Analysis of multiple factors influencing the survival of patients with advanced gastric cancer.

OBJECTIVE: The aim of this study was to investigate the main factors influencing the survival of patients with advanced gastric cancer. METHODS: The clinicopathological data of 120 patients with advanced gastric cancer were analyzed retrospectively, and clinical and pathological data were collected. Tumor tissue staging and grading were re-evaluated, and 5-year overall survival was followed up. The classified data were described by percentages, and the continuous data were described by standard deviations or medians. Univariate analysis was performed using the χ2 test or rank-sum test, followed by Kaplan-Meier survival analysis to calculate the median survival time and 5-year cumulative survival. A multivariate Cox regression model was used to evaluate the independent risk factors affecting survival. The test level was α = 0.05. RESULTS: Patients were followed up for 0 to 60 months, the 5-year overall survival rate was 36.2%, and the median survival time was 53.0 ± 1.461 months. K-M and log-rank test results revealed that tumor location, degree of differentiation, depth of invasion, regional lymph node involvement, and postoperative tumor stage were correlated with a decreased 5-year survival rate (P < 0.05). A multivariate Cox risk regression model was used to analyze the degree of histological differentiation (HR = 1.441; 95% CI = 1.049-1.979; P = 0.024), regional lymph node (HR = 1.626; 95% CI = 1.160-2.279; P = 0.005), and pTNM stage (HR = 2.266; 95% CI = 1.335-3.847; P = 0.002), which are independent risk factors for poor survival. Tumor location (P = 0.191), invasion depth (P = 0.579) and tumor size (P = 0.324) were not found to be independent risk factors. CONCLUSION: The degree of tumor differentiation, regional lymph node metastasis and postoperative pathological stage were found to be independent risk factors for 5-year overall survival in patients with advanced gastric cancer. Standardized and reasonable lymph node dissection and accurate postoperative pathological staging were very important.

Gastric Ganglioneuroblastoma in an Elderly man: A Case Report and Literature Review.

Background. Ganglioneuroblastoma is a borderline tumor of sympathetic origin that is considered a childhood disease, with the majority of patients occurring in children less than five years old and few patients occurring in adults. There are no treatment guidelines for adult ganglioneuroblastoma. Here, we report a rare patient of adult gastric ganglioneuroblastoma that was completely resected by a laparoscopic approach. Case presentation. A 73-year-old man presented with dull pain in the upper abdomen along with abdominal distension for one month. Gastroscopy examination revealed chronic gastritis and submucosal tumors of the gastric antrum. Endoscopic ultrasonography showed a hypoechoic mass in the gastric antrum arising from the muscularis propria. An abdominal computed tomography scan revealed an irregular soft tissue mass in the gastric antrum with heterogeneous enhancement in the arterial phase. The mass was completely resected by laparoscopic surgery. Postoperative histopathology revealed that the mass contained differentiated neuroblasts, mature ganglion cells and ganglioneuroma components. The pathological diagnosis was ganglioneuroblastoma intermixed, and the patient was determined to be in stage I. The patient received no adjuvant chemotherapy or radiotherapy. At his two-year follow-up, the patient was doing well and showed no signs of recurrence. Conclusion. Despite the rarity of gastric ganglioneuroblastoma as a primary site of origin, it should be considered in the differential diagnosis of gastric masses in adults. Radical surgery is sufficient for the treatment of ganglioneuroblastoma intermixed, and long-term follow-up should be performed.

The Safety and Antiaging Effects of Nicotinamide Mononucleotide in Human Clinical Trials: an Update.

The importance of nicotinamide adenine dinucleotide (NAD+) in human physiology is well recognized. As the NAD+ concentration in human skin, blood, liver, muscle, and brain are thought to decrease with age, finding ways to increase NAD+ status could possibly influence the aging process and associated metabolic sequelae. Nicotinamide mononucleotide (NMN) is a precursor for NAD+ biosynthesis, and in vitro/in vivo studies have demonstrated that NMN supplementation increases NAD+ concentration and could mitigate aging-related disorders such as oxidative stress, DNA damage, neurodegeneration, and inflammatory responses. The promotion of NMN as an antiaging health supplement has gained popularity due to such findings; however, since most studies evaluating the effects of NMN have been conducted in cell or animal models, a concern remains regarding the safety and physiological effects of NMN supplementation in the human population. Nonetheless, a dozen human clinical trials with NMN supplementation are currently underway. This review summarizes the current progress of these trials and NMN/NAD+ biology to clarify the potential effects of NMN supplementation and to shed light on future study directions.

