An extensive network of cutaneous nerves, neuropeptides, and specific receptors richly innervates the skin and influences a variety of physiological and pathological processes. The sensory and autonomic nerve fibers secrete a variety of neuropeptides that are essential to the different phases of wound healing. In addition to initiating a neurogenic inflammatory response in the early stages of healing, neuropeptides also control wound healing by influencing immune cells, repair cells, and the growth factor network. However, the precise mechanism by which they accomplish these roles in the context of cutaneous wound healing is still unknown. Investigating the mechanisms of action of neuropeptides in wound healing and potential therapeutic applications is therefore urgently necessary. The present review discusses the process of wound healing, types of neuropeptides, potential mechanisms underlying the role of neuropeptides in cutaneous wound healing, as well as some neuropeptide-derived treatment strategies, such as hydrogels, new dressings, electro stimulation, and skin-derived precursors. Future in-depth mechanistic studies of neuropeptides in cutaneous wound healing may provide opportunities to develop therapeutic technologies that harness the roles of neuropeptides in the wound healing process.

Brain injury poses a heavy disease burden in the world, resulting in chronic deficits. Therapies for brain injuries have been focused on pharmacologic, small molecule, endocrine and cell-based therapies. Endogenous neural stem cells (eNSCs) are a group of stem cells which can be activated in vivo by damage, neurotrophic factors, physical factor stimulation, and physical exercise. The activated eNSCs can proliferate, migrate and differentiate into neuron, oligodendrocyte and astrocyte, and play an important role in brain injury repair and neural plasticity. The roles of eNSCs in the repair of brain injury include but are not limited to ameliorating cognitive function, improving learning and memory function, and promoting functional gait behaviors. The activation and mobilization of eNSCs is important to the repair of injured brain. In this review we describe the current knowledge of the common character of brain injury, the roles and mechanism of eNSCs in brain injury. And then we discuss the current mobilization strategy of eNSCs following brain injury. We hope that a comprehensive awareness of the roles and mobilization strategy of eNSCs in the repair of cerebral ischemia may help to find some new therapeutic targets and strategy for treatment of stroke.

Background. S100 Calcium Binding Protein A8 (S100A8) is beneficial for cancer immunotherapy. However, the processes underlying its therapeutic potential have not been completely studied. Methods. The Cancer Genome Atlas provides raw data on 33 different cancer types. GEO made available GSE67501, GSE78220, and IMvigor210. We investigated S100A8s genetic changes, expression patterns, and survival studies. The linkages between S100A8 and TME, as well as its association with immunological processes/elements and the major histocompatibility complex, were explored to effectively understand the role of S100A8 in cancer immunotherapy. Three distinct immunotherapeutic cohorts were employed to examine the relationship between S100A8 and immunotherapeutic response. Results. S100A8 expression was high in tumor tissue. The overexpression of S100A8 is associated with poor clinical outcome in patients with overall survival. S100A8 is associated with immune cell infiltration, immunological modulators, and immunotherapeutic indicators. S100A8 overexpression is connected to immune-related pathways. However, no statistically significant connection between S100A8 and immunotherapeutic response was identified. Conclusions. S100A8 may be a reliable biomarker for tumor prognosis and a viable prospective therapeutic target for human cancer immunotherapy (e.g., GBM, KIRC, LGG, and LIHC).

Background. Stomach adenocarcinoma (STAD) is a kind of cancer that begins in the stomach cells and has a poor overall survival rate. Following resection surgery, chemotherapy has been suggested as a curative method for stomach cancer. However, it is ineffective. Pyroptosis, a kind of inflammatory programmed cell death, has been shown to play a significant role in the development and progression of STAD. However, whether pyroptosis-related genes (PRGs) can be utilized to predict the diagnosis and prognosis of gastric cancer remains unknown. Method. The research measured at predictive PRGs in STAD samples from TCGA and GEO. Lasso regression was used to build the prediction model. Coexpression analysis revealed that gene expression was linked to pyroptosis. PRGs were found to be overexpressed in high-risk individuals, implying that they could be used in a model to predict STAD prognosis. Result. Immunological and tumor-related pathways were discovered using GSEA. In STAD patients, the genes GPX3, PDGFRL, RGS2, and SERPINE1 may be connected to the cancer process. The levels of expression also differed between the two risk groups. Conclusion. The purpose of this study is to identify and verify STAD-associated PRGs that can effectively guide prognosis and the immunological milieu in STAD patients as well as offer evidence for the development of pyroptosis-related molecularly targeted therapeutics. Therefore, PRGs and the link between immunological and PRGs in STAD may be therapeutic targets.

Osteoporosis is a global high prevalence of chronic metabolic disease with serious disability-adjusted life years losing. Acupuncture is used to treat osteoporosis broadly in China and other countries although the evidence on effectiveness cannot give a certain answer. The aim of this systematic review protocol is to appraise the efficacy and safety of acupuncture for osteoporosis. A literature search of randomized controlled trials focusing on acupuncture for osteoporosis will be performed in the databases of Medline, Cochrane Library, Web of Science, EBASE, Springer, WHO International Clinical Trials Registry Platform (ICTRP), China National Knowledge Infrastructure (CNKI), Wan fang, Chinese Biomedical Literature Database (CBM), Chinese Scientific Journal Database (VIP), and other possible resources with a valid search strategy. Outcomes of pain, bone mineral density, fracture, mortality, improvement proportion, biochemical indicators, quality of life, adverse event, and other valid will be extracted and merged for quantitative analysis using Review Manager software (V.5.3.5) or descriptive analysis correspondingly. This is the first systematic review to estimate the effect of acupuncture on osteoporosis, and the result may provide evidence to clinical doctor. PROSPERO CRD42016037829

Background. Gastric carcinoma (GC) is a kind of digestive tract tumor that is highly malignant and has a very poor prognosis. Although both Astragalus mongholicus (AM, huáng qí) and Curcuma phaeocaulis Valeton (CPV, é zhú) can slow the onset and progression of GC, the mechanism by which AM-CPV works in the treatment of GC is uncertain. Materials and Methods. The traditional Chinese medicine network databases TCMSP, TCMID, and ETCM were used to identify the key functional components and associated targets of AM and CPV. To establish a theoretical foundation, the development of gastric cancer (GC) was predicted utilizing a GEO gene chip and TCGA difference analysis mixed with network pharmacology. A herbal-ingredient-target network and a core target-signal pathway network were created using GO and KEGG enrichment analyses. The molecular docking method was used to evaluate seventeen main targets and their compounds. Results. Cell activity, reactive oxygen species modification, metabolic regulation, and systemic immune activation may all be involved in the action mechanism of the AM-CPV drug-pair in the treatment of GC. It inhibits the calcium signaling route, the AGE-RAGE signaling system, the cAMP signaling pathway, the PI3K-Akt signaling network, and the MAPK signaling pathway, slowing the progression of GC. The number of inflammatory substances in the tumor microenvironment is reduced, GC cell proliferation is deprived, apoptosis is promoted, and GC progression is retarded through controlling the IL-17 signaling route, TNF signaling pathway, and other inflammation-related pathways. Conclusions. The AM-CPV pharmaceutical combination regulates GC treatment via a multitarget, component, and signal pathway with a cooperative and bidirectional regulatory mechanism. Its active constituents may treat GC by regulating the expression of STAT1, MMP9, IL6, HSP90AA1, JUN, CCL2, IFNG, CXCL8, and other targets, as well as activating or inhibiting immune-inflammatory and cancer signaling pathways.