A probe into the acid deposition mitigation path in China over the last four decades and beyond.

China currently has the highest acid deposition globally, yet research on its status, impacts, causes and controls is lacking. Here, we compiled data and calculated critical loads regarding acid deposition. The results showed that the abatement measures in China have achieved a sharp decline in the emissions of acidifying pollutants and a continuous recovery of precipitation pH, despite the drastic growth in the economy and energy consumption. However, the risk of ecological acidification and eutrophication showed no significant decrease. With similar emission reductions, the decline in areas at risk of acidification in China (7.0%) lags behind those in Europe (20%) or the USA (15%). This was because, unlike Europe and the USA, China's abatement strategies primarily target air quality improvement rather than mitigating ecological impacts. Given that the area with the risk of eutrophication induced by nitrogen deposition remained at 13% of the country even under the scenario of achieving the dual targets of air quality and carbon dioxide mitigation in 2035, we explored an enhanced ammonia abatement pathway. With a further 27% reduction in ammonia by 2035, China could largely eliminate the impacts of acid deposition. This research serves as a valuable reference for China's future acid deposition control and for other nations facing similar challenges.

Assessment of atmospheric heavy metal pollution in Qinghai-Tibet Plateau: Using mosses as biomonitor.

Atmospheric heavy metal (HM) pollution may pose a significant threat to the fragile ecosystem of Qinghai-Tibet Plateau (QTP). To investigate potential atmospheric HM pollution within the QTP region of China, mosses, along with other higher plants and soil, were collected from 33 sites for heavy metal measurement. The concentration ranges of Zn, Pb, Cd, and Cu in mosses were 6.07-69.9, 5.36-23.9, 0.60-1.05, and 14.4-50.5 mg·kg-1 (dry weight), respectively, significantly higher than those in other higher plants, except for Zn. The spatial distribution of relative concentrations (RCs; moss to top soil) of HMs varied considerably, indicating distinct differences in atmospheric Zn and Cu pollution levels between the northern and southern QTP. This study first reported that moderate regional atmospheric Cu pollution, primarily due to large-scale mining in recent years, had occurred, particularly in southern QTP. Pb also presented slight pollution due to anthropogenic activities. However, Cd showed almost no atmospheric pollution, while Zn concentrations were relatively high in southern QTP. Although less severe than atmospheric pollution levels in Chinese inland or coastal cities, the atmospheric pollution of Pb and Cu in QTP indicated by mosses were far more severe than global background areas, or even worse than most European cities.

Differentiated emission control strategy based on comprehensive evaluation of multi-media pollution: Case of mercury emission control.

In order to comprehensively evaluate the environmental impact of multi-media mercury pollution under differentiated emission control strategies in China, a literature review and case studies were carried out. Increased human exposure to methylmercury was assessed through the dietary intake of residents in areas surrounding a typical coal-fired power plant and a zinc (Zn) smelter, located either on acid soil with paddy growth in southern China, or on alkaline soil with wheat growth in northern China. Combined with knowledge on speciated mercury in flue gas and the fate of mercury in the wastewater or solid waste of the typical emitters applying different air pollution control devices, a simplified model was developed by estimating the incremental daily intake of methylmercury from both local and global pollution. Results indicated that air pollution control for coal-fired power plants and Zn smelters can greatly reduce health risks from mercury pollution, mainly through a reduction in global methylmercury exposure, but could unfortunately induce local methylmercury exposure by transferring more mercury from flue gas to wastewater or solid waste, then contaminating surrounding soil, and thus increasing dietary intake via crops. Therefore, tightening air emission control is conducive to reducing the comprehensive health risk, while the environmental equity between local and global pollution control should be fully considered. Rice in the south tends to have higher bioconcentration factors than wheat in the north, implying the great importance of strengthening local pollution control in the south, especially for Zn smelters with higher contribution to local pollution.

Structural network efficiency mediates the association between glymphatic function and cognition in mild VCI: a DTI-ALPS study.