ULK1 Depletion Protects Mice from Diethylnitrosamine-Induced Hepatocarcinogenesis by Promoting Apoptosis and Inhibiting Autophagy.

Purpose: The uncoordinated-51 like kinase 1 (ULK1) is an important serine/threonine protein kinase involved in autophagy, especially for the initiation stage. Previous studies have shown that ULK1 could be used as a prognostic marker in predicting poor progression-free survival and a therapeutic target for hepatocellular carcinoma (HCC) when treated with sorafenib; however, its role during hepatocarcinogenesis remains to be elucidated. Methods: CCK8 and colony formation assay were used to detect cell growth ability. Western blotting was performed to determine expression level of protein. Data from public database were downloaded to analyze expression of ULK1 at mRNA level and predict survival time. RNA-seq was conducted to reveal disturbed gene profile orchestrated by ULK1 depletion. A diethylnitrosamine (DEN)-induced HCC mice model was used to uncover the role of ULK1 in hepatocarcinogenesis. Results: ULK1 was up-regulated in liver cancer tissues and cell lines, and knockdown of ULK1 promoted apoptosis and suppressed proliferation of liver cancer cells. In in vivo experiments, Ulk1 depletion attenuated starvation-induced autophagy in mice liver, reduced diethylnitrosamine (DEN)-induced hepatic tumor number and size, and prevented tumor progression. Further, RNA-seq analysis revealed a close relationship between Ulk1 and immunity with significant changes in gene sets enriched in the interleukin and interferon pathways. Conclusion: ULK1 deficiency prevented hepatocarcinogenesis and inhibited hepatic tumor growth, and might be a molecular target for the prevention and treatment of HCC.

Toxicogenomics scoring system: TGSS, a novel integrated risk assessment model for chemical carcinogenicity prediction.

BACKGROUND: Given the increasing exposure of humans to environmental chemicals and the limitations of conventional toxicity test, there is an urgent need to develop next-generation risk assessment methods. OBJECTIVES: This study aims to establish a novel computational system named Toxicogenomics Scoring System (TGSS) to predict the carcinogenicity of chemicals coupling chemical-gene interactions with multiple cancer transcriptomic datasets. METHODS: Chemical-related gene signatures were derived from chemical-gene interaction data from the Comparative Toxicogenomics Database (CTD). For each cancer type in TCGA, genes were ranked by their effects on tumorigenesis, which is based on the differential expression between tumor and normal samples. Next, we developed carcinogenicity scores (C-scores) using pre-ranked GSEA to quantify the correlation between chemical-related gene signatures and ranked gene lists. Then we established TGSS by systematically evaluating the C-scores in multiple chemical-tumor pairs. Furthermore, we examined the performance of our approach by ROC curves or prognostic analyses in TCGA and multiple independent cancer cohorts. RESULTS: Forty-six environmental chemicals were finally included in the study. C-score was calculated for each chemical-tumor pair. The C-scores of IARC Group 3 chemicals were significantly lower than those of chemicals in Group 1 (P-value = 0.02) and Group 2 (P-values = 7.49 ×10-5). ROC curves analysis indicated that C-score could distinguish "high-risk chemicals" from the other compounds (AUC = 0.67) with a specificity and sensitivity of 0.86 and 0.57. The results of survival analysis were also in line with the assessed carcinogenicity in TGSS for the chemicals in Group 1. Finally, consistent results were further validated in independent cancer cohorts. CONCLUSION: TGSS highlighted the great potential of integrating chemical-gene interactions with gene-cancer relationships to predict the carcinogenic risk of chemicals, which would be valuable for systems toxicology.

TCN1 Deficiency Inhibits the Malignancy of Colorectal Cancer Cells by Regulating the ITGB4 Pathway.

