Structural Relationships between Counselors' Sense of Calling, Meaning of Work, Living a Calling, and Psychological Burnout.

This study examined the influence of counselors' sense of calling on psychological burnout, mediated by meaning of work and living a calling, based on the work as a calling theory (WCT) and preceding studies. Furthermore, the sequential mediating effects of meaning of work and living a calling were investigated. Data were collected from 420 Korean counselors working in counseling centers located nationwide and analyzed using Partial Least Squares Structural Equation Modeling (PLS-SEM). The results revealed that a sense of calling negatively impacted psychological burnout. Second, the sense of calling did not affect psychological burnout through the mediation of meaning of work. Third, the sense of calling negatively impacted psychological burnout through the mediation of living a calling. Fourth, the sense of calling negatively affected psychological burnout through the sequential mediation of meaning of work and living a calling. Based on this study's findings, implications can be provided to enhance counselors' professional calling and reduce psychological burnout, thereby aiding them in resolving their psychological issues during counseling practice and providing higher-quality psychological services to clients. Suggestions for improvements and future research are also discussed.

[p53-dependent antiproliferation and apoptosis of H22 cell induced by melatonin].

BACKGROUND & OBJECTIVE: It has been shown that melatonin has a direct inhibitory effect on the proliferation of H22 mouse hepatoma cells in our research. This study was designed to investigate its molecular mechanism. METHODS: (1) Animal models were established by transplanting H22 cells and treated with melatonin, and then the p53 and cyclin E of the tumor tissue were determined by immunohistochemical analysis. (2) After treatment of H22 cells with melatonin in vitro, the percentage of cells in each cell cycle phase and apoptosis rate were analyzed by flow cytometry. p53 and cyclin E were determined again by immunohistochemical analysis. The level of Fas mRNA was examined by real time polymerase chain reaction (RT-PCR). RESULTS: (1) After treated with melatonin (1 x 10(-6) mol/L), the number of the H22 cells in phase G(0)/G(1) were elevated from 75.24% to 85.46%, while which in phase S almost decreased from 10.32% to 0, and at the same time, the number of apoptotic cells increased from 5.07% to 12.77%. (2) Compared with the control, the level of p53 elevated 42.5% (in vitro) and 19.5% (in vivo), however, the level of cyclin E decreased 31.7% (in vitro) and 39.9% (in vivo). (3) Fas mRNA increased about 44.2% after melatonin treatment (P< 0.01). CONCLUSION: Melatonin inhibits the proliferation of H22 cells by arrest and apoptosis, and the mechanism perhaps interferes with increasing p53 that results in down-regulation of cyclin E indirectly and stimulates the expression of Fas gene.

Inhibitory effect of melatonin on the growth of H22 hepatocarcinoma cells by inducing apoptosis.

Whether melatonin not only inhibits the growth of H22 hepatocarcinoma cells but also induces apoptosis in vitro was assessed. The anti-proliferative effects of melatonin on tumor cells was observed by MTT assay and tumor cells growth curve assay. And the apoptosis of the cells was studied by acridine orange fluorescence assay and flow cytometry. The cell cycle of the tumor cells was also observed by flow cytometry. It was found that melatonin could significantly inhibit the growth of H22 hepatocarcinoma cells. Incubated with melatonin, chromatin condensation of the tumor cells was observed by fluorescence microscopy. Compared with control, the percentage of apoptotic cells was increased, and the proportion of G0/S increased but that of G2/M decreased. It was suggested that melatonin could directly inhibit the growth of H22 hepatocarcinoma cells by inducing apoptosis and extending the length of cell cycle of the tumor cells.

Role of mitochondria in neuron apoptosis during ischemia-reperfusion injury.

To investigate the role of mitochondria in neuronal apoptosis, ischemia-reperfusion mediated neuronal cell injury model was established by depriving of glucose, serum and oxygen in media. DNA fragmentation, cell viability, cytochrome C releasing, caspase3 activity and mitochondrial transmembrane potential were observed after N2a cells suffered the insults. The results showed that N2a cells in ischemic territory exhibited survival damage, classical cell apoptosis change, DNA ladder and activation of caspase3. Apoptosis-related alterations in mitochondrial functions, including release of cytochrome C and depression of mitochondrial transmembrane potential (deltapsim) were testified in N2a cells after mimic ischemia-reperfusion. Moreover, activation of caspase3 occurred following the release of cytochrome C. However, the inhibitor of caspase3, Ac-DEVD-CHO, couldn't completely rescue N2a cells from apoptosis. Administration of cyclosporine A, an inhibitor of mitochondria permeability transition pore only partly inhibited caspase3 activity and reduced DNA damage. Interestingly, treatment of Z-IETD-FMK, an inhibitor of caspase8 could completely reverse DNA fragmentation, but can't completely inhibit caspase3 activity. It was concluded that there were caspase3 dependent and independent cellular apoptosis pathways in N2a cells suffering ischemia-reperfusion insults. Mitochondria dysfunction may early trigger apoptosis and amplify apoptosis signal.

Elevated levels of phosphorylated neurofilament proteins in cerebrospinal fluid of Alzheimer disease patients.

Neurofilament (NF) subunits NF-H, NF-M and NF-L are hyperphosphorylated and elevated in Alzheimer disease (AD) brain. We investigated the level and phosphorylation states of NF subunits in lumbar cerebrospinal fluid (CSF) from living patients by bienzyme substrate-recycle enzyme-linked immunosorbent assay. We found: (i), that the levels of phosphorylated NF-H/M (pNF-H/M), non-phosphorylated NF-H/M (npNF-H/M) and NF-L were significantly higher (pNF-H/M, approximately 12-24-fold; npNF-H/M, approximately 3-4-fold) in neurologically healthy aged people than young control individuals; (ii), that in AD, the levels of npNF-H/M, and NF-L were similar to vascular dementia (VaD), and higher than in age-matched controls; and (iii), that the levels of pNF-H/M were significantly higher than in aged controls, non-AD neurological disorders and VaD. Based on these findings, it is suggested that the increased level of total NF proteins in CSF could be used as a marker for brain aging and neurodegenerative disorders in general, and the levels of pNF-H/M as a marker to discriminate AD from normal brain aging and as well as neurological conditions including VaD.