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557 result(s) for "Wang, Jianling"
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Climate change, vulnerability, and its impacts in rural Pakistan: a review
Pakistan is one of the most vulnerable countries especially in Southeast Asia experiencing floods and droughts as a result of climate change. Variation in climate adversely affects agriculture sector, ground water, nutrition, soil quality and soil organic matter, health conditions, and poverty. The main purpose of this study is to review the impact of climate change and adaptation strategies used at farm level in response to variation in temperature and precipitation. As per literature, Pakistani farmers adopt several adaptation strategies in response to climate change, like change in fertilizer, change in crop variety, pesticide, seed quality, water storage, farm diversification, plant shade trees, irrigation practices, off-farm activities, permanent and temporary migration, and selling of assets. Literature also showed that farmers living wetland area perceived less variation in climate than farm households living in dry area.
The optimized Fenton-like activity of Fe single-atom sites by Fe atomic clusters—mediated electronic configuration modulation
The performance optimization of isolated atomically dispersed metal active sites is critical but challenging. Here, TiO₂@Fe species-N-C catalysts with Fe atomic clusters (ACs) and satellite Fe-N₄ active sites were fabricated to initiate peroxymonosulfate (PMS) oxidation reaction. The AC-induced charge redistribution of single atoms (SAs) was verified, thus strengthening the interaction between SAs and PMS. In detail, the incorporation of ACs optimized the HSO₅⁻oxidation and SO₅ ·− desorption steps, accelerating the reaction progress. As a result, the Vis/TiFeAS/PMS system rapidly eliminated 90.81% of 45 mg/L tetracycline (TC) in 10 min. The reaction process characterization suggested that PMS as an electron donor would transfer electron to Fe species in TiFeAS, generating ¹O₂. Subsequently, the hVB⁺ can induce the generation of electron-deficient Fe species, promoting the reaction circulation. This work provides a strategy to construct catalysts with multiple atom assembly–enabled composite active sites for high-efficiency PMS-based advanced oxidation processes (AOPs).
SLC39A10 promotes malignant phenotypes of gastric cancer cells by activating the CK2-mediated MAPK/ERK and PI3K/AKT pathways
Solute carrier family 39 member 10 (SLC39A10) belongs to a subfamily of zinc transporters and plays a key role in B-cell development. Previous studies have reported that its upregulation promotes breast cancer metastasis by enhancing the influx of zinc ions (Zn 2+ ); however, its role in gastric cancer remains totally unclear. Here, we found that SLC39A10 expression was frequently increased in gastric adenocarcinomas and that SLC39A10 upregulation was strongly associated with poor patient outcomes; in addition, we identified SLC39A10 as a direct target of c-Myc. Functional studies showed that ectopic expression of SLC39A10 in gastric cancer cells dramatically enhanced the proliferation, colony formation, invasiveness abilities of these gastric cancer cells and tumorigenic potential in nude mice. Conversely, SLC39A10 knockdown inhibited gastric cancer cell proliferation and colony formation. Mechanistically, SLC39A10 exerted its carcinogenic effects by increasing Zn 2+ availability and subsequently enhancing the enzyme activity of CK2 (casein kinase 2). As a result, the MAPK/ERK and PI3K/AKT pathways, two major downstream effectors of CK2, were activated, while c-Myc, a downstream target of these two pathways, formed a vicious feedback loop with SLC39A10 to drive the malignant progression of gastric cancer. Taken together, our data demonstrate that SLC39A10 is a functional oncogene in gastric cancer and suggest that targeting CK2 is an alternative therapeutic strategy for gastric cancer patients with high SLC39A10 expression. Gastric cancer: Zinc transporter protein fuels disease progression A zinc transporter protein that is upregulated in gastric and other cancers offers a potential treatment target. Zinc is a vital trace element in the body, and a structural and catalytic component of many enzymes. Scientists know that the upregulation of the zinc transporter protein SLC39A10 enhances the influx of zinc ions into breast and liver cancer cells, boosting proliferation and metastasis. However, the role of SLC39A10 in other cancers is unclear. Xiaojuan Ren and co-workers at Xi’an Jiaotong University in Xi’an, China, found that SLC39A10 is upregulated in human gastric cancer cells and this increase is linked to poor prognosis. SLC39A10 increased the invasiveness of gastric cancer cells and their tumorigenic potential in mouse models. The team outlined the mechanisms behind SLC39A10 activity, highlighting two key pathways and identifying a possible treatment route.
