Cystatin SA attenuates gastric cancer cells growth and increases sensitivity to oxaliplatin via PI3K/AKT signaling pathway.

PURPOSE: Cystatin SA (CST2) belongs to the superfamily of cysteine protease inhibitors. Emerging research indicates that CST2 is often dysregulated across various cancers. Its role and molecular mechanisms in gastric cancer remain underexplored. This study aims to explore the expression and function of CST2 in gastric cancer. METHODS: CST2 expression was analyzed and validated through Western blot. CST2 overexpression was induced by lentivirus in GC cells, and the correlation between CST2 expression levels and downstream signaling pathways was assessed. In addition, multiple assays, including cell proliferation, colony formation, wound-healing, and transwell migration/invasion, were considered to ascertain the influence of CST2 overexpression on gastric cancer. The cell cycle and apoptosis were detected by flow cytometry. RESULTS: CST2 expression at the protein level was decreased to be reduced in both gastric cancer tissues and cell lines, and CST2 expression attenuate gastric cancer growth, an effect restricted to gastric cancer cells and absent in gastric epithelial GES-1 cells. Furthermore, CST2 was demonstrated to improve chemosensitivity to Oxaliplatin in gastric cancer cells through the PI3K/AKT signaling pathway. CONCLUSION: These findings indicate that CST2 is downregulated at the protein level in gastric cancer tissues and cell lines. Additionally, CST2 was found to attenuate the growth of gastric cancer cells and to enhance sensitivity to Oxaliplatin through the PI3K/AKT signaling pathway, specific to gastric cancer cell lines. CST2 may serve as a tumor suppressor gene increasing sensitivity to Oxaliplatin in gastric cancer.

Reliability and Validity of the Chinese Version of the Revised Sociosexual Orientation Inventory.

The Revised Sociosexual Orientation Inventory (SOI-R) is a measurement tool for assessing an individual's willingness to engage in uncommitted sexual relations. Despite its widespread use in various contexts, no studies have validated the use of this instrument in China. Therefore, the current study aimed to assess the reliability and validity of an existing Chinese translation of the SOI-R. A total of 2,209 participants were recruited and randomly divided into two groups: exploratory factor analysis was conducted on one group and confirmatory factor analysis on the other, with 161 participants from the total sample recruited to assess the test-retest reliability. Criterion validity was measured by testing the correlations between sociosexuality and sexual desire, mate value, sexual attitudes, and personality traits. The results confirmed a three-factor structure (sociosexual behaviors, attitudes, and desire) for the SOI-R. Furthermore, the findings demonstrated good reliability (internal consistency and test-retest stability) and validity (criterion validity, convergent validity, and discriminant validity) of the SOI-R, supporting its suitability as an assessment tool for sociosexual orientation in China.

The nanobody targeting PD-L1 and CXCR4 counteracts pancreatic stellate cell-mediated tumour progression by disrupting tumour microenvironment.

Pancreatic ductal adenocarcinoma (PDAC) is the most lethal malignancy worldwide owing to its complex tumour microenvironment and dense physical barriers. Stromal-derived factor-1 (SDF-1), which is abundantly secreted by tumour stromal cells, plays a pivotal role in promoting PDAC growth and metastasis. In this study, we investigated the impact and molecular mechanisms of the anti-PD-L1&CXCR4 bispecific nanobody on the TME and their consequent interference with PDAC progression. We found that blocking the SDF-1/CXCR4 signalling pathway delayed the epithelial-mesenchymal transition in pancreatic cancer cells. Anti-PD-L1&CXCR4 bispecific nanobody effectively suppress the secretion of SDF-1 by pancreatic stellate cells and downregulate the expression of smooth muscle actin alpha(α-SMA), thereby preventing the activation of cancer-associated fibroblasts by downregulating the PI3K/AKT signaling pathway. This improves the pancreatic tumour microenvironment, favouring the infiltration of T cells into the tumour tissue. In conclusion, our results suggest that the anti-PD-L1&CXCR4 bispecific nanobody exerts an antitumor immune response by changing the pancreatic tumour microenvironment. Hence, the anti-PD-L1&CXCR4 bispecific nanobody is a potential candidate for pancreatic cancer treatment.

