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تقويم برامج الموهوبين : دليل للمدربين والمنسقين
تواجه مناطق تعليمية كثيرة صعوبات مالية لا تمكنها من تعيين خبير خارجي لتقويم برامج الموهوبين لديها. لذا بإمكان هذه المناطق إجراء تقويم داخلي خاص بها، بوصفه حلا مؤقتا. وبذلك جاء هذا الكتاب : (تقويم برامج الموهوبين دليل للمديرين والمنسقين) لمساعدة المديرين على تصميم تقويم برامج الموهوبين داخليا، وتطبيقه، وإعداد التقارير عنه، وقد أعدت المؤلفتان هذا الكتاب آخذتين في الحسبان ضغط الوقت الذي يتعرض له المديرون، وعليه، فإن هذا الدليل يشتمل على عملية تفصيلية لتقويم العناصر الأولية لبرامج الموهوبين، وكذلك نماذج أوراق العمل، واستطلاعات الرأي والمصادر القابلة للنسخ ؛ وذلك لتسهيل إجراء تقويم شامل مبني على أفضل الممارسات في تربية الموهوبين.
Book
Elevated brain cannabinoid CB1 receptor availability in post-traumatic stress disorder: a positron emission tomography study
Endocannabinoids and their attending cannabinoid type 1 (CB
1
) receptor have been implicated in animal models of post-traumatic stress disorder (PTSD). However, their specific role has not been studied in people with PTSD. Herein, we present an
in vivo
imaging study using positron emission tomography (PET) and the CB
1
-selective radioligand [
11
C]OMAR in individuals with PTSD, and healthy controls with lifetime histories of trauma (trauma-exposed controls (TC)) and those without such histories (healthy controls (HC)). Untreated individuals with PTSD (
N
=25) with non-combat trauma histories, and TC (
N
=12) and
HC
(
N
=23) participated in a magnetic resonance imaging scan and a resting PET scan with the CB
1
receptor antagonist radiotracer [
11
C]OMAR, which measures the volume of distribution (
V
T
) linearly related to CB
1
receptor availability. Peripheral levels of anandamide, 2-arachidonoylglycerol, oleoylethanolamide, palmitoylethanolamide and cortisol were also assessed. In the PTSD group, relative to the HC and TC groups, we found elevated brain-wide [
11
C]OMAR
V
T
values (F(2,53)=7.96,
P
=0.001; 19.5% and 14.5% higher, respectively), which were most pronounced in women (F(1,53)=5.52,
P
=0.023). Anandamide concentrations were reduced in the PTSD relative to the TC (53.1% lower) and HC (58.2% lower) groups. Cortisol levels were lower in the PTSD and TC groups relative to the HC group. Three biomarkers examined collectively—OMAR
V
T
, anandamide and cortisol—correctly classified nearly 85% of PTSD cases. These results suggest that abnormal CB
1
receptor-mediated anandamide signaling is implicated in the etiology of PTSD, and provide a promising neurobiological model to develop novel, evidence-based pharmacotherapies for this disorder.
Journal Article
Serotonin versus catecholamine deficiency: behavioral and neural effects of experimental depletion in remitted depression
Despite immense efforts into development of new antidepressant drugs, the increases of serotoninergic and catecholaminergic neurotransmission have remained the two major pharmacodynamic principles of current drug treatments for depression. Consequently, psychopathological or biological markers that predict response to drugs that selectively increase serotonin and/or catecholamine neurotransmission hold the potential to optimize the prescriber’s selection among currently available treatment options. The aim of this study was to elucidate the differential symptomatology and neurophysiology in response to reductions in serotonergic versus catecholaminergic neurotransmission in subjects at high risk of depression recurrence. Using identical neuroimaging procedures with [
18
F] fluorodeoxyglucose positron emission tomography after tryptophan depletion (TD) and catecholamine depletion (CD), subjects with remitted depression were compared with healthy controls in a double-blind, randomized, crossover design. Although TD induced significantly more depressed mood, sadness and hopelessness than CD, CD induced more inactivity, concentration difficulties, lassitude and somatic anxiety than TD. CD specifically increased glucose metabolism in the bilateral ventral striatum and decreased glucose metabolism in the bilateral orbitofrontal cortex, whereas TD specifically increased metabolism in the right prefrontal cortex and the posterior cingulate cortex. Although we found direct associations between changes in brain metabolism and induced depressive symptoms following CD, the relationship between neural activity and symptoms was less clear after TD. In conclusion, this study showed that serotonin and catecholamines have common and differential roles in the pathophysiology of depression.
