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Diabetes is a disorder of glucose metabolism, and over 90% are type 2 diabetes. Diabetic cardiomyopathy (DCM) is one of the type 2 diabetes complications, usually accompanied by changes in myocardial structure and function, together with cardiomyocyte apoptosis. Our study investigated the effect of curcumin on regulating oxidative stress (OS) and apoptosis in DCM. In vivo, diabetes was induced in an experimental rat model by streptozoticin (STZ) together with high‐glucose and high‐fat (HG/HF) diet feeding. In vitro, H9c2 cardiomyocytes were cultured with high‐glucose and saturated free fatty acid palmitate. Curcumin was orally or directly administered to rats or cells, respectively. Streptozoticin ‐induced diabetic rats showed metabolism abnormalities and elevated markers of OS (superoxide dismutase [SOD], malondialdehyde [MDA], gp91phox, Cyt‐Cyto C), enhanced cell apoptosis (Bax/Bcl‐2, Cleaved caspase‐3, TUNEL‐positive cells), together with reduced Akt phosphorylation and increased Foxo1 acetylation. Curcumin attenuated the myocardial dysfunction, OS and apoptosis in the heart of diabetic rats. Curcumin treatment also enhanced phosphorylation of Akt and inhibited acetylation of Foxo1. These results strongly suggest that apoptosis was increased in the heart of diabetic rats, and curcumin played a role in diabetic cardiomyopathy treatment by modulating the Sirt1‐Foxo1 and PI3K‐Akt pathways.

Coal-based porous materials for supercapacitors were successfully prepared using Taixi anthracite (TXA) by multi-stage activation. The characterization and electrochemical tests of activated carbons (ACs) prepared in different stages demonstrated that the AC from the third-stage activation (ACIII) shows good porous structures and excellent electrochemical performances. ACIII exhibited a fine specific capacitance of 199 F g−1 at a current density of 1 A g−1 in the three-electrode system, with 6 mol L−1 KOH as the electrolyte. The specific capacitance of ACIII remained 190 F g−1 even despite increasing the current density to 5 A g−1, indicating a good rate of electrochemical performance. Moreover, its specific capacitance remained at 98.1% of the initial value after 5000 galvanostatic charge-discharge (GCD) cycle tests at a current density of 1 A g−1, suggesting that the ACIII has excellent cycle performance as electrode materials for supercapacitors. This study provides a promising approach for fabricating high performance electrode materials from high-rank coals, which could facilitate efficient and clean utilization of high-rank coals.

DNA 5-hydroxymethylcytosine (5hmC) modification is known to be associated with gene transcription and frequently used as a mark to investigate dynamic DNA methylation conversion during mammalian development and in human diseases. However, the lack of genome-wide 5hmC profiles in different human tissue types impedes drawing generalized conclusions about how 5hmC is implicated in transcription activity and tissue specificity. To meet this need, we describe the development of a 5hmC tissue map by characterizing the genomic distributions of 5hmC in 19 human tissues derived from ten organ systems. Subsequent sequencing results enabled the identification of genome-wide 5hmC distributions that uniquely separates samples by tissue type. Further comparison of the 5hmC profiles with transcriptomes and histone modifications revealed that 5hmC is preferentially enriched on tissue-specific gene bodies and enhancers. Taken together, the results provide an extensive 5hmC map across diverse human tissue types that suggests a potential role of 5hmC in tissue-specific development; as well as a resource to facilitate future studies of DNA demethylation in pathogenesis and the development of 5hmC as biomarkers. DNA 5-hydroxymethylcytosine (5hmC) modification is associated with gene transcription and used as a mark of mammalian development. Here the authors report a comprehensive 5hmC tissue map and analysis of 5hmC genomic distributions in 19 human tissues derived from 10 organ systems, thus providing insights into the role of 5hmC in tissue-specific development.

The combination of linezolid and opioid drugs such as fentanyl may increase the risk of serotonin syndrome, but its impact on in-hospital mortality is not yet clear. The aim of this study is to investigate the effect of simultaneous use of fentanyl and linezolid on in-hospital mortality in mechanically ventilated patients. Based on the MIMIC-IV database, 3339 patients receiving mechanical ventilation were enrolled and divided into three groups: the group receiving linezolid simultaneously (n = 43), the group receiving linezolid within 14 days (n = 22) and the group that did not use linezolid (n = 3274). Use multivariate Cox regression analysis to analyze in-hospital mortality rates and adjust for confounding factors. The in-hospital mortality rate of the group receiving linezolid simultaneously was 37.2% (16/43), the group receiving linezolid within 14 days was 40.9% (9/22), and the group that did not use linezolid was 22.9% (751/3274). The in-hospital mortality rate of the group receiving linezolid simultaneously was significantly higher than that of the group that did not use linezolid (hazard ratio [HR], 1.56; 95% CI, 1 ~ 2.43; P = 0.049). There was no statistically significant difference in in-hospital mortality rate among the group receiving linezolid within 14 days and the group that did not use linezolid (hazard ratio [HR], 1.01; 95% CI, 0.5 ~ 2.05; P = 0.968). Subgroup analysis showed that there was no interaction between different groups at baseline (age, gender, race, BMI, liver disease, and kidney disease) (interaction p-value > 0.05). In this post-hoc analysis, we found an association between the combined use of fentanyl and linezolid and increased in-hospital mortality among mechanically ventilated patients. However, this finding is based on studies with small sample sizes and requires further validation through larger, multicenter investigations. In clinical practice, the potential risks of this drug interaction should be carefully evaluated.

