The impact of rural e-commerce participation on farmers' entrepreneurial behavior: Evidence based on CFPS data in China.

The "Three Rural Issues", encompass challenges related to agriculture, farmer, and rural area, which hold significant importance in driving comprehensive rural revitalization efforts in China. Farmer entrepreneurship, as a crucial means to enhance productivity, create job opportunities, and increase residents' income, has gradually become a key driving force in promoting rural revitalization in the new stage of development in China. With the rapid development of rural e-commerce, farmer entrepreneurship has encountered new opportunities. This study utilizes the 2020 China Family Panel Studies (CFPS) data and employs a structural equation model (SEM) to analyze the direct impact of rural e-commerce participation on farmer entrepreneurial behavior, considering factors such as human capital, social capital, and network infrastructure. This study further explores the indirect effects and mechanisms of e-commerce participation as a mediating variable and analyzes the impact and mechanisms on agricultural entrepreneurship behavior. The findings are as follows: (1) E-commerce participation significantly promotes farmer entrepreneurial behavior; (2) E-commerce participation as a mediating variable has a positive indirect effect on the relationship between social trust, network infrastructure, human capital, and farmer entrepreneurial behavior; (3) E-commerce participation has a significant positive influence on farmer entrepreneurship in the agricultural sector, and farmers with higher levels of network infrastructure and human capital have a higher probability of choosing agricultural entrepreneurship under the influence of e-commerce participation. Finally, this study provides policy recommendations in terms of infrastructure construction, entrepreneurial policy environment, and education level, aiming to optimize the situation of farmer entrepreneurship and contribute to the comprehensive promotion of rural revitalization.Overall, the research in this paper effectively combines theory and empirical evidence to outline the direct and indirect impact mechanisms of rural e-commerce participation on farmers' entrepreneurial behavior and agriculture-related entrepreneurial behavior and to test the effects of their impacts. First, most of the existing literature deals with farmers in individual sample areas, while the sample selected in this paper is farmers in the whole country, which is relatively more generalizable; second, most of the previous studies explore the level of e-commerce in the inter-provincial or county areas, while this paper expands the empirical study of rural e-commerce on the entrepreneurial behavior of farmers and the micro-period of agricultural entrepreneurial behavior, and focuses on the impacts of the e-commerce activities of farmers on their entrepreneurial behavior.

Genotypic and phenotypic features of 39 Chinese patients with glycogen storage diseases type I, VI, and IX.

Glycogen storage diseases (GSDs) are abnormally inherited glycogen metabolism mainly affecting the liver, muscles, and heart. Deficiency of proteins involved in glycogen metabolism caused by genetic mutations are responsible for different subtype of GSDs. However, there are still some challenges in diagnosing GSD. This study includes 39 suspected GSDs patients from unrelated families in China. Next-generation sequencing (NGS) was used to investigate the reason for their diseases at the genetic level. Finally, all 39 patients were diagnosed with GSDs, including 20 GSD-Ia, 4 GSD-VI, and 15 GSD IX (12 GSD-IXa patients and 3 GSD-IXb patients). Thirty-two mutations in G6PC1, PYGL, PHKA2, and PHKB genes were identified, with 14 of them being novel variants. The pathogenicity of novel variants was classified according to ACMG guildlines and predicted by in slico algorithms. Mutations p.L216L and p.R83H in G6PC1 gene may be the hot spot mutation in Chinese. Hearing impairment is a rare clinical feature of GSD Ia, which has also been observed in our cohort. The severity of GSD VI and IX was indicated by our patients. Close follow-up should be applied to GSD VI and IX patients. Our findings provided evidence for building the phenotype-genotype of GSDs and expanded the mutation spectrum of related genes.

Recurrent abdominal pain and vomiting with elevated triglyceride and positive antinuclear antibody in a girl aged 12 years. / 12å²å¥³å­©åå¤è ¹ç—›ã€å‘•åä¼´ä¸‰é °ç”˜æ²¹å‡é«˜ã€æŠ—æ ¸æŠ—ä½“é˜³æ€§.

