Supervisors’ reports of the effects of supervisor self-disclosure on supervisees

Abstract

Using consensual qualitative research, researchers interviewed 16 supervisors regarding their use of self-disclosure in supervision. Supervisors reported that their prior training in supervisor self-disclosure (SRSD) came via didactic sources and encouraged judicious use of SRSD. Supervisors used SRSD to enhance supervisee development and normalize their experiences; supervisors did not use SRSD when it derailed supervision or was developmentally inappropriate for supervisees. In describing specific examples of the intervention, SRSD occurred in good supervision relationships, was stimulated by supervisees struggling, was intended to teach or normalize, and focused on supervisors’ reactions to their own or their supervisees’ clients. SRSD yielded largely positive effects on supervisors, supervisees, the supervision relationship, and supervisors’ supervision of others.     

Sexual differences of the effects of prenatal stress on the expression of extracellular signal-regulated kinaseas in the hippocampus of offspring rats

IN T R O D U C T IO N Anim als that are stressed during the prenatal period display w idespread neurobiological,behavioraland cognitive changes.Prenat alstress (PN S) has been associated w ith disturbances in the hy- pothalam ic-pituitary-adrenal (H PA) a…     

Monitoring the cognitive effects of antiepileptic pharmacotherapy — approaching the individual patient

Cognitive side effects of antiepileptic drugs are common and can negatively affect tolerability, compliance, and long-term retention of the treatment. Furthermore, adverse cognitive effects of pharmacotherapy significantly affect everyday functioning and quality of life. Consequently, preservation of cognitive functions is an important aspect of epilepsy therapy. Knowledge of the patient’s neuropsychological status before and after pharmacological interventions can help to decide on the appropriate treatment and, thus, can potentially improve individual medical care. Here, we suggest that cognitive monitoring of antiepileptic pharmacotherapy – like the assessment of seizure frequency, blood serum levels, electroencephalography or structural imaging – should be carried out as a matter of routine. In contrast to subjective measures, there are only very few neuropsychological instruments explicitly validated for the assessment of cognition along with antiepileptic pharmacotherapy. This review (1.) outlines indications and requirements for individual cognitive monitoring, (2.) discusses available diagnostic tools, and (3.) discloses relevant pitfalls. Neuropsychology, as demonstrated, provides evidence-based methods for monitoring cognitive effects of individual pharmacological treatments and, therefore, serves as a valuable tool for the quality and outcome control of antiepileptic therapies.This article is part of a Special Issue entitled “The Future of Translational Epilepsy Research”.     

The effects of Guillain-Barré syndrome on the close relatives of patients during the first year

OBJECTIVE: To study the impact of Guillain-Barré Syndrome (GBS) on the psychosocial functioning of the closest relative and on family functioning during the first year after GBS. METHOD: At 1 (=T1), 3 (=T3), 6 (=T6), and 12 months (=T12) after the onset of GBS, relatives of patients received the General Health Questionnaire (GHQ28) and the Family Assessment Device (FAD). Sixty-three relatives returned the GHQ28 at all four designated intervals. At T1 the relatives also received a questionnaire that contained questions on the impact on their daily life. The answers to these questions yielded a Daily Living Impact index. From the 110 relatives, 86 returned this questionnaire. RESULTS: 72% of the 86 relatives reported one or more problems in daily living. At T1 the scores of the GHQ subscales ranged from normal to mildly disturbed. The relatives showed significant improvement in their somatic complaints and anxiety during the first half year. Social dysfunction remained somewhat less than normal, severe depression was not found. At T1 and T3 the scores of the GHQ28 and some subscales differed significantly depending on the severity of the functional status of the patient, but not at T6 and T12. Relatives of patients with severe residua at 1 month score worse on the GHQ28 and most subscales at 6 months. The FAD was normal at all moments measured. CONCLUSIONS: Psychological morbidity of close relatives is significantly higher in the first months after the onset of GBS. The patient's condition has an important impact on the psychosocial functioning of close relatives. Therefore, a family approach is recommended to neurologist and other medical personnel during the first period of the disease. Also patient support groups may play a beneficial role for the relatives of GBS patients.     

