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While there has been great interest in species characteristics that promote invasiveness, still little is known about the characteristics that distinguish invasive from non‐invasive insects. Using a database on the naturalised distributions of alien insects and expert opinions about their impacts, we identified the world's 100 worst invasive insect species.By comparing species characteristics reported in the literature using a meta‐analysis, between the 100 worst invasive species and related non‐invasive species, we found that invasive insects overall have more pathways of introduction, occur in more habitats, have higher fecundities, higher voltinism, more genes, shorted lifespans and faster development from egg to adult. Some of the differences in species characteristics related to propagule pressures, life‐histories and biotic interactions, conditional on whether the non‐invasive species compared is known to be naturalised somewhere, whether the invasive species is globally distributed, and the climatic region of the species.Synthesis and applications. We show for the first time, using a multi‐species comparative approach, that invasive insects differ in several characteristics from related non‐invasive insects. Our results show that invasive species, such as Spodoptera frugiperda, typically are habitat generalists with a high fecundity, a short lifespan and fast development, whereas the importance of female body size and number of enemies are context dependent. Our study can guide and improve existing screening tools for assessing the invasion potential of alien insects. [ABSTRACT FROM AUTHOR]

Accumulation of lipid droplets (LDs) induces cardiac dysfunctions in type 2 diabetes patients. Recent studies have shown that hydrogen sulphide (H2S) ameliorates cardiac functions in db/db mice, but its regulation on the formation of LDs in cardiac tissues is unclear. Db/db mice were injected with NaHS (40 μmol·kg‐1) for twelve weeks. H9c2 cells were treated with high glucose (40 mmol/L), oleate (200 µmol/L), palmitate (200 µmol/L) and NaHS (100 µmol/L) for 48 hours. Plasmids for the overexpression of wild‐type Hrd1 and Hrd1 mutated at Cys115 were constructed. The interaction between Hrd1 and DGAT1 and DGAT2, the ubiquitylation level of DGAT1 and 2, the S‐sulfhydration of Hrd1 were measured. Exogenous H2S ameliorated the cardiac functions, decreased ER stress and reduced the number of LDs in db/db mice. Exogenous H2S could elevate the ubiquitination level of DGAT 1 and 2 and increased the expression of Hrd1 in cardiac tissues of db/db mice. The S‐sulfhydration of Hrd1 by NaHS enhanced the interaction between Hrd1 and DGAT1 and 2 to inhibit the formation of LD. Our findings suggested that H2S modified Hrd1 S‐sulfhydration at Cys115 to reduce the accumulation of LDs in cardiac tissues of db/db mice. [ABSTRACT FROM AUTHOR]

Muscle atrophy occurs in many pathological states, including cancer, diabetes and sepsis, whose results primarily from accelerated protein degradation and activation of the ubiquitin‐proteasome pathway. Expression of Muscle RING finger 1 (MuRF1), an E3 ubiquitin ligase, was increased to induce the loss of muscle mass in diabetic condition. However, hydrogen sulphide (H2S) plays a crucial role in the variety of physiological functions, including antihypertension, antiproliferation and antioxidant. In this study, db/db mice and C2C12 myoblasts treated by high glucose and palmitate and oleate were chose as animal and cellular models. We explored how exogenous H2S attenuated the degradation of skeletal muscle via the modification of MuRF1 S‐sulfhydration in db/db mice. Our results show cystathionine‐r‐lyase expression, and H2S level in skeletal muscle of db/db mice was reduced. Simultaneously, exogenous H2S could alleviate ROS production and reverse expression of ER stress protein markers. Exogenous H2S could decrease the ubiquitination level of MYOM1 and MYH4 in db/db mice. In addition, exogenous H2S reduced the interaction between MuRF1 with MYOM1 and MYH4 via MuRF1 S‐sulfhydration. Based on these results, we establish that H2S prevented the degradation of skeletal muscle via MuRF1 S‐sulfhydration at the site of Cys44 in db/db mice. [ABSTRACT FROM AUTHOR]