Molecular characterization, expression pattern and immunologic function of CD82a in large yellow croaker (Larimichthys crocea).

Visceral white spot disease (VWND) caused by Pseudomonas plecoglossicida poses a major threat to the sustainable development of large yellow croaker (Larimichthys crocea) aquaculture. Genome-wide association analysis (GWAS) and RNA-seq research indicated that LcCD82a play an important role in resistance to visceral white spot disease in L. crocea, but the molecular mechanism of LcCD82a response to P. plecoglossicida infection is still unclear. In this study, we cloned and validated the Open Reading Frame (ORF) sequence of LcCD82a and explored the expression profile of LcCD82a in various tissues of L.crocea. In addition, two different transcript variants (LcCD82a-L and LcCD82a-S) of LcCD82a were identified that exhibit alternative splicing patterns after P. plecoglossicida infection, which may be closely related to the immune regulation during pathogenetic process of VWND. In order to explore the function of LcCD82a, we purified the recombinant protein of LcCD82a-L and LcCD82a-S. The bacterial agglutination and apoptosis function analysis showed that LcCD82a may involve in extracellular bacterial recognition, agglutination, and at the same time participate in the process of antigen presentation and induction of cell apoptosis. Collectively, our studies demonstrate that LcCD82a plays a crucial role in regulating apoptosis and antimicrobial immunity.

An All-Protein Multisensory Highly Bionic Skin.

To achieve a highly realistic robot, closely mimicking human skin in terms of materials and functionality is essential. This paper presents an all-protein silk fibroin bionic skin (SFBS) that emulates both fast-adapting (FA) and slow-adapting (SA) receptors. The mechanically different silk film and hydrogel, which exhibited skin-like properties, such as stretchability (>140%), elasticity, low modulus (<10 kPa), biocompatibility, and degradability, were prepared through mesoscopic reconstruction engineering to mimic the epidermis and dermis. Our SFBS, incorporating SA and FA sensors, demonstrated a highly sensitive (1.083 kPa-1) static pressure sensing performance (in vitro and in vivo), showed the ability to sense high-frequency vibrations (50-400 Hz), could discriminate materials and sliding, and could even identify the fine morphological differences between objects. As proof of concept, an SFBS-integrated rehabilitation glove was synthesized, which could help stroke patients regain sensory feedback. In conclusion, this work provides a practical approach for developing skin equivalents, prostheses, and smart robots.

Celecoxib alleviates the DSS-induced ulcerative colitis in mice by enhancing intestinal barrier function, inhibiting ferroptosis and suppressing apoptosis.

INTRODUCTION: Ulcerative colitis (UC) is an inflammatory intestine disease characterized by dysfunction of the intestinal mucosal barrier, ferroptosis, and apoptosis. Previous researches suggest that celecoxib, a nonsteroidal anti-inflammatory drug, holds promise in alleviating inflammation in UC. Therefore, this study aims to investigate the effects and mechanisms of celecoxib in UC. METHODS: To identify ferroptosis-related drugs and genes associated with UC, we utilized the Gene Expression Omnibus (GEO), FerrDb databases, and DGIdb database. Subsequently, we established a 2.5% DSS (Dextran sulfate sodium)-induced colitis model in mice and treated them with 10 mg/kg of celecoxib to validate the bioinformatics results. We evaluated histological pathologies, inflammatory response, intestinal barrier function, ferroptosis markers, and apoptosis regulators. RESULTS: Celecoxib treatment significantly ameliorated DSS-induced UC in mice, as evidenced by the body weight change curve, colon length change curve, disease activity index (DAI) score, and histological index score. Celecoxib treatment reduced the level of pro-inflammatory factors and promoted the expressions of intestinal tight junction proteins such as Claudin-1 and Occludin, thereby restoring the integrity of the intestinal mucosal barrier. Furthermore, celecoxib treatment reversed the ferroptosis characteristics in DSS-induced mice by increasing glutathione (GSH), decreasing malondialdehyde (MDA), and increasing the expression of GPX-4 and xCT. Additionally, apoptosis was induced in mice with UC, as evidenced by increased Caspase3, BAD, P53, BAX, Caspase9 and Aifm1 production, and decreased expression of BCL-XL and BCL2. Celecoxib treatment significantly reversed the apoptotic changes in DSS-induced mice. CONCLUSION: Our findings suggest that celecoxib effectively treats DSS-induced UC in mice by inhibiting ferroptosis and apoptosis.