Low-normal free thyroxine is associated with a higher prevalence of lower extremity arterial disease in euthyroid type 2 diabetes mellitus
Recent studies suggest that high-normal concentrations of free triiodothyronine (FT3) were associated with a lower prevalence of microangiopathy in adult euthyroid people with type 1 diabetes. This study was performed to identify the association between thyroid hormones and lower extremity arterial disease (LEAD) in euthyroid patients with type 2 diabetes mellitus (T2DM). A total of 1052 euthyroid T2DM patients were enrolled, including 704 patients with LEAD as observation group and 348 patients with T2DM alone as control group. The differences in clinical characteristics, biochemical indexes, thyroid hormone between the two groups were compared. At the same time, the association between the incidence of LEAD and thyroid hormone was analyzed. The data demonstrated that FT4 levels were significantly lower in the LEAD patients than in the without LEAD patients (16.1 vs. 16.5 pmol/L). The logistic regression analysis revealed that free thyroxine (FT4) was significantly associated with the incidence of LEAD in T2DM patients, and the prevalence of LEAD increased gradually from the highest FT4 quartile to the lowest FT4 quartile ( P  < 0.05). In conclusion, patients with low-normal FT4 had a higher prevalence of diabetic LEAD, suggesting that adjusting FT4 levels may better regulate metabolism and thus reduce lower extremity arterial injury.
Gas chromatography-time-of-flight mass spectrometry (GC-TOFMS)-based metabonomic response of Salvia miltiorrhiza flowers to cadmium stress
Cadmium (Cd) poses a threat to plants and humans. As a commonly used Chinese medicinal material, (SM) roots have been investigated in many studies, but few studies have investigated SM flowers. In particular, there is a lack of research on the response of SM flowers to Cd stress. Here, the metabolomic mechanisms underlying the response of SM flowers to Cd stress were analyzed. Six kinds of metabolites were detected: amino acids, organic acids, sugars, lipids, alcohols, and others. Among them, organic acids accounted for the largest proportion, followed by sugars and amino acids. Principal component analysis (PCA) and orthogonal partial least squares discriminant analysis (OPLS-DA) clearly differentiated the control from the Cd-treated groups. A total of 31, 40, and 49 differential metabolites (DMs) were detected in 25 (HT1), 50 (HT2), and 100 (HT3) mg·kg Cd-treated groups, respectively. These DMs were mainly enriched in alanine, aspartate and glutamate metabolism, glyoxylate and dicarboxylate metabolism, butanoate metabolism, citrate cycle (TCA cycle), and glycine, serine and threonine metabolism. Among the metabolites, oxamic acid and citric acid contributed most to the down-regulated differential amino acids and differential organic acids, respectively; xylose and 1-kestose contributed most to the up-regulated differential sugars; tryptophan and arachidic acid contributed most to the up-regulated amino acids and organic acids, respectively. These findings suggested that SM flowers might resist Cd stress through restructuring the cell-wall framework, modulating membrane fluidity, and regulating intracellular soluble components. These findings provide new avenues for exploring how medicinal plant resources cope with heavy-metal stress.
Has corporate involvement in government-initiated corporate social responsibility activities increased corporate value?—Evidence from China’s Targeted Poverty Alleviation
Poverty remains the biggest challenge facing the world today. In 2016, the Chinese government launched a national campaign to eradicate poverty by 2020, among which Chinese listed companies have made significant contributions to. This paper focuses on the targeted poverty alleviation (TPA) and investigates the relationship between corporate participation in TPA and its corporate value. As compared to firm’s own corporate social responsibility (CSR) initiatives, participating in government-initiated CSR activities can better enhance corporate value. This is especially so when firms engage in penetrative “integrated poverty alleviation” rather than the direct approach of “donative poverty alleviation”. This paper adopts the Mediating Effect Model to explain the relationship between corporate participation in TPA and their corporate value, with the shareholding ratio of institutional investors, government subsidies and corporate reputation as mediating factors. Findings suggest that corporations’ active implementation of TPA actions can increase the shareholding ratio of institutional investors and government subsidies and improve corporate reputation, thereby significantly increasing their corporate value. However, the impact of participation in TPA on corporate value is limited by factors including the nature of property rights, the intensity of competition in the industry and the degree of marketization. The impact is generally more significant in state-owned enterprises, areas with lesser industry competition and higher marketization. This study provides a fresh perspective for theories related to CSR, poverty eradication and corporate value of listed companies.
Litigation Risk and Corporate Social Responsibility—Evidence from a Poverty Alleviation Campaign in China
This paper investigates the impact of an external uncertain factor, litigation risk, on corporate participation in Targeted Poverty Alleviation (TPA) activities. It proposes and explores three possible mechanisms, namely, restore legitimacy, send positive signals, and maintain corporate reputation, for corporations to manage their litigation risk via the participation in TPA. Using a sample of Chinese listed firms from 2016 to 2020, it shows that for corporations with high legitimacy pressure, high stakeholder concern, and strong reputation protection motive, litigation risk increases corporate investment in TPA. After litigation cases arise, corporations can manage their litigation risk through participation in TPA, thereby restoring legitimacy, sending positive signals, and maintaining corporate reputation. Furthermore, participation in TPA can also moderate the negative impact of litigation risk on enterprise value. The results remain significant after robustness tests on endogeneity, variable and measurement errors, and firm fixed effects. This paper is insightful for future studies relating to the economic consequences of litigation risk. Concurrently, by exploring the role of China’s legal environment in promoting the effect of corporate participation in TPA, this paper not only expands the scope of factors influencing corporate TPA inputs, but also provides policy implications for the formulation of China’s upcoming Rural Revitalization Strategy.
