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Under the principle of similar compatibility, researchers have developed various polarity extractants corresponding to a class of chemicals. Separating different polarities chemicals with one extractant effectively has become a novel research trend in separation science. Given the complexity of environmental sample matrices and the significant differences in polarity and solubility of various compounds, the introduction of hydrophilic groups to hydrophobic material skeletons can lead to sorbents with hydrophilic-lipophilic balance (HLB) property and thus improve their extraction performance for substances with different polarities. In this work, a hypercrosslinked polymer (HCP Pz-TPB ), designated as HLB, was synthesized by incorporating polar pyrazine and nonpolar triphenylbenzene molecules within each other. Subsequently, a core-shell magnetic composite material was obtained by encapsulating magnetic Fe 3 O 4 nanoparticles in HCP Pz-TPB . The material was applied as an adsorbent for magnetic solid phase extraction (MSPE) and combined with a high-performance liquid chromatography-photodiode array detector (HPLC-PDA) to enrich, separate, and detect seven polar contaminants in environmental water samples. The proposed approach, Fe 3 O 4 @SiO 2 @HCP Pz-TPB -MSPE-HPLC-PDA, is characterized by its outstanding high sensitivity, low detection limits, wide linear range, and good reproducibility. The method demonstrated satisfactory linearity in the range of 0.05-2 μg mL -1 with R 2 values between 0.9969 and 0.9997; the limits of detection (LOD) were observed to be within the range of 0.0019-0.016 μg L -1 , and limits of quantification (LOQ) was observed to be within the range of 0.0064-0.054 μg L -1 range with good precision. The recoveries of the different contaminants in the environmental samples ranged from 83.61 to 116.46% (RSD≤10.56, n = 5). The new hydrophilic-lipophilic balance extractant is highly efficient, sensitive, and precise for extracting different polar pollutants. The findings demonstrate that the Fe 3 O 4 @SiO 2 @HCP Pz-TPB display a remarkable affinity for multiple targets, driven by complex interactions including multi-stackings and hydrogen bonding as a sorbent. The synthesized Fe 3 O 4 @SiO 2 @HCP Pz-TPB may be employed in diverse applications, including extraction, removal, and determination of diverse trace multi-target analytes in complex media., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

