[Theory and Practice of Empowerment for Family Members of Patients Under Custodial Protection Sentence].

Empowerment not only benefits patients but also provides support and assistance to their family members, especially in cases when patients are subject to custodial protection sentences. The positive effects of empowerment on patients' family members may be summarized into three main aspects, including: enhancing their engagement in healthcare, alleviating their anxiety, and enhancing their caregiving skills. With regard to enhancing engagement in healthcare, family members receive health education that provides an overview of the illness, treatment options, prognosis, and key nursing points and allows them to better understand the patient's condition and actively participate in decision-making. With regard to alleviating anxiety, patients under custodial protection sentences are involved in legal problems, which results in higher levels of stress for family members compared to their peers caring for general patients. Through emotional support and active listening, nurses provide opportunities for family members to express their concerns and offer comfort and encouragement, helping them cope with difficulties and pressures. With regard to enhancing caregiving skills, the purpose of custodial protection sentences is to prevent recidivism, and family members bear significant responsibility for caregiving after discharge. Nurses can share similar caregiving experiences from their ward, educate family members about observing symptoms, and provide guidance, thereby strengthening their caregiving capabilities. In addition, with regard to the disposition of patients, nurses assist family members to understand the medical process and provide necessary guidance, ensuring family members have a clear understanding and are respected during the preparations for discharge. Based on related theoretical frameworks and practical experiences, this research highlights the positive role of empowerment in enhancing the caregiving abilities and satisfaction of the family members of patients, particularly those subject to custodial protection sentences.

Sertraline alleviated osmophobia caused by partial hypopituitarism with isolated ACTH deficiency.

OBJECTIVE: Hyperosmia may be an early manifestation of hypocortisolism and may be mistakenly diagnosed as osmophobia. However, sertraline therapy incidentally alleviated the phobic symptoms and hindered accurate diagnosis. CASE REPORT: A 41-year-old man was diagnosed as having osmophobia. Initial sertraline treatment relieved the symptoms, but its cessation resulted in recurrence of osmophobia. Endocrinological examinations revealed severe hypocortisolism and partial hypopituitarism with isolated adrenocorticotropic hormone deficiency. After prednisolone supplementation, his condition dramatically improved. CONCLUSION: We recommend that, before intervention with selective serotonin reuptake inhibitors is performed, the hypothalamic-pituitary-adrenal axis be evaluated in psychiatric patients presenting with co-occurring olfactory change.

Fluoxetine depresses glutamate exocytosis in the rat cerebrocortical nerve terminals (synaptosomes) via inhibition of P/Q-type Ca2+ channels.

Fluoxetine, an antidepressant that is used clinically in the treatment of mood disorders, is a selective serotonin reuptake inhibitor. In the present study we investigated the effects of fluoxetine on 4-aminopyridine (4AP)-evoked glutamate release in cerebrocortical nerve terminals (synaptosomes). Fluoxetine suppressed the release of glutamate evoked by 4AP in a concentration-dependent manner. This effect was associated with a reduction in the depolarization-evoked increase in cytosolic free calcium levels in the absence of significant effect on the synaptosomal membrane potential. In addition, both ionomycin- and sucrose-evoked glutamate releases were not affected by fluoxetine, indicating that fluoxetine-mediated inhibition of glutamate release is not a direct effect on the exocytotic machinery. Furthermore, the inhibitory action of fluoxetine was completely abolished in synaptosomes pretreated with P/Q type Ca(2+) channel blocker omega-agatoxin IVA (omega-AgTX IVA) or protein kinase C (PKC) stimulator 4beta-phorbol 12, 13-dibutyrate (PDBu). These results suggest that, in cerebrocortical nerve terminals, fluoxetine inhibits glutamate release through the suppression of P/Q type Ca(2+) channel activity. The presynaptic action of fluoxetine is mediated by a PKC-sensitive signaling pathway. Synapse 48:170-177, 2003.