Metallic MoS2 (i.e., 1T‐MoS2) is considered as the most promising precious‐metal‐free electrocatalyst with outstanding hydrogen evolution reaction (HER) performance in acidic media comparable to Pt. However, sluggish kinematics of HER in alkaline media and its inability for the oxygen evolution reaction (OER), hamper its development as bifunctional catalysts. The instability of 1T‐MoS2 further impedes its applications for scaling up, calling an urgent need for simple synthesis to produce stable 1T‐MoS2. In this work, the challenge of 1T‐MoS2 synthesis is first addressed using a direct one‐step hydrothermal method by adopting ascorbic acid. 1T‐MoS2 with flower‐like morphology is obtained, and transition metals (Ni, Co, Fe) are simultaneously doped into 1T‐MoS2. Ni‐1T‐MoS2 achieves an enhanced bifunctional catalytic activity for both HER and OER in alkaline media, where the key role of Ni doping as single atom is proved to be essential for boosting HER/OER activity. Finally, a Ni‐1T‐MoS2||Ni‐1T‐MoS2 electrolyzer is fabricated, reaching a current density of 10 mA cm−2 at an applied cell voltage of only 1.54 V for overall water splitting.

Several members of the sirtuin family (SIRT1-7), which are a highly conserved family of NAD+-dependent enzymes, play an important role in tumor formation. Recent studies indicate that SIRT4 acts as a tumor suppressor by regulating glutamine metabolism. In the present study, we investigated the expression and activity of SIRT4 in colorectal cancer. Using a tissue microarray of 89 colorectal cancer cases, we found that SIRT4 was significantly downregulated in colorectal cancer tissues compared with that noted in the corresponding normal tissue (P<0.001). Lower SIRT4 levels were associated with worse pathological differentiation (P=0.031) and poorer post-operative overall survival rate (P=0.041). We found that SIRT4 overexpression inhibited the proliferation of colorectal cancer cells in vitro and in vivo. SIRT4 inhibited the glutamine metabolism of colorectal cancer cells and synergistically with glycolysis inhibitors induced cell death. SIRT4 also increased the sensitivity of colorectal cancer cells to chemotherapeutic drug 5-fluorouracil by inhibiting the cell cycle. Together, these results highlight the prognostic value of SIRT4 in colorectal cancer and the potential application of SIRT4 in colorectal cancer treatment.

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The family is a group of plant-specific transcription factors. genes encode proteins harboring bHLH structure, which is implicated in DNA binding and protein-protein interactions and known as the TCP domain. TCP genes play important roles in plant development and have been evolutionarily and functionally elaborated in various plants, however, no overall phylogenetic analysis or expression profiling of genes in has been reported. In the present study, a systematic analysis of molecular evolution and functional prediction of family genes in maize (. L.) has been conducted. We performed a genome-wide survey of genes in maize, revealing the gene structure, chromosomal location and phylogenetic relationship of family members. Microsynteny between grass species and tissue-specific expression profiles were also investigated. In total, 29 genes were identified in the maize genome, unevenly distributed on the 10 maize chromosomes. Additionally, genes were categorized into nine classes based on phylogeny and purifying selection may largely be responsible for maintaining the functions of maize genes. What's more, microsynteny analysis suggested that genes have been conserved during evolution. Finally, expression analysis revealed that most genes are expressed in the stem and ear, which suggests that genes influence stem and ear growth. This result is consistent with the previous finding that maize genes represses the growth of axillary organs and enables the formation of female inflorescences. Altogether, this study presents a thorough overview of family in maize and provides a new perspective on the evolution of this gene family. The results also indicate that family genes may be involved in development stage in plant growing conditions. Additionally, our results will be useful for further functional analysis of the gene family in maize.

Several members of the sirtuin (SIRT) family, a highly conserved family of NAD+-dependent enzymes, have been shown to play a critical role in both promoting and/or suppressing tumorigenesis. In this study, recent progress in the field concerning SIRT4 and cancer was reviewed, and the relationship between SIRT4 and tumors was investigated. Subsequently, we evaluated the role of SIRT4 with oncogenic or tumor-suppressive activity in cancer, which may provide insight in identifying the underlying mechanism of action of SIRT4 in cancer. Finally, we explored the potential of SIRT4 as a therapeutic target in cancer therapy.

Retinoblastoma binding protein 6 (RBBP6) plays an important role in chaperone-mediated ubiquitination and interacts with TP53 in carcinogenesis. However, the clinicopathologic significance of RBBP6 expression in colon cancer is unknown; in particular, the prognostic value of RBBP6 combined with TP53 expression has not been explored. Therefore, quantitative real-time PCR and western blot analyses were performed to detect RBBP6 expression in colon cancer tissues. RBBP6 and TP53 expression were assessed by immunohistochemistry in a tissue microarray format, in which the primary colon cancer tissue was paired with noncancerous tissue. Tissue specimens were obtained from 203 patients. We found that RBBP6 was overexpressed in colon tumorous tissues and was significantly associated with clinical stage, depth of tumor invasion, lymph node metastasis (LNM), distant metastasis, and histologic grade. Further studies revealed that a corresponding correlation between RBBP6 overexpression and mutant TP53 was evident in colon cancer (r = 0.450; P<0.001). RBBP6 expression was an independent prognostic factor for overall survival (OS) and disease free survival (DFS). Interestingly, patients with tumors that had both RBBP6 overexpression and mutant TP53 protein accumulation relapsed and died within a significantly short period after surgery (P<0.001). Multivariate analysis showed that patients with LNM and patients with both RBBP6- and TP53-positive tumors had extremely poor OS (HR 6.75; 95% CI 2.63–17.35; P<0.001) and DFS (HR 8.08; 95% CI 2.80–23.30; P<0.001). These clinical findings indicate that the assessment of both RBBP6 and mutant TP53 expression will be helpful in predicting colon cancer prognosis.