There is a growing body of evidence suggesting that dietary polysaccharides play a crucial role in preventing metabolic syndrome (MetS) through their interaction with gut microbes. Tea (Camellia sinensis L.) flower polysacchride (TFPS) is a novel functional compound known for its diverse beneficial effects in both vivo and vitro. To further investigate the effects of TFPS on MetS and gut microbiota, and the possible association between gut microbiota and their activities, this study was carried out on mice that were fed a high-fat diet (HFD) and given oral TFPS at a dose of 400 and 800 mg/kg·body weight (BW)/d, respectively. TFPS treatment significantly mitigated HFD-induced MetS, evidenced by reductions in body weight, fat accumulation, plasma levels of total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), and pro-inflammatory cytokines tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and IL-1β, along with an increase in plasma IL-10 levels. Furthermore, TFPS induced alterations in the diversity and composition of HFD-induced gut microbiota. Specifically, TFPS influenced the relative abundance of 11 genera, including Lactobacillus and Lactococcus, which showed strong correlations with metabolic improvements and likely contributed to the amelioration of MetS. In conclusion, TFPS exhibits promising prebiotic properties in preventing MetS and regulating gut microbiota., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Aims: This study aimed to examine the therapeutic effects and response mechanisms of 4-OI in Alzheimer's disease (AD)., Methods: In this study, network pharmacology was employed to analyze potential targets for AD drug therapy. Immunofluorescence and quantitative reverse transcription polymerase chain reaction (qRT-PCR) techniques were utilized to detect inflammatory phenotypes in a 4-OI-resistant mouse microglia cell line (BV2). We conducted four classical behavioral experiments, namely the open field test, new object recognition test, Y maze test, and Morris water maze, to assess the emotional state and cognitive level of APPswe/PS1dE9 (referred to as APP/PS1) mice after 4-OI treatment. Hematoxylin and eosin (HE) staining, along with immunofluorescence staining, were performed to detect amyloid (Aβ) deposition in mouse brain tissue. To explore the potential molecular mechanisms regulating the effects of 4-OI treatment, we performed RNA-SEQ and transcription factor prediction analyses. Additionally, mouse BV2 cells underwent Western blotting analysis to elucidate potential molecular mechanisms underlying the observed effects., Results: We discovered that 4-OI exerts an inhibitory effect on neuroinflammation by promoting autophagy. This effect is attributed to the activation of the AMPK/mTOR/ULK1 pathway, achieved through enhanced phosphorylation of AMPK and ULK1, coupled with a reduction in mTOR phosphorylation. Furthermore, 4-OI significantly enhances neuronal recovery in the hippocampus and diminishes Aβ plaque deposition in APP/PS1 mice, improved anxiety in mice, and ultimately led to improved cognitive function., Conclusions: Overall, the results of this study demonstrated that 4-OI improved cognitive deficits in AD mice, confirming the therapeutic effect of 4-OI on AD., Competing Interests: Declaration of competing interest The authors declare that there are no known competing financial interests or personal relationships that could have appeared to influence this work., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Ulcerative colitis (UC) is a complicated inflammatory disease with a continually growing incidence. In this study, resistant starch was obtained from purple sweet potato (PSPRS) by the enzymatic isolation method. Then, the structural properties of PSPRS and its protective function in dextran sulfate sodium (DSS)-induced colitis were investigated. The structural characterization results revealed that the crystallinity of PSPRS changed from C A -type to A-type, and the lamellar structure was totally destroyed during enzymatic hydrolysis. Compared to DSS-induced colitis mice, PSPRS administration significantly improved the pathological phenotype and colon inflammation in a dose-dependent manner. ELISA results indicated that DSS-induced colitis mice administered with PSPRS showed higher IL-10 and IgA levels but lower TNF-α, IL-1β, and IL-6 levels. Meanwhile, high doses (300 mg/kg) of PSPRS significantly increased the production of acetate, propionate, and butyrate. 16S rDNA high-throughput sequencing results showed that the ratio of Firmicutes to Bacteroidetes and the potential probiotic bacteria levels were notably increased in the PSPRS treatment group, such as Lactobacillus , Alloprevotella , Lachnospiraceae &#95;NK4A136&#95;group, and Bifidobacterium . Simultaneously, harmful bacteria like Bacteroides , Staphylococcus , and Akkermansia were significantly inhibited by the administration of a high dose of PSPRS ( p < 0.05). Therefore, PSPRS has the potential to be a functional food for promoting intestinal health and alleviating UC.