Does cannabidiol protect against the negative effects of THC?

A recent study by Morgan and colleagues found that cannabidiol attenuates the acute cognitive effects of delta-9-tetrahydrocannabinol (THC). This is of interest as THC has been associated with the detrimental effects of cannabis on mental health in at-risk users, and the potency of cannabis is increasing across Europe.     

Additive effects of fatty acid mixtures on the levels and ratio of amyloid β40/42 peptides differ from the effects of individual fatty acids

Several studies have shown the protective and/or deleterious effects of dietary enrichment of single fatty acids (FAs) in several animal and cell-culture models of Alzheimer's disease (AD). However, potential interactions among dietary fatty acids are traditionally ignored. None of these studies has examined and compared the differential effects of FAs in combination, as well as alone, for their effects on amyloid β production or AD. Here we investigated the effects of omega-9 (oleic acid) and omega-6 (linoleic and arachidonic acids) fatty acids, either alone or combined, on Aβ production by APP-695 and SP-C99 transfected COS-7 cells. Overall, our results are the first to demonstrate that mixtures of FAs alter the production of Aβ40 and Aβ42 peptides and consequently the Aβ40:42 ratio differently from individual FAs. Here we show that the effects of a single lipid on Aβ production are not attributed to that single FA alone. Rather, the overall lipid composition influences the specificity and level of the regulated intramembranous proteolysis of APP by the γ-secretase complex. Our results reinforce the importance of studying composite lipids/nutrients rather than single lipids or nutrients.     

Are purines mediators of the anticonvulsant/neuroprotective effects of ketogenic diets?

Abnormal neuronal signaling caused by metabolic changes characterizes several neurological disorders, and in some instances metabolic interventions provide therapeutic benefits. Indeed, altering metabolism either by fasting or by maintaining a low-carbohydrate (ketogenic) diet might reduce epileptic seizures and offer neuroprotection in part because the diet increases mitochondrial biogenesis and brain energy levels. Here we focus on a novel hypothesis that a ketogenic diet-induced change in energy metabolism increases levels of ATP and adenosine, purines that are critically involved in neuron-glia interactions, neuromodulation and synaptic plasticity. Enhancing brain bioenergetics (ATP) and increasing levels of adenosine, an endogenous anticonvulsant and neuroprotective molecule, might help with understanding and treating a variety of neurological disorders.     

The effects of the co-administration of the α₁-adrenoreceptor antagonist prazosin on the anxiolytic effect of citalopram in conditioned fear stress in the rat

Several studies have shown that the α₁-adrenoreceptor is involved in controlling extracellular serotonin levels. The administration of the α₁-adrenoreceptor antagonist prazosin was shown to decrease extracellular serotonin levels in the hippocampus, the prefrontal cortex and the raphe nucleus, while the administration of the α₁-adrenoreceptor agonist cirazoline was shown to increase serotonin levels. Furthermore, the elevation of serotonin levels induced by the selective serotonin reuptake inhibitor (SSRI) citalopram was attenuated by prazosin. Thus, α₁-adrenoreceptor antagonists may affect SSRI-induced increases in extracellular serotonin levels and their antidepressive and anxiolytic effects. However, little is known about the influence of α₁-adrenoreceptor antagonists on the behavioral pharmacological effects of SSRIs. The conditioned fear stress-induced freezing behavior is an animal model of anxiety and can detect the anxiolytic effect of SSRIs. To clarify whether an α₁-adrenoreceptor antagonist affects the anxiolytic action of SSRIs, we examined the effects of the co-administration of the α₁-adrenoreceptor antagonist prazosin and the SSRI citalopram using the contextual conditioned fear stress model. Low-dose prazosin (0.03 mg/kg) significantly attenuated the citalopram (3 mg/kg)-induced decrease in conditioned freezing. Moreover, high-dose (0.5 mg/kg), but not low-dose (0.03 mg/kg), prazosin significantly attenuated citalopram (10 mg/kg)-induced decreases in conditioned freezing. These drugs did not affect the spontaneous motor activity of the rats. Therefore, these results suggest that blocking the α₁-adrenoreceptor decreases the anxiolytic effect of citalopram.     

