In mammals, the microbiota can be transmitted from the placenta, uterus, and vagina of the mother to the infant. Unlike mammals, development of the avian embryo is a process isolated from the mother and thus in the avian embryo the gut microbial developmental process remains elusive. To explore the establishment and inheritance of the gut microbiome in the avian embryo, we used the chicken as the model organism to investigate the gut microbial composition in embryos, chicks, and maternal hens. We observed: (1) 28 phyla and 162 genera of microbes in embryos where the dominated genus was Halomonas (79%). (2) 65 genera were core microbiota in all stages with 42% and 62% gut microbial genera of embryo were found in maternal hen and chick, respectively. There was a moderate correlation (0.40) between the embryo and maternal, and 0.52 between the embryo and chick at the family level. (3) Gut microbes that are involved in substance metabolism, infectious disease, and environmental adaptation are enriched in embryos, chicks, and maternal hens, respectively. (4) 94% genera of gut microbial composition were similar among three different chicken breeds which were maintained under similar conditions. Our findings provide evidence to support the hypothesis that part of the microbial colonizers harbored in early embryos were inherited from maternal hens, and the gut microbial abundance and diversity were influenced by environmental factors and host genetic variation during development.

Proanthocyanidins (PCs) are naturally occurring polyphenolic compounds abundant in many vegetables, plant skins (rind/bark), seeds, flowers, fruits, and nuts. Numerous in vitro and in vivo studies have demonstrated myriad effects potentially beneficial to human health, such as antioxidation, anti-inflammation, immunomodulation, DNA repair, and antitumor activity. Accumulation of prooxidants such as reactive oxygen species (ROS) exceeding cellular antioxidant capacity results in oxidative stress (OS), which can damage macromolecules (DNA, lipids, and proteins), organelles (membranes and mitochondria), and whole tissues. OS is implicated in the pathogenesis and exacerbation of many cardiovascular, neurodegenerative, dermatological, and metabolic diseases, both through direct molecular damage and secondary activation of stress-associated signaling pathways. PCs are promising natural agents to safely prevent acute damage and control chronic diseases at relatively low cost. In this review, we summarize the molecules and signaling pathways involved in OS and the corresponding therapeutic mechanisms of PCs.

Establishing and maintaining beneficial interactions between the host and associated gut microbiota are pivotal requirements for host health. Autophagy is an important catabolic recycling pathway that degrades long-lived proteins and some organelles by lysosome to maintain cellular homeostasis. Although impaired autophagy is thought to be closely correlated with Crohn's disease (CD), the functional role of autophagy in the maintenance of gut microbiota is poorly understood. As autophagy-related 5 () is a key gene associated with the extension of the phagophoric membrane in autophagic vesicles, we established a gut-specific knockout mouse model, and we found that the disruption of autophagic flux in the intenstinal epithelium cells dramatically altered the composition of the gut microbiota and reduced alpha diversity. Microbial function prediction indicated that the pathway allocated for infectious diseases was enriched in mice. " Arthromitus" and the family were increased in mice, whereas and the family were reduced. Transcriptome analysis revealed that two key inflammatory bowel disease (IBD)-related transcription factors, RORC and TBX21, of host cells were upregulated in mice, thus elevating the Muc2-related immunological response. The findings suggest that intestinal autophagy plays a vital role in modulating the diversity and composition of gut microbiota. The homeostasis of host-microbiota interactions is of great importance to host health. Previous studies demonstrated that disruption of autophagy was linked to inflammatory bowel disease. However, the interaction mechanism of gut microbiota regulated by autophagy was obscure. In an intestinal epithelium-specific autophagy-related 5 () knockout mouse model, we observed a significant alteration and decreased diversity in the gut microbiota of -deficient mice compared with that of wild-type mice. Although the numbers of some organisms (e.g., and members of the family) associated with the control of inflammation decreased, those of proinflammationory bacteria (e.g., " Arthromitus") and potential pathogens (the family) increased in mice. Differential gene expression analysis revealed that two key genes, and, involved in inflammatory bowel disease were upregulated in mice. Our study suggests that deficiency results in an imbalance of the host-microbe interaction and deterioration of the gut microenvironment.