Celecoxib enhancing intestinal barrier functionCelecoxib alleviates ferroptosis in DSS-induces ulcerative colitisCelecoxib effectively alleviates apoptosis signaling pathway.

Tousled-like kinase 1 promotes gastric cancer progression by regulating the tumor growth factor-beta signaling pathway.

BACKGROUND: The role of Tousled-like kinase 1 (TLK1) in in gastric cancer (GC) remains unclear. AIM: To investigate the expression, biological function, and underlying mechanisms of TLK1 in GC. METHODS: We measured TLK1 protein expression levels and localized TLK1 in GC cells and tissues by western blot and immunofluorescence, respectively. We transfected various GC cells with lentiviruses to create TLK1 overexpression and knockdown lines and established the functional roles of TLK1 through in vitro colony formation, 5-ethynyl-2`-deoxyuridine, and Transwell assays as well as flow cytometry. We applied bioinformatics to elucidate the signaling pathways associated with TLK1. We performed in vivo validation of TLK1 functions by inducing subcutaneous xenograft tumors in nude mice. RESULTS: TLK1 was significantly upregulated in GC cells and tissues compared to their normal counterparts and was localized mainly to the nucleus. TLK1 knockdown significantly decreased colony formation, proliferation, invasion, and migration but increased apoptosis in GC cells. TLK1 overexpression had the opposite effects. Bioinformatics revealed, and subsequent experiments verified, that the tumor growth factor-beta signaling pathway was implicated in TLK1-mediated GC progression. The in vivo assays confirmed that TLK1 promotes tumorigenesis in GC. CONCLUSION: The findings of the present study indicated that TLK1 plays a crucial role in GC progression and is, therefore, promising as a therapeutic target against this disease.

Red Rice Seed Coat Targeting SPHK2 Ameliorated Alcoholic Liver Disease via Restored Intestinal Barrier and Improved Gut Microbiota in Mice.

Alcoholic liver disease (ALD), leading to the most common chronic liver diseases, is increasingly emerging as a global health problem, which is intensifying the need to develop novel treatments. Herein, our work aimed to estimate the therapeutic efficacy of red rice (Oryza sativa L.) seed coat on ALD and further uncover the underlying mechanisms. Red rice seed coat extract (RRA) was obtained with citric acid-ethanol and analyzed via a widely targeted components approach. The potential targets of RRA to ALD were predicted by bioinformatics analysis. Drunken behavior, histopathological examination, liver function, gut microbiota composition and intestinal barrier integrity were used to assess the effects of RRA (RRAH, 600 mg/kg·body weight; RRAL, 200 mg/kg·body weight) on ALD. Oxidative stress, inflammation, apoptosis associated factors and signaling pathways were measured by corresponding kits, Western blot and immunofluorescence staining. In ALD model mice, RRA treatment increased sphingosine kinase 2 (SPHK2) and sphingosine-1-phosphate (S1P) levels, improved gut microbiota composition, restored intestinal barrier, decreased lipopolysaccharide (LPS) levels in plasma and the liver, cut down Toll-like receptor 4 (TLR4)/Nuclear factor kappa B (NF-κB) pathways, alleviated liver pathological injury and oxidative stress, attenuated inflammation and apoptosis and enhanced liver function. To sum up, RRA targeting SPHK2 can ameliorate ALD by repairing intestinal barrier damage and reducing liver LPS level via the TLR4/NF-κB pathway and intestinal microbiota, revealing that red rice seed coat holds potential as a functional food for the prevention and treatment of ALD.

Oryza sativa L. Indica Seed Coat Ameliorated Concanavalin A-Induced Acute Hepatitis in Mice via MDM2/p53 and PKCα/MAPK1 Signaling Pathways.

