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Responding to tissue injury, skeletal muscles undergo the tissue destruction and reconstruction accompanied with inflammation. The immune system recognizes the molecules released from or exposed on the damaged tissue. In the local minor tissue damage, tissue-resident macrophages sequester pro-inflammatory debris to prevent initiation of inflammation. In most cases of the skeletal muscle injury, however, a cascade of inflammation will be initiated through activation of local macrophages and mast cells and recruitment of immune cells from blood circulation to the injured site by recongnization of damage-associated molecular patterns (DAMPs) and activated complement system. During the inflammation, macrophages and neutrophils scavenge the tissue debris to release inflammatory cytokines and the latter stimulates myoblast fusion and vascularization to promote injured muscle repair. On the other hand, an abundance of released inflammatory cytokines and chemokines causes the profound hyper-inflammation and mobilization of immune cells to trigger a vicious cycle and lead to the cytokine storm. The cytokine storm results in the elevation of cytolytic and cytotoxic molecules and reactive oxygen species (ROS) in the damaged muscle to aggravates the tissue injury, including the healthy bystander tissue. Severe inflammation in the skeletal muscle can lead to rhabdomyolysis and cause sepsis-like systemic inflammation response syndrome (SIRS) and remote organ damage. Therefore, understanding more details on the involvement of inflammatory factors and immune cells in the skeletal muscle damage and repair can provide the new precise therapeutic strategies, including attenuation of the muscle damage and promotion of the muscle repair.

Heart failure (HF) is a major public health problem worldwide, especially coronary heart disease (myocardial infarction)-induced HF with reduced ejection fraction (HFrEF), which accounts for over 50% of all HF cases. An estimated 6 million American adults have HF. As a major feature of HF, cardiac sympathetic overactivation triggers arrhythmias and sudden cardiac death, which accounts for nearly 50–60% of mortality in HF patients. Regulation of cardiac sympathetic activation is highly integrated by the regulatory circuitry at multiple levels, including afferent, central, and efferent components of the sympathetic nervous system. Much evidence, from other investigators and us, has confirmed the afferent and central neural mechanisms causing sympathoexcitation in HF. The stellate ganglion is a peripheral sympathetic ganglion formed by the fusion of the 7th cervical and 1st thoracic sympathetic ganglion. As the efferent component of the sympathetic nervous system, cardiac postganglionic sympathetic neurons located in stellate ganglia provide local neural coordination independent of higher brain centers. Structural and functional impairments of cardiac postganglionic sympathetic neurons can be involved in cardiac sympathetic overactivation in HF because normally, many effects of the cardiac sympathetic nervous system on cardiac function are mediated via neurotransmitters (e.g., norepinephrine) released from cardiac postganglionic sympathetic neurons innervating the heart. This review provides an overview of cardiac sympathetic remodeling in stellate ganglia and potential mechanisms and the role of cardiac sympathetic remodeling in cardiac sympathetic overactivation and arrhythmias in HF. Targeting cardiac sympathetic remodeling in stellate ganglia could be a therapeutic strategy against malignant cardiac arrhythmias in HF.

Autism spectrum disorder (ASD) is a common neurodevelopmental disorder. The mechanisms underlying ASD are unclear. Astrocyte alterations are noted in ASD patients and animal models. However, whether astrocyte dysfunction is causal or consequential to ASD-like phenotypes in mice is unresolved. Type 2 inositol 1,4,5-trisphosphate 6 receptors (IP3R2)-mediated Ca 2+ release from intracellular Ca 2+ stores results in the activation of astrocytes. Mutations of the IP3R2 gene are associated with ASD. Here, we show that both IP3R2-null mutant mice and astrocyte-specific IP3R2 conditional knockout mice display ASD-like behaviors, such as atypical social interaction and repetitive behavior. Furthermore, we show that astrocyte-derived ATP modulates ASD-like behavior through the P2X2 receptors in the prefrontal cortex and possibly through GABAergic synaptic transmission. These findings identify astrocyte-derived ATP as a potential molecular player in the pathophysiology of ASD. Astrocytes contribute to autism spectrum disorder (ASD) pathophysiology. Here, the authors show that IP3R2 conditional KO mice show ASD-like behaviours and identify astrocyte-derived ATP as a modulator of these behaviours in mice.

Sclerotinia sclerotiorum (Lib.) de Bary is an unusual pathogen which has the broad host range, diverse infection modes, and potential double feeding lifestyles of both biotroph and necrotroph. It is capable of infecting over 400 plant species found worldwide and more than 60 names have agriculturally been used to refer to diseases caused by this pathogen. Plant defense to S. sclerotiorum is a complex biological process and exhibits a typical quantitative disease resistance (QDR) response. Recent studies using Arabidopsis thaliana and crop plants have obtained new advances in mechanisms used by plants to cope with S. sclerotiorum infection. In this review, we focused on our current understanding on plant defense mechanisms against this pathogen, and set up a model for the defense process including three stages: recognition of this pathogen, signal transduction and defense response. We also have a particular interest in defense signaling mediated by diverse signaling molecules. We highlight the current challenges and unanswered questions in both the defense process and defense signaling. Essentially, we discussed candidate resistance genes newly mapped by using high-throughput experiments in important crops, and classified these potential gene targets into different stages of the defense process, which will broaden our understanding of the genetic architecture underlying quantitative resistance to S. sclerotiorum . We proposed that more powerful mapping population(s) will be required for accurate and reliable QDR gene identification.