Background/Aims: This study aimed to investigate the biological function and regulatory mechanism of TCN1 in colorectal cancer (CRC). Methods: We studied the biological function of TCN1 by performing gain-of-function and loss-of-function analyses in HCT116 cell lines; examined the effects of TCN1 on the proliferation, apoptosis, and invasion of CRC cells; and determined potential molecular mechanisms using HCT116 and SW480 CRC lines and mouse xenotransplantation models. Tumor xenograft and colonization assays were performed to detect the tumorigenicity and metastatic foci of cells in vivo. Results: TCN1 knockdown attenuated CRC cell proliferation and invasion and promoted cell apoptosis. Overexpression of TCN1 yielded the opposite effects. In addition, TCN1-knockdown HCT116 cells failed to form metastatic foci in the peritoneum after intravenous injection. Molecular mechanism analyses showed that TCN1 interacted with integrin subunit ß4 (ITGB4) to positively regulate the expression of ITGB4. TCN1 knockdown promoted the degradation of ITGB4 and increased the instability of ITGB4 and filamin A. Downregulation of ITGB4 at the protein level resulted in the disassociation of the ITGB4/plectin complex, leading to cytoskeletal damage. Conclusions: TCN1 might play an oncogenic role in CRC by regulating the ITGB4 signaling pathway.

Comparing bariatric surgery and medical therapy for obese adolescents with type 2 diabetes.

BACKGROUND: Mounting evidence in recent years has demonstrated that the number of obese adolescents has continued to rise. Obese adolescents are more likely to be diagnosed with type 2 diabetes, which causes additional harm. This study aimed to compare the clinical outcomes of bariatric surgery and medical treatment. METHODS: We conducted a multicenter, nonrandomized, retrospective study on 202 obese adolescents with type 2 diabetes who received surgery or medical treatment in three hospitals from 2017 to 2019. We analyzed the effects of surgery and medical treatment in terms of weight loss, glycemic control and the remission of type 2 diabetes. Propensity score matching was conducted to balance the confounding factors. RESULTS: Among the 202 adolescents, 109 adolescents underwent surgery, and the remaining 93 adolescents received nonsurgical treatment. Both in the entire cohort and in the propensity-score matching cohort, the mean body mass index (BMI) and total weight in the surgery group notably decreased. Similarly, the effect of surgery on glycemic control (with respect to HBG, HbA1c, HOMA-IR) was superior to that of medical treatment. In the surgery group, the remission rate of diabetes was 76.1% in the entire cohort and 80.5% in the matched group, which was significantly higher than that in the control group (6.5% and 5.7%, respectively). In addition, LRYGB had better effects on weight loss and glycemic control than LSG. CONCLUSION: Bariatric surgery is more effective in the control of weight loss and type 2 diabetes than medical treatment. The effects between different types of bariatric surgeries remain to be further investigated, and longer follow-up times are needed.

Quench-Induced Surface Engineering Boosts Alkaline Freshwater and Seawater Oxygen Evolution Reaction of Porous NiCo2 O4 Nanowires.

The electrochemical oxygen evolution reaction (OER) by efficient catalysts is a crucial step for the conversion of renewable energy into hydrogen fuel, in which surface/near-surface engineering has been recognized as an effective strategy for enhancing the intrinsic activities of the OER electrocatalysts. Herein, a facile quenching approach is demonstrated that can simultaneously enable the required surface metal doping and vacancy generation in reconfiguring the desired surface of the NiCo2 O4 catalyst, giving rise to greatly enhanced OER activities in both alkaline freshwater and seawater electrolytes. As a result, the quenched-engineered NiCo2 O4 nanowire electrode achieves a current density of 10 mA cm-2 at a low overpotential of 258 mV in 1 m KOH electrolyte, showing the remarkable catalytic performance towards OER. More impressively, the same electrode also displays extraordinary activity in an alkaline seawater environment and only needs 293 mV to reach 10 mA cm-2 . Density functional theory (DFT) calculations reveal the strong electronic synergies among the metal cations in the quench-derived catalyst, where the metal doping regulates the electronic structure, thereby yielding near-optimal adsorption energies for OER intermediates and giving rise to superior activity. This study provides a new quenching method to obtain high-performance transition metal oxide catalysts for freshwater/seawater electrocatalysis.

