The comparative burden of brain and central nervous system cancers from 1990 to 2019 between China and the United States and predicting the future burden.

Background: Brain and central nervous system (CNS) cancers represent a major source of cancer burden in China and the United States. Comparing the two countries' epidemiological features for brain and CNS cancers can help plan interventions and draw lessons. Methods: Data were extracted from the Global Burden of Disease repository. The average annual percentage change (AAPC) and relative risks of cancer burdens were calculated using joinpoint regression analysis and age-period-cohort (APC) models, respectively. Moreover, a Bayesian APC model was employed to predict the disease burden over the next decade. Results: From 1990 to 2019, the number of incidences, deaths, and disability-adjusted life-years (DALYs) increased in China and the US, with a larger increase in China. Age-standardized incidence rates in China and the United States have shown an increasing trend over the past three decades, with AAPCs of 0.84 and 0.16%, respectively. However, the rates of age-standardized mortality and age-standardized DALYs decreased in both countries, with a greater decrease in China. Overall, age trends in cancer burden were similar for males and females, with two peaks in the childhood and elderly groups, respectively. The period and cohort effects on incidence showed an overall increasing trend in China and limited change in the US. However, the period effects for mortality and DALY were decreasing in both countries, while the cohort effects tended to increase and then decrease. Moreover, we predicted that the cancer burdens would continue to rise in China over the next decade. Conclusion: The burden of brain and CNS cancers is substantial and will continue to increase in China. Comprehensive policy and control measures need to be implemented to reduce the burden.

[Valproate up-regulates the expression of NKG2DL through the MEK/ERK signaling pathway to enhance the killing effect of NK cells on A375 human melanoma cells].

Objective To investigate the effect of sodium valproate (VPA) on the expression of NKG2D ligand and the killing effect of NK cells on melanoma cells through MEK/ERK signaling pathway. Methods In the group with A375 cells in logarithmic phase treated with 1 mmol/L of VPA for 24 hours, the protein expression levels of MICA, MICB, phosphorylated MEK (p-MEK), MEK, phosphorylated ERK1/2 (p-ERK1/2), and ERK1/2 were detected by Western blotting, the expressions of MICA and MICB were detected by flow cytometry, and the killing effect of NK92 cells on A375 cells was detected by lactate dehydrogenase (LDH) release assay. In the group with A375 cells treated with the MEK/ERK signaling pathway inhibitor PD98059 combined with VPA, the protein expressions of MICA and MICB were detected by Western blotting, the expressions of MICA and MICB were detected by flow cytometry, and the killing effect of NK92 cells on A375 cells was detected by LDH release assay. The changes of melanoma volume in non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mice were detected by tumor formation assay, and the expression of MICA and MICB was detected by immunohistochemical staining. Results Compared with those in the control group, the expressions of MICA and MICB of A375 cells, the killing effect of NK92 cells on A375 cells, and the ratios of p-MEK/MEK and p-ERK1/2/ERK1/2 were increased in the VPA group. Compared with those in the VPA group, the expressions of MICA and MICB of A375 cells and the killing effect of NK92 cells on A375 cells were decreased in the group of VPA combined with PD98059. Compared with those in the group of NK92 cells, the tumor volume of NOD/SCID mice was reduced, and the expressions of MICA and MICB were increased in the group of NK92 cells with VPA. Compared with those in the group of NK92 cells with VPA, the tumor volume of NOD/SCID mice was increased, and the expressions of MICA and MICB were decreased in the group of NK92 cells with VPA and PD98059. Conclusion VPA up-regulates the expression of MICA and MICB in melanoma cells and enhances the killing effect of NK92 cells on melanoma, which may be related to the activation of MEK/ERK signaling pathway.

Anthocyanin from Lycium ruthenicum Murr. in the Qaidam Basin Alleviates Ultraviolet-Induced Apoptosis of Human Skin Fibroblasts by Regulating the Death Receptor Pathway.