Aims: To determine the availability and the potential molecular mechanisms underlying the therapeutic effect of omaveloxolone (RTA408) on Alzheimer's Disease (AD)., Materials and Methods: This study employed network pharmacology to assess the feasibility of drug treatment of AD. To determine the cognitive status and emotional state of APPswe/PS1dE9 (APP/PS1) mice after the RTA408 treatment, three classical behavioral experiments (water maze, Y-maze, and open field test) were conducted. Immunofluorescence and immunohistochemical staining were utilized to evaluate hippocampal neuronal status and amyloid (Aβ) deposition in mice. RNA-seq and transcription factor prediction analyses were performed to explore the potential molecular mechanisms regulating the therapeutic effects of RTA408. Molecular docking was employed to predict the direct drug targets. To validate these molecular mechanisms, quantitative reverse transcription PCR (qRT-PCR), Western blotting, and immunofluorescence analyses were performed in two instrumental cell lines, i.e., mouse hippocampal neuronal cells (HT22) and microglia (BV2)., Results: RTA408 was revealed with the capability to reduce Aβ plaque deposition and to restore damaged neurons in the hippocampal region of APP/PS1 mice, ultimately leading to an improvement in cognitive function. This beneficial effect was achieved by balancing the STAT3 pathway. Specifically, RTA408 facilitated the activations of both STAT3/OXR1 and NRF2/ARE axes, thereby enhancing the compromised resistance in neurons to oxidative stress. RTA408 inhibited the NFκB/IL6/STAT3 pathway, effectively countering the neuroinflammation triggered by microglial activation., Conclusion: RTA408 is revealed with promising potential in the treatment of AD based on preclinical data., Competing Interests: Declaration of competing interest The authors declare that there are no conflicts of interest., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Glucose 6 phosphatase dehydrogenase (G6PD) is a key regulator of the pentose phosphate pathway (PPP). However, the exact role of G6PD in gastrointestinal cancers remains unclear. The purpose of this study is to explore the correlation of G6PD with clinical features, pathological stages, diagnosis and prognosis of gastrointestinal cancers, as well as uncover possible mechanisms of G6PD on mutations, immunity and signaling pathways., Methods: G6PD mRNA expression data were downloaded from TCGA and GEO databases. Protein expression was examined by the HPA database. The correlation of G6PD expression with clinical and pathological characteristics was explored. The pROC package in R language was used to evaluate the diagnostic value of G6PD expression in gastrointestinal cancers. We accessed the correlation of disease-free survival (DFS) with G6PD online by Kaplan-Meier plotter. Univariate Cox regression and stepwise multiple Cox regression analysis were performed to determine the association between G6PD and patient's overall survival. In addition, genomic alterations, mutation profiles, immune infiltration, drug sensitivity and enrichment analysis related with G6PD were visualized., Results: After a pan-cancerous genomic analysis, we found that G6PD expression was the highest in African American esophageal carcinoma (ESCA) patients ( P <0.05). G6PD was correlated with age, weight, disease stage, lymph node metastasis and pathological grade. Notably, G6PD showed an excellent predictive diagnosis ability for liver hepatocellular carcinoma (LIHC) (AUC=0.949, 95% CI=0.925-0.973, P <0.001). G6PD can improve the DFS of esophageal adenocarcinoma (EAC) and pancreatic adenocarcinoma (PAAD) patients ( P <0.05). Both Univariate Cox regression and stepwise multiple Cox regression analysis in R language determined that G6PD expression was closely related with LIHC ( P <0.001). G6PD was found to have a high mutation rate in colon adenocarcinoma and ESCA and gene amplification in ESCA, Cholangiocarcinoma, PAAD and LIHC. Copy number of G6PD was missing in LIHC. G6PD was also related to mutation of TP53 ( P <0.05). Particularly, it was positively correlated with CD276 in all gastrointestinal cancers and negatively with HERV-H LTR-associating 2 in ESCA and stomach adenocarcinoma. The abnormal expression of G6PD was related to the increase of CD4+ Th2 subsets and the decrease of CD4+ (non-regulatory) of T cells. G6PD was sensitive to FK866, Phenformin, AICAR etc., while resistant to RO-3306, CGP-082996, TGX221 etc. G6PD was found to closely interact with TALDO1, GAPDH and TP53. G6PD related biological processes included aging, nutritional response and daunorubicin metabolism, and related pathways included PPP, cytochrome P450 metabolism of exogenous substances and glutathione metabolism., Conclusion: G6PD is highly expressed in gastrointestinal cancers. It is a carcinogenic indicator related to prognosis and can be used as a potential diagnostic marker of gastrointestinal cancers, so as to provide new strategy for cancer treatment., Competing Interests: None., (AJTR Copyright © 2023.)