Clinicopathological Analysis and Prognostic Assessment of TCN1 in Patients with Gastric Cancer.

BACKGROUND: Stomach cancer is the fourth most common type of cancer worldwide. TCN1 mainly encodes the vitamin B12 transporter, transcobalamin. TCN1 is a marker of gastrointestinal tumor progression, but the impact of TCN1 on survival is unclear. MATERIAL/METHODS: Gastrointestinal tumor records were reviewed and analyzed, clinicopathological data were summarized, immunohistochemical detection of TCN1 was performed again, and the protein expression in tumor tissue, non-tumor tissue, and lymph nodes was semi-quantitatively analyzed. Patients were followed up for 5 years to determine the 5-year survival rates. RESULTS: The strong immune reactivity of the TCN1 protein was significantly correlated with tumor invasion depth, regional lymph nodes, and a tumor diameter of >5 cm (Z = -2.531 and P = .016; Z = 3.785 and P < .001; Z = 2.541 and P = .049). Kaplan-Meier survival analysis showed that the total survival time of patients in the low-expression TCN1 group was significantly longer than that in the high-expression TCN1 group (P = .001; Table 2 and Figure 5). The mean survival time of all patients was 49.774 months (95% CI: 47.871-51.676; Table 4) and the 5-year overall survival rates were 73.3, 50.8, and 34.0%, respectively. Multivariate analysis revealed that regional lymph nodes (HR = 1.253; 95% CI: 1.031-1.747, P = .012), TCN1 immune expression status (HR = 2.707; 95% CI: 1.068-1.886, P = .016), and pTNM staging (HR = 2.293; 95% CI: 1.583-3.321; P = .001) were independent risk factors for poor survival. CONCLUSION: The high expression of TCN1 in gastric tumor tissues was found to be associated with the clinicopathological factors of patients, and the high expression of TCN1 was shown to indicate a poor clinical prognosis.

Complete chloroplast genome of Hordeum brevisubulatum: Genome organization, synonymous codon usage, phylogenetic relationships, and comparative structure analysis.

BACKGROUND: Hordeum brevisubulatum, known as fine perennial forage, is used for soil salinity improvement in northern China. Chloroplast (cp) genome is an ideal model for assessing its genome evolution and the phylogenetic relationships. We de novo sequenced and analyzed the cp genome of H. brevisubulatum, providing a fundamental reference for further studies in genetics and molecular breeding. RESULTS: The cp genome of H. brevisubulatum was 137,155 bp in length with a typical quadripartite structure. A total of 130 functional genes were annotated and the gene of accD was lost in the process of evolution. Among all the annotated genes, 16 different genes harbored introns and the genes of ycf3 and rps12 contained two introns. Parity rule 2 (PR2) plot analysis showed that majority of genes had a bias toward T over A in the coding strand in all five Hordeum species, and a slight G over C in the other four Hordeum species except for H. bogdanil. Additionally, 52 dispersed repeat sequences and 182 simple sequence repeats were identified. Moreover, some unique SSRs of each species could be used as molecular markers for further study. Compared to the other four Hordeum species, H. brevisubulatum was most closely related to H. bogdanii and its cp genome was relatively conserved. Moreover, inverted repeat regions (IRa and IRb) were less divergent than other parts and coding regions were relatively conserved compared to non-coding regions. Main divergence was presented at the SSC/IR border. CONCLUSIONS: This research comprehensively describes the architecture of the H. brevisubulatum cp genome and improves our understanding of its cp biology and genetic diversity, which will facilitate biological discoveries and cp genome engineering.

Huanglianjiedu Decoction as an effective treatment for oral squamous cell carcinoma based on network pharmacology and experimental validation.