Acute hepatitis (AH) is a common liver disease with an increasing number of patients each year, requiring the development of new treatments. Hence, our work aimed to evaluate the therapeutic effect of Oryza sativa L. indica (purple rice) seed coat on concanavalin A (ConA)-induced AH and further reveal its potential mechanisms. Purple rice seed coat extract (PRE) was extracted with hydrochloric acid ethanol and analyzed through a widely targeted components method. We evaluated the effects of PRE on AH through histopathological examination, liver function, gut microbiota composition, and the intestinal barrier. The potential targets of PRE on AH were predicted by bioinformatics. Western blotting, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining, and corresponding kits were used to investigate PRE effects on predicting targets and associated signaling pathways in AH mice. In AH model mice, PRE treatment increased transformed mouse 3T3 cell double minute 2 (MDM2) expression to inhibit apoptosis; it also markedly downregulated protein kinase C alpha (PKCα), prostaglandin-endoperoxide synthase 1 (PTGS1), and mitogen-activated protein kinase 1 (MAPK1) activity to alleviate inflammation. Thus, PRE treatment also recovered the intestinal barrier, decreased the lipopolysaccharide (LPS) levels of plasma and the liver, enhanced liver function, and improved the composition of intestinal microbiota. In general, PRE targeting MDM2, PKCα, MAPK1, and PTGS1 ameliorated ConA-induced AH by attenuating inflammation and apoptosis, restoring the intestinal barrier, enhancing the liver function, and improving the gut microbiota, which revealed that the purple rice seed coat might hold possibilities as a therapeutic option for AH.

Effective degradation of anthraquinones in Folium Sennae with Monascus fermentation for toxicity reduce and efficacy enhancement.

Folium Sennae are widely used around the world, mainly in purging and removal of endogenous active substances, such as anthraquinone and its derivatives. However, the potential toxicity of anthraquinones to the liver, kidney, and intestinal limits the application of Folium Sennae. In this study, we aimed at safe regulation of Folium Sennae to degrade anthraquinones, boosting medicinal properties and reducing toxicity and potency with Monascus fermentation. Monascus strains H1102 for Folium Sennae fermentation were selected as the initial strain which was capable of producing high yields of functional pigment and low yields of hazardous citrinin. The anthraquinone degradation rate reached 41.2%, with 212.2 U mL-1 of the pigment and approximately 0.038 mg L-1 of the citrinin under optimal fermentation conditions followed by response surface streamlining, which met the requirements of reducing toxicity, increasing efficiency of Monascus fermented Folium Sennae. Furthermore, the Monascus/Folium Sennae culture had no observable toxic effect on HK-2 and L-02 cells in vitro and further inhibited cell apoptosis and necrosis. Overall, our results showed that Monascus fermentation could provide an alternative strategy for toxicity reduction of herbal medicines as well as efficacy enhancement.

MGST1 Expression Is Associated with Poor Prognosis, Enhancing the Wnt/ß-Catenin Pathway via Regulating AKT and Inhibiting Ferroptosis in Gastric Cancer.

BACKGROUND: The role of microsomal glutathione S-transferase 1 (MGST1) underlying gastric cancer (GC) is unclear. The purpose of this research was to study the expression level and biological functions of MGST1 in GC cells. METHODS: Expression of MGST1 was detected by RT-qPCR, Western blot (WB), and immunohistochemical staining. MGST1 was knockdown and overexpression by short hairpin RNA lentivirus in GC cells. Cell proliferation was evaluated by the CCK-8 assay and EDU assay. The cell cycle was detected by flow cytometry. The TOP-Flash reporter assay was used to examine the activity of T-cell factor/lymphoid enhancer factor transcription based on ß-catenin. WB was performed to assess the protein levels involved in the cell signaling pathway and ferroptosis. The MAD assay and C11 BODIPY 581/591 lipid peroxidation probe assay were performed to determine the reactive oxygen species lipid level in GC cells. RESULTS: MGST1 expression was upregulated in GC and it was correlated with poor overall survival of GC patients. MGST1 knockdown significantly inhibited GC cell proliferation and cell cycle by regulating the AKT/GSK-3ß/ß-catenin axis. In addition, we found that MGST1 inhibits ferroptosis in GC cells. CONCLUSION: These findings suggested that MGST1 played a confirmed role in promoting GC development and serving as a possible independent prognostic factor for GC.

Increased ATF2 expression predicts poor prognosis and inhibits sorafenib-induced ferroptosis in gastric cancer.