The objective of this research is to use metabolomic techniques to discover and validate plasma metabolite biomarkers for the diagnosis of early-stage non-small cell lung cancer (NSCLC). The study included plasma samples from 156 patients with biopsy-confirmed NSCLC along with age and gender-matched plasma samples from 60 healthy controls. A fully quantitative targeted mass spectrometry (MS) analysis (targeting 138 metabolites) was performed on all samples. The sample set was split into a discovery set and validation set. Metabolite concentration data, clinical data, and smoking history were used to determine optimal sets of biomarkers and optimal regression models for identifying different stages of NSCLC using the discovery sets. The same biomarkers and regression models were used and assessed on the validation models. Univariate and multivariate statistical analysis identified β-hydroxybutyric acid, LysoPC 20:3, PC ae C40:6, citric acid, and fumaric acid as being significantly different between healthy controls and stage I/II NSCLC. Robust predictive models with areas under the curve (AUC) > 0.9 were developed and validated using these metabolites and other, easily measured clinical data for detecting different stages of NSCLC. This study successfully identified and validated a simple, high-performing, metabolite-based test for detecting early stage (I/II) NSCLC patients in plasma. While promising, further validation on larger and more diverse cohorts is still required. Tissue Bank, which is the site of the Respiratory Health Network Tissue Bank of the Fonds de la Recherché du Quebec-Sante in Quebec, Canada. Dates of sample collection range from 2005 to 2017. Frozen (−80 • C) aliquots of 200-400 µL of plasma were assembled and shipped to The Metabolomic Innovation Centre (TMIC) at the University of Alberta, Canada for quantitative metabolomic analysis. The plasma samples were collected from 156 patients with biopsy-proven and biopsy-graded NSCLC and 60 healthy controls with comparable age and gender profiles. Healthy controls consisted of both smokers and non-smokers. The cancer samples had detailed data on cancer stage, lung cancer histology, age, weight, height, body mass index, smoking status (never/former/current), smoking history (cig/day and period of smoking in years), sex, survival history, medical condition history, personal history of cancer, lung disease status, treatment, tumor size (in mm), tumor grading, details of positive nodules, as well as data collected on each cancer patient's transthoracic needle biopsy, transbronchial biopsy, endobronchial biopsy, bronchoalveolar lavage, bronchial brushing, bronchial aspiration, endobronchial ultrasound, transesophageal echocardiography, bone scintigraphy, abdominal ultrasound, abdominal CT scan, thoracic CT scan, cerebral CT scan, thoracic X-ray, mediastinoscopy, thoracic MRI, cerebral MRI, and PET scan. Healthy controls had data on age, weight, height, body mass index, smoking status (never/former/current), smoking history (cig/day and period of smoking...

Background SIRT4, a protein localized in the mitochondria, is one of the least characteristic members of the sirtuin family. It is known that SIRT4 has deacetylase activity and plays a role in energy metabolism, but little is known about its possible role in carcinogenesis. Recently, several studies have suggested that SIRT4 may function as either a tumor oncogene or a tumor suppressor gene. However, its relationship with thyroid cancer remains unclear. Methods We stably overexpressed SIRT4 or silenced its expression in the human thyroid cancer cell line BCPAP by means of lentiviral vectors. We conducted a variety of tests, such as CCK-8, wound healing, migration, and invasion assays, to investigate the role of SIRT4 in the proliferation, migration, and invasion abilities of thyroid cancer cells. We also investigated the effects of SIRT4 overexpression on cell cycle progression and apoptosis of BCPAP cells and studied the role of glutamine metabolism in the effects of SIRT4 on BCPAP cell migration and invasion. Finally, we analyzed SIRT4 expression levels in thyroid cancer specimens by immunohistochemistry and investigated their association with clinicopathological features. Results Overexpression of SIRT4 inhibited the proliferation, migration, and invasion abilities of BCPAP thyroid cancer cells, blocked the cell cycle in the G0/G1 phase, and induced apoptosis. Mechanistically, SIRT4 inhibited BCPAP migration and invasion by inhibiting glutamine metabolism. Moreover, we found that SIRT4 protein levels in thyroid cancer tissues were markedly lower than in their non-neoplastic tissue counterparts ( P <0.001). Conclusion SIRT4 plays a pivotal role in the growth and metastasis of thyroid cancer cells and could be a potential therapeutic target in thyroid cancer.