Meridian energy analysis may predict the prognosis of patients with advanced cancers receiving palliative care.

Background and aim: A better understanding of irreversible prognoses in palliative care is crucial for improving patients' quality of life and their sense of dignity. We examined whether measurements of meridian electrical conductance can noninvasively and objectively predict survival time in a hospice patient population. Experimental procedure: This was a single-center cohort study. Between 2019 and 2020, we measured skin conductance from 24 representative acupoints of 12 meridians on both sides of the body in 181 advanced cancer patients within 48 h of hospitalization and monitored their survival time. The Palliative Prognostic Score (PaP Score) was calculated for each patient, classifying them into one of three prognosis groups: Group A, B, or C. Factors associated with short-term and long-term survival were identified using multivariate regression analysis. Statistical differences in survival times were analyzed between the meridian electrical conductance measurements and PaP Scores. Results and conclusion: Analyses of the clinicopathological data from terminal cancer patients revealed that male sex, mean meridian electrical conductance measurements of ≤8.8 µA, and PaP Scores in Group C were independent predictors of short-term survival. Mean meridian electrical conductance measurements of ≤8.8 µA demonstrated good sensitivity (85.1%) and adequate specificity (60.6%) for short-term survival. A survival curve analysis revealed a mortality rate of 90.6% at 30 days among patients with meridian electrical conductance measurements of ≤8.8 µA. A mean meridian electrical conductance measurement of ≤8.8 µA can objectively assess short-term survival with advanced cancer and reduce nonbeneficial medical treatment.

Polysaccharides of Grifola frondosa ameliorate oxidative stress and hypercholesterolaemia in hamsters fed a high-fat, high-cholesterol diet.

OBJECTIVES: This study was to evaluate the antioxidant and anti-hypercholesterolaemia activities of Grifola frondosa in hamsters fed a high-fat, high-cholesterol (HFHC) diet. METHODS: G. frondosa, including fruiting bodies (FGF), fermented mycelia (MGF) and polysaccharides extracted from fruiting bodies (FPS), fermented mycelia (MIP) and fermented broth (BEP) were received intragastrically. Lipid profile and antioxidant status in the blood and liver of hamsters were assessed. KEY FINDINGS: FGF decreased weight gain, serum triglycerides and cholesterol and increased hepatic mRNA expression of cholesterol-7α-hydroxylase expression. FGF, MGF, FPS and MIP decreased the HFHC diet-increased area under the curve (AUC) of serum cholesterol. FGF and FPS further decreased AUC of serum triglycerides. When evaluating the redox status of erythrocytes, FPS and MIP increased non-protein sulfhydryl (NP-SH) groups, reduced glutathione (GSH) and catalase activity and FPS further increased GSH peroxidase activity. In the liver, MGF increased NP-SH groups and GSH and decreased triglycerides content. FPS, MIP and BEP decreased oxidized GSH and triglycerides content. Moreover, all treatments alleviated HFHC diet-increased LDL oxidation. CONCLUSIONS: Fruiting bodies of G. frondosa may improve hypercholesterolaemia via increased bile acid synthesis. Additionally, fermented biomass and polysaccharides of G. frondosa may have the potential to prevent hepatic lipid accumulation.

Anticancer Effects and Molecular Mechanisms of Apigenin in Cervical Cancer Cells.

Cervical cancer is the fourth most frequent malignancy in women. Apigenin is a natural plant-derived flavonoid present in common fruit, vegetables, and herbs, and has been found to possess antioxidant and anti-inflammatory properties as a health-promoting agent. It also exhibits important anticancer effects in various cancers, but its effects are not widely accepted by clinical practitioners. The present study investigated the anticancer effects and molecular mechanisms of apigenin in cervical cancer in vitro and in vivo. HeLa and C33A cells were treated with different concentrations of apigenin. The effects of apigenin on cell viability, cell cycle distribution, migration potential, phosphorylation of PI3K/AKT, the integrin ß1-FAK signaling pathway, and epithelial-to-mesenchymal transition (EMT)-related protein levels were investigated. Mechanisms identified from the in vitro study were further validated in a cervical tumor xenograft mouse model. Apigenin effectively inhibited the growth of cervical cancer cells and cervical tumors in xenograft mice. Furthermore, the apigenin down-regulated FAK signaling (FAK, paxillin, and integrin ß1) and PI3K/AKT signaling (PI3K, AKT, and mTOR), inactivated or activated various signaling targets, such as Bcl-2, Bax, p21cip1, CDK1, CDC25c, cyclin B1, fibronectin, N-cadherin, vimentin, laminin, and E-cadherin, promoted mitochondrial-mediated apoptosis, induced G2/M-phase cell cycle arrest, and reduced EMT to inhibit HeLa and C33A cancer cell migration, producing anticancer effects in cervical cancer. Thus, apigenin may act as a chemotherapeutic agent for cervical cancer treatment.

Metformin induces apoptosis and inhibits migration by activating the AMPK/p53 axis and suppressing PI3K/AKT signaling in human cervical cancer cells.

Human cervical cancer is the fourth most common malignancy among women worldwide, and it is expected to result in 460,000 deaths per year by 2040. Moreover, patients with cervical cancer often display drug resistance and severe side effects; therefore, the development of effective novel chemotherapeutic agents is important. In the present study, the effects of metformin, a first­line therapeutic drug for type 2 diabetes mellitus, were evaluated in cervical cancer. Compared with the control group, metformin significantly inhibited cell viability and migration, and induced apoptosis and cell cycle arrest in human cervical cancer cell lines (CaSki and HeLa). Following metformin treatment, the protein expression levels of p­AMP­activated protein kinase (p­AMPK), which promotes cell death, and the tumor suppressor protein p­p53 were remarkably upregulated in CaSki and C33A cells compared with the control group. Furthermore, compared with the control group, metformin significantly suppressed the PI3K/AKT signaling pathway in CaSki, C33A and HeLa cells. Compound C (an AMPK inhibitor) significantly reversed the effects of metformin on CaSki, C33A and HeLa cell viability, and AMPK and p53 phosphorylation. The results of the present study suggested that metformin induced AMPK­mediated apoptosis, thus metformin may serve as a chemotherapeutic agent for human cervical cancer.

