[Water Environmental Characteristics and Water Quality Assessment of Lakes in Tibetan Plateau].

Lakes are an important water resource and biological habitat in the Tibetan Plateau. Owing to the combined influence of climate, topography, and other natural factors as well as human factors, the water environment of the lakes on the Tibetan Plateau is facing more and more severe problems and challenges. To clarify the present status, distribution pattern, main characteristic factors of water quality, and important factors affecting the water quality of lakes on the Tibetan Plateau, the water environment of 12 typical lakes on the Tibet Plateau was investigated in summer (July-August) and autumn (October-November) in 2020. The field sampling and laboratory test data comprehensive analysis showed that:① several physical and chemical parameters of typical lakes on the Tibetan Plateau differed in spatiotemporal distribution. ② Salinity was the main characteristic of water quality in the typical lakes on the Tibetan Plateau. ③ The spatiotemporal distribution of lake eutrophication index showed little diversity and basically ranged from poor nutrition to moderate nutrition. The spatial and temporal distributions in the lake water quality index (WQI) were significantly different. The lake WQI grade decreased from "Moderate" to "Very poor" with the increase in salinity area, and the lake water quality in autumn was better than that in summer. ④ The spatiotemporal differences in lake water quality on the Tibetan Plateau were mainly controlled by precipitation, evapoconcentration, and human activities. This study will provide scientific basis for water environment protection and improvement of water ecosystems on the Tibetan Plateau.

Melatonin attenuates manganese-induced mitochondrial fragmentation by suppressing the Mst1/JNK signaling pathway in primary mouse neurons.

Manganese (Mn) toxicity is mainly caused by excessive Mn content in drinking water and occupational exposure. Moreover, overexposure to Mn can impair mental, cognitive, memory, and motor capacities. Although melatonin (Mel) can protect against Mn-induced neuronal damage and mitochondrial fragmentation, the underlying mechanism remains elusive. Here, we examined the related molecular mechanisms underlying Mel attenuating Mn-induced mitochondrial fragmentation through the mammalian sterile 20-like kinase-1 (Mst1)/JNK signaling path. To test the role of Mst1 in mitochondrial fragmentation, we treated mouse primary neurons overexpressing Mst1 with Mel and Mn stimulation. In normal neurons, 10 µM Mel reduced the effects of Mn (200 µM) on Mst1 expression at the mRNA and protein levels and on phosphorylation of JNK and Drp1, Drp1 mitochondrial translocation, and mitochondrial fragmentation. Conversely, overexpression of Mst1 hindered the protective effect of Mel (10 µM) against Mn-induced mitochondrial fragmentation. Anisomycin (ANI), an activator of JNK signaling, was similarly found to inhibit the protective effect of Mel on mitochondria, while Mst1 levels were not significantly changed. Thus, our results demonstrated that 10 µM Mel negatively regulated the Mst1-JNK pathway, thereby reducing excessive mitochondrial fission, maintaining the mitochondrial network, and alleviating Mn-induced mitochondrial dysfunction.

Preparation of Magnesium Hydroxide Flame Retardant from Hydromagnesite and Enhance the Flame Retardant Performance of EVA.

In this study, hydromagnesite, a rare natural hydrated alkaline magnesium carbonate, was used to synthesize magnesium hydroxide (MH) as a flame retardant for ethylene-vinyl acetate (EVA) to enhance its fire resistance and smoke suppression. Various concentrations of sodium hydroxide (NaOH) were used to alter the morphology and the flame-retardant efficiency of synthesized MH. EVA/MH composites were prepared through melt blending, and the influence of NaOH on the flame retardancy and mechanical properties was investigated by means of the limiting oxygen index (LOI), cone calorimeter test (CCT) and tensile test. The flame retardancy results demonstrated that composites exhibited remarkably improved flame retardant properties after introducing MH, reflected by an increase in the LOI value from 20% for neat EVA to roughly 38%. Additionally, the peak of heat release rate (pHRR), the total heat release (THR) and the peak of the smoke production rate for EVA3 were decreased by 37.6%, 20.7% and 44.4% compared with neat EVA, respectively. In the meantime, increasing char residues were also observed. The incorporation of different MH concentrations had a limited effect on the mechanical properties of the EVA/MH composites.

