The psychological and physiological effects of integrated cognitive-behavioral and biofeedback therapy on panic disorder: A randomized controlled trial.

BACKGROUND: Cognitive-behavioral therapy (CBT) and biofeedback therapy are commonly regarded as effective treatment modalities for panic disorder. The aim of this study was to establish a Taiwanese version of an integrated cognitive-behavioral and biofeedback therapy (ICB) and examine its effects on panic disorder using psychological and physiological indicators. METHODS: Thirty patients with panic disorder were enrolled in this study. They were randomly assigned to either the ICB group (n = 15) or the treatment as usual (TAU) group (n = 15). The intervention consisted of six sessions, conducted once a week. Psychological indicators were measured at baseline (prior to intervention), week 3, and week 6, while physiological indicators were measured at baseline and week 6. The psychological indicators included five scales, with the Panic Disorder Severity Scale (PDSS) being the primary measure. The physiological indicators included respiratory sinus arrhythmia (RSA) and skin conductance, which respectively represent parasympathetic and sympathetic activity. RESULTS: Considering all participants, PDSS scores significantly decreased over time, but the difference between the ICB and TAU groups did not reach statistical significance. Among the physiological indicators, resting-state RSA and RSA under relaxation showed significant between-group differences over time, with the ICB group demonstrating a more pronounced improvement in RSA. CONCLUSION: In the context of existing pharmacological treatments, the benefits of ICB for panic disorder may not be observable through psychological indicators. However, it can lead to enhancement of parasympathetic activity as evidenced by the physiological indicators.

Identifying dopamine supersensitivity through a randomized controlled study of switching to aripiprazole from other antipsychotic agents in patients with schizophrenia.

BACKGROUND: Aripiprazole has been reported to worsen psychotic symptoms when switching from other antipsychotics, possibly due to dopamine supersensitivity psychosis. OBJECTIVE: This study aimed to explore the predictors and possible underlying mechanisms of aripiprazole-related psychotic exacerbation. METHODS: We conducted an 8-week, open-label, randomized controlled study from October 2007 to September 2009, assigning patients with a primary diagnosis of schizophrenia or schizoaffective disorder to switch from other antipsychotics to aripiprazole with 2-week dual administration, and then to taper off the original agents in fast (n = 38, within 1 week) or slow (n = 41, within 4 weeks) strategies. Positive and Negative Syndrome Scale (PANSS) was examined at day 0, 7, 14, 28, 56. Aripiprazole-related exacerbation (ARE) was defined positive as a 2-point increase in delusion/hallucination dimension score within 28 days compared with baseline. Baseline demographic, clinical and intervention-related variables were compared between the ARE+ and ARE- groups. RESULTS: Of the 79 randomized patients, 21 fulfilled the criteria of ARE+ , and 46 were classified as ARE-. Fourteen patients in the ARE+ group had worsening psychotic symptoms in the first and second weeks. Compared with the ARE- group, the ARE+ group had a higher baseline chlorpromazine equivalent dose (405.8 ± 225.8 mg vs 268.1 ± 165.4 mg, p = 0.007) and was associated with prescription of first-generation antipsychotics (p = 0.038). CONCLUSIONS: A higher dose of original antipsychotics and prescription of first-generation antipsychotics may be associated with a higher risk of ARE. The underlying mechanism might be covert dopamine supersensitivity psychosis. These findings may help to identify high-risk patients and guide appropriate treatment strategies. TRIAL REGISTRATION: ClinicalTrials.gov, identifier: NCT00545467.

Validation of the Mediation Effect Between Cross-Cultural Management and Employee Identification.

PURPOSE: Corporate culture faces a variety of cross-cultural challenges across the globe. Every culture retains and maintains different norms and customs, which are totally unique and different from other cultures. Consequently, employees from different cultures often experience various cross-cultural issues and challenges while working in transnational organizations where employees are needed to understand how people from diverse cultures must work together. PATIENTS AND METHODS: The study used mixed research methodology for meeting the paper goals. Both positivism and phenomenology look relevant in a sense that they individually and collectively satisfy the paper objectives. To test mediation and moderation, the authors have used various hypotheses through collecting the sample size of 600 out of 6000 employees working for an Asian group encompassing more than 200 companies. Moderation and mediation strategic management research methods were used with the American Industrial Group in Asia as the setup of the study. Hypotheses were tested on effects of new corporate culture-based learning on the perception of social norms, learning attitude, self-efficacy, and social values. Additional hypotheses were also tested on the effects of perception of social norms, learning attitude, self-efficacy, social values, and psychological control on change intention. RESULTS: Perceived social norms directly affect the willingness to change as they have been used as mediating variables. Therefore, social norms affect corporate norms. CONCLUSION: The paper shows how mediation and moderation are understood and applied through understanding the relationship between local culture and corporate culture. The findings reveal how local culture affects corporate culture. However, there are certain limitations of the study; this includes that the study scope has mostly focused on an Asian context, therefore, it may not be applicable to other continents.

Specific personality traits and associated psychosocial distresses among individuals with heroin or methamphetamine use disorder in Taiwan.