Sorafenib, a tyrosine kinase inhibitor, has an important antitumor effect as a ferroptosis inducer in multiple cancers, including gastric cancer (GC). However, the status of sorafenib as a ferroptosis inducer has recently been questioned. There is very limited information about the relationship between ferroptosis and ATF2, and the role of ATF2 in sorafenib-induced ferroptosis has not been studied. In this study, we investigated the role and underlying molecular mechanisms of ATF2 in sorafenib-induced ferroptosis in GC. We found that ATF2 was significantly upregulated in GC tissues and predicted a poor clinical prognosis. Silencing ATF2 significantly inhibited the malignant phenotype of GC cells. In addition, we observed that ATF2 was activated during sorafenib-induced ferroptosis in GC cells. ATF2 knockdown promoted sorafenib-induced ferroptosis, while ATF2 overexpression showed the opposite results in GC cells. Using ChIP-Seq and RNA-Seq, we identified HSPH1 as a target of ATF2 and further validated it by ChIP‒qPCR analysis. HSPH1 can interact with SLC7A11 (cystine/glutamate transporter) and increase its protein stability. Importantly, knockdown of HSPH1 partly reversed the effects caused by ATF2 overexpression on sorafenib-induced ferroptosis in GC cells. In addition, the results from the tumor xenograft model showed that ATF2 knockdown can effectively enhance sorafenib sensitivity in vivo. Collectively, our study reveals a novel mechanism by which sorafenib induces ferroptosis in GC.

Fusion of Oligopeptide to the C Terminus of α-Glucuronidase from Thermotoga maritima Improves the Catalytic Efficiency for Hemicellulose Biotransformation.

Fusion protein combined the oligopeptide (HQAFFHA) with the C terminus of α-glucuronidase from Thermotoga maritima was produced in E. coli and purified for characterization and applications of glucuronic and glucaric acid production. The fusion protein with oligopeptide exhibited a 2.97-fold higher specific activity than individual protein. Their catalytic efficiency kcat/Km and kcat increased from 469.3 ± 2.6 s-1 (g mL-1)-1 and 62.4 ± 0.9 s-1 to 2209.5 ± 26.3 s-1 (g mL-1)-1 and 293.9 ± 4.9 s-1, respectively. Fusion protein had similar temperature and pH profiles to those without oligopeptide, but the thermal stability decreases and the pH stability shifts to alkaline. Using beech xylan hydrolysate as a substrate, the glucuronic acid yield of fusion enzyme increased by 9.94% compared with its parent at 65 °C pH 8.5 for 10 h, and can hydrolyze corn cob xylan with xylanase to obtain glucuronic acid, and can be combined with uronate dehydrogenase to obtain high-added value glucaric acid. Homologous modeling analysis revealed the factors contributing to the high catalytic efficiency of fusion enzyme. These results show that the peptide fusion strategy described here may be useful for improving the catalytic efficiency and stability of other industrial enzymes, and has great potential for producing high value-added products from agricultural waste.

Tumour inhibitory activity on pancreatic cancer by bispecific nanobody targeting PD-L1 and CXCR4.

BACKGROUND: Antibodies and derivative drugs targeting immune checkpoints have been approved for the treatment of several malignancies, but there are fewer responses in patients with pancreatic cancer. Here, we designed a nanobody molecule with bi-targeting on PD-L1 and CXCR4, as both targets are overexpressed in many cancer cells and play important roles in tumorigenesis. We characterized the biochemical and anti-tumour activities of the bispecific nanobodies in vitro and in vivo. METHODS: A nanobody molecule was designed and constructed. The nanobody sequences targeting PD-L1 and CXCR4 were linked by the (G4S)3 flexible peptide to construct the anti-PD-L1/CXCR4 bispecific nanobody. The bispecific nanobody was expressed in E. coli cells and purified by affinity chromatography. The purified nanobody was biochemically characterized by mass spectrometry, Western blotting and flow cytometry to confirm the molecule and its association with both PD-L1 and CXCR4. The biological function of the nanobody and its anti-tumour effects were examined by an in vitro tumour cell-killing assay and in vivo tumour inhibition in mouse xenograft models. RESULTS: A novel anti-PD-L1/CXCR4 bispecific nanobody was designed, constructed and characterized. The molecule specifically bound to two targets on the surface of human cancer cells and inhibited CXCL12-induced Jurkat cell migration. The bispecific nanobody increased the level of IFN-γ secreted by T-cell activation. The cytotoxicity of human peripheral blood mononuclear cells (hPBMCs) against pancreatic cancer cells was enhanced by the molecule in combination with IL-2. In a human pancreatic cancer xenograft model, the anti-PD-L1/CXCR4 nanobody markedly inhibited tumour growth and was superior to the combo-treatment by anti-PD-L1 nanobody and anti-CXCR4 nanobody or treatment with atezolizumab as a positive control. Immunofluorescence and immunohistochemical staining of xenograft tumours showed that the anti-tumour effects were associated with the inhibition of angiogenesis and the infiltration of immune cells. CONCLUSION: These results clearly revealed that the anti-PD-L1/CXCR4 bispecific nanobody exerted anti-tumour efficacy in vitro and inhibited tumour growth in vivo. This agent can be further developed as a therapeutic reagent to treat human pancreatic cancer by simultaneously blocking two critical targets.