Resveratrol reduces DRP1-mediated mitochondrial dysfunction via the SIRT1-PGC1α signaling pathway in manganese-induced nerve damage in mice.

Excessive manganese (Mn) exposure can cause nerve damage and mitochondrial dysfunction, which may involve defects in mitochondrial dynamics. Resveratrol (RSV) exerts a wide range of beneficial effects via activation of sirtuin 1 (SIRT1) and thus may positively impact Mn-induced mitochondrial damage through the regulation of peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α) by SIRT1. In this study, we investigated the molecular mechanisms by which RSV alleviates the nerve injury and mitochondrial fragmentation caused by Mn in C57 BL/6 mice. Our results demonstrated that RSV activated the deacetylase activity of SIRT1 and protected against the surge of mitochondrial reactive oxygen species, the loss of mitochondrial membrane potential, and the attenuation of ATP caused by Mn. RSV, therefore, inhibits mitochondrial fragmentation and safeguards neural cells. Increased deacetylase activity led to a reduction in the acetylation of PGC-1α, which directly regulates DRP1 expression by binding to the DRP1 promoter. The resultant attenuation of DRP1-mediated mitochondrial fragmentation in RSV-pretreated mice was abolished by the addition of the SIRT1 inhibitor EX527. Taken together, these findings indicate that RSV alleviates Mn-induced mitochondrial dysfunction mediated by DRP1 by modulating the SIRT1/PGC-1α signaling pathway.

Resveratrol attenuates manganese-induced oxidative stress and neuroinflammation through SIRT1 signaling in mice.

Exposure to excess levels of manganese (Mn) leads to neurotoxicity. Increasing evidence demonstrates that oxidative stress and neuroinflammation are important pathological causes of neurotoxicity. Resveratrol (Rsv), a sirtuin-1 (SIRT1) activator, plays an important role in neuroprotection. However, the molecular mechanisms of Rsv alleviating Mn-induced oxidative stress and neuroinflammation are not fully understood. To evaluate whether Rsv treatment relieves the oxidative stress and neuroinflammation in the hippocampus after Mn exposure through SIRT1 signaling, C57BL/6 adult mice were exposed to MnCl2 (200 µmol/kg), Rsv (30 mg/kg), and EX527 (5 mg/kg). Our results showed that administering MnCl2 for 6 weeks caused behavioral impairment and nerve cell injury in hippocampal tissue, which was related to oxidative stress and neuroinflammation. Activating Mn-induced JNK and inhibiting SIRT1 increased the phosphorylated and acetylated levels of NF-κB and STAT3, respectively. However, Rsv reduced the phosphorylated and acetylated levels of NF-κB and STAT3, and attenuated Mn-induced oxidative stress and inflammatory cytokines by activating SIRT1 signaling. Most importantly, EX527, a potent SIRT1 inhibitor, inactivated SIRT1, which prevented Rsv from exerting its beneficial effects. Taken together, our findings revealed that Rsv alleviated Mn-induced oxidative stress and neuroinflammation in adult mice by activating SIRT1.

Manganese-induced alpha-synuclein overexpression aggravates mitochondrial damage by repressing PINK1/Parkin-mediated mitophagy.