BACKGROUND: Oral squamous cell carcinoma (OSCC) is one of malignant tumors in oral and maxillofacial region with high fatality. Huanglianjiedu Decoction (HLJDD) is a well-known traditional Chinese medicinal prescription, which consists of Coptis chinensis Franch, Scutellaria baicalensis Georgi, Phellodendron amurense Rupr and Gardenia jasminoides J.Ellis. Some clinical studies showed HLJDD had good effectiveness on OSCC, but the mechanism is unclear. METHODS: In this study, potential components of HLJDD and putative targets were screened by Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). Combining with potential targets of OSCC searched from Therapeutic Target Database (TTD) and Online Mendelian Inheritance in Man (OMIM), we drew protein-protein interaction (PPI) network by Cytoscape v3.2.0 software. After topological analysis we got core targets and further did Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Then we did the in vitro experiments to verify the major biological processes (cell cycle, apoptosis and proliferation) and signaling pathways (mitogen-activated protein kinase (MAPK), nuclear factor-kappa B (NF-κB), protein kinase B (AKT)) on OSCC cell lines, SCC-25 and CAL-27. RESULTS: The potential component targets number of Coptis chinensis Franch, Scutellaria baicalensis Georgi, Phellodendron amurense Rupr and Gardenia jasminoides J.Ellis were 39, 93, 81and 88, respectively. Then we got 52 core targets which enriched in cell cycle, apoptosis, proliferation, MAPK activation etc. and obtained TOP30 pathways. On SCC-25 and CAL-27, HLJDD suppressed cell proliferation, induced late apoptosis and inhibited cell invasion and migration which were consistent with the results from network pharmacology analysis. Additionally, in cell cycle, we confirmed HLJDD inhibited G1 phase and arrested in S phase to reduce cell proliferation on SCC-25. In signaling pathways, HLJDD inhibited the phosphorylation of extracellular regulatory protein kinase 1/2 (ERK1/2) and NF-κB p65 (S468) on SCC-25 and CAL-27. CONCLUSIONS: HLJDD played a potential therapeutic role on OSCC via inhibiting p-ERK1/2 and p-NF-κB p65 (S468).

Aspartame and sucralose extend the lifespan and improve the health status of C. elegans.

Aspartame (ASP) and sucralose (SUC) are non-nutritive sweeteners which are widely consumed worldwide. They are considered safe for human consumption, but their effects on certain physiological aspects, such as the lifespan or health status, of the organism have not yet been studied in depth and only limited data are available in the literature. The objectives of this study were to evaluate the effects of ASP and SUC on the lifespan and health indexes using Caenorhabditis elegans (C. elegans) as a model system. Interestingly, it was shown that at the concentrations tested, ASP (0.03-3 mg mL-1) showed an increasing trend of the mean lifespan of C. elegans, with a significant increase of 27.6% compared to the control at 3 mg mL-1. Similarly, SUC (ranging from 0.03 to 10 mg mL-1) also significantly increased the mean lifespan by 20.3% and 22.3% at 0.03 and 0.3 mg mL-1, respectively. However, 10 mg mL-1 SUC had a negative effect on the lifespan, though it did not reach a statistically significant level. In addition, ASP and SUC decreased lipofuscin accumulation and transiently improved motility, indicating improved health status. Nonetheless, they had different effects on food intake and intestinal fat deposition (IFD) at different intervals of time. Taken together, our findings revealed that ASP and SUC can prolong the lifespan and improve the health status of C. elegans.

Low-dose mono(2-ethylhexyl) phthalate promotes ovarian cancer development through PPARα-dependent PI3K/Akt/NF-κB pathway.

