The Protective Effect of Traditional Chinese Medicine on Liver Ischemia-Reperfusion Injury.

Liver ischemia-reperfusion (I/R) injury occurs during transplantation and major hepatic surgery, which may lead to postoperative liver dysfunction. More and more traditional Chinese medicines (TCMs) have been used to treat liver ischemia-reperfusion injury. The purpose of this review is to evaluate the different protective effects of TCMs in the treatment of liver ischemia-reperfusion injury and to summarize its possible mechanisms. The results indicate that TCMs attenuate liver I/R injury via multiple mechanisms, including antioxidation stress, anti-inflammatory response, antiapoptosis, and inhibiting endoplasmic reticulum stress. However, the in-depth mechanism of the protective effects of these traditional Chinese medicines still remains unknown

A mobile signal transported over a long distance induces systemic transcriptional gene silencing in a grafted partner

Transcriptional gene silencing (TGS) can be induced by promoter-targeted small interfering RNA (siRNA). Long-distance transmission of TGS by viral infection in plants has been reported. However, systemic TGS has not been observed in the case of using an inverted repeat transgene as the silencing trigger. Here it is reported that a mobile signal, presumably the siRNA, produced from a hairpin structure transgene controlled by a companion cell-specific promoter can also induce transmissible TGS in both a modified agroinfiltration and a grafting system. Although the transmissible TGS occurred only in cells located in the vicinity of a leaf vein in the scion, very strong silencing was observed in the root system, especially the lateral roots, including the root apical meristem. The transmissible TGS was maintained through tissue culture and subsequently inherited by the progeny. The results suggest the potential application of mobile promoter-targeting siRNA in horticulture for improvement of plant cultivars by grafting

Performance analysis and optimization for workflow authorization

Many workflow management systems have been developed to enhance the performance of workflow executions. The authorization policies deployed in the system may restrict the task executions. The common authorization constraints include role constraints, Separation of Duty (SoD), Binding of Duty (BoD) and temporal constraints. This paper presents the methods to check the feasibility of these constraints, and also determines the time durations when the temporal constraints will not impose negative impact on performance. Further, this paper presents an optimal authorization method, which is optimal in the sense that it can minimize a workflow’s delay caused by the temporal constraints. The authorization analysis methods are also extended to analyze the stochastic workflows, in which the tasks’ execution times are not known exactly, but follow certain probability distributions. Simulation experiments have been conducted to verify the effectiveness of the proposed authorization methods. The experimental results show that comparing with the intuitive authorization method, the optimal authorization method can reduce the delay caused by the authorization constraints and consequently reduce the workflows’ response time

Cardiac-to-adipose axis in metabolic homeostasis and diseases: special instructions from the heart

Abstract Adipose tissue is essential for maintaining systemic metabolic homeostasis through traditional metabolic regulation, endocrine crosstalk, and extracellular vesicle production. Adipose dysfunction is a risk factor for cardiovascular diseases. The heart is a traditional pump organ. However, it has recently been recognized to coordinate interorgan cross-talk by providing peripheral signals known as cardiokines. These molecules include specific peptides, proteins, microRNAs and novel extracellular vesicle-carried cargoes. Current studies have shown that generalized cardiokine-mediated adipose regulation affects systemic metabolism. Cardiokines regulate lipolysis, adipogenesis, energy expenditure, thermogenesis during cold exposure and adipokine production. Moreover, cardiokines participate in pathological processes such as obesity, diabetes and ischemic heart injury. The underlying mechanisms of the cardiac-to-adipose axis mediated by cardiokines will be further discussed to provide potential therapeutic targets for metabolic diseases and support a new perspective on the need to correct adipose dysfunction after ischemic heart injury

Improved Analytical Model for Thermal Softening in Aluminum Alloys Form Room Temperature to Solidus

In advanced solid-state manufacturing processes such as friction stir welding, the metal’s temperature ranges from room temperature to the solidus temperature. The material strength in the temperature range is generally required for investigating the mechanical behaviors. In this communication paper, an analytical model is proposed for describing the thermal softening of aluminum alloys for room temperature to solidus temperature, in which the concept of temperature-dependent transition between two thermal softening regimes is implemented. It is demonstrated that the proposed model compares favorably to the well-known Sellars–Tegart model and Johnson–Cook model. The constants of the proposed model for nine typical engineering commercial aluminum alloys are documented

Proanthocyanidins in seed coat tegmen and endospermic cap inhibit seed germination in Sapium sebiferum