Type 2 diabetes mellitus (T2DM) is one of the most significant health issues worldwide, with associated healthcare costs estimated to surpass USD 1054 billion by 2045. The leading cause of death in T2DM patients is the development of cardiovascular disease (CVD). In the early stages of T2DM, patients develop cardiovascular autonomic dysfunction due to the withdrawal of cardiac parasympathetic activity. Diminished cardiac parasympathetic tone can lead to cardiac arrhythmia-related sudden cardiac death, which accounts for 50% of CVD-related deaths in T2DM patients. Regulation of cardiovascular parasympathetic activity is integrated by neural circuitry at multiple levels including afferent, central, and efferent components. Efferent control of cardiac parasympathetic autonomic tone is mediated through the activity of preganglionic parasympathetic neurons located in the cardiac extensions of the vagus nerve that signals to postganglionic parasympathetic neurons located in the intracardiac ganglia (ICG) on the heart. Postganglionic parasympathetic neurons exert local control on the heart, independent of higher brain centers, through the release of neurotransmitters, such as acetylcholine. Structural and functional alterations in cardiac parasympathetic postganglionic neurons contribute to the withdrawal of cardiac parasympathetic tone, resulting in arrhythmogenesis and sudden cardiac death. This review provides an overview of the remodeling of parasympathetic postganglionic neurons in the ICG, and potential mechanisms contributing to the withdrawal of cardiac parasympathetic tone, ventricular arrhythmogenesis, and sudden cardiac death in T2DM. Improving cardiac parasympathetic tone could be a therapeutic avenue to reduce malignant ventricular arrhythmia and sudden cardiac death, increasing both the lifespan and improving quality of life of T2DM patients.

Red mud discharged during alumina production via the Bayer process is characterized by high contents of sodium carbonate, sodium sulfate, and other soluble salts, and it remains poorly utilized and accumulates in long-term stockpiles. Sodium percarbonate has found extensive industrial applications, and its synthesis via the salting-out method represents one of the dominant industrial routes. In this context, sodium sulfate was employed as a salting-out agent. On the basis of relevant ternary systems, the phase equilibrium of the quaternary system Na2CO3–Na2SO4–H2O2–H2O at 5 °C was systematically investigated and calculated. The objective was to utilize red mud as a waste resource and develop a novel integrated process that favored the wet synthesis of sodium percarbonate while enabling the efficient separation of sodium salts. The solubility data for the ternary subsystems constituting the above quaternary system were correlated using the Pitzer model, yielding the corresponding ion interaction parameters and activity coefficients. The validated model was then applied to predict the phase equilibrium data of the quaternary system. Verification results indicate that the calculated values are in satisfactory agreement with the experimental data. On the basis of the phase equilibrium data of the Na2CO3–Na2SO4–H2O2–H2O system at 5 °C, a phase diagram was constructed. Along with five solid-phase crystallization fields, three invariant points were identified: the co-saturation point of Na2SO4·10H2O, Na2CO3·10H2O, and Na2CO3·1.5H2O2·H2O; the co-saturation point of Na2SO4·10H2O, Na2CO3·1.5H2O2·H2O, and Na2SO4·0.5H2O2·H2O; and the co-saturation point of Na2CO3·1.5H2O2·H2O, Na2SO4·0.5H2O2·H2O, and Na2CO3·2H2O2·H2O. From phase diagram analysis, a novel wet process route for sodium percarbonate production using waste red mud is proposed. The process involves chemical reaction, crystallization, separation, and drying to obtain the final product. A new process flow diagram for the value-added production of sodium percarbonate is also presented.

Abstract Rapid adaptation to novel environments may drive changes in genomic regions through natural selection. However, the genetic architecture underlying these adaptive changes is still poorly understood. Using population genomic approaches, we investigated the genomic architecture that underlies rapid parallel adaptation of Coilia nasus to fresh water by comparing four freshwater-resident populations with their ancestral anadromous population. Linkage disequilibrium network analysis and population genetic analyses revealed two putative large chromosome inversions on LG6 and LG22, which were enriched for outlier loci and exhibited parallel association with freshwater adaptation. Drastic frequency shifts and elevated genetic differentiation were observed for the two chromosome inversions among populations, suggesting that both inversions would undergo divergent selection between anadromous and resident ecotypes. Enrichment analysis of genes within chromosome inversions showed significant enrichment of genes involved in metabolic process, immunoregulation, growth, maturation, osmoregulation, and so forth, which probably underlay differences in morphology, physiology and behavior between the anadromous and freshwater-resident forms. The availability of beneficial standing genetic variation, large optimum shift between marine and freshwater habitats, and high efficiency of selection with large population size could lead to the observed rapid parallel adaptive genomic change. We propose that chromosomal inversions might have played an important role during the evolution of rapid parallel ecological divergence in the face of environmental heterogeneity in C. nasus. Our study provides insights into the genomic basis of rapid adaptation of complex traits in novel habitats and highlights the importance of structural genomic variants in analyses of ecological adaptation.