Background and Purpose: Hydrogen sulfide (H2 S) plays important roles as a gasotransmitter in pathologies. Increased expression of the E3 ubiquitin ligase, muscle RING finger-1 (MuRF1), may be involved in diabetic cardiomyopathy. Here we have investigated whether and how exogenous H2 S alleviates cardiac muscle degradation through modifications of MuRF1 S-sulfhydration in db/db mice.Experimental Approach: Neonatal rat cardiomyocytes were treated with high glucose (40 mM), oleate (100 μM), palmitate (400 μM), and NaHS (100 μM) for 72 hr. MuRF1 was silenced with siRNA technology and mutation at Cys44 . Endoplasmic reticulum stress markers, MuRF1 expression, and ubiquitination level were measured. db/db mice were injected with NaHS (39 μmol·kg-1 ) for 20 weeks. Echocardiography, cardiac ultrastructure, cystathionine-γ-lyase, cardiac structure proteins expression, and S-sulfhydration production were measured.Key Results: H2 S levels and cystathionine-γ-lyase protein expression in myocardium were decreased in db/db mice. Exogenous H2 S reversed endoplasmic reticulum stress, including impairment of the function of cardiomyocytes and structural damage in db/db mice. Exogenous H2 S could suppress the levels of myosin heavy chain 6 and myosin light chain 2 ubiquitination in cardiac tissues of db/db mice, and MuRF1 was modified by S-sulfhydration, following treatment with exogenous H2 S, to reduce the interaction between MuRF1 and myosin heavy chain 6 and myosin light chain 2.Conclusions and Implications: Our findings suggest that H2 S regulates MuRF1 S-sulfhydration at Cys44 to prevent myocardial degradation in the cardiac tissues of db/db mice.Linked Articles: This article is part of a themed section on Hydrogen Sulfide in Biology & Medicine. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.4/issuetoc. [ABSTRACT FROM AUTHOR]

The current prognostic long noncoding RNA (lncRNA) signatures for hepatocellular carcinoma (HCC) are still controversial and need to be optimized by systematic bioinformatics analyses with suitable methods and appropriate patients. Therefore, we performed the study to establish a credible lncRNA signature for HCC outcome prediction and explore the related mechanisms. Based on the lncRNA profile and the clinical data of carefully selected HCC patients (n = 164) in TCGA, six of 12727 lncRNAs, MIR22HG, CTC‐297N7.9, CTD‐2139B15.2, RP11‐589N15.2, RP11‐343N15.5, and RP11‐479G22.8 were identified as the independent predictors of patients' overall survival in HCC by sequential univariate Cox and 1000 times Cox LASSO regression with 10‐fold CV, and multivariate Cox analysis with 1000 times bootstrapping. In the Kaplan‐Meier analysis with patients trichotomized by the six‐lncRNA signature, high‐risk patients showed significantly shorter survival than mid‐ and low‐risk patients (log‐rank test P < 0.0001). According to the ROCs, the six‐lncRNA signature showed superior predictive capacity than the two existing four‐lncRNA combinations and the traditional prognostic clinicopathological parameter TNM stage. Furthermore, low MIR22HG and CTC‐297N7.9, but high CTD‐2139B15.2, RP11‐589N15.2, RP11‐343N15.5, and RP11‐479G22.8, were, respectively, demonstrated to be related with the malignant phenotypes of HCC. Functionally, the six lncRNAs were disclosed to involve in the regulation of multiple cell cycle and stress response‐related pathways via mediating transcription regulation and chromatin modification. In conclusion, our study identified a novel six‐lncRNA signature for resectable HCC prognosis prediction and indicated the underlying mechanisms of HCC progression and the potential functions of the six lncRNAs awaiting further elucidation. By systematic bioinformatics analyses, a novel six‐lncRNA signature including MIR22HG, CTC‐297N7.9, CTD‐2139B15.2, RP11‐589N15.2, RP11‐343N15.5, and RP11‐479G22.8 was established for HCC prognosis prediction and demonstrated to have superior prediction capacity than the two established four‐lncRNA groups and the traditional prognostic TNM stage. Functionally, the six lncRNAs were disclosed to involve in the regulation of multiple cell cycle and stress response‐related pathways via mediating transcription regulation and chromatin modification. [ABSTRACT FROM AUTHOR]

Toll-like receptor 3 and RIG-I like receptors (RLRs; MDA5, RIG-I) are involved in cell growth inhibition and apoptosis. However, the toll-like receptor 3-related apoptotic pathway is insensitive to direct polyinosinic-polycytidylic acid (dsRNA analog) stimulation in hepatoma cells. To determine whether the strategy of transferring polyinosinic-polycytidylic acid into cells (polyinosinic-polycytidylic acid-liposome) could induce apoptosis in hepatoma cells through cytoplasm receptors, we examined the responses of innate immune receptors RLRs and toll-like receptor 3 in response to different stimulation. We found that the apoptosis could exclusively be detected under polyinosinic-polycytidylic acid-liposome stimulation, which involved the activation of the caspase pathway. Besides, the expression of RIG-I, MDA5, IFNβ and interferon-stimulated gene 15 was increased significantly at an early stage. Moreover, the growth inhibition of polyinosinic-polycytidylic acid-liposome was confirmed in a mouse model. Taken together, these results suggest polyinosinic-polycytidylic acid-liposome could be used as a potential apoptotic agent in hepatocellular carcinoma cells and imply a potential therapeutic strategy. ( Cancer Sci 2009; 100: 529–536) [ABSTRACT FROM AUTHOR]

Investigates the transport behavior, thermophysical properties and reaction kinetics of cellular poly(urethane-isocyanurate). Reaction temperature profiles and computational fluid dynamics simulations; Reaction kinetics; Heat capacity; Thermal conductivity; Heat of reaction by differential scanning calorimetry.