Background: Alzheimer's disease (AD) is a progressive, neurodegenerative disorder with insidious onset. Some scholars believe that there is a close relationship between pyroptosis and AD. However, studies with evidence supporting this relationship are lacking., Materials and Methods: The microarray data of AD were retrieved from the Gene Expression Omnibus (GEO) database with the datasets merged using the R package inSilicoMerging. R software package Limma was used to perform the differential expression analysis to identify the differentially expressed genes (DEGs). We further performed the enrichment analyses of the DEGs based on Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) databases to identify the metabolic pathways with a significant difference. The Gene Set Enrichment Analysis (GSEA) was applied to identify the significant pathways. The protein-protein interaction (PPI) network was constructed based on the STRING database with the hub genes identified. Quantitative real-time PCR (qRT-PCR) analyses based on HT22 cells were performed to validate the findings based on the microarray analysis. Gene expression correlation heatmaps were generated to evaluate the relationships among the genes., Results: A new dataset was derived by merging 4 microarray datasets in the hippocampus of AD patients in the GEO database. Differential gene expression analysis yielded a volcano plot of a total of 20 DEGs (14 up-regulated and 6 down-regulated). GO analysis revealed a group of GO terms with a significant difference, e.g., cytoplasmic vesicle membrane, vesicle membrane, and monocyte chemotaxis. KEGG analysis detected the metabolic pathways with a significant difference, e.g., Rheumatoid arthritis and Fluid shear stress and atherosclerosis. The results of the Gene Set Enrichment Analysis of the microarray data showed that gene set ALZHEIMER&#95;DISEASE and the gene set PYROPTOSIS were both up-regulated. PPI network showed that pyroptosis-related genes were divided into two groups. In the Aβ-induced HT22 cell model, three genes (i.e., BAX, IL18, and CYCS) were revealed with significant differences. Gene expression correlation heatmaps revealed strong correlations between pyroptotic genes and AD-related genes., Conclusion: The pyroptosis-related genes BAX, IL18, and CYCS were significantly different between AD patients and normal controls., (© 2023. The Author(s).)

Background: Metastasis was the major cause of the high mortality in ovarian cancer. Although some mechanisms of metastasis in ovarian cancer were proposed, few have been targeted in the clinical practice. In the study, we aimed to identify novel genes contributing to metastasis and poor clinical outcome in ovarian cancer from bioinformatics databases., Methods: Studies collecting matched primary tumors and metastases from ovarian cancer patients were searched in the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were screened by software R language. Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis for the DEGs were implemented by Metascape. Venn diagram was plotted to present overlapping DEGs. The associations between the overlapping DEGs and prognosis were tested by Cox proportional hazard regression model using a cohort of ovarian cancer patients from the TCGA database. Genes affecting patients' outcomes significantly were served as hub genes. The mechanisms of the hub genes in promoting ovarian cancer metastasis were then predicted by R software., Results: Two gene expression profiles (GSE30587 and GSE73168) met the inclusion criteria and were finally analyzed. A total of 259 genes were significantly differentially expressed in GSE30587, whereas 712 genes were in GSE73168. In GSE30587, DEGs were mainly involved in extracellular matrix (ECM) organization; For GSE73168, most of DEGs showed ion trans-membrane transport activity. There were 9 overlapping genes between the two datasets (RUNX2, FABP4, CLDN20, SVEP1, FAM169A, PGM5, ZFHX4, DCN and TAS2R50). ZFHX4 was proved to be an independent adverse prognostic factor for ovarian cancer patients (HR = 1.44, 95%CI: 1.13-1.83, p = 0.003). Mechanistically, ZFHX4 was positively significantly correlated with epithelial-mesenchymal transition (EMT) markers (r = 0.54, p = 2.59 × 10 -29 ) and ECM-related genes (r = 0.52, p = 2.86 × 10 -27 )., Conclusions: ZFHX4 might promote metastasis in ovarian cancer by regulating EMT and reprogramming ECM. For clinical applications, ZFHX4 was expected to be a prognostic biomarker for ovarian cancer metastasis., (© 2022. The Author(s).)

Carboxymethyl chitosan (CMCS) is a useful polysaccharide with potential applications in food, cosmetic and biomedical industries. Nonetheless, CMCS is unfavorable for maintaining intestinal flora balance. In this study, gallic acid (GA) was grafted with CMCS through ascorbic acid/hydrogen peroxide initiated graft copolymerization reaction, producing GA grafted CMCS (GA-g-CMCS). The digestive and fermentative behavior of CMCS and GA-g-CMCS were investigated by using in vitro simulated gastrointestinal digestion and colonic fermentation models. Results showed that the average molecular weight (M w ) of CMCS gradually decreased during saliva-gastro-intestinal digestion, changing from original sheet-like morphology to porous and rod-like fragments. However, the M w and morphology of GA-g-CMCS were almost unchanged under saliva-gastro-intestinal digestion. Meanwhile, the grafted GA moiety was not released from GA-g-CMCS during saliva-gastro-intestinal digestion. As compared with CMCS fermentation, GA-g-CMCS fermentation significantly suppressed the relative abundance of Escherichia-Shigella, Paeniclostridium, Parabacteroides, Lachnoclostridium, Clostridium&#95;sensu&#95;stricto&#95;1, UBA1819 and Butyricimonas, while facilitated the relative abundance of Enterobacter, Enterococcus, Fusobacterium and Lachnospira. In addition, GA-g-CMCS fermentation significantly enhanced the production of short-chain fatty acids. These findings suggested that the digestive stability and prebiotic effect of CMCS were improved by grafting with GA., (Copyright © 2022 Elsevier B.V. All rights reserved.)

