Nonlinear effect of wind velocity on mumps in Shenzhen, China, 2013-2016.

OBJECTIVES: Plenty of studies have shown that wind velocity has an influence on airborne diseases. There is, however, no consistent conclusion found on the relationship between wind velocity and mumps, and the regional heterogeneity has been largely neglected in previous studies. This study aims to explore the association between wind velocity and mumps in Shenzhen. STUDY DESIGN: Ecological study. METHODS: Sixteen subdistricts with the highest incidence rates of mumps were selected from Shenzhen city, and the multilevel distributed lag-nonlinear model was conducted to explore the relationship between mumps cases and wind velocity via the dlnm and lme4 packages of the software R 3.4.3. RESULTS: In Shenzhen, a total of 16,997 mumps cases were reported between 2013 and 2016, and the means of daily rainfall, temperature, relative humidity, and 10 min wind velocity were 5.74 mm, 23.27 °C, 76.31% and 1.87 m/s, respectively. Obvious nonlinear correlation relationships of wind velocity and mumps risk were found, where a reverse-V curved shape was shown in the exposure dimension with the logRR value of mumps peaking at 2 m/s, and the type of nonlinear correlation varying with the levels of wind velocity in lag dimension with a peak at two lag weeks. CONCLUSIONS: The lag and nonlinear association between wind velocity and number of mumps cases were examined, while there was no statistically significant associations for other meteorological factors accounting for the regional heterogeneity. Results from this study indicated that public health administrators could strengthen health education in schools on ventilation management to prevent and control mumps outbreaks.

Mitochondrial calcium dysfunction contributes to autophagic cell death induced by MPP+ via AMPK pathway.

Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra. Prevailing evidence suggests that abnormal autophagy and mitochondrial dysfunction participate in the process of PD. However, many damages of neuronal functions are regulated by intracellular Ca2+ signaling and the contribution of mitochondrial Ca2+ to the process of neurodegeneration is still unclear. MPP+, the metabolite of a neurotoxin MPTP, causes symptom of PD in animal models by selectively destroying dopaminergic neurons in substantia nigra. Here we report that mitochondrial Ca2+ uniporter (MCU) participated in MPP+-induced autophagic cell death in SH-SY5Y cells. Pharmacological agonist of MCU or exogenous expressed MCU can partially reduce MPP+-induced autophagic cell death. Down-regulation of MCU enhanced autophagic cell death via AMPK activation, which was independent of Beclin1 and PI3K. These findings show that the mitochondrial calcium dyshomeostasis contributes to MPP+-induced neuronal degeneration, and MCU may be a potential therapeutic target of PD through the prevention of pathological autophagy.

Polyelectrolyte modified black phosphorus/titania nanosheet heterojunction enhanced photocatalysis: Synergistic enhancement effect of interface affinity and electron transport channel.

The instability and high electron-hole recombination have limited the application of black phosphorus (BP) as an excellent photocatalyst. To address these challenges, poly dimethyl diallyl ammonium chloride (PDDA), poly (allylamine hydrochloride) (PAH), and polyethyleneimine (PEI) are introduced to the functionalization of BP (F-BP), which can not only enhance its stability, but also boost the carrier transfer. Furthermore, a high-performance heterojunction photocatalyst is fabricated using F-BP and titania nanosheets (TNs) via a layer-by-layer self-assembly approach. The experimental outcomes unequivocally indicate that F-BP exhibits fast charge migration compared to BP. The density functional theory (DFT), in situ Kelvin-probe force microscopy (KPFM) and other advanced characterization techniques collectively unfold that PDDA modified BP can notably boost separation and propagation of charges, along with an enhanced carrier abundance. In summary, this novel strategy of using polyelectrolytes to enhance the electron transfer and the stability of BP permits immense potential in building next-generation BP-based high efficiency photocatalysts.

Phosphorylation of Parkin at serine 131 by p38 MAPK promotes mitochondrial dysfunction and neuronal death in mutant A53T α-synuclein model of Parkinson's disease.

α-synuclein abnormal accumulation and mitochondria dysfunction are involved in the pathogenesis of Parkinson's disease. Selective autophagy of mitochondria (mitophagy) is a crucial component of the network controlling the mitochondrial homeostasis. However, the underlying mechanism that mutant α-synuclein induces mitochondrial abnormality through mitophagy impairment is not fully understood. Here, we showed that mutant A53T α-synuclein accumulation impaired mitochondrial function and Parkin-mediated mitophgy in α-synucleinA53T model. α-synucleinA53T overexpression caused p38 MAPK activation, then p38 MAPK directly phosphorylated Parkin at serine 131 to disrupt the Parkin's protective function. The p38 MAPK inhibition significantly reduced cellular apoptosis, restored mitochondrial membrane potential as well as increased synaptic density both in SN4741 cells and primary midbrain neurons. These findings show that the p38 MAPK-Parkin signaling pathway regulates mitochondrial homeostasis and neuronal degeneration, which may be a potential therapeutic strategy of PD via enhancing mitochondrial turn-over and maintenance.

Mitochondrial calcium uniporter-mediated inhibition of 1-methyl-4-phenylpyridinium ions neurotoxicity in PC12 cells.

Parkinson's disease (PD) is one of the most debilitating neurodegenerative disorders. The etiology of sporadic PD remains unknown. One prominent hypothesis is that impaired mitochondrial function may underlie slow and progressive neurodegeneration. Mitochondrial calcium uniporter (MCU) is a crucial component that regulates the intramitochondrial Ca level. Ca uptake to the mitochondria by MCU, resulting in activation of mitochondrial dehydrogenases and stimulation of ATP synthesis, but excessive Ca uptake to the mitochondria resulting in cell apoptosis. Therefore, this study focused on whether MCU was involved in the apoptosis induced by 1-methyl-4-phenylpyridinium ions (MPP) in PC12 cells. Our results showed that the viability of PC12 cells was inhibited by MPP in a concentration-dependent and time-dependent manner. The expression of MCU was decreased gradually with a certain concentration of MPP. Meanwhile, MPP decreased the mitochondrial transmembrane potential and increased the apoptosis in PC12 cells. Notably, preincubated with Spermine, an MCU-specific agonist, or exogenously expressed MCU significantly alleviated cell apoptosis and decreased the reactive oxygen species production in PC12 cells that is induced by MPP treatment. Knockdown of endogenous MCU expression or preincubation with a specific inhibitor of MCU enhances the cell apoptosis and the reactive oxygen species in PC12. Thus, MCU is involved in the apoptosis in PC12 induced by MPP.