α2-Adrenoceptor antagonists potentiate the anticonflict and the rotarod impairing effects of benzodiazepines

Summary Putative interactions between the specific ₂-adrenoceptor antagonist idazoxan and benzodiazepines (BDZs) were examined in two different rat conflict models; Vogel's drinking conflict test (VT) and Montgomery's conflict test (MT) (the elevated +-maze). In the MT, idazoxan (0.031mg/kg) produced anxiogenic-like effects, which were counteracted both by the triazolo-BDZ alprazolam (APZ; 0.2mg/kg) and the conventional BDZ diazepam (DIZ; 0.2mg/ kg). In fact, the anxiolytic-like effects of APZ were significantly potentiated when co-administering idazoxan. A tendency to such a phenomenon was seen also in rats treated with DIZ and idazoxan. In the VT, the anxiolytic-like effects both of APZ (1.0 mg/kg) and DIZ (4.0 mg/kg) were significantly enhanced when co-administering idazoxan (1.0 mg/kg) in a dose not affecting the behaviorper se. Similar potentiating phenomena by behaviorally inert doses of ₂-adrenoceptor antagonists (idazoxan 1.0 mg/kg; yohimbine 2.0 mg/kg) were seen with regard to the ataxic/sedative effects of the BDZs (APZ 0.25 mg/kg; DIZ 1.5 mg/ kg). The present results provide further support for the notion that the anxiolytic-like effects of BDZs are not related to attenuation of Locus Coeruleus activity. In addition, it is suggested that the potentiation caused by the ₂-adrenoceptor antagonist is mediated via a noradrenaline induced increase in signal-to-noise ratio in target neurons of the brain noradrenergic system.     

Are gender differences important for the clinical effects of antidepressants?

OBJECTIVE: Gender differences in antidepressant treatment response, side effects, dropout rates, and plasma concentrations were examined in patients with major and predominantly melancholic depression. METHOD: The study included a subgroup of 292 inpatients (96 men, 196 women) from three Danish double-blind, randomized, controlled trials. All patients completed a 5-week treatment period and fulfilled the DSM-III or DSM-III-R criteria for major depression. Clomipramine (150 mg/day) was the reference treatment, and comparable treatments were citalopram (40 mg/day), paroxetine (30 mg/day), and moclobemide (400 mg/day). Assessments were performed by using the 17-item Hamilton Depression Rating Scale and the Udvalg for Kliniske Unders?gelser Side Effect Rating Scale. In a subgroup of 110 patients, weekly measurements of clomipramine plasma concentrations were obtained. Nonparametric statistical tests and multiple linear and logistic regression models were used for statistical evaluations. RESULTS: Both genders had similar remission rates (Hamilton depression scale score <8) when treated with clomipramine and had significantly higher remission rates with clomipramine than with the comparable treatments. The plasma concentrations of clomipramine were significantly higher for female than for male patients. No gender differences were found in posttreatment Hamilton depression scale scores, nor did the therapeutic effects of treatment depend on gender. Rates of dropout and side effects were similar for men and women. No relationship between plasma concentrations, gender, and therapeutic outcome was found. CONCLUSIONS: In a group of patients with major and predominantly melancholic depression, differentiation according to gender was not important in treatment with common antidepressants. Women appeared to have higher plasma concentrations of tricyclic antidepressants than men. The consequences of this difference for clinical effects are unclear. Gender-specific recommendations for dosing of tricyclic antidepressants may be considered.     

Improved effects of word‐retrieval treatments subsequent to addition of the orthographic form

Background: The participant, an individual with moderate–severe Wernicke's aphasia, had not benefited from two word‐retrieval cueing treatments in a previous investigation. The participant insisted that her performance would have been improved if the written word had been provided as part of the cueing process.

Aims: The purpose of this investigation was to examine the effects of adding the orthographic form of targeted action names to a semantic cueing treatment (SCT) and a phonologic cueing treatment (PCT).