Chronic manganese (Mn) exposure is related to elevated risks of neurodegenerative diseases, and mitochondrial dysfunction is considered a critical pathophysiological feature of Mn neurotoxicity. Although previous research has demonstrated Mn-induced alpha-synuclein (α-Syn) overexpression, the role of α-Syn in mitochondrial dysfunction remains unclear. Here, we used Wistar rats and human neuroblastoma cells (SH-SY5Y cells) to elucidate the molecular mechanisms underlying how α-Syn overexpression induced by different doses of Mn (15, 30, and 60 mg/kg) results in mitochondrial dysfunction. We found that Mn-induced neural cell injury was associated with mitochondrial damage. Furthermore, Mn upregulated α-Syn protein levels and increased the interaction between α-Syn and mitochondria. We then used a lentivirus vector containing α-Syn shRNA to examine the effect of Mn-induced α-Syn protein on PINK1/Parkin-mediated mitophagy in SH-SY5Y cells. Our data demonstrated that the knockdown of α-Syn decreased the interaction between α-Syn and PINK1. The enhanced level of phosphorylated Parkin (p-Parkin) was due to the decrease of the interaction between α-Syn and PINK1. Moreover, the knockdown of α-Syn increased recruitment of p-Parkin to mitochondria. Collectively, these observations revealed that Mn-induced α-Syn overexpression repressed PINK1/Parkin-mediated mitophagy and exacerbated mitochondrial damage.

Wideband composite planar spiral antenna for generation of tunable angular momentum wave.

In this paper, a composite planar spiral antenna consisting of an eight-arm equiangular spiral antenna and eight Archimedean spiral antennas has been designed to radiate electromagnetic wave carrying tunable angular momenta in a wide band. A tunable eight-way Wilkinson power divider network is used to offer three kinds of feeding modes for the equiangular spiral antenna, and thus the composite antenna can radiate the electromagnetic waves with angular momenta of the modes l=1, 2, and 3, respectively. The Archimedean spiral is introduced to improve the gain of the composite antenna in the case of the angular momentum of l=3. By analyzing axis ratio (AR) of the proposed antenna, the generated angular momentum of l=1 is spin angular momentum (SAM), and the angular momenta of both l=2 and 3 include SAM and orbital angular momentum (OAM). Simulated and measured results are given to demonstrate good performance including tunable modes, good purity and wide band.

LncRNA SNHG1 promotes EMT process in gastric cancer cells through regulation of the miR-15b/DCLK1/Notch1 axis.

BACKGROUND: Gastric cancer (GC) is a malignant tumour originating from the gastric mucosa epithelium that seriously threatens human health. DCLK1, miR-15b and lncRNA SNHG1 play potential roles in the occurrence of GC, but the mechanism remains unclear. METHODS: Gene expression of DCLK1, miR-15b and lncRNA SNHG1 was investigated by qRT-PCR. Protein expression was detected by Western blotting. Migration and invasion of gastric cancer cells was tested by a Transwell assay and wound healing assay. Cell proliferation was measured by an MTT assay. Finally, the correctness of the prediction results was confirmed by a dual-luciferase reporter assay. RESULTS: The expression of DCLK1, Notch1, and SNHG1 was increased in GC tissues, while the expression of miR-15b was decreased. Overexpression of lncRNA SNHG1 promoted the expression of DCLK1 and Nothc1 in GC cells. Moreover, miR-15b targeted DCLK1 to regulate Notch1 expression and inhibited the EMT process in GC cells. SNHG1 enhanced the effects of DCLK1/Notch1 on the EMT process through regulating miR-15b expression. CONCLUSION: SNHG1 enhances the EMT process in GC cells through DCLK1-mediated Notch1 pathway, which can be a potential target for treating GC.

MiR-185-3p regulates epithelial mesenchymal transition via PI3K/Akt signaling pathway by targeting cathepsin D in gastric cancer cells.