Cell osteogenic bioactivity mediated precisely by varying scaled micro-pits on ordered micro/nano hierarchical structures of titanium.

Hierarchical surface structures with micro-nano scale play a crucial role in regulation of cell proliferation and osteogenic differentiation. It has been proven that cells are extremely sensitive to the nanoscaled structure and show multifarious phenotypes. Though a vital function of microstructure on osseointegration has been confirmed, the cell performances response to different microscaled structure is needed to be further dissected and in depth understood. In this work, the ordered micro-nano hierarchical structures with varying micro-scaled pits were precisely fabricated on titanium successfully by the combination of electrochemical, chemical etching and anodization as well. In vitro systematical assessments indicated that the micro-nano multilevel structures on titanium exhibited excellent cells adhesion and spreading ability, as well as steerable proliferation and osteogenic differentiation behaviors. It is shown that smaller micro-pits and lower roughness of the hierarchical structures enabled faster cell propagation. Despite cell growth was delayed on micro-nano titanium with relatively larger cell-match-size micro-pits and roughness, osteogenic-specific genes were significantly elevated. Furthermore, the alkaline phosphatase activity, collagen secretion and extracellular matrix mineralization of MC3T3-E1 on multi-scaled titanium were suppressed by a large margin after adding IWP-2 (an inhibitor of Wnt/ß-catenin signal pathway), indicating this pathway played a crucial part in cell osteogenic differentiation modulated by micro-nano structures.

Combined Non-Invasive Prediction and New Biomarkers of Oral and Fecal Microbiota in Patients With Gastric and Colorectal Cancer.

Background: There is no information on the commonality and specificity of oral and fecal microbiota in patients with gastric cancer (GC) and colorectal cancer (CRC). Methods: The high-throughput 16S rRNA gene V4 region sequencing was used to perform bioinformatics analysis of oral, fecal, and tissue microbiota in GC (76 subjects), CRC (53), and healthy controls (HC, 70). Furthermore, we determined the microbial characteristics of each part, constructed and verified three classifiers for GC and CRC, and evaluated curves of receiver operating characteristic and precision-recall with probability of disease. Results: Compared to HC, the microbial richness and diversity of GC and CRC decreased in oral cavity and increased in stool; additionally, these indexes in GC tissue were higher than those in CRC tissue. In GC and CRC patients, Haemophilus, Neisseria, Faecalibacterium, and Romboutsia were significantly reduced compared to the relative abundance value of oral or fecal bacterial genera in the HC group, while the Streptococcus, Gemella, Escherichia-Shigella, and Fusobacterium were significantly increased. The oral and tissue microbiota have similar and abundant shared bacterial networks. The single and combined microbial detection have good AUC values based on POD indices for predicting GC, CRC, and gastrointestinal (GI) cancers (GC and CRC). Conclusion: This study is the first to examine the characteristics of oral, fecal, and tumor microbiota in GC and CRC patients, and the similarities and differences in their microbial changes are reported. These oral or fecal bacteria (Haemophilus, Neisseria, Faecalibacterium, Romboutsia, Streptococcus, Gemella, Escherichia-Shigella, and Fusobacterium) may be involved in tumor evolution as potentially characteristic genera. In addition, both oral and fecal microbial detection may provide a solid theoretical foundation for the non-invasive prediction of these cancers.