Salt stress directly affects the growth of plants. The limitation of leaf grow is among the earliest visible effects of salt stress. However, the regulation mechanism of salt treatments on leaf shape has not been fully elucidated. We measured the morphological traits and anatomical structure. In combination with transcriptome analysis, we analyzed differentially expressed genes (DEGs) and verified the RNA-seq data by qRT-PCR. Finally, we analyzed correlation between leaf microstructure parameters and expansin genes. We show that the leaf thickness, the width, and the leaf length significantly increased at elevated salt concentrations after salt stress for 7 days. Low salt mainly promoted the increase in leaves length and width, but high salt concentration accelerated the leaf thickness. The anatomical structure results indicated that palisade mesophyll tissues contribute more to leaf thickness than spongy mesophyll tissues, which possibly contributed to the increase in leaf expansion and thickness. Moreover, a total of 3,572 DEGs were identified by RNA-seq. Notably, six of the DEGs among 92 identified genes concentrated on cell wall synthesis or modification were involved in cell wall loosening proteins. More importantly, we demonstrated that there was a strong positive correlation between the upregulated EXLA2 gene and the thickness of the palisade tissue in L. barbarum leaves. These results suggested that salt stress possibly induced the expression of EXLA2 gene, which in turn increased the thickness of L. barbarum leaves by promoting the longitudinal expansion of cells of the palisade tissue. This study lays a solid knowledge for revealing the underlying molecular mechanisms of leaf thickening in L. barbarum in response to salt stresses.

Stem cell therapy is a promising strategy for tissue regeneration. The therapeutic benefits of cell therapy are mediated by both direct and indirect mechanisms. However, the application of stem cell therapy in the clinic is hampered by several limitations. This concise review provides a brief introduction into stem cell therapies for ischemic heart disease. It summarizes cell‐based and cell‐free paradigms, their limitations, and the benefits of using them to target disease. Stem Cells Translational Medicine 2018;7:354–359 Summary outlining barriers and solutions to cell therapy. Stem cell therapy is a promising strategy for cardiac tissue regeneration. However, the application of stem cell therapy in the clinic is hampered by several limitations. Despite these hurdles, a number of alternative and ever‐evolving solutions involving cell based and cell free paradigms, offer promising therapy options for patients with cardiac disease.

This report describes a novel tickborne orthonairovirus species identified in patients presenting with an acute febrile illness in China.

Oncogene‐derived metabolic reprogramming is important for anabolic growth of cancer cells, which is now considered to be not simply rely on glycolysis. Pentose phosphate pathway and tricarboxylic acid cycle also play pivotal roles in helping cancer cells to meet their anabolic and energy demands. The present work focused on gankyrin, a relatively specific oncogene in hepatocellular carcinoma (HCC), and its impact on glycolysis and mitochondrial homeostasis. Metabolomics, RNA‐seq analysis, and subsequent conjoint analysis illustrated that gankyrin regulated the pentose phosphate pathway (PPP), tricarboxylic acid (TCA) cycle, and mitochondrial function and homeostasis, which play pivotal roles in tumor development. Mechanistically, gankyrin was found to modulate HCC metabolic reprogramming via TIGAR. Gankyrin positively regulated the transcription of TIGAR through Nrf2, which bound to the antioxidant response elements (AREs) in the promoter of TIGAR. Interestingly, TIGAR feedback regulated the transcription of Nrf2 and subsequently gankyrin by promoting nuclear importation of PGC1α. The loop between gankyrin, Nrf2, and TIGAR accelerated glucose metabolism toward the PPP and TCA cycle, which provided vital building blocks, such as NADPH, ATP, and ribose of tumor and further facilitated the progression of HCC. Gankyrin positively regulated the transcription of TIGAR through Nrf2, which bound to the antioxidant response elements (AREs) in the promoter of TIGAR. Interestingly, TIGAR feedback regulated the transcription of Nrf2 and subsequently gankyrin by promoting nuclear importation of PGC1a. The loop between gankyrin, Nrf2, and TIGAR accelerated glucose metabolism toward the pentose phosphate pathway (PPP) and tricarboxylic acid (TCA) cycle, which provided vital building blocks, such as NADPH, ATP, and ribose of tumor and further facilitated tumorigenesis of hepatocellular carcinoma (HCC).

The 3′-end processing machinery for metazoan replication-dependent histone precursor messenger RNAs (pre-mRNAs) contains the U7 small nuclear ribonucleoprotein and shares the key cleavage module with the canonical cleavage and polyadenylation machinery. We reconstituted an active human histone pre-mRNA processing machinery using 13 recombinant proteins and two RNAs and determined its structure by cryo–electron microscopy. The overall structure is highly asymmetrical and resembles an amphora with one long handle. We captured the pre-mRNA in the active site of the endonuclease, the 73-kilodalton subunit of the cleavage and polyadenylation specificity factor, poised for cleavage. The endonuclease and the entire cleavage module undergo extensive rearrangements for activation, triggered through the recognition of the duplex between the authentic pre-mRNA and U7 small nuclear RNA (snRNA). Our study also has notable implications for understanding canonical and snRNA 3′-end processing.

Anaplasma capra is an emerging tickborne human pathogen initially recognized in China in 2015; it has been reported in ticks and in a wide range of domestic and wild animals worldwide. We describe whole-genome sequences of 2 A. capra strains from metagenomic sequencing of purified erythrocytes from infected goats in China. The genome of A. capra was the smallest among members of the genus Anaplasma. The genomes of the 2 A. capra strains contained comparable G+C content and numbers of pseudogenes with intraerythrocytic Anaplasma species. The 2 A. capra strains had 54 unique genes. The prevalence of A. capra was high among goats in the 2 endemic areas. Phylogenetic analyses revealed that the A. capra strains detected in this study were basically classified into 2 subclusters with those previously detected in Asia. Our findings clarify details of the genomic characteristics of A. capra and shed light on its genetic diversity.