Wall thickness analysis method for judging the degree of lower extremity long bone healing
To evaluate the possibility of judging the degree of bone healing by wall thickness analysis provide reference for quantitative analysis of bone healing. Patients with lower limb fracture from April 2014 to October 2019 were recruited and divided into bone healing (group A), poor bone healing (group B), and nonunion (group C). Models were built in Mimics 20.0 with DICOM 3.0 data obtained from patient’s CT. Three-dimensional geometric models of unaffected limb and affected limb after simulated removal of internal fixation were established, corresponding to basic phase and simulated phase, respectively. Wall thickness analysis was performed to obtain median wall thickness after meshing. R2 (median wall thickness ratio), R4 (CT value ratio), and R5 (healing index ratio) were obtained by calculating the ratio of each value in simulated phase to that in basic phase. Receiver operating characteristic curve analysis was used to evaluate the ability of Wall Thickness Analysis to indicate fracture healing. 112 CT scans of 79 patients were included in the study. The frequency of categorization in groups A, B, and C was 49, 37 and 26, respectively. The median R2 in groups A, B, and C was 0.91, 0.80, and 0.67, respectively (group A > group B > group C, all P  < 0.05). The best cutoff point for R2 in predicting bone healing was 0.84, and predicting bone nonunion was 0.74. The Wall Thickness Analysis can be used to quantitatively evaluate fracture healing state, with median wall thickness ratio as a more intuitive and reliable judgment index.
A preliminary study of serum metabolomic profiling in male patients with acute brucellosis
Brucellosis is a significant zoonotic disease that may lead to metabolic profile changes, which remain insufficiently studied. This study utilized an ultra-high performance liquid chromatography coupled with Q Exactive-Orbitrap mass spectrometry (UHPLC-QE xactive -Orbitrap MS/MS) to investigate serum samples of acute brucellosis in 32 male patients against 32 well-matched healthy controls. The results revealed nine differential metabolites that correlated with human acute brucellosis, all showing increased levels, except cis-4-hydroxy-D-proline, inosine, hypoxanthine and azelaic acid. These differential metabolites were predominantly involved in metabolic pathways, such as primary bile acid biosynthesis, purine metabolism, taurine and hypotaurine metabolism, and d-amino acid metabolism. This study identified potential metabolite biomarkers of acute brucellosis and laid the foundation for its early diagnosis and prognostic assessment, thus helping to prevent the chronicity of acute brucellosis.
Thyrotropin exacerbates insulin resistance by triggering macrophage inflammation in subclinical hypothyroidism
In subclinical hypothyroidism, the levels of serum thyroid-stimulating hormone (TSH) are positively correlated with insulin resistance; however, the precise mechanism is unclear. Except for thyroid follicular epithelial cells, macrophages express the highest levels of TSHR . Thus, we speculate that TSH may promote insulin resistance by triggering macrophage inflammation. Here we established a mouse model of TSH receptor ( Tshr ) myeloid-specific knockout ( Tshr MKO ) and found that Tshr MKO mice showed improvement on high-fat diet-induced obesity and insulin resistance compared with wild-type mice ( Tshr f/f ). In addition, Tshr MKO mice exhibited decreased infiltration and M1 polarization of macrophages in liver, adipose and skeletal muscle. Co-culture experiments proved that Tshr -deficient macrophages decreased gluconeogenesis in hepatocytes but increased glucose uptake in adipocytes and skeletal muscle cells by improving the insulin signaling pathway. Mechanistically, increased TSH levels in subclinical hypothyroidism promoted the secretion of cytokines IL-1α, IL-1β and IL-6 by inducing macrophage M1 polarization, which upregulated EGR1 to transcriptionally activate LCN2 and SOCS3 in insulin target cells, thereby exacerbating insulin resistance. These effects could be reversed by IL-1 and IL-6 blockers IL-1RA and IL-6ST. Thus, we provided mechanistic insights into the predisposition to insulin resistance in subclinical hypothyroidism and revealed the role of TSH in metabolic disorders. TSH induces macrophage inflammation linked to insulin resistance Subclinical hypothyroidism is a condition in which the thyroid-stimulating hormone (TSH) levels are high, but thyroid hormone levels are normal, and the levels of serum TSH are positively correlated with insulin resistance. Researchers investigated this by using mice with a specific genetic modification that affects TSH receptors in macrophages. The study found that high TSH levels can cause these macrophages to become more inflammatory, which, in turn, worsens insulin resistance. The researchers used a mouse model to show that, when TSH receptors were removed from macrophages, the mice had better insulin sensitivity and less inflammation. This suggests that TSH plays a role in promoting inflammation and insulin resistance. The findings indicate that managing TSH levels in patients with subclinical hypothyroidism could help to reduce their risk of developing insulin resistance and related conditions such as type 2 diabetes. This summary was initially drafted using artificial intelligence, then revised and fact-checked by the author.