A novel actinomycete, designated strain NEAU-GRX11(T), was isolated from muddy soil collected from a stream of Jinlong Mountain in Harbin, north China. The organism was found to have morphological and chemotaxonomic characteristics typical of the genus Micromonospora. The 16S rRNA gene sequence of strain NEAU-GRX11(T) showed highest similarity to Micromonospora zamorensis CR38(T) (99.2 %), Micromonospora saelicesensis Lupac 09(T) (99.0 %), Micromonospora chokoriensis 2-19/6(T) (98.7 %), Micromonospora coxensis 2-30-b/28(T) (98.5 %), Micromonospora aurantiaca ATCC 27029(T) (98.4 %) and Micromonospora lupini lupac 14N(T) (98.3 %). Phylogenetic analysis based on the 16S rRNA gene and gyrB gene demonstrated that strain NEAU-GRX11(T) was a member of the genus Micromonospora and supported the closest phylogenetic relationship to M. zamorensis CR38(T), M. saelicesensis Lupac 09(T), M. chokoriensis 2-19/6(T) and M. lupini lupac 14N(T). A combination of DNA-DNA hybridization and some phenotypic characteristics indicated that the novel strain could be readily distinguished from these closest phylogenetic relatives. Therefore, it is proposed that NEAU-GRX11(T) represents a novel species of the genus Micromonospora, for which the name Micromonospora jinlongensis sp. nov. is proposed. The type strain is NEAU-GRX11(T) (=CGMCC 4.7103(T)=DSM 45876(T)).

LF-rTMS and HF-rTMS are both beneficial to the recovery of linguistic function in patients with post-stroke non-fluent aphasia. LF-rTMS produced immediate benefits that persisted long-term, while HF-rTMS only produced long-term benefits. In addition, the benefits produced with LF-rTMS were more marked than those produced by HF-rTMS.

Pruritus, the most common cutaneous symptom, is widely seen in many skin complaints. It is an uncomfortable feeling on the skin and sometimes impairs patients' quality of life. At present, the specific mechanism of pruritus still remains unclear. Antihistamines, which are usually used to relieve pruritus, ineffectively work in some patients with itching. Recent evidence has suggested that, apart from histamine, many mediators and signaling pathways are involved in the pathogenesis of pruritus. Various therapeutic options for itching correspondingly have been developed. In this review, we summarize the updated pathogenesis and therapeutic strategies for pruritus.

The crosstalk between the gut microbiota and immune state of the host is an essential focus in academia and clinics. To explore the dynamic role of the microbiota in response to immune deficiency, we comprehensively assessed the microbiome of 90 mouse fecal samples, across three time points including two immunodeficiency models, namely severe combined immunodeficient (SCID) mice and non-obese diabetic SCID (NOD/SCID) mice, with BALB/cA as a control strain. Metagenomic analysis revealed a decrease in alpha diversity and the existence of a clear structural separation in the microbiota of immunodeficient mice. Although nuances exist between SCID and NOD/SCID mice, an increase in the protective microbiota, in particular Lactobacillus, contributed the most to the discrimination of immunodeficient and control mice. Further data regarding the red blood cell (RBC) concentration and serum IgA level during different stages of development support the concept of the microbiota alleviating the advancement of immune deficiency, which is called microbial compensation. Taken together, these results demonstrate the dynamic impact of immunodeficiency on the gut microbiota and the adaptive alteration of the microbiota that may influence the host state.

Psoriasis is a common, chronic, inflammatory skin disease that affects 2%-4% of the global population. Recent studies have shown that increased oxidative stress (OS) and T-cell abnormalities are central to the pathogenesis of this disease. The resulting reactive oxygen species (ROS) induces proliferation and differentiation of Th17/Th1/Th22 cells and inhibits the anti-inflammatory activities of regulatory T lymphocytes (Treg). Subsequent secretions of inflammatory cytokines, such as interleukin (IL)-17, IL-22, tumor necrosis factor alpha (TNF-α), and interferon-gamma (IFN-γ), and vascular endothelial growth factor (VEGF), stimulate keratinocyte proliferation and angiogenesis. Proanthocyanidins are a class of flavonoids from plants and fruits, and have various antioxidant, anti-inflammatory, and anti-angiogenic properties. Numerous reports have demonstrated therapeutic effects of proanthocyanidins for various diseases. Among clinical activities, proanthocyanidins suppress cell proliferation, prevent OS, and regulate Th17/Treg cells. Because the pathogenesis of psoriasis involves OS and T cells dysregulation, we reviewed the effects of proanthocyanidins on OS, Th17 and Treg