A girl aged 12 years and 2 months presented with recurrent abdominal pain and vomiting for more than 2 years and arthrodynia for 3 months. She was diagnosed with recurrent acute pancreatitis with unknown causes and had been admitted multiple times. Laboratory tests showed recurrent significant increases in fasting serum triglyceride, with elevated immunoglobulin and positive antinuclear antibody. The girl was improved after symptomatic supportive treatment. The girl developed arthrodynia with movement disorders 3 months before, and proteinuria, hematuria, and positive anti-double-stranded DNA antibody were observed. The renal biopsy was performed, and the pathological examination and immunofluorescence assay suggested diffuse lupus nephritis (type Ⅳ). She was finally diagnosed with systemic lupus erythematosus (SLE), lupus nephritis (type Ⅳ), and recurrent acute pancreatitis. Pancreatitis was suspected to be highly associated with SLE. She was treated with oral hydroxychloroquine sulfate and intravenous methylprednisolone sodium succinate and cyclophosphamide. Arthrodynia was partially relieved. She was then switched to oral prednisone acetate tablets. Intravenous cyclophosphamide and pump infusion of belimumab were regularly administered. Now she had improvement in arthrodynia and still presented with proteinuria and hematuria. It is concluded that recurrent acute pancreatitis may be the first clinical presentation of SLE. For pancreatitis with unknown causes, related immunological parameters should be tested, and symptoms of the other systems should be closely monitored to avoid delaying the diagnosis.

Case Report: Identification of a Novel Homozygous Mutation in GPD1 Gene of a Chinese Child With Transient Infantile Hypertriglyceridemia.

Transient infantile hypertriglyceridemia is a rare autosomal recessive disorder characterized by hypertriglyceridemia, hypohepatia, hepatomegaly, hepatic steatosis and fibrosis in infancy. Mutations in GPD1 gene are considered the causative factor but the underlying mechanism of this disorder is still enigmatic. To date, only 24 different GPD1 mutations have been reported in the literature worldwide with transient infantile hypertriglyceridemia or relevant conditions. Here we report a Chinese girl who developed hepatomegaly hepatic steatosis, elevated transaminase and hypertriglyceridemia from the age of 4 months. A novel homozygous variant c.454C>T (p.Q152*) was found in GPD1 gene by next-generation sequencing. This patient is the 3rd Asian reported with transient infantile hypertriglyceridemia. We summarized the clinical presentations of transient infantile hypertriglyceridemia and also expanded the spectrum of disease-causing mutations in GPD1.

Nerve growth factor regulates liver cancer cell polarity and motility.

Nerve growth factor (NGF), a prototypical neurotrophic factor essential for neuronal cell proliferation and survival, has been implicated as a marker of tumor progression, as well as a potential target for novel therapeutic approaches in cancer. To investigate the functional potential of NGF in liver cancer in the present study, a stable NGF­overexpressing HepG2 cell line was generated. The scratch­wound assay was used to investigate cell motility and polarity. Western blotting was performed to evaluate the expression levels of epithelial­mesenchymal transition (EMT)­related proteins, including E­cadherin, N­cadherin and vimentin. Moreover, immunofluorescence was performed to investigate the arrangement of the actin cytoskeleton. Cell anoikis resistance was examined using a suspension culture model and cell apoptosis was examined via flow cytometry. The present results indicated that NGF overexpression in HepG2 cells disrupted HepG2 cell polarity and promoted cell motility. Furthermore, NGF overexpression induced EMT and actin cytoskeleton rearrangement in HepG2 cells, as well as enhanced anoikis resistance and prevented cellular apoptosis. Notably, a tropomyosin receptor kinase A receptor inhibitor blocked NGF­induced cell motility and apoptosis. Therefore, it was suggested that NGF serves a critical role in the invasion and metastasis of liver cancer. The use of NGF as a biomarker or potential new target could lead to the development of novel factors for diagnosis or for improving therapeutic strategies in liver cancer.

lncRNA BG981369 Inhibits Cell Proliferation, Migration, and Invasion, and Promotes Cell Apoptosis by SRY-Related High-Mobility Group Box 4 (SOX4) Signaling Pathway in Human Gastric Cancer.