Background The short-snout icefish, Neosalanx brevirostris , a member of the Salangidae family, is an economically important fishery species in China. Understanding the mechanisms underlying sex determination in this species has crucial implications for conservation, ecology and evolution. Meanwhile, there is a shortage of rapid and cost-effective genetic methods for sex identification, which poses challenges in identifying the sex of immature individuals in sex determination mechanism studies and aquaculture breeding applications. Results Based on whole genome resequencing data, sex-specific loci and regions were found to be concentrated in a region on chromosome 2. All sex-specific loci exhibited excess heterozygosity in females and complete homozygosity in males. This sex determining region contains seven genes, including cytochrome P450 aromatase CYP19B , which is involved in steroidogenesis and is associated with 24 sex-specific loci and two W-deletions. A haploid female-specific sequence was identified as paralogous to a diploid sequence with a significant length difference, making it suitable for rapid and cost-effective genetic sex identification by traditional PCR and agarose gel electrophoresis, which were further validated in 24 females and 24 males with known phenotypic sexes. Conclusions Our results confirm that N. brevirostris exhibits a female heterogametic sex determination system (ZZ/ZW), with chromosome 2 identified as the putative sex chromosome containing a relatively small sex determining region (~ 48 Kb). The gene CYP19B is proposed as a candidate sex determining gene. Moreover, the development of PCR based method enables genetic sex identification at any developmental stage, thereby facilitating further studies on sex determination mechanisms and advancing aquaculture breeding applications for this species.

Cardiac sympathetic overactivation is involved in arrhythmogenesis in patients with chronic heart failure (CHF). Inflammatory infiltration in the stellate ganglion (SG) is a critical factor for cardiac sympathoexcitation in patients with ventricular arrhythmias. This study aims to investigate if macrophage depletion in SGs decreases cardiac sympathetic overactivation and ventricular arrhythmogenesis in CHF. Surgical ligation of the coronary artery was used for induction of CHF. Clodronate liposomes were microinjected into bilateral SGs of CHF rats for macrophage depletion. Using cytokine array, immunofluorescence staining, and Western blot analysis, we found that macrophage expansion and expression of TNFα and IL-1β in SGs were markedly increased in CHF rats. Flow cytometry data confirmed that the percentage of macrophages in SGs was higher in CHF rats than that in sham rats. Clodronate liposomes significantly reduced CHF-elevated proinflammatory cytokine levels and macrophage expansion in SGs. Clodronate liposomes also reduced CHF-increased N-type Ca2+ currents and excitability of cardiac sympathetic postganglionic neurons and inhibited CHF-enhanced cardiac sympathetic nerve activity. ECG data from 24-h, continuous telemetry recording in conscious rats demonstrated that clodronate liposomes not only restored CHF-induced heterogeneity of ventricular electrical activities, but also decreased the incidence and duration of ventricular tachycardia/fibrillation in CHF. Macrophage depletion with clodronate liposomes attenuated CHF-induced cardiac sympathetic overactivation and ventricular arrhythmias through reduction of macrophage expansion and neuroinflammation in SGs.

Background The clearhead icefish, Protosalanx hyalocranius , is an economically important fishery species in China. Since 1980s, P. hyalocranius was widely introduced into lakes and reservoirs of northern China for aquaculture. However, the lack of a rapid and cost-effective sex identification method based on sex specific genetic markers has hindered study on sex determination mechanisms and breeding applications. Results Female-specific genomic regions were discovered by comparing whole genome re-sequencing data of both males and females. Two female-specific genomic regions larger than 50 bp were identified, and one (598 bp) contained a putative FOXI gene, which was paralogous to another FOXI gene with sex-associated SNPs. The two FOXI sequences displayed significant length difference with nine deletions of total length of 230 bp. This deletion-type structural variation could be easily and efficiently detected by traditional PCR and agarose gel electrophoresis with one 569 bp band for males and two bands (569 and 339 bp) for females, which were validated in 50 females and 40 males with known phenotypic sexes. Conclusions The results provided structural genomic evidence for the ZZ/ZW sex determination system in P. hyalocranius discovered in our previous study with association analysis of SNPs. Moreover, the female-specific markers and rapid and cost-effective PCR-based genetic sex identification method should have applications in further studies of sex determination mechanism for this species.