Background: Studies have suggested that many down-regulated miRNAs identified in the brain tissue or serum of Alzheimer's disease (AD) patients were involved in the formation of senile plaques and neurofibrillary tangles. Specifically, our previous study revealed that microRNA-22-3p (miR-22-3p) was significantly down-regulated in AD patients. However, the molecular mechanism underlying the down-regulation of miR-22-3p has not been comprehensively investigated., Methods: The ameliorating effect of miR-22-3p on apoptosis of the Aβ-treated HT22 cells was detected by TUNEL staining, flow cytometry, and western blotting. The cognition of mice with stereotaxic injection of agomir or antagomir of miR-22-3p was assessed by Morris water maze test. Pathological changes in the mouse hippocampus were analyzed using hematoxylin and eosin (HE) staining, Nissl staining, and immunohistochemistry. Proteomics analysis was performed to identify the targets of miR-22-3p, which were further validated using dual-luciferase reporter analysis and western blotting analysis., Results: The miR-22-3p played an important role in ameliorating apoptosis in the Aβ-treated HT22 cells. Increased levels of miR-22-3p in the mouse hippocampus improved the cognition in mice. Although the miR-22-3p did not cause the decrease of neuronal loss in the hippocampus, it reduced the Aβ deposition. Proteomics analysis revealed Sox9 protein as the target of miR-22-3p, which was verified by the luciferase reporter experiments., Conclusion: Our study showed that miR-22-3p could improve apoptosis and reduce Aβ deposition by acting on Sox9 through the NF-κB signaling pathway to improve the cognition in AD mice. We concluded that miR-22-3p ameliorated AD by targeting Sox9 through the NF-κB signaling pathway in the hippocampus., (© 2022. The Author(s).)

It is still uncertain whether the consumption of Lachnum sp. polysaccharides (LEP) alleviates colorectal cancer (CRC) through the gut microbiota. In this study, our efforts are focused on the influence of LEP on CRC, intestinal barrier and inflammation, and fecal microbiota and the metabolites, in azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced CRC mice. Results showed that LEP inhibited CRC mouse colon shortening and weight loss, decreased tumor incidence, restored intestinal barrier integrity, and reduced excessive inflammation. LEP consumption significantly altered microbiota overall structure and community, with reduced pernicious bacteria (such as Parabacteroides, Escherichia&#95;Shigella, Desulfovibrio and Helicobacter), and increased beneficial bacterium (such as Alistipes, Alloprevotella and Ruminiclostridium). Fecal-metabolome profile indicated that a total of 43 metabolites were clearly changed, with 10 down-regulated and 33 up-regulated metabolites. In addition, short-chain fatty acids (SCFAs), including acetic acid, propionic acid and n-butyric acid, were significantly increased after LEP administration. Moreover, a strong correlation between the fluctuant gut microbiota and metabolites was found. These findings provided not only deeper insights into the responsibility of LEP for CRC alleviation, and but also the potential of LEP as a promising candidate for CRC prevention and treatment., (Copyright © 2022. Published by Elsevier B.V.)