Journal Article
The MCP-4/MCP-1 ratio in plasma is a candidate circadian biomarker for chronic post-traumatic stress disorder
Post-traumatic stress disorder (PTSD) is psychiatric disease, which can occur following exposure to traumatic events. PTSD may be acute or chronic, and can have a waxing and waning course of symptoms. It has been hypothesized that proinflammatory cytokines and chemokines in the cerebrospinal fluid (CSF) or plasma might be mediators of the psychophysiological mechanisms relating a history of trauma exposure to changes in behavior and mental health disorders, and medical morbidity. Here we test the cytokine/chemokine hypothesis for PTSD by examining levels of 17 classical cytokines and chemokines in CSF, sampled at 0900 hours, and in plasma sampled hourly for 24 h. The PTSD and healthy control patients are from the NIMH Chronic PTSD and healthy control cohort, initially described by Bonne
et al.
(2011), in which the PTSD patients have relatively low comorbidity for major depressive disorder (MDD), drug or alcohol use. We find that in plasma, but not CSF, the bivariate MCP4 (CCL13)/ MCP1(CCL2) ratio is ca. twofold elevated in PTSD patients compared with healthy controls. The MCP-4/MCP-1 ratio is invariant over circadian time, and is independent of gender, body mass index or the age at which the trauma was suffered. By contrast, MIP-1β is a candidate biomarker for PTSD only in females, whereas TARC is a candidate biomarker for PTSD only in males. It remains to be discovered whether these disease-specific differences in circadian expression for these specific immune signaling molecules are biomarkers, surrogates, or drivers for PTSD, or whether any of these analytes could contribute to therapy.
Journal Article
Elevated brain cannabinoid CB.sub.1 receptor availability in post-traumatic stress disorder: a positron emission tomography study
Endocannabinoids and their attending cannabinoid type 1 ([CB.sub.1]) receptor have been implicated in animal models of post-traumatic stress disorder (PTSD). However, their specific role has not been studied in people with PTSD. Herein, we present an in vivo imaging study using positron emission tomography (PET) and the [CB.sub.1]-selective radioligand [[sup.11]C]OMAR in individuals with PTSD, and healthy controls with lifetime histories of trauma (trauma-exposed controls (TC)) and those without such histories (healthy controls (HC)). Untreated individuals with PTSD (N = 25) with non-combat trauma histories, and TC (N = 12) and HC (N = 23) participated in a magnetic resonance imaging scan and a resting PET scan with the [CB.sub.1] receptor antagonist radiotracer [[sup.11]C]OMAR, which measures the volume of distribution ([V.sub.T]) linearly related to [CB.sub.1] receptor availability. Peripheral levels of anandamide, 2-arachidonoylglycerol, oleoylethanolamide, palmitoylethanolamide and cortisol were also assessed. In the PTSD group, relative to the HC and TC groups, we found elevated brain-wide [[sup.11]C]OMAR [V.sub.T] values ([F.sub.(2,53)] = 7.96, P = 0.001;19.5% and 14.5% higher, respectively), which were most pronounced in women ([F.sub.(1,53)] = 5.52, P = 0.023). Anandamide concentrations were reduced in the PTSD relative to the TC (53.1% lower) and HC (58.2% lower) groups. Cortisol levels were lower in the PTSD and TC groups relative to the HC group. Three biomarkers examined collectively--OMAR [V.sub.T], anandamide and cortisol--correctly classified nearly 85% of PTSD cases. These results suggest that abnormal [CB.sub.1] receptor-mediated anandamide signaling is implicated in the etiology of PTSD, and provide a promising neurobiological model to develop novel, evidence-based pharmacotherapies for this disorder.