BACKGROUND Human gastric cancer (GC) is a leading primary cause of cancer-associated deaths in both males and females worldwide. However, there are few effective diagnostic and therapeutic measures for GC patients due to the complicated underlying mechanisms of GC. Recently, increasing research has indicated that lncRNAs may play a critical role in the progression of GC. MATERIAL AND METHODS AI769947, AK054978, DB077273, BG981369, AK054588, and AF131784 expressions were analyzed by qRT-PCR assay in GC tissues and corresponding normal tissues (n=44). BG981369 expression was detected by qRT-PCR assay in GC cells. BG981369 was overexpressed and silenced in AGS and SNU-5 cells. The proliferation ability was detected by MTT and colony formation assays. Cell cycle distribution and cell apoptosis rate were analyzed by flow cytometry. The migration and invasion abilities were measured by Transwell assay. In addition, SOX4 expression was analyzed by qRT-PCR in GC tissues. The correlation between SOX4 and BG981369 was analyzed by Pearson analysis. RESULTS The results indicated that lncRNA BG981369 was significantly higher in GC tissues than in normal tissues. Overexpression of BG981369 inhibited the proliferation, migration, and invasion and promoted apoptosis of gastric adenocarcinoma (AGS) cells, and silencing of BG981369 promoted proliferation, migration, and invasion, and inhibited cell apoptosis of SNU-5 cells. Furthermore, we found that SOX4 may act as a downstream mediator of BG981369, suggesting that BG981369 inhibits proliferation, migration, and invasion, and promotes apoptosis by targeting SOX4 in the GC cell lines. CONCLUSIONS Our results suggest that BG981369 and SOX4 are potentially effective therapeutic targets for GC.

Fibrinogen-like protein 2 prothrombinase may contribute to the progression of inflammatory bowel disease by mediating immune coagulation.

Inflammation and coagulation are interdependent processes that enable each process to activate and propagate the other in inflammatory bowel disease (IBD). Thus, we investigated the role of a novel immune coagulant, fibrinogen-like protein 2 prothrombinase (FGL2), in patients and mice with IBD. 83 IBD patients and 40 normal controls were enrolled, and trinitro-benzene-sulfonic acid (TNBS)-induced colitis mice were used. Expression of FGL2 in the intestine was detected by immunohistochemistry. Using serial sections, staining was performed to detect tumor necrosis factor α (TNF-α) expression, and to demonstrate co-localization of FGL2 with macrophages and fibrin. Correlations between FGL2 expression with some common laboratory parameters were examined. FGL2 was seen primarily in inflammatory infiltrating cells, mainly macrophages, and microvascular vessels and had a strong co-localization with fibrin deposition. IBD patients and mice had increased expression of FGL2 compared with controls. Furthermore, FGL2 expression was correlated with intestinal and plasmatic TNF-α expression, mean platelet volume (MPV), platelet count (PLT), platelet-crit (PCT), and fibrinogen. Our data indicate that FGL2 may mediate immune coagulation in IBD patients. It may be considered as a novel molecule that contributes to the onset and development of IBD.

Total glucosides of paeony ameliorates TNBS­induced colitis by modulating differentiation of Th17/Treg cells and the secretion of cytokines.

The imbalance between effector CD4+ T helper 17 (Th17) and regulatory CD4+ T cells (Treg) cells and their associated cytokines, have been associated with the pathogenesis of inflammatory bowel disease (IBD). Total glycosides of paeony (TGP) is an alternative immunomodulatory agent that is widely used for the treatment of autoimmune diseases. The present study aimed to evaluate the modulatory effect of TGP in a rat model of colitis induced by 2,4,6­trinitrobenzene sulfonic acid (TNBS). TGP was administered intragastrically 24 h after the TNBS intrarectal instillation for 7 days. TGP treatment ameliorated the clinical status and reversed the histopathologic severity of acute TNBS colitis. Furthermore, TGP inhibited the levels of Th17­associated cytokines interleukin (IL)­17, IL­6, tumor necrosis factor­α, whereas the expression levels of Treg­associated cytokines IL­10, transforming growth factor­ß in the plasma, colon, spleen and mesenteric lymph nodes (MLN). Additionally, TGP reduced the percentage of Th17 cells; however, the proportion of Treg cells in the spleen and MLN was increased. The present study also observed a suppression of Th17­associated transcription factor, termed retinoid­related orphan receptor­Î³t (ROR­Î³t). However, expression of the Treg­associated transcription factor forkhead boxp3 was increased in the TGP treatment group. Therefore, the present findings suggest that TGP has a regulatory role in modulating the balance of Th17 and Treg cells to ameliorate the TNBS­induced colitis and support the strategy of using TGP to treat IBD.

Elevated fibrinogen­like protein 2 in TNBS­induced colitis mice: Association with Th17 and regulatory T cells.