Methods & Procedures: The participant received SCT and PCT applied to the retrieval of action names. The treatments both provided the written word form paired with the pictured action in conjunction with cueing hierarchies. Two, sequential multiple baseline designs across behaviours were employed to examine the acquisition and response generalisation effects of treatment.

Outcomes & Results: Improved accuracy of action naming was found for both treatments. Gains were limited to trained items; no changes were observed in naming of untrained actions.

Conclusions: It appeared that the participant utilised the orthographic word form to develop associations between the visual object recognition system and the orthographic input lexicon, thus facilitating access to the phonological output lexicon.     

Mechanisms of antinociceptive effects of ouabain in combination with neostigmine in the rat***★

BACKGROUND： It has been previously shown that intrathecal administration of either ouabain or neosdgmine can produce antinociceptive effects. Moreover, ouabain and neostigmine are differently associated with acetylcholine.
OBJECTIVE： It has been hypothesized that intrathecal administration of ouabain, in combination with neostigmine, can produce antinociceptive synergistic effects. Atropine, as a competitive antagonist, was pre-injected to verify the mechanisms of action.
DESIGN, TIME AND SETTING： This study was a randomized, controlled, animal experiment, performed at the State Key Laboratory of Oncology in Southern China between May 2006 and February 2007.
MATERIALS： A total of 102 healthy, adult, Sprague Dawley rats were included. Ouabain and neostigmine （Sigma, USA）, as well as atropine （Tanabe Seiyaku, Japan）, were also used.
METHODS： Varied doses of ouabain, neostigmine, and a combination of the two were intrathecally injected into rats. Six rats were allotted for each dose group. Intrathecal pretreatment with atropine was tested 10 minutes prior to intrathecal administration of neostigmine or the combination of ouabain and neostigmine.
MAIN OUTCOME MEASURES： Tail-flick tests were performed to measure tail-flick latency （seconds） prior to and after administration. The response in the tail-flick test was expressed as the percentage of maximum possible effect （% MPE）, where % MPE = [tail-flick latency after administration （seconds） -mean baseline value for tail-flick latency]/[ 10 seconds - the mean baseline value for tail-flick latency （seconds）] x 100%.
RESULTS： Rat spinal intrathecal administration of either ouabain or neostigmine alone produced antinociceptive effects in a dose-dependent manner. Intrathecally administration of neostigmine （0.05, 0.1, 0.3 μg ） in combination with ouabain （1 μ g ） produced enhanced antinociceptive effects, with a % MPE of 29%, 78%, and 95%, respectively （P 〈 0.05）. Intrathecally administration of 0.3μg neost     

BDNF–ERK–CREB signalling mediates the role of miR-132 in the regulation of the effects of oleanolic acid in male mice

Background

Although previous study has demonstrated that brain-derived neurotrophic factor (BDNF) is involved in the antidepressant-like effect of oleanolic acid, there is little information regarding the details of the molecular mechanism involved in this effect.

Methods

We used a chronic unpredictable mild stress (CUMS) model to test the antidepressant-like effect of oleanolic acid on depressant-like behaviour, miR-132 expression and synaptic protein expression in the male mouse hippocampus. Furthermore, we explored the possible signalling pathways associated with miR-132 expression that mediate the effect of oleanolic acid on neuronal proliferation.

Results

The results demonstrated that a 3-week treatment with oleanolic acid ameliorated CUMS-induced anhedonic and anxiogenic behaviours. Furthermore, we found that oleanolic acid led to the BDNF-related phosphorylation and activation of extracellular signal-regulated kinases (ERK) and cyclic adenosine monophosphate response element binding protein (CREB), which was associated with the upregulation of miR-132 and hippocampal neuronal proliferation. Moreover, experiments with an miR-132 antagomir revealed that targeting miR-132 led to inhibition of neuronal proliferation and the postsynaptic density protein 95, but did not affect presynaptic protein synapsin I.

Limitations

Several other stimuli can also induce CREB phosphorylation in the hippocampus. Thus, regulation of miR-132 may not be restricted to neurotrophic signalling.