Journal Article
A polymorphism (5-HTTLPR) in the serotonin transporter promoter gene is associated with DSM-IV depression subtypes in seasonal affective disorder
Serotonergic mechanisms are thought to play an important role in the pathogenesis of seasonal affective disorder (SAD). The expression of the serotonin transporter (5-HTT) is regulated in part by an insertion/deletion polymorphism in the serotonin transporter gene promoter region (5-HTTLPR). The 5-HTTLPR short allele
(s)
has been associated with anxiety-related personality traits and depression, and one study observed an association between the 5-HTTLPR
s
-allele and SAD and the trait of seasonality. We genotyped 138 SAD patients and 146 healthy volunteers with low seasonality for 5-HTTLPR. No difference between patients and controls was found for genotype distribution and
s
-allele frequency. However, genotype distribution and allele frequencies were strongly associated with DSM-IV depression subtypes. Melancholic depression was associated with the 5-HTTLPR long
(l)
allele and atypical depression with the 5-HTTLPR
s
-allele (two-sided Fisher's exact test: genotype distribution:
P
=0.0038; allele frequencies:
P
=0.007). Our data are compatible with the hypothesis of a disease process that is not causally related to 5-HTTLPR, but involves 5-HT neurotransmission and 5-HTTLPR somewhere on its way to phenotypic disease expression.
Journal Article
Dopamine transporter availability in symptomatic depressed patients with seasonal affective disorder and healthy controls
Background. During recent years hypotheses about the pathophysiology of seasonal affective disorder/winter type (SAD) have focused monoaminergic mechanisms. There is substantial evidence that serotonergic systems play an important role. The potential role of catecholaminergic pathways has not been fully explored. Methods. Eleven drug-free, symptomatic depressed patients with SAD and 11 healthy age- and gender-matched healthy controls were invited to participate in a 123Iβ-CIT single photon emission computed tomography (SPECT) study to assess striatal density of dopamine transporters (DATs). The cerebellum was used as reference region. Ratios were calculated between mean counts in left and right striatum and cerebellum. These ratios minus 1 represent specific/non-displaceable binding and are assumed to be directly related to DAT availability at the time of binding equilibrium. Results. Displaceable 123Iβ-CIT binding in the area corresponding to the left striatum was significantly reduced in SAD patients compared to healthy controls (10·49±0·91 v. 11·95±1·54, respectively; 2-tailed P = 0·017, Mann–Whitney U test). Conclusions. These data suggest reductions in the availability of striatal DAT binding sites in untreated symptomatic depressed SAD patients. It remains unclear whether these reductions represent a primary defect or an attempt to overcome a state of possible lowered dopamine availability in the synaptic cleft during a depressive episode of SAD. However, these findings provide evidence that brain dopaminergic systems may be involved in the pathophysiology of SAD.
Journal Article
PET imaging of norepinephrine transporter in cocaine abuser using ( S, S)- 11CMRB
Introduction The role of the norepinephrine transporter (NET) in the reinforcing effects of stimulants, such as cocaine (COC), and the mechanisms responsible for their addictive and toxic effects has long been recognized; however, it has never been demonstrated via in vivo imaging due to the lack of suitable NET radioligands. [...]ROIs for small brain regions including locus coeruleus (LC), brainstem nuclei, hypothalamus (hypoTH), and thalamic (TH) subnuclei such as dorsomedial (DM), pulvinar (PU), and ventrolateral (VL) were also defined.
Journal Article