The plasticizer di(2-ethylhexyl) phthalate (DEHP) and its hydrolysate mono(2-ethylhexyl) phthalate (MEHP) are major toxicants from plastics, but their association with hormone-dependent cancers has been controversial. We treated the human ovarian cancer cell lines SKOV3 and A2780 with low concentrations of DEHP/MEHP, and found that although no significant effect on cell proliferation was observed, ovarian cancer cell migration, invasion, and epithelial-mesenchymal transition (EMT) were promoted by submicromolar MEHP but not DEHP. Next, ovarian cancer patient data from The Cancer Genome Atlas (TCGA) were obtained and subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) supported enrichment and Kaplan-Meier survival analyses, which identified PI3K/Akt pathway as a pivotal signaling pathway in ovarian cancer. We found that 500 nM MEHP treatment significantly increased PIK3CA expression, which could be reversed by the knockdown of peroxisome proliferator-activated receptor alpha (PPARα). Silencing PIK3CA significantly suppressed the MEHP-induced migration, invasion and EMT. In addition, we validated that MEHP treatment promoted phosphorylation of Akt and degradation of IκB-α, thereby activating NF-κB and enhancing NF-κB nuclear translocation. In nude mice, MEHP exposure significantly promoted the metastasis of ovarian cancer xenografts, which could be suppressed by the treatment of PPARα inhibitor GW6471. Our findings showed that low-dose MEHP promoted ovarian cancer progression through activating PI3K/Akt/NF-κB pathway, in a PPARα-dependent manner.

Boosting supercapacitive performance of flexible carbon via surface engineering.

The relatively low specific capacitance of flexible carbons hinders their practical application for fabricating high-performance flexible supercapacitors. In this work, a surface engineering method is proposed to boost the supercapacitive performance of the flexible carbon. In this method, a flexible carbon was fabricated from carbon felt via co-activation with potassium argininate and potassium hydroxide (KOH) as activators, and the resulting material is abbreviated as AKCF. Unlike traditional KOH activation processes, the addition of potassium argininate can produce a micro-graphitized carbon layer to be the outer layer of AKCF fibers for achieving better electronic transfer. Due to the improved conductivity and lower charge transfer resistance endowed by a thin micro-graphitized carbon layer, the capacitance of the AKCF-0.1 (0.1 M arginine was used) electrode obtained by the co-activation process is elevated to a 1.8-fold higher value of 403 C·g-1 (2583 mC·cm-2) relative to the AKCF-0 (0 M arginine was used) electrode prepared by KOH activation alone (222 C·g-1 or 1369 mC·cm-2). Moreover, this AKCF-0.1 electrode also displays satisfactory rate capability (66% capacitance retention after a 20-fold current increase) and highly stable cycling performance (no capacitance decline after 20,000 cycles). In addition, the asymmetric supercapacitors constructed with this AKCF-0.1 electrode as the flexible negative electrode expresses high energy densities of 68.4 Wh·kg-1 and 0.139 mWh·cm-2 in aqueous and gel electrolytes, respectively.

Photosynthesis, fluorescence, and nutrition of Zhonglan No. 2, a new alfalfa cultivar.

BACKGROUND: The years after planting play an important role in the above-ground biomass and nutritive value of alfalfa. Zhonglan No. 2 (Medicago sativa L. cv. Zhonglan No. 2) is a new breeding alfalfa cultivar characterized by high drought tolerance and high yield. To determine the optimum time for utilization of Zhonglan No. 2, we examined growth traits, chlorophyll content, photosynthetic and fluorescence parameters, and composition and nutritive values at the late vegetative and early flowering stages of the first stubble in the second, third, fourth, sixth, and eleventh years after planting. RESULTS: In general, the height and leaf area decreased with increasing number of years after planting. At the late vegetative stage, the fourth-year alfalfa exhibited higher stomatal conductance (Gs) and intercellular CO2 concentration (Ci), and better water use efficiency, and at the early flowering stage, the fourth-year alfalfa had the highest (P < 0.05) leaf net photosynthetic rate (Pn) and carboxylation efficiency (CE). Total digestible nutrients did not differ among years, but, in the early flowering stage, crude protein content decreased with years (P < 0.05). Malondialdehyde (MDA) content and total antioxidant capacity did not differ among years after planting, suggesting aging did not impose oxidative stress on this alfalfa cultivar. CONCLUSIONS: Based on height, chlorophyll content, crude protein (CP) content, and photosynthetic and fluorescence parameters, the fourth year after planting, at the early flowering stage, was the best for using Zhonglan No. 2. © 2021 Society of Chemical Industry.

Gentle fabrication of colorful superhydrophobic bamboo based on metal-organic framework.