BACKGROUND/PURPOSE: Previous studies showed the association between substance use disorders (SUDs) and borderline and antisocial personality disorders. Substance abusers may have emotional, somatic and interpersonal distresses. This study aimed to investigate the associations between substance, personality and psychosocial distresses. METHODS: This cross-sectional, questionnaire-based study recruited 39 individuals with heroin use disorder (HUD), 111 with methamphetamine use disorder (MUD) and 101 as the control group in a rural area of Taiwan. The Tridimensional Personality Questionnaire (TPQ) and Opiate Treatment Index were used to assess the association between personality and psychosocial conditions. Deviations of the three personality dimensions of TPQ (novelty seeking, harm avoidance, and reward dependence) could reflect eight personality patterns. RESULTS: We found SUD was associated with high novelty seeking and harm avoidance traits and explosive (borderline) personality pattern, whereas HUD was also linked with sensitive (narcissistic) pattern. Subjects with HUD tended to have more deviant personality traits than subjects with MUD. For subjects with SUDs, all three personality dimensions and sensitive (narcissistic) personality patterns were associated with emotional and somatic distresses, and those with explosive (borderline) and sensitive (narcissistic) patterns had poor social functioning. CONCLUSION: Our results indicate substance abusers with high novelty seeking and harm avoidance, corresponding to explosive (borderline) or sensitive (narcissistic) patterns, to have a higher tendency to suffer from somatic and psychosocial distresses.

Two Cases of De Novo Pathological Gambling Associated With Aripiprazole.

OBJECTIVES: Pathological gambling can be potentiated by treatment with dopamine agonists. Aripiprazole, bearing a partial agonist activity at dopamine D2 and D3 receptors, has also been linked to such a behavioral aberration, usually on subjects predisposed with tendency of impulsive or addictive behaviors. METHODS: Review of patient's medical records and literature review. RESULTS: Two young patients' pathological gambling emerged simply due to exposure to aripiprazole, neither related to manic or psychotic symptoms nor with history of addictive or impulsive behaviors. Their pathological gambling disappeared soon after switching aripiprazole to other antipsychotics. One patient has tested such a relationship by reexposure to aripiprazole while his compulsion to gamble recurred. CONCLUSIONS: In addition to previously recognized risk factors, pathological gambling might occur in young patients whose history did not reveal an addictive tendency while they were sensitive to the pharmacological effect, as well as adverse effects, of psychotropic agents.

Ubiquitin Ligase RNF138 Promotes Episodic Ataxia Type 2-Associated Aberrant Degradation of Human Cav2.1 (P/Q-Type) Calcium Channels.

Voltage-gated CaV2.1 channels comprise a pore-forming α1A subunit with auxiliary α2δ and ß subunits. CaV2.1 channels play an essential role in regulating synaptic signaling. Mutations in the human gene encoding the CaV2.1 subunit are associated with the cerebellar disease episodic ataxia type 2 (EA2). Several EA2-causing mutants exhibit impaired protein stability and exert dominant-negative suppression of CaV2.1 wild-type (WT) protein expression via aberrant proteasomal degradation. Here, we set out to delineate the protein degradation mechanism of human CaV2.1 subunit by identifying RNF138, an E3 ubiquitin ligase, as a novel CaV2.1-binding partner. In neurons, RNF138 and CaV2.1 coexist in the same protein complex and display notable subcellular colocalization at presynaptic and postsynaptic regions. Overexpression of RNF138 promotes polyubiquitination and accelerates protein turnover of CaV2.1. Disrupting endogenous RNF138 function with a mutant (RNF138-H36E) or shRNA infection significantly upregulates the CaV2.1 protein level and enhances CaV2.1 protein stability. Disrupting endogenous RNF138 function also effectively rescues the defective protein expression of EA2 mutants, as well as fully reversing EA2 mutant-induced excessive proteasomal degradation of CaV2.1 WT subunits. RNF138-H36E coexpression only partially restores the dominant-negative effect of EA2 mutants on CaV2.1 WT functional expression, which can be attributed to defective membrane trafficking of CaV2.1 WT in the presence of EA2 mutants. We propose that RNF138 plays a critical role in the homeostatic regulation of CaV2.1 protein level and functional expression and that RNF138 serves as the primary E3 ubiquitin ligase promoting EA2-associated aberrant degradation of human CaV2.1 subunits.SIGNIFICANCE STATEMENT Loss-of-function mutations in the human CaV2.1 subunit are linked to episodic ataxia type 2 (EA2), a dominantly inherited disease characterized by paroxysmal attacks of ataxia and nystagmus. EA2-causing mutants may exert dominant-negative effects on the CaV2.1 wild-type subunit via aberrant proteasomal degradation. The molecular nature of the CaV2.1 ubiquitin-proteasome degradation pathway is currently unknown. The present study reports the first identification of an E3 ubiquitin ligase for CaV2.1, RNF138. CaV2.1 protein stability is dynamically regulated by RNF138 and auxiliary α2δ and ß subunits. We provide a proof of concept that protecting the human CaV2.1 subunit from excessive proteasomal degradation with specific interruption of endogenous RNF138 function may partially contribute to the future development of a novel therapeutic strategy for EA2 patients.