Conclusion

Our results show that oleanolic acid induces the upregulation of miR-132, which serves as an important regulator of neurotrophic actions, mainly through the activation of the hippocampal BDNF–ERK–CREB signalling pathways.     

The adjustment of children of Australian Vietnam veterans: is there evidence for the transgenerational transmission of the effects of war-related trauma?

OBJECTIVE: The presence of posttraumatic stress disorder (PTSD) in trauma survivors has been linked with family dysfunction and symptoms in their children, including lower self-esteem, higher disorder rates and symptoms resembling those of the traumatized parent. This study aims to examine the phenomenon of intergenerational transfer of PTSD in an Australian context. METHOD: 50 children (aged 16-30) of 50 male Vietnam veterans, subgrouped according to their fathers' PTSD status, were compared with an age-matched group of 33 civilian peers. Participants completed questionnaires with measures of self-esteem, PTSD symptomatology and family functioning. RESULTS: Contrary to expectations, no significant differences were found between the self-esteem and PTSD symptomatology scores for any offspring groups. Unhealthy family functioning is the area in which the effect of the veteran's PTSD appears to manifest itself, particularly the inability of the family both to experience appropriate emotional responses and to solve problems effectively within and outside the family unit. CONCLUSION: Methodological refinements and further focus on the role of wives/mothers in buffering the impact of veterans' PTSD symptomatology on their children are indicated. Further effort to support families of Veterans with PTSD is also indicated.     

Neuroprotective and neurodegenerative effects of the chronic expression of tumor necrosis factor α in the nigrostriatal dopaminergic circuit of adult mice

Tumor necrosis factor (TNF)-α, a pro-inflammatory cytokine, has been implicated in both neuronal death and survival in Parkinson's disease (PD). The substantia nigra (SN), a CNS region affected in PD, is particularly susceptible to inflammatory insults and possesses the highest density of microglial cells, but the effects of inflammation and in particular TNF-α on neuronal survival in this region remains controversial. Using adenoviral vectors, the CRE/loxP system and hypomorphic mice, we achieved chronic expression of two levels of TNF-α in the SN of adult mice. Chronic low expression of TNF-α levels reduced the nigrostriatal neurodegeneration mediated by intrastriatal 6-hydroxydopamine administration. Protective effects of low TNF-α level could be mediated by TNF-R1, GDNF, and IGF-1 in the SN and SOD activity in the striatum (ST). On the contrary, chronic expression of high levels of TNF-α induced progressive neuronal loss (63% at 20 days and 75% at 100 days). This effect was accompanied by gliosis and an inflammatory infiltrate composed almost exclusively by monocytes/macrophages. The finding that chronic high TNF-α had a slow and progressive neurodegenerative effect in the SN provides an animal model of PD mediated by the chronic expression of a single cytokine. In addition, it supports the view that cytokines are not detrimental or beneficial by themselves, i.e., their level and time of expression among other factors can determine its final effect on CNS damage or protection. These data support the view that new anti-parkinsonian treatments based on anti-inflammatory therapies should consider these dual effects of cytokines on their design.     

The effects of 1 Hz rTMS over the hand area of M1 on movement kinematics of the ipsilateral hand

1 Hz rTMS applied over primary motor cortex (M1) reduces cortical excitability outlasting the stimulation period. Healthy right-handed subjects performed finger and hand tapping and a reach-to-grasp movement prior to (baseline) and after 1 Hz rTMS applied over (1) M1 of either the right or the left hemisphere, and (2) the vertex (control stimulation). 1 Hz rTMS applied over the left M1, but not over the vertex, improved movement kinematics of finger and hand tapping as well as grasping with the left hand. 1 Hz rTMS applied over the right M1, but not over the vertex, improved only the kinematics of hand tapping performed with the right hand. These data suggest that 1 Hz rTMS induced inhibition of ipsilateral M1 reduces transcallosal inhibition of contralateral M1 and thereby improves motor performance at the ipsilateral hand. The impact on motor performance of the ipsilateral hand is most pronounced after 1 Hz rTMS over the left M1.