating this trait are warranted.
Pituitary gland volume in adolescent and young adult bipolar and unipolar depression
Authors: MacMaster Frank P , Leslie Ronald , Rosenberg David R , Kusumakar Vivek 
Published: September 2010

Objectives:  Few studies have examined pituitary gland size in mood disorders, particularly in adolescents. We hypothesized increase in the pituitary gland size in early‐onset mood disorders.Methods:  Thirty subjects between the ages of 13 and 20 years participated in the study. Three groups (control, bipolar I depression and unipolar depression) of 10 subjects each (4 male, 6 female) underwent volumetric magnetic resonance imaging at 1.5 T.Results:  Analysis of covariance (covarying for age, sex and intracranial volume) revealed a significant difference in pituitary gland volume amongst the groups [F(2,24) = 7.092, p = 0.014]. Post hoc analysis revealed that controls had a significantly smaller pituitary gland volume than both bipolar patients (p = 0.019) and depressed patients (p = 0.049). Bipolar and depressed subjects did not differ significantly from each other with regard to pituitary gland volume (p = 0.653). Control females had larger pituitary glands than control males [F(1,8) = 10.523, p = 0.012], but no sex differences were noted in the mood disorder groups.Conclusions:  Pituitary glands are enlarged in adolescents with mood disorders compared to controls. Healthy young females have larger pituitary glands than males, but such a difference is not evident in individuals with unipolar depression or bipolar disorder. These findings provide new evidence of abnormalities of the pituitary in early onset mood disorders, and are consistent with neuroendocrine dysfunction in early stages of such illnesses.
Psychotic phenomena in 257 young children and adolescents with bipolar I disorder: delusions and hallucinations (benign and pathological)
Authors: Tillman Rebecca , Geller Barbara , Klages Tricia , Corrigan Meg , Bolhofner Kristine , Zimerman Betsy 
Published: September 2010

Objectives:  In contrast to studies of adult bipolar I disorder (BP‐I), there is a paucity of data on psychotic phenomena in child BP‐I. Therefore, the aim of this work was to describe delusions and hallucinations in pediatric BP‐I.Methods:  Subjects were 257 participants, aged 6–16, in either of two large, ongoing, NIMH‐funded studies, ‘Phenomenology and Course of Pediatric Bipolar Disorders’ or ‘Treatment of Early Age Mania (TEAM)’. All subjects had current DSM‐IV BP‐I (manic or mixed phase) with a Children’s Global Assessment Scale score ≤60 (definite clinical impairment), and all had cardinal mania symptoms (i.e., elation and/or grandiosity). Comprehensive assessments included the Washington University in St. Louis Kiddie Schedule for Affective Disorders and Schizophrenia (WASH‐U‐KSADS), which was administered to parents about their children and separately to children about themselves by experienced research clinicians. The WASH‐U‐KSADS contains modules for developmentally child‐age‐specific manifestations of numerous categories of psychotic phenomena.Results:  Psychosis was present in 76.3% (n = 196) of subjects, which included 38.9% (n = 100) with delusions, 5.1% (n = 13) with pathological hallucinations, and 32.3% (n = 83) with both. The most common delusion was grandiose (67.7%, n = 174), and the most common pathological hallucination was visual (16.0%, n = 41). Benign hallucinations occurred in 43.6% (n = 112). A median split by age yielded 6–9 year‐olds (n = 139) and 10–16 year‐olds (n = 118). Analyses of these two groups, and of 6, 7, 8, and 9 year‐olds separately, found no significant differences in psychotic phenomena.Conclusions:  Counterintuitively, psychosis was equally prevalent in 6–9 compared to 10–16 year‐olds. High prevalence of psychosis in child BP‐I warrants focus in intervention strategies and is consistent with increasing evidence of the severity of child‐versus adult‐onset BP‐I.
Homicidal ideation with intent during a manic episode triggered by antidepressant medication in a man with brain injury
Authors: Dealberto Marie‐José , Marino Josie , Bourgon Luc 
Published: September 2010