BACKGROUND: Recently research reported that miR-185-3p could serve as an independent prognosis factor in gastric cancer (GC). However, the functional role and underlying mechanism of miR-185-3p in GC and epithelial-mesenchymal transition (EMT) progression remains largely elusive. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was carried out to analyze the expression of miR-185-3p and cathepsin D in patient-derived GC samples and various GC cell lines. Scratch assay and Transwell assay were used to evaluate the migration ability. The influence of miR-185-3p on the cell cycle distribution and cell apoptosis was evaluated using flow cytometry. Western blotting assay was performed to detect the expression of EMT associated proteins and the activity of PI3K/Akt signaling pathway. Furthermore, the interaction between miR-185-3p and cathepsin D was explored by dual-luciferase reporter assay. RESULTS: Our data revealed that miR-185-3p was down-regulated, while cathepsin D was up-regulated in both patient-derived GC samples and GC cells. Apart from inducing apoptosis, overexpression of miR-185-3p also inhibited EMT process and migration of GC cells. Mechanically, we firstly verified that miR-185-3p directly targeted the cathepsin D. Furthermore, miR-185-3p exerted its function on EMT process and migration via inhibiting cathepsin D to mediated PI3K/Akt signaling pathway. CONCLUSIONS: Our findings suggested that miR-185-3p targeted cathepsin D inhibiting EMT process via PI3K/Akt signaling, which may serve as a potential prognosis factor and therapeutic target to reduce the malignancy of GCs.

MAPK/AP-1 pathway regulates benzidine-induced cell proliferation through the control of cell cycle in human normal bladder epithelial cells.

Bladder cancer is the most common malignancy of the urinary tract. Long-term exposure to benzidine is one of the major causes of bladder cancer. However, the mechanism of benzidine-induced bladder cancer is not yet sufficiently characterized. Dysregulated cell proliferation serves a critical role in cancer initiation and development; whether benzidine promotes cell proliferation, and the role of MAPKs in this process, have not previously been investigated. The present study aimed to investigate the benzidine-induced modulation of intracellular mitogen-activated protein kinases (MAPKs) and activator protein-1 (AP-1) signaling cascades on cell proliferation in SV-40 immortalized human uroepithelial cells (SV-HUC-1). It was identified that benzidine exposure enhanced the proliferation of SV-HUC-1 cells, promoted the transition of cells from G1 to S phase and altered the expression level of cell cycle-associated genes at the mRNA and protein levels. Furthermore, exposure of the SV-HUC-1 cells to benzidine was associated with the activation of MAPKs, including extracellular regulated protein kinases 1 and 2, p38 and Jun N-terminal kinase. The downstream target of MAPKs, AP-1 monomers, was also activated. Benzidine-induced proliferation was reversed by MAPK-specific inhibitors. Thus, the present study demonstrated that benzidine enhances the proliferation of bladder cells via activating the MAPK/AP-1 pathway, which may provide novel insights into the molecular mechanisms of benzidine-initiated bladder tumorigenesis, as well as cancer prevention.

A Geometry Effect of Carbon Nanomaterials on Flame Retardancy and Mechanical Properties of Ethylene-Vinyl Acetate/Magnesium Hydroxide Composites.

This study was aimed at investigating the effects of carbon nanomaterials with different geometries on improving the flame retardancy of magnesium hydroxide⁻filled ethylene-vinyl acetate (EM). The thermal stability and flame retardancy were studied by thermogravimetric analysis (TGA), limiting oxygen index (LOI), UL-94 test, and cone calorimeter test (CCT). The in situ temperature monitoring system and interrupted combustion offered direct evidence to link flame retardancy and composite structure. Results demonstrated that carbon nanomaterials enhanced the thermal stability and fire safety of EM. The geometry of carbon nanomaterials played a key role in synergistic flame retardancy of EM, with the flame-retardant order of carbon nanotube > nanoscale carbon black > graphene. Based on an online temperature monitoring system and interrupted combustion test, one-dimensional carbon nanotube was more inclined to form the network structure synergistically with magnesium hydroxide in ethylene-vinyl acetate, which facilitated the generation of more continuous char structure during combustion. In parallel, the mechanical property was characterized by a tensile test and dynamic mechanical analysis (DMA). The incorporation of carbon nanomaterials presented a limited effect on the mechanical properties of the EM system.