Background and objective: Vascular cognitive impairment (VCI) can be caused by multiple types of cerebrovascular pathology and is considered a network disconnection disorder. The heterogeneity hinders research progress in VCI. Glymphatic failure has been considered as a key common pathway to dementia recently. The emergence of a new method, Diffusion Tensor Image Analysis Along the Perivascular Space (DTI-ALPS), makes it possible to investigate the changes of the glymphatic function in humans non-invasively. We aimed to investigate alterations of glymphatic function in VCI and its potential impact on network connectivity. Methods: We recruited 79 patients with mild VCI, including 40 with cerebral small vessel disease cognitive impairment (SVCI) and 39 with post-stroke cognitive impairment (PSCI); and, 77 normal cognitive (NC) subjects were recruited. All subjects received neuropsychological assessments and multimodal magnetic resonance imaging scans. ALPS-index was calculated and structural networks were constructed by deterministic tractography, and then, the topological metrics of these structural connectivity were evaluated. Results: The ALPS-index of VCI patients was significantly lower than that of NC subjects (P < 0.001). Multiple linear regression analysis showed that ALPS-index affects cognitive function independently (ß = 0.411, P < 0.001). The results of correlation analysis showed that the ALPS-index was correlated with overall vascular risk factor burden (r = -0.263, P = 0.001) and multiple cerebrovascular pathologies (P < 0.05). In addition, global efficiency (Eg) of network was correlated with ALPS-index in both SVCI (r = 0.348, P = 0.028) and PSCI (r = 0.732, P < 0.001) patients. Finally, the results of mediation analysis showed that Eg partially mediated in the impact of glymphatic dysfunction on cognitive impairment (indirect effect = 7.46, 95% CI 4.08-11.48). Conclusion: In both major subtypes of VCI, the ALPS-index was decreased, indicating impaired glymphatic function in VCI. Glymphatic dysfunction may affect cognitive function in VCI by disrupting network connectivity, and, may be a potential common pathological mechanism of VCI. ALPS-index is expected to become an emerging imaging marker for VCI.

Oxidation and coagulation/adsorption dual effects of ferrate (VI) pretreatment on organics removal and membrane fouling alleviation in UF process during secondary effluent treatment.

Ultrafiltration (UF) has been widely used in water and advanced sewage treatment. Unfortunately, membrane fouling is still the main obstacle to further improvement in the system. Fe (III) salt, a type of traditional coagulant, is often applied to mitigate UF membrane fouling. However, low molecule organic weight cannot be effectively removed, thus the water quality after single coagulation treatment does not effectively meet the standard of subsequent water reuse during secondary effluent treatment. Recently, it has been found that potassium ferrate (Fe (VI)) has multiple functions of oxidation, sterilization and coagulation, with other studies proving its good performance in organics removal and membrane fouling mitigation. However, the respective contributions of oxidation and coagulation/adsorption have not yet been fully understood. The oxidation and coagulation/adsorption effects of Fe (VI) during membrane fouling mitigation were investigated here. The oxidation effect of Fe (VI) was the main reason for organics with the MW of 8-20 kDa removal, and its coagulation/adsorption mainly accounted for the smaller amounts of molecular organics removed. The oxidation of Fe (VI) was the main method for overcoming membrane fouling in the initial filtration; it largely alleviated the standard blockage. The formation of a cake layer transformed the main membrane fouling alleviation mechanism from oxidation to coagulation/adsorption and further removed smaller amounts of molecule organics with the increase of filtration cycles and Fe (VI) dosages. The main fouling mechanism altered from standard blocking and cake filtration to only cake filtration after Fe (VI) treatment. Overall, the mechanism of the oxidation and coagulation/adsorption of Fe (VI) were differentiated, and would provide a reference for future Fe (VI) pretreatment in UF membrane fouling control during water and wastewater treatments.

Senkyunolide A inhibits the progression of osteoarthritis by inhibiting the NLRP3 signalling pathway.