The efficient use of abundant renewable bamboo as high value-added decoration and building materials is of great significance for mitigating carbon dioxide emissions and maintaining sustainable development. The key challenge is to explore efficient and gentle methods to improve the undesirable surface properties of bamboo. Herein, a colorful and superhydrophobic bamboo is gently fabricated by a facile in-situ growth and conversion method based on metal-organic framework (for constructing micro-nano composite structures) and subsequent coating of sodium laurate (for reducing surface energy) at room temperature. The resulting sodium laurate-coated cobalt-nickel double hydroxide layer (CoNi-DH-La) is demonstrated as an efficient superhydrophobic layer to exhibit excellent chemical and mechanical stability. Impressively, the as-obtained CoNi-DH-La-coated bamboo sheet (BS-CoNi-DH-La) shows positive performances in terms of mildew resistance, flame retardancy, and self-cleaning. More importantly, this gentle method can endow bamboo with multiple unfading colors by changing the type of inorganic salts during the preparation process and display good potential for large-scale production.

CD31 and D2-40 Contribute to Peritoneal Metastasis of Colorectal Cancer by Promoting Epithelial-Mesenchymal Transition.

BACKGROUND/AIMS: Colorectal cancer (CRC) patients often exhibit peritoneal metastasis, which negatively impacts their prognosis. CD31 and D2-40 have recently been suggested to be predictors of breast cancer prognosis, but their role in colorectal peritoneal metastasis (CRPM) remains unknown. METHODS: The expression profiles of CD31 and D2-40 were analyzed in CRC patients with or without CRPM and in CRC cell lines with increasing metastatic potential. Overexpression and short hairpin RNA knockdown assays were performed in CRC cells, and the effects of these alterations on epithelial-mesenchymal transition (EMT) in vitro, growth of xenograft tumors in vivo, and peritoneal metastasis potential in a mouse model of CRPM were examined. RESULTS: The expressions of CD31 and D2-40 were upregulated in CRC tumor tissues and was elevated further in tumor tissues from patients with CRPM. CD31 and D2-40 expression levels exhibited increasing trends parallel to the EMT potential of CRC cells. CD31 and D2-40 are essential for CRC cell EMT in vitro as well as for xenograft tumor growth and peritoneal metastasis in vivo. CONCLUSIONS: CD31 and D2-40 contribute to CRPM by promoting EMT and may serve as prognostic markers and therapeutic targets for CRC, particularly in patients with peritoneal metastasis.

Rational design of cobalt-nickel double hydroxides for flexible asymmetric supercapacitor with improved electrochemical performance.

Rational design of micro-nano morphology and suitable crystalline structure are highly desired for metal hydroxides to achieve overall high-performance in the advanced electrodes for flexible supercapacitors. Herein, a novel wisteria flower-like microstructure of cobalt-nickel double hydroxide (CoNi-DH) is successfully constructed on carbon cloth (CC) using an in-situ hydrolysis-induced exchange process between hydroxide ions and organic ligands of the Co-MOF in four different kinds of solutions containing Ni2+. The as-prepared wisteria flower-like microstructure grown on CC shows vertically aligned arrays with high specific area and abundant active sites, which not only guarantee the CoNi-DH active materials to be thoroughly exposed in the electrolyte, resulting in highly effective pseudocapacitive energy storage, but also are beneficial to rapid and reversible redox kinetics and thus give rise to high-rate capability. In addition, compared to Ni(NO3)2, NiCl2, and Ni(CH3COO)2 solutions, the Ni2SO4 solution is found to facilitate the formation of the most regular morphology and the largest interlayer spacing on (003) plane of the layered nickel hydroxide phase in the resultant CoNi-DH. As a result, the optimal CoNi-DH-S@CC (CoNi-DH prepared in Ni2SO4) serves as an advanced electrode to show high-rate capability (only 13% Cs decay after a 15-fold current elevation) and a superior specific capacity (Cs) of 929.4 C g-1, which remarkably exceeds those of CoNi-DH-N (823.1 C g-1, in Ni(NO3)2), CoNi-DH-Cl (798.4 C g-1, in NiCl2), CoNi-DH-C (803.8 C g-1, in Ni(CH3COO)2), and other similar metal hydroxides. Moreover, with this CoNi-DH-S electrode as the positive electrode, the as-prepared asymmetric supercapacitor (ASC) delivers an impressive capacity of 204.8 C g-1, a superior energy density of 42.5 Wh kg-1, and satisfactory cycle life (81.5% reservation after 7500 cycles). As a proof-of-concept application, a quasi-solid-state ASC is further successfully fabricated based on the CoNi-DH-S electrode to exhibit encouraging application potential.