The role of glucocorticoids in ovarian development of sleep deprived rats.

OBJECTIVE: Sleep deprivation (SD) adversely affects female reproductive function. In this study, we investigated the role of glucocorticoids in ovarian development in sleep deprived rats. MATERIALS AND METHODS: Female rats were subjected to SD for 1-4 days. Concentrations of serum estradiol and corticosterone were assessed. Betamethasone (BET) and/or recombinant human follicle-stimulating hormone (FSH) were administered to 21-day-old female rats for 2 days to evaluate ovarian status for follicular development. Intact preantral follicles were mechanically dissected from the rat's ovaries and cultured for 72 h with or without FSH in the presence or absence of BET to evaluate follicular development. RESULTS: SD led to a significant difference in serum estradiol concentrations between the sham and SD groups, and corticosterone concentrations were significantly elevated in groups with more than 2 days of SD (P < 0.05). FSH stimulated ovarian growth in immature rats, whereas BET inhibited ovarian development caused by the FSH treatment. Treatment of the preantral follicles with FSH induced an increase in both follicle size and follicular cell number, while follicular cell differentiation was accompanied by enhanced inhibin-α and connexin 43 expression. Inhibition of FSH-stimulated follicular growth through BET treatment exhibited a dose-dependent reciprocal trend; as the BET dose increased (0.001-1 µg/mL), preantral follicular growth decreased. This decrease was associated with a decrease in follicular cell numbers and suppression of a proliferating cell nuclear antigen, inhibin-α, and connexin 43 expression. CONCLUSION: The findings suggest that the adverse effects of SD may inhibit follicular development during ovarian hyperstimulation by corticosterone elevation in rat.

Effect of morphokinetics and morphological dynamics of cleavage stage on embryo developmental potential: A time-lapse study.

OBJECTIVE: Using a non-invasive method to select the most competent embryo is essential in in vitro fertilization (IVF). Since the beginning of clinical application of time-lapse technology, several studies have proposed models using the time-lapse imaging system for predicting the IVF outcome. This study used both morphokinetic and morphological dynamic parameters to select embryos with the highest developmental potential. MATERIALS AND METHODS: A total of 23 intracytoplasmic sperm injection treatment cycles with 138 fertilized oocytes were included in this study. All embryos were cultured to the blastocyst stage, and embryo development was recorded every 10 min by using a time-lapse imaging system. Morphokinetic parameters and eight major abnormal division behaviors were studied to determine their effects on blastocyst formation. The most influential variables were used in hierarchical classification for blastocyst formation prediction. RESULTS: Several parameters were significantly related to the developmental potential. Embryos with the timing of pronuclear fading (tPNF) of >26.4 h post insemination (hpi), the timing of division to two cells (t2) of >29.1 hpi, and the timing of division to four cells (t4) of >41.3 hpi showed the lowest blastocyst formation rate. The abnormal division behaviors of fragmentation >50%, direct cleavage, reverse cleavage, and delayed division or developmental arrest were found to be detrimental to blastocyst formation. On the basis of these results, we propose a hierarchical model classification, in which embryos are classified into groups A-D according to their developmental potential. The blastocyst formation rates of groups A, B, C, and D were 80.0%, 77.8%, 53.7%, and 22.2% (p < 0.001). The good blastocyst rates of groups A, B, C, and D were 60.0%, 44.4%, 14.6%, and 11.1% (p = 0.007). CONCLUSION: We propose a hierarchical classification system for blastocyst formation prediction, which provides information for embryo selection by using a time-lapse imaging system.

Sleep deprivation enhances peripheral serotonin secretion to regulate the large follicle steroidogenesis of rats.

OBJECTIVE: Sleep deprivation (SD) leads to the disturbance of the estrous cycle. Serotonin, the levels of which increase with SD, has been shown to inhibit luteinizing hormone production and the receptor has been found in the follicles. In this study, the serotonin effect on preovulatory follicular steroidogenesis is investigated and the underlying mechanisms are elucidated. MATERIALS AND METHODS: Female rats were subjected to SD for a time span of 1-4 days using the dish-over-water-method with a Rechtschaffen apparatus. Serum estradiol and serotonin concentrations were assessed; thereafter, they were evaluated with the effect of serotonin on the estradiol production and steroidogenic acute regulatory (StAR) protein expression in a serum-free culture system. Preovulatory follicles were dissected mechanically from the ovaries of 21-day-old rats, which induced follicle growth, and cultured for 24 hours with or without recombinant human follicle-stimulating hormone (FSH) in the presence or absence of serotonin. RESULTS: SD, led to a significant decrease in serum estradiol concentrations, while serotonin concentrations were significantly elevated (all p < 0.05). Follicles were cultured with a constant dose of FSH (50 mIU/mL) and increasing doses of serotonin, estradiol production was reduced by 20%. The inhibitory effect of serotonin was concentration dependent. The addition of serotonin (0.1 µg/mL) decreased FSH-induced estradiol production and attenuated FSH-stimulated follicular StAR protein expression. The inhibitory effects of serotonin could be reduced by the serotonin receptor antagonist ketanserin. CONCLUSION: These findings suggest that decreased serum estradiol concentrations in SD rats may be the result of serotonin-related inhibition of estradiol production and decreased large follicle expression of StAR protein.