CONTEXT: Osteoarthritis (OA) is a degenerative disease. Senkyunolide A (SenA) is an important phthalide from Ligusticum chuanxiong Hort (Umbelliferae) with anti-spasmodic and neuroprotective effects. OBJECTIVE: We explored the effect of SenA on IL-1ß-stimulated chondrocytes and OA mice. MATERIALS AND METHODS: Chondrocytes were stimulated by IL-1ß (10 ng/mL) to establish an OA model in vitro. Cells were treated with SenA (20, 40, 80 and 160 µg/mL) for 48 h. The in vivo OA model was established by cutting off the medial meniscus tibial ligament (MMTL) at right knee incision of male C57BL/6 mice. One week after surgery, mice were injected with SenA (intraperitoneally one week) and divided into four groups (n = 6 per group): Sham, OA, OA + SenA 20 mg/kg and OA + SenA 40 mg/kg. The OA progression was examined by haematoxylin and eosin (H&E) staining. RESULTS: SenA treatment increased cell viability (33%), proliferation (71%), inhibited apoptosis (21%), decreased levels of catabolic marker proteins (MMP13, 23%; ADAMTS4, 31%; ADAMTS5, 19%), increased levels of anabolic marker proteins (IGF-1, 57%; aggrecan, 75%; Col2a1, 48%), reduced levels of inflammation cytokines (TNF-α, 31%; IL-6, 19%; IL-18, 20%) and decreased levels of NLRP3 (21%), ASC (20%) and caspase-1 (29%) of chondrocytes. However, NLRP3 agonist nigericin increased levels of MMP13 (55%), ADAMTS4 (70%), ADAMTS5 (53%), decreased levels of IGF-1 (36%), aggrecan (26%), Col2a1 (25%), inhibited proliferation (61%) and promoted apoptosis (76%). DISCUSSION AND CONCLUSIONS: SenA alleviates OA progression by inhibiting NLRP3 signalling pathways. These findings provide an experimental basis for the clinical application of drugs in the treatment of OA.

Critical loads of headwater streams in China using SSWC model modified by comprehensive F-factor.

In order to evaluate the potential risk of surface water acidification in regions with historically-elevated acid deposition and to measure the recovery of such ecosystems after policy changes, critical loads and their exceedances were estimated for 349 headwater streams across China using a modified SSWC model. Such a model considered the acid-neutralizing capacity derived from high base cation deposition and the robust retention of sulfate and nitrate. Results indicated that China's streams had higher critical loads (averaged at 4.7 keq·ha-1·yr-1) and were less sensitive to acid deposition as compared to Europe and North America. The proportion of surveyed streams with acid deposition exceeded critical load decreased from 40.4% in 2005 to 29.5% in 2018, indicating a significant decrease in risk of surface water acidification, and thus a benefit from the emission abatement in recent years. Nonetheless, a relatively high risk of acidification still existed in southeast China with lower critical loads and most critical load exceedances. More efforts should be put into implementing emission control policies in the future.

Nuclear receptor TLX may be through regulating the SIRT1/NF-κB pathway to ameliorate cognitive impairment in chronic cerebral hypoperfusion.