Aluminum-doping-based method for the improvement of the cycle life of cobalt-nickel hydroxides for nickel-zinc batteries.

The unsatisfactory cycle life of nickel-based cathodes hinders the widespread commercial usage of nickel-zinc (Ni-Zn) batteries. The most frequently used methods to improve the cycle life of Ni-based cathodes are usually complicated and/or involve using organic solvents and high energy consumption. A facile process based on the hydrolysis-induced exchange of the cobalt-based metal-organic framework (Co-MOF) was developed to prepare aluminum (Al)-doped cobalt-nickel double hydroxides (Al-CoNiDH) on a carbon cloth (CC). The entire synthesis process is highly efficient, energy-saving, and has a low negative impact on the environment. Compared to undoped cobalt-nickel double hydroxide (Al-CoNiDH-0%), the as-prepared Al-CoNiDH as the electrode material displays a remarkably improved cycling stability because the Al-doping successfully depresses the transition in the crystal phase and microstructure during the long cycling. Benefiting from the improved performance of the optimal Al-CoNiDH electrode (Al-CoNiDH-5% electrode), the as-constructed aqueous Ni-Zn battery with Al-CoNiDH-5% as the cathode (Al-CoNiDH-5%//Zn) displays more than 14% improvement in the cycle life relative to the Al-CoNiDH-0%//Zn battery. Moreover, this Al-CoNiDH-5%//Zn battery achieves a high specific capacity (264 mAh g-1), good rate capability (72.4% retention at a 30-fold higher current), high electrochemical energy conversion efficiency, superior fast-charging ability, and strong capability of reversible switching between fast charging and slow charging. Furthermore, the as-assembled quasi-solid-state Al-CoNiDH-5%//Zn battery exhibits a decent electrochemical performance and satisfactory flexibility.

TRPM2 expression levels are associated with histological grading in patients with tongue squamous cell carcinoma.

Tongue squamous cell carcinoma (TSCC) accounts for a large proportion of cases of head and neck cancer. Transient receptor potential melastatin 2 (TRPM2) is a non­selective cation channel sensitive to oxidative stress. High TRPM2 expression has been reported in various types of cancer, including neuroblastoma, glioblastoma, non­small cell lung cancer and breast cancer. However, whether expression levels of TRPM2 are associated with aggressive clinical features in TSCC remains unclear. A total of 26 clinical sample tissues with TSCC were collected in the present study. The expression levels of the TRPM2 channel were determined by immunohistochemistry, western blot, and qPCR analysis. The content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) were measured to reveal oxidative stress levels in TSCC tissues with different degrees of differentiation. The protein expression levels of caspase­8, Bcl­xL, Bax, caspase­9, cleaved caspase­9, caspase­3, cleaved caspase­3, poly [ADP­ribose] polymerase (PARP) and cleaved PARP were detected by western blot analysis. Analysis of the tissue specimens from 26 patients with TSCC showed that TRPM2 was not upregulated in all specimens. Notably, the expression levels of TRPM2 were associated with the histological grading of different tissues. The specimens with low TRPM2 expression were significantly associated with moderate or poor differentiation (P=0.003), and exhibited increased lipid peroxidation level and decreased SOD activity. Furthermore, the altered expression of pro­ and anti­apoptotic proteins indicated a significant upregulation of apoptosis in TSCC tissues with low TRPM2 expression. These results suggested that low TRPM2 expression in TSCC may inhibit the ability of cells to adapt to or resist the oxidative stress, resulting in increased susceptibility to apoptosis. Therefore, the oxidative stress­sensitive TRPM2 channel may serve as a potent biomarker, and the present study provides insights into the underlying mechanisms of tumor cell differentiation.