The Omicron variant of SARS-CoV-2 infected many vaccinated and convalescent individuals 1-3 . Despite the reduced protection from infection, individuals who received three doses of an mRNA vaccine were highly protected from more serious consequences of infection 4 . Here we examine the memory B cell repertoire in a longitudinal cohort of individuals receiving three mRNA vaccine doses 5,6 . We find that the third dose is accompanied by an increase in, and evolution of, receptor-binding domain (RBD)-specific memory B cells. The increase is due to expansion of memory B cell clones that were present after the second dose as well as the emergence of new clones. The antibodies encoded by these cells showed significantly increased potency and breadth when compared with antibodies obtained after the second dose. Notably, the increase in potency was especially evident among newly developing clones of memory cells, which differed from persisting clones in targeting more conserved regions of the RBD. Overall, more than 50% of the analysed neutralizing antibodies in the memory compartment after the third mRNA vaccine dose neutralized the Omicron variant. Thus, individuals receiving three doses of an mRNA vaccine have a diverse memory B cell repertoire that can respond rapidly and produce antibodies capable of clearing even diversified variants such as Omicron. These data help to explain why a third dose of a vaccine that was not specifically designed to protect against variants is effective against variant-induced serious disease., (© 2022. The Author(s).)

Protocatechualdehyde (PCA), an important component of Salvia miltiorrhiza , has many activities, such as anti-inflammatory and antisepsis activities. However, the role of PCA in osteoclasts is not clear. We used RAW264.7 cells (a mouse leukemic monocyte/macrophage cell line) and bone marrow macrophages (BMMs) to probe the role of PCA in osteoclasts and the underlying mechanism. The effects of PCA on cell activity were evaluated with CCK-8 assays. TRAP staining detected mature osteoclasts. Corning Osteo Assay Surface plates were used to examine absorption. The levels of RNA and protein were analyzed, respectively, using RT-PCR and Western blotting. PCA (5  μ g/ml) was not toxic to the two cell types but reduced the formation of osteoclasts and bone absorption. Furthermore, PCA restrained the expression of mRNAs encoding proteins associated with osteoclasts and reduced the phosphorylation of proteins in important signaling pathways. The results indicate that PCA inhibits osteoclast differentiation by suppressing NF- κ B and MAPK activity., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2021 Yunyun Qu et al.)

Therapeutic strategies that targeting tumor-associated macrophages (TAMs) reprogramming play a crucial role in ameliorating the immunosuppressive tumor microenvironment and boosting anti-tumor immune responses. In this study, we demonstrated that Lachnum polysaccharide (LEP) could work as an immunomodulator to reset TAMs from pro-tumor M2 to anti-tumor M1 phenotype. Mechanistically, LEP promoted Th1 polarization and the secretion of IFN-γ, which played a key role in M1 phenotype polarization. In parallel, LEP might directly activate M1 macrophages via TLR4 mediated NF-κB signaling pathway. Moreover, LEP also resulted in the accumulation of anti-tumor immune cells and decreased the infiltration of immunosuppressive cells such as myeloid-derived suppressor cells (MDSCs) and Treg cells, thereby potentiating anti-tumor immunity. In summary, these results revealed a novel mechanism of the anti-tumor effect of LEP and provided a potential new avenue targeting TAMs and cancer immunotherapy., Competing Interests: Declaration of Competing Interest The authors declare that there are no conflicts of interest., (Copyright © 2019. Published by Elsevier B.V.)

Carboxymethyl chitosan (CMC) is widely used in food and medicine as a biodegradable polymer. However, its effects on inflammation profile and colon health are not well investigated. In the present study, CMC was given to mice to evaluate its possible effects on body weight, blood glucose level, inflammation factors, intestinal permeability and colon microbiota. Results showed that blood glucose level of CMC treated mice was relatively higher than control ones. Glucose tolerance test revealed that CMC treated mice presented higher peak glucose level and lower lag level. CMC treatment increased serum LDL-c level, decreased serum HDL-c and IL-10 level in the fat tissue. Moreover, CMC treatment downregulated the expression of tight junction protein, occludin and ZO-1, in colon as evaluated by Western blot. Colon microbiota analysis demonstrated that CMC treatment significantly decreased the OTUs and relative species abundance. The level of Enterobacteriaceae, Lachnospiraceae and several other bacteria were much higher in the colon content of CMC treated mice. The results collectively suggest that CMC treatment induces disturbance of glucose and fat metabolism, affects the inflammation profile, perturbs colon microbiota balance., (Copyright © 2019. Published by Elsevier Taiwan LLC.)