Chinese Version of the Vestibular Disorders Activities of Daily Living Scale.

OBJECTIVES/HYPOTHESIS: To translate and cross-culturally adapt vestibular disorders activities of daily living (VADL) scale to Chinese population, and verify its psychometric characteristics. STUDY DESIGN: A methodology study to translate, validate, and verify the reliability of the VADL scale. METHODS: The translation of the VADL from English to Chinese was carried out in accordance with the recommendations proposed by the Process of Cross-Cultural Adaptation guideline. All 185 Subjects with chief complaints of dizziness or vertigo were continuously invited to the study from January 2021 to June 2021. Investigation using the Chinese version of VADL (VADL-C) was completed by all the participants. Complete data from all 124 participants were used for reliability and internal consistency analysis by using SPSS 22.0. RESULTS: Through careful and complete translation and adaptation, the VADL-C was successfully created. The content validity of the VADL-C was 0.887, the internal consistency was 0.951, and the test-retest reliability was 0.989. CONCLUSIONS: The VADL-C has an excellent internal consistency, test-retest reliability, and content validity. It will be a new tool to be used in China and for overseas Chinese speakers to explore the functional capacity of individuals with vestibular diseases and guide therapy planning, particularly in vestibular rehabilitation training program. Laryngoscope, 132:1446-1451, 2022.

Elevated expression of NFE2L3 promotes the development of gastric cancer through epithelial-mesenchymal transformation.

Gastric cancer (GC) is a malignant tumor with high mortality, but research on its molecular mechanisms remain limited. This study is the first to explore the biological role of nuclear factor NFE2L3 (nuclear factor, erythroid 2 like 3) in GC. We used Western blot and RT-qPCR to detect gene expression at the protein or mRNA level. Short hairpin RNA (shRNA) transfection was used to inhibit NFE2L3 expression. CCK-8 and colony formation assays were used to detect cell proliferation. Cell migration, invasion, cell cycle and apoptosis were detected by Transwell assays and flow cytometry. The results showed that NFE2L3 was highly expressed in gastric cancer tissues and promoted gastric cancer cell proliferation and metastasis. Inhibiting NFE2L3 expression blocks the cell cycle and increases the proportion of apoptotic cells, whereas NFE2L3 expression promotes the epithelial-mesenchymal transformation (EMT) process. In summary, NFE2L3 is highly expressed in gastric cancer and promotes gastric cancer cell proliferation and metastasis and the EMT process.

Erratum: Construction of a Competitive Endogenous RNA Network in Uterine Corpus Endometrial Carcinoma.

There was an error in Figure 4. The correct Figure 4 is provided below. The picture error would not affect the conclusion of the paper. Reference: Dong Ouyang, Ruyi Li, Yaxian Li, Xueqiong Zhu. Construction of a Competitive Endogenous RNA Network in Uterine Corpus Endometrial Carcinoma. Med Sci Monit 2019; 25:7998-8010. DOI: 10.12659/MSM.915798.

Long-Term Observation of the Quasi-3-Hour Large-Scale Traveling Ionospheric Disturbances by the Oblique-Incidence Ionosonde Network in North China.

The oblique-incidence ionosonde network in North China is a very unique system for regional ionospheric observation. It contains 5 transmitters and 20 receivers, and it has 99 ionospheric observation points between 22.40° N and 33.19° N geomagnetic latitudes. The data of the ionosonde network were used to investigate the statistical characteristics of the quasi-3-h large-scale traveling ionospheric disturbances (LSTIDs). From September 2009 to August 2011, 157 cases of the quiet-time LSTIDs were recorded; 110 cases traveled southward, 46 cases traveled southwestward and only 1 case traveled southeastward. The LSTIDs mainly appeared between 10:00 and 19:00 LT in the months from September to the following May. We compared the data of the Beijing, Mohe and Yakutsk digisondes and found that the LSTIDs are most likely to come from the northern auroral region. These LSTIDs may be induced by the atmospheric gravity waves (AGWs) and presented obvious seasonal and diurnal varying features, indicating that the thermospheric wind field has played an important role.