Purpose: The study aimed to investigate the potential protective role of anthocyanin from Lycium ruthenicum Murr. in the Qaidam Basin against ultraviolet B (UVB)-induced apoptosis of human skin fibroblasts (HSFs). Methods: HSFs cultured in vitro were randomly divided into a control group, UVB group, and anthocyanin groups (0.1, 0.5, and 1.0 mg/mL). HSFs in the UVB and anthocyanin groups were exposed to 30 mJ/cm2 UVB to establish a photoaging model. Then, apoptosis rate, tumor necrosis factor-α (TNF-α), cysteinyl aspartate specific proteinase-3 (caspase-3), cysteinyl aspartate specific proteinase-7 (caspase-7), and survivin expression were evaluated. Results: UVB irradiation can increase the apoptosis rate of HSFs and expression of TNF-α, caspase-7, and survivin. Anthocyanin pretreatment (0.1, 0.5, and 1.0 mg/mL) decreased UVB-induced apoptosis rate and TNF-α and caspase-7 expression and increased survivin expression. Compared with the control group, the apoptosis rate and expression of TNF-α, caspase-7, and survivin of anthocyanin groups in UVB-irradiated HSFs were high. Among the three doses of anthocyanin (0.1, 0.5, and 1.0 mg/mL) groups, the apoptosis rate and TNF-α expression of anthocyanin at 1.0 mg/mL were the lowest. There was no significant change in caspase-3 expression in each group. Conclusion: Anthocyanin from Lycium ruthenicum Murr. in the Qaidam Basin could alleviate UVB-induced apoptosis by regulating the death receptor pathway.

Effect of beta-cypermethrin exposure on embryo implantation in mice.

The aim of this study was to investigate the effect of ß-CP on embryo implantation in mice. Forty female mice were randomly assigned to four groups of 10 mice each: one control group and three ß-CP treated groups. The control group was administered corn oil only, while the three ß-CP-treated groups were given corn oil containing 5, 10, and 20 mg/kg bw d ß-CP for 3 months through intragastric administration. The results indicated that the administration of ß-CP decreased the rate of embryo implantation (all p < 0.05), E2 level in the serum, and the expression of Homeobox A10 (HoxA10) protein. In addition, ß-CP significantly increased ERa and PRA protein expression levels. These results suggest that ß-CP can disrupt the balance of E2 and P, influence ERa and PRA expression and their downstream-related molecule Hoxa10, and decrease embryo implantation.

Saussurea tridactyla Sch. Bip.-derived polysaccharides and flavones reduce oxidative damage in ultraviolet B-irradiated HaCaT cells via a p38MAPK-independent mechanism.

OBJECTIVE: To investigate whether Saussurea tridactyla Sch. Bip.-derived polysaccharides and flavones exert apoptosis-inhibiting effects in ultraviolet B (UVB)-irradiated HaCaT cells. METHODS: We divided HaCaT cells into low radiation UVB and high radiation UVB groups. Low radiation UVB and high radiation UVB groups were further divided into a control group, UVB radiation group (UVB group), S. tridactyla Sch. Bip.-derived polysaccharides and flavones low-dose group, and S. tridactyla Sch. Bip.-derived polysaccharides and flavones high-dose group. Cell viability and morphology were assayed by MTT and trypan blue staining. Superoxide dismutase activity, glutathione content, malondialdehyde content, and catalase activity test kits were used to detect superoxide dismutase activity, glutathione content, malondialdehyde content, and catalase activity, respectively. Cell apoptosis, intracellular Ca(2+) levels, and mitochondrial membrane potential (Δψ) were detected by flow cytometry. Protein levels were analyzed by Western blotting and immunofluorescence. RESULTS: S. tridactyla Sch. Bip.-derived polysaccharides and flavones were found to increase the absorbance of MTT, decrease cell death, alleviate the degree of cell edema, restore the cell morphology, reduce cell death fragments and chip phenomenon, increase superoxide dismutase activity, glutathione content, and catalase activity while decreasing the content of malondialdehyde, lowering the population of apoptotic cells, reducing the intracellular Ca(2+) fluorescence, increasing the mitochondrial membrane potential (Δψ), increasing the expressions of p-38, p-53, Bcl-2, and decreasing the expressions of Bax and active-caspase-3. CONCLUSION: S. tridactyla Sch. Bip.-derived polysaccharides and flavones can reduce cell apoptosis to protect HaCaT cells from oxidative damage after UVB irradiation; however, this effect does not occur via the p38MAPK pathway.