BACKGROUND: Chronic cerebral hypoperfusion (CCH) is a common pathophysiological mechanism in neurodegenerative diseases, such as Alzheimer's disease and vascular dementia. The orphan nuclear receptor TLX plays an important role in neural development, adult neurogenesis and cognition. The aim of this study was to investigate the neuroprotective effects of TLX on cognitive dysfunction, hippocampal neurogenesis and neuroinflammation in a rat model of CCH and to assess the possible mechanisms. METHODS: Permanent bilateral common carotid artery occlusion (2-VO) was used to establish a model of CCH. Stereotaxic injection of an adeno-associated virus vector expressing TLX was used to overexpress TLX in the hippocampus. Cognitive function was evaluated by the Morris Water Maze test. Immunofluorescent staining was used to assess hippocampal neurogenesis. The effects of overexpression of TLX on SIRT1 and inflammatory cytokines were analyzed with qRT-PCR and western blot. RESULT: After 2-VO, CCH rats exhibited cognitive impairment and reduction of hippocampal TLX levels. Overexpression of TLX ameliorated cognitive impairments with increasing number of BrdU + cells and BrdU + NeuN + cells in DG. Furthermore, TLX rescued the reduced SIRT1 usually induced by CCH. Additionally, TLX also inhibited the expression of inflammatory cytokines such as NF-κB and IL-1ß. CONCLUSIONS: The present findings suggested that TLX exerted protective effects against cognitive deficits induced by CCH. The possible mechanisms of TLX may be through regulating the SIRT1/NF-κB pathway, promoting hippocampal neurogenesis and inhibiting the neuroinflammatory response.

Neurological Implications of Non-critically Ill Patients With Coronavirus Disease 2019 in a Fangcang Shelter Hospital in Wuhan, China.

Background: Coronavirus disease 2019 (COVID-19) is a new viral respiratory disease and has become a pandemic. Fever, weakness, and dry cough are the main clinical manifestations. However, little is known about neurological symptoms of non-critically ill COVID-19 patients. Objective: To investigate the neurological symptoms and implications of patients with non-critically ill COVID-19 patients. Materials and Methods: This retrospective cohort study investigated all COVID-19 patients admitted to Wuhan East-West Lake Fangcang shelter hospital. Demographic data, clinical manifestations, comorbidities, radiological data, the result of nucleic acid test, and treatments were collected and analyzed. Results: Among 1,682 patients with confirmed non-critically ill COVID-19, 509 patients (30.3%) had neurological symptoms, including myalgia (311, 18.5%), headache (216, 12.8%), fatigue (83, 4.9%), and dizziness (15, 0.9%). One hundred and fourteen patients (6.8%) were the expansion of pulmonary infection according to their chest CT images and medical history. Compared with patients without neurological symptoms, patients with neurological symptoms had a significantly longer length of hospital stay, time of nucleic acid turning negative, and the mean time from onset of symptom to hospital admission (p < 0.05). Patients with neurological symptoms were more likely to occur the expansion of pulmonary infection compared with the patients without neurological symptoms (46/509 [9.0%] vs. 68/1,173 [5.8%]). Conclusions: Non-critically ill COVID-19 patients commonly have neurological symptoms. Neurological symptoms are significantly associated with the processes of COVID-19. Early identification and aggressive treatment are particularly important for COVID-19 patients with neurological symptoms.

Antitumor effects of ß-elemene via targeting the phosphorylation of insulin receptor.

Ewing sarcoma family tumors (ESFTs) are a group of aggressive and highly metastatic tumors lacking efficient therapies. Insulin-like growth factor 1 receptor (IGF1R) blockade is one of the most efficient targeting therapy for ESFTs. However, the appliance is obstructed by drug resistance and disease recurrence due to the activation of insulin receptor (IR) signaling induced by IGF1R blockade. Herein ß-elemene, a compound derived from natural plants, exhibited a remarkable proliferation repression on ESFT cells, which was weakened by a caspase inhibitor Z-VAD. ß-elemene in combination with IGF1R inhibitors enhanced markedly the repression on cellular proliferation and mTOR activation by IGF1R inhibitors and suppressed the PI3K phosphorylation induced by IGF1R inhibitors. To investigate the mechanisms, we focused on the effects of ß-elemene on IR signaling pathway. ß-elemene significantly suppressed the insulin-driven cell growth and the activation of mTOR and PI3K in tumor cells, while the toxicity to normal hepatocytes was much lower. Further, the phosphorylation of IR was found to be suppressed notably by ß-elemene specifically in tumor cells other than normal hepatocytes. In addition, ß-elemene inhibited the growth of ESFT xenografts in vivo, and the phosphorylation of IR and S6 ribosomal protein was significantly repressed in the ß-elemene-treated xenografts. These data suggest that ß-elemene targets IR phosphorylation to inhibit the proliferation of tumor cells specifically and enhance the effects of IGF1R inhibitors. Thus, this study provides evidence for novel approaches by ß-elemene alone or in combination with IGF1R blockades in ESFTs and IR signaling hyperactivated tumors.