Sapium sebiferum, an ornamental and bio-energetic plant, is propagated by seed. Its seed coat contains germination inhibitors and takes a long time to stratify for germination. In this study, we discovered that the S. sebiferum seed coat (especially the tegmen) and endospermic cap (ESC) contained high levels of proanthocyanidins (PAs). Seed coat and ESC removal induced seed germination, whereas exogenous application with seed coat extract (SCE) or PAs significantly inhibited this process, suggesting that PAs in the seed coat played a major role in regulating seed germination in S. sebiferum. We further investigated how SCE affected the expression of the seed-germination-related genes. The results showed that treatment with SCE upregulated the transcription level of the dormancy-related gene, gibberellins (GAs) suppressing genes, abscisic acid (ABA) biosynthesis and signalling genes. SCE decreased the transcript levels of ABA catabolic genes, GAs biosynthesis genes, reactive oxygen species genes and nitrates-signalling genes. Exogenous application of nordihydroguaiaretic acid, gibberellic acid, hydrogen peroxide and potassium nitrate recovered seed germination in seed-coat-extract supplemented medium. In this study, we highlighted the role of PAs, and their interactions with the other germination regulators, in the regulation of seed dormancy in S. sebiferum

CD38 deficiency alleviates Ang II-induced vascular remodeling by inhibiting small extracellular vesicle-mediated vascular smooth muscle cell senescence in mice

Abstract CD38 is the main enzyme for nicotinamide adenine dinucleotide (NAD) degradation in mammalian cells. Decreased NAD levels are closely related to metabolic syndromes and aging-related diseases. Our study showed that CD38 deficiency significantly alleviated angiotensin II (Ang II)-induced vascular remodeling in mice, as shown by decreased blood pressures; reduced vascular media thickness, media-to-lumen ratio, and collagen deposition; and restored elastin expression. However, our bone marrow transplantation assay showed that CD38 deficiency in lymphocytes led to lack of protection against Ang II-induced vascular remodeling, suggesting that the effects of CD38 on Ang II-induced vascular remodeling might rely primarily on vascular smooth muscle cells (VSMCs), not lymphocytes. In addition, we observed that CD38 deficiency or NAD supplementation remarkably mitigated Ang II-induced vascular senescence by suppressing the biogenesis, secretion, and internalization of senescence-associated small extracellular vesicles (SA-sEVs), which facilitated the senescence of neighboring non-damaged VSMCs. Furthermore, we found that the protective effects of CD38 deficiency on VSMC senescence were related to restoration of lysosome dysfunction, particularly with respect to the maintenance of sirtuin-mediated mitochondrial homeostasis and activation of the mitochondria–lysosomal axis in VSMCs. In conclusion, our findings demonstrated that CD38 and its associated intracellular NAD decline are critical for Ang II-induced VSMC senescence and vascular remodeling

Genetic boundaries delineate the potential human pathogen Salmonella bongori into discrete lineages: divergence and speciation

Abstract Background Salmonella bongori infect mainly cold-blooded hosts, but infections by S. bongori in warm-blooded hosts have been reported. We hypothesized that S. bongori might have diverged into distinct phylogenetic lineages, with some being able to infect warm-blooded hosts. Results To inspect the divergence status of S. bongori, we first completely sequenced the parakeet isolate RKS3044 and compared it with other sequenced S. bongori strains. We found that RKS3044 contained a novel T6SS encoded in a pathogenicity island-like structure, in addition to a T6SS encoded in SPI-22, which is common to all S. bongori strains so far reported. This novel T6SS resembled the SPI-19 T6SS of the warm-blooded host infecting Salmonella Subgroup I lineages. Genomic sequence comparisons revealed different genomic sequence amelioration events among the S. bongori strains, including a unique CTAG tetranucleotide degeneration pattern in RKS3044, suggesting non-overlapping gene pools between RKS3044 and other S. bongori lineages/strains leading to their independent accumulation of genomic variations. We further proved the existence of a clear-cut genetic boundary between RKS3044 and the other S. bongori lineages/strains analyzed in this study. Conclusions The warm-blooded host-infecting S. bongori strain RKS3044 has diverged with distinct genomic features from other S. bongori strains, including a novel T6SS encoded in a previously not reported pathogenicity island-like structure and a unique genomic sequence degeneration pattern. These findings alert cautions about the emergence of new pathogens originating from non-pathogenic ancestors by acquiring specific pathogenic traits