Differentiated embryonic chondrocyte expressed gene 2 (DEC2; BHLHE41/Sharp1) is a helix-loop-helix (bHLH) transcription factor, and its deregulation has been observed in several tumors. However, this gene's effects on tumor progression are controversial, and its roles in gastric cancer (GC) remain unclear. In the present study, we found that DEC2 expression level is lower in GC tissues compared with adjacent non-tumor tissues, and negatively correlated with tumor invasion, lymph node metastasis, TNM stage, and poor survival of GC patients. Positive clinical correlations of DEC2 with EMT regulator, E-cadherin, were also observed in the tissue sections. Overexpression of DEC2 inhibits cell proliferation and EMT in vitro, as well as tumor growth and metastasis in vivo. DEC2 expression also induces cell apoptosis. Furthermore, the anti-metastatic effect of DEC2 was mediated by inhibiting ERK/NF-κB/EMT axis. After treatment with ERK1/2 chemical inhibitor (U0126), DEC2's inhibitory effect on ERK/NF-κB/EMT was further decreased. Collectively, these data helped to characterize DEC2, which might be a potential molecular target for diagnostic and therapeutic approaches for GC.

The aim of the present study was to investigate the effects of PS-341 on vascular remodeling in an experimental rat model of high blood flow-induced pulmonary arterial hypertension (PAH), as well as to elucidate its mechanisms of action. We established the PAH model by a surgical method that implanted a left-to-right shunt. Three days post-surgery, the animals were randomly assigned to 3 groups (n=15 in each group): sham-operated (control), shunt (model) and PS-341 (treated) groups. Eight weeks post-surgery, hemodynamic parameters were significantly improved in the PS-341 group compared with the shunt group (P<0.05). Immunohistochemical analysis indicated that the expression levels of ubiquitin and nuclear factor-κB (NF-κB) p65 were significantly higher in the shunt group compared with the sham-operated group (P<0.05). Semi-quantitative western blot analysis further confirmed that the levels of ubiquitin and NF-κB p65 were decreased, while those of IκB-α (an inhibitor of NF-κB) were significantly increased in the PS-341 group compared with the shunt group (P<0.05). In conclusion, PS-341 attenuates high blood flow-induced pulmonary artery remodeling in rats via inhibition of the NF-κB pathway.

An influenza virus, A/canine/Shandong/JT01/2009, has been isolated from a dog exhibiting classical flu signs in China. HAI and NAI assays subtyped A/canine/Shandong/JT01/2009 as a H5N2 like virus. Phylogenetic reconstructions indicated strong relationships with viruses from various hosts and dispersed geographic locations. These analyses indicate A/canine/Shandong/JT01/2009 is a novel virus generated by complex reassortment of the viral segments., (Copyright © 2011 Elsevier B.V. All rights reserved.)

Hydroxyl radical molecular beam was generated by DC pulsed high voltage discharge. The rotational resolution excitation fluorescence spectra of the OH A 2sigma+ -X 2pi (1, 0) band were observed by using second harmonious output of a nanosecond dye laser (around 282 nm). The rotational temperature of the (1, 0) band was determined to be (30 +/- 1) K based on the analysis of the intensity distribution of the OH spectra. Moreover, the fluorescence decay curves of the (1, 1) band and the (0, 0) band and were obtained and the fluorescence lifetimes of A 2sigma+ (v' = 1) state and the X 2pi (v" = 0) state were fitted to be (637 +/- 16) and (675 +/- 13) ns, respectively.

In this paper, a new concept 'seed geography' was provided, and its definition, research contents, and scientific issues were put forward. Seed geography is a newly developed interdisciplinary science from plant geography, seed ecology, and phytosociology, which studies the geographic variation patterns of seed biological traits as well as their relationships with environmental factors from macroscopic to microscopic, and the seed formation, development, and change trends. The main research contents would include geography of seed mass, geography of seed chemical components, geography of seed morphology, geography of seed cell biological characteristics, geography of seed physiological characteristics, geography of seed genetic characteristics, and geography of flower and fruit. To explore the scientific issues in seed geography would help us to better understand the long-term adaptation and evolution of seed characteristics to natural environments.