Rosiglitazone ameliorates astrocyte over-activation and inflammatory cytokine release induced by global cerebral ischemia/reperfusion.

Global cerebral ischemia (GCI) is a leading cause of mortality worldwide and remains the primary cause of long-term neurological disability. Astrocyte over-activation and extensive neuron loss in the ischemic brain are the characteristic pathological features of cerebral ischemia. Rosiglitazone (RSG) is a peroxisome-proliferating activating receptor-γ agonist known for its anti-inflammatory activity. Previous studies have suggested that RSG is able to exert neuroprotection in numerous acute and chronic brain injury models. However, whether RSG treatment is involved in astrocyte over-activation and inflammatory reaction in the cortex remains unclear. The aim of the present study was to investigate whether RSG treatment improved functional impairment induced following GCI and protected against cortex neuron loss, and to elucidate the potential mechanisms underlying these functions. Rats were randomly divided into three groups: Sham-operated, GCI and RSG treatment groups. The RSG treatment group was treated with 2 mg/kg RSG immediately following GCI. The results demonstrated that RSG treatment significantly reduced infarct volume and neuron survival rates in addition to increasing function recovery. Furthermore, these results correlate with a reduction in astrocyte over-activation and inflammatory cytokines in the rat cortex. However, no significant changes in glutamate transporter-1 expression levels were observed following RSG treatment compared with the GCI rats. The results of this investigation provide in vivo evidence that RSG significantly protected rats against ischemia-reperfusion-induced brain injury. In addition, RSG may exert neuroprotective effects by inhibiting astrocyte over-activation, and thereby reducing the levels of inflammatory cytokines in the GCI-injured brain. All data revealed that RSG may be a potential neuroprotective agent for cerebral ischemia.

Meta-analysis of BACE1 gene rs638405 polymorphism and the risk of Alzheimer's disease in Caucasion and Asian population.

Recent studies showed the ß-site amyloid precursor protein cleaving enzyme (BACE) is associated with Alzheimer's disease (AD). However, studies investigating the association of single-nucleotide polymorphism (SNP) in exon 5 of BACE1 (rs638405, C786G, Val262) with AD are controversial. Therefore we conducted this meta-analysis to clarify the association. Relevant studies were identified on PubMed, Cochrane library and CNKI from established through July 2015 according to the inclusion criteria. Odds ratios (ORs) with 95% confidence intervals (CIs) and five genetic models were applied to assess the association. A total of 13 studies composed of 2538 AD patients and 3020 controls were included in this study. Significant association of SNP rs638405 with AD was found in overall population among allelic genetic model (G vs. C: OR=1.11, 95%CI=1.02-1.20, P=0.01), codominant genetic model (GG vs. CC: OR=1.22, 95%CI=1.04-1.44, P=0.02) and recessive genetic model (GG vs. GC+ CC: OR=1.25, 95%CI=1.10-1.42, P=0.0008). Besides, subgroup analysis indicated significant association among Asian population (allelic genetic model, G vs. C, OR=1.18, 95%CI=1.04-1.34, P=0.01; codominant genetic model, GG vs. CC, OR=1.43, 95%CI=1.08-1.89, P=0.01 and recessive genetic model, GG vs. GC+ CC, OR=1.40, 95%CI=1.09-1.78, P=0.008) and Caucasion population (recessive genetic model, GG vs. GC+ CC, OR=1.20, 95%CI=1.02-1.39, P=0.02). Our analysis demonstrated that GG genotype and G allele of BACE1 gene rs638405 probably increase the risk of AD.