Background:  Mood disorders are more frequent after brain injury and both depressive and manic episodes are associated in these patients with an increased risk of aggression. Antidepressant medications are associated with a risk of manic induction.Case report:  We describe a case of homicidal ideation with intent during the onset of a manic episode in a patient with prior brain injury on antidepressant medication at low dosage. The manic episode could have been secondary to brain injury and/or triggered by antidepressant medications. This case raises the possibility of the sensitizing role of brain injury for antidepressant‐induced mania.Conclusions:  Further studies are needed to assess the role of brain injury as a risk factor for antidepressant‐induced mania. Physicians should be cautious when prescribing antidepressants to patients with prior brain injury and inform them and their relatives of the possibility of a switch into mania.
Proceedings of the Symposium ‘Angiotensin AT1Receptors: From Molecular Physiology to Therapeutics’: REGULATION OF RENAL TUBULAR SODIUM TRANSPORT BY ANGIOTENSIN II AND ATRIAL NATRIURETIC FACTOR
Authors: Harris Peter J , Hiranyachattada Siriphun , Antoine Arianne M , Walker Lesley , Reilly Angela M , Eitle Eveline 
Published: September 2010

SUMMARYThe effects of angiotensin II (AngII) on water and electrolyte transport are biphasic and dose‐dependent, such that low concentrations (10−12to 10−9mol/L) stimulate reabsorption and high concentrations (10−7to 10−6mol/L) inhibit reabsorption. Similar dose‐response relationships have been obtained for luminal and peritubular addition of AngII.The cellular responses to AngII are mediated via AT1receptors coupled via G‐regulatory proteins to several possible signal transduction pathways. These include the inhibition of adenylyl cyclase, activation of phospholipases A2, C or D and Ca2+release in response to inositol‐1,4,5,‐triphosphate or following Ca2+channel opening induced by the arachidonic acid metabolite 5,6,‐epoxy‐eicosatrienoic acid. In the brush border membrane, transduction of the AngII signal involves phospholipase A2, but does not require second messengers.Angiotensin II affects transepithelial sodium transport by modulation of Na+/H+exchange at the luminal membrane and Na+/HCO3cotransport, Na+/K+‐ATPase activity and K+conductance at the basolateral membrane.Atrial natriuretic factor (ANF) does not appear to affect proximal tubular sodium transport directly, but acts via specific receptors on the basolateral and brush border membranes to raise intracellular cGMP levels and inhibit AngII‐stimulated transport.It is concluded that there is a receptor‐mediated action of ANF on proximal tubule reabsorption acting via elevation of cGMP to inhibit AngII‐stimulated sodium transport. This effect is exerted by peptides delivered at both luminal and peritubular sides of the epithelium and provides a basis for the modulation by ANF of proximal glomerulotubular balance. The evidence reviewed supports the concept that in the proximal tubule, AngII and ANF act antagonistically in their roles as regulators of extracellular fluid volume.
Proceedings of the Symposium ‘Angiotensin AT1Receptors: From Molecular Physiology to Therapeutics’: EXPERIENCE WITH ANGIOTENSIN II ANTAGONISTS IN HYPERTENSIVE PATIENTS
Authors: Waeber Bernard , Burnier Michel , Nussberger Jürg , Brunner Hans R 
Published: September 2010

SUMMARYThe availability of orally active specific angiotensin receptor antagonists (AT1antagonists) has opened new therapeutic choices and provided probes to test the specific role of the renin‐angiotensin system in the pathogenesis of cardiovascular disease.The data available so far suggest that the antihypertensive efficacy of angiotensin receptor antagonists is comparable to that of angiotensin‐converting enzyme (ACE) inhibitors. This provides further evidence that this latter class of drugs exerts its effect mainly through blockade of the renin‐angiotensin enzymatic cascade. As expected, the association of a diuretic exerts an equally strong additive effect to the antihypertensive efficacy of both classes of drugs.The most common side effect of ACE inhibitors, dry cough, does not occur with AT1antagonists, which confirms the long‐held view that this untoward effect of the ACE inhibitors is due to renin‐angiotensin‐independent mechanisms.Long‐term studies with morbidity/mortality outcome results are needed, before a definite position can be assigned to this newcomer in the orchestra of modern antihypertensive drugs. Notwithstanding, this new class of agents already represents an exciting new addition to our therapeutic armamentarium.
EFFECTS OF TAIL FAT ON HALOTHANE BIOTRANSFORMATION IN FAT‐TAILED SHEEP
Authors: Sharifi S , Vesal N 
Published: September 2010

