Search

Abstract Nurses play a pivotal role in the delivery of medical services. Professional commitment is crucial for nursing professionals’ long-term, healthy, and sustainable development. However, nursing students’ professional commitment levels are currently unsatisfactory in China, especially given that the COVID-19 pandemic has posed unprecedented challenges to the profession. Therefore, studies investigating the professional commitment levels of nursing students and the underlying influencing factors are urgently required. This study explored how nursing students’ risk perceptions, negative emotions, and psychological capital affected their professional commitment during the COVID-19 pandemic. A cross-sectional study was conducted among nursing students using risk perception, professional commitment, negative emotions, and psychological capital scales. An analysis of 1142 Chinese nursing students suggested that nursing students’ risk perception positively impacted professional commitment and that negative emotions mediated this association. Importantly, psychological capital moderates the mediating effect of negative emotions and can buffer the negative emotions caused by risk perception. This study demonstrated that effective intervention strategies should be implemented in multiple dimensions such as education, individual, public and society to improve the professional commitment of nursing students.

Antipsychotic drugs alter the activity of dopamine neurons in the ventral tegmental area (A10) and substantia nigra pars compacta (A9). As there is a dense projection of orexin neurons from the lateral hypothalamus to A10 dopaminergic neurons, and some antipsychotics have been shown to increase the expression of c-fos in orexin-containing cells in the hypothalamus, we hypothesized that stimulation of orexin receptors plays a role in the effects of antipsychotics on the activity of A9 and A10 dopamine cells. Single-unit recordings in anesthetized rats demonstrated the central effects of the selective orexin-1 receptor antagonist SB-334867 (2 mg/kg, intravenous), as it reversed the excitatory effects of orexin-A administration (6 μg, intracerebroventricular) on the activity of locus coeruleus (LC) cells. Recordings from midbrain dopamine neurons showed that acute administration of SB-334867 alone did not alter the number of spontaneously active A9 or A10 cells, but did reverse: (1) the increase in the number of spontaneously active A9 and/or A10 dopamine cells caused by the acute administration of haloperidol (1 mg/kg, subcutaneous) or olanzapine (10 mg/kg, s.c.) and (2) the decrease in the number of spontaneously active A9 and/or A10 dopamine cells caused by the chronic administration of haloperidol (1 mg/kg/day × 21 days, s.c.) or olanzapine (10 mg/kg/day × 21 days, s.c.). However, SB-334867 did not block a different electrophysiological effect of olanzapine, as it did not block the olanzapine-induced activation of LC cells. These results indicate that activation of orexin-1 receptors plays an important role on the effects of antipsychotic drugs on dopamine neuronal activity and may play an important role in the clinical effects of antipsychotic drugs.Neuropsychopharmacology (2007) 32, 786–792. doi:10.1038/sj.npp.1301239; published online 25 October 2006 [ABSTRACT FROM AUTHOR]

The tumor suppressor p53 is tightly controlled at low levels in cells by constant ubiquitination and proteasomal degradation. In response to stresses, ubiquitination of p53 is inhibited through diverse pathways, depending on the nature of the stimulus and cell type. This leads to the accumulation and activation of p53, which induces cell cycle arrest and/or apoptosis to prevent cells from transformation. Many studies have indicated that defects of the p53 system are present in most, if not all, human tumor cells. Meanwhile, significant progress has been made in understanding the molecular mechanisms of p53 ubiquitination and the regulation of the p53 system. Therefore, it is possible now to consider targeting ubiquitination as a means to regulate and reactivate p53 in tumors. Emerging evidence suggests that inhibiting the E3 activity of Mdm2, blocking the interaction of p53 and Mdm2, and restoring the function of mutated p53 are potential effective strategies to kill certain tumor cells selectively. It is conceivable that new chemotherapeutic agents based on these studies will be generated in the not-so-distant future.Oncogene (2004) 23, 2096-2106. doi:10.1038/sj.onc.1207411 [ABSTRACT FROM AUTHOR]

Examines the role of tumor necrosis factor-alpha on the signalling components. Concentration of proteasome inhibitor lactacystin; Activation of N-terminal kinase; Inhibition of calpain-like protease activity.