The etiology and pathogenesis of inflammatory bowel disease (IBD) is complex and remains to be completely elucidated. Numerous cytokines are associated with the initiation and development of IBD. Fibrinogen­like protein 2 (FGL2), an immunosuppressive cytokine expressed by regulatory cluster of differentiation (CD)4+ T (Treg) cells, has been identified to be important for immunomodulatory activity in the inflammatory state. Therefore, the present study investigated the expression of FGL2 and interleukin (IL)­17 in trinitro­benzene­sulfonic acid (TNBS)­induced colitis mice to identify the function of FGL2, based on the effector CD4+ T helper (Th)17/Treg balance, in IBD. Compared with control mice, TNBS­induced mice exhibited marked alterations in clinical manifestation, including macroscopic and histopathological damage. Intestinal and peripheral expression of FGL2 was upregulated in TNBS­induced mice, while the level of FGL2 in the spleen was decreased. Expression of IL­17 in the plasma, colon and spleen was increased in TNBS­induced mice. The percentage of Treg cells was markedly decreased, although Th17 cells were increased following TNBS induction. The results of the present study indicated that, in the colitis model, FGL2 was associated with the immunopathogenesis of IBD.

Tolvaptan regulates aquaporin-2 and fecal water in cirrhotic rats with ascites.

AIM: To investigate the role of tolvaptan in regulating aquaporin (AQP)-2 expression and fecal water content in cirrhotic rats with ascites. METHODS: Cirrhosis with ascites was induced in rats by repetitive dorsal injection of CCl4 for 14 wk. In total, 84 cirrhotic rats with ascites divided into three groups (vehicle, 3 mg/kg and 5 mg/kg tolvaptan), and then further divided into five subgroups (days 1, 2, 3, 4, and 5). Blood samples were obtained to measure vasopressin and sodium concentrations. Rats were killed and colonic mucosa was scraped for analysis of protein expression and AQP-2 transcriptional level. The whole layer was fixed for hematoxylin&eosin (HE) staining and feces were collected for determination of fecal water content. CONCLUSION: Compared with vehicle, vasopressin decreased significantly in the tolvaptan groups from day 2 to a similar level in each treatment group. AQP-2 showed significant upregulation in cirrhotic rats with ascites compared with an untreated control group (100% ± 22.9% vs 22.2% ± 10.23%, P < 0.01). After administration of tolvaptan, AQP-2 expression began to decrease significantly from day 2 in each treatment group, but no significant difference was finally found between the treatment groups. Fecal water content in the distal colon was increased by 5 mg/kg tolvaptan on day 1 (66.8% ± 9.3% vs 41.4% ± 6.3%, in the vehicle group, P < 0.05). Fecal water content returned to baseline at day 4 at the latest in both treatment groups, and did not correspond to the change in AQP-2 expression. HE staining of the colonic mucosa showed no mucosal damage related to tolvaptan. CONCLUSION: Upregulation of AQP-2 in the distal colon is found in cirrhotic rats with ascites. Tolvaptan inhibits its expression and may decrease water reabsorption and induce diarrhea.

Serum uric acid levels in patients with myasthenia gravis are inversely correlated with disability.

Uric acid (UA), the final product of purine metabolism, has been reported to be reduced in patients with various neurological disorders and is considered to be a possible indicator for monitoring the disability and progression of multiple sclerosis. However, it remains unclear whether there is a close relationship between UA and myasthenia gravis (MG), or whether UA is primarily deficient or secondarily reduced because of its peroxynitrite scavenging activity. We investigated the correlation between serum UA levels and the clinical characteristics of MG. We assessed 338 serum UA levels obtained in 135 patients with MG, 47 patients with multiple sclerosis, and 156 healthy controls. In addition, we compared serum UA levels when MG patients were stratified according to disease activity and classifications performed by the Myasthenia Gravis Foundation of America, age of onset, duration, and thymus histology (by means of MRI or computed tomography). MG patients had significantly lower serum UA levels than the controls (P<0.001). Moreover, UA levels in patients with MG were inversely correlated with disease activity and disease progression (P=0.013). However, UA levels did not correlate significantly with disease duration, age of onset, and thymus histology. Our findings suggest that serum level of UA was reduced in patients with MG and serum UA might be considered a surrogate biomarker of MG disability and progression.