SUMMARY1. The aim of the present study was to evaluate the effects of tail fat on halothane biotransformation following similar anaesthetic exposure in intact sheep and sheep with a ligated median sacral artery.2. A prospective randomized experimental study was performed using 12 healthy, 10–12‐month‐old female sheep.3. Sheep were randomly divided into two groups of six animals each and were anaesthetized twice at 2 weekly intervals. After mask induction with halothane in 100% oxygen, sheep were intubated and anaesthesia was maintained for 3 h using a rebreathing system. Serum fluoride concentration (SFC) was measured at 0, 1, 3, 6, 12, 24, 48 and 72 h following the induction of anaesthesia. Serum biochemistry was also evaluated at baseline and 72 h after anaesthesia. Induction and extubation times and time to sternal recumbency were also recorded during anaesthetic induction and recovery. Prior to the second anaesthesia (2 weeks later), the median sacral artery (MSA) was ligated under epidural anaesthesia in the experimental group. Sheep in the control group underwent sham operation. All sheep were anaesthetized as before.4. Following the first halothane anaesthesia, SFC was significantly increased from 3 to 48 h compared with baseline. In the second stage of the experiment, the increases in SFC in the control group were similar to those seen in the first stage of the experiment. However, in MSA‐ligated sheep, the increases in SFC were only significant between 3 and 12 h compared with baseline. The SFC was significantly higher in intact sheep from 3 to 72 h compared with the MSA‐ligated group. Extubation and sternal recumbency times were significantly longer in intact sheep.5. Ligation of the MSA in fat‐tailed sheep induced a significant reduction in SFC, suggesting that the presence of tail fat substantially affects halothane metabolism during the peri‐anaesthetic period in sheep. The greater extent of halothane biotransformation may be clinically important in, otherwise normal, obese patients.
EFFECTS OF MELATONIN ON LIPID PEROXIDATION and ANTI‐OXIDANT ENZYME ACTIVITY IN RATS WITH EXPERIMENTALLY INDUCED HYPERTHYROIDISM
Authors: Baydas Burhanettin , Meral Ismail 
Published: September 2010

SUMMARY1. The present study was designed to investigate the effects of high‐dose melatonin on lipid peroxidation and anti‐oxidant enzyme activity in rats with experimentally induced hyperthyroidism.2. Twenty‐four albino male rats, weighing 240–260 g, were randomly allotted into one of three experimental groups (control, hyperthyroid and hyperthyroid + melatonin treatment), with each group containing eight animals. Hyperthyroidism was induced by a daily with i.p. injection of 200 µg l‐thyroxine for 30 days. In addition to l‐thyroxin treatment, rats in the hyperthyroid + melatonin treatment group were also given daily i.p. injections of 10 mg/kg melatonin on the last 10 days of l‐thyroxine treatment. Control animals received injections of an equivalent volume of saline solution. Rats received the last injection 24 h before being killed.3. At the end of the experiment, rats in all three groups were fasted for 12 h and killed by cardiac puncture under ether anaesthesia. Blood samples were taken for the determination of malondialdehyde (MDA), glutathione (GSH) and superoxide dismutase (SOD) levels and concentrations of tri‐iodothyronine (T3) and thyroxine (T4).4. It was found that MDA and SOD levels and concentrations of T3 and T4 were higher and the GSH level was lower in rats with hyperthyroidism compared with controls. Melatonin treatment decreased the elevated MDA and SOD levels and increased the lowered GSH level to control levels in rats with hyperthyroidism, but did not ameliorate the concentrations of T3 and T4.5. It was concluded that high‐dose melatonin treatment may decrease the hyperthyroidism‐induced disturbances of lipid peroxidation and anti‐oxidant enzyme activity and oxidative damage.