A review of the genus Neopsocopsis (Psocodea, "Psocoptera", Psocidae), with one new species from China.

A review of species of the genus Neopsocopsis Badonnel, 1936 is presented. Four species are redescribed, viz. Neopsocopsis hirticornis (Reuter, 1893), Neopsocopsis quinquedentata (Li & Yang, 1988), Neopsocopsis profunda (Li, 1995), and Neopsocopsis flavida (Li, 1989), as well as the description of one new species, Neopsocopsis convexasp. n. Seven new synonymies are proposed as follows: Pentablaste obconica Li syn. n. and Pentablaste clavata Li syn. n. of Neopsocopsis hirticornis, Pentablaste tetraedrica Li syn. n. of Neopsocopsis longiptera, Neoblaste schizopetala Li syn. n. and Neoblaste flavae Li syn. n. of Neopsocopsis profunda, Blastopsocidus pini Li syn. n. and Pentablaste lanceolata Li syn. n. of Neopsocopsis flavida. Neopsocopsis hirticornis (Reuter, 1893) is recorded from Japan and China for the first time, and Neopsocopsis longiptera Vishnyakova, 1986 is newly recorded from China. Illustrated keys to adult males and females are presented.

Long-term administration of salicylate enhances prestin expression in rat cochlea.

Salicylate, a common drug frequently used long term in the clinic, is well known for causing reversible hearing loss and tinnitus. Our previous study, however, demonstrated that chronic administration of salicylate progressively raised the amplitude of distortion product of otoacoustic emissions (DPOAEs), which are mainly caused by (outer hair cell) OHC electromotility. How salicylate affects OHC electromotility to cause this paradoxical increase remains unclear. One possibility is that it could affect prestin, which is a motor protein that contributes to the mechano-electrical properties of OHCs. In this experiment, we assessed the effect of acute and chronic salicylate treatment on prestin expression. Interestingly, after long-term salicylate injection (200 mg/kg, twice daily for 14 days), prestin gene and protein levels were up-regulated about twofold. These levels returned to baseline 14 days after treatment stopped. Acute injection of salicylate (single injection, 400 mg/kg) did not affect prestin levels. These data reveal that chronic salicylate administration markedly, but reversibly, increased prestin levels which may contribute to the enhanced DPOAE amplitudes we observed previously with similar salicylate treatment, which may be responsible for salicylate-induced tinnitus generation.

[Application of ischemic preconditioning before hepatic vascular exclusion for resection of hepatocellular carcinoma].

OBJECTIVE: To assess the value of clinical application of ischemic preconditioning (IP) before hepatic vascular exclusion for resection of hepatocellular carcinoma (HCC) accompanied by cirrhosis and explore the possible mechanism underlying the protective effect of this maneuver. METHODS: Thirty-four consecutive patients with resectable HCC were randomized into IP group to receive IP with a 5-min ischemia followed by 5-min perfusion before hepatic vascular exclusion and the control group with simply hepatic vascular exclusion. The liver function, hepatic Fas mRNA expression, caspase-3 activity, apoptosis of the hepatocytes were compared between the two groups. RESULTS: In the IP group, the aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels on postoperative day 1, 3 and 7 were all significantly higher than those of the control group (t=6.985, P<0.01). The total bilirubin levels were also higher in the former group on postoperative day 3 and 7 (t=3.447, P<0.05). The IP group had higher albumin levels on postoperative day 1 than the control group (t=3.360, P<0.05). After 1 hour's reperfusion, the hepatic mRNA expression of Fas, caspase-3 activity and apoptotic sinusoidal endothelial cells were all significantly higher than those of the control group (t=3.771, P<0.05). CONCLUSION: IP has a protective effect on liver function after hepatic resection with hepatic vascular exclusion in HCC patients, possibly due to the inhibition of hepatocyte apoptosis by down-regulating hepatic Fas mRNA expression and caspase-3 activity, and is a convenient technique applicable in such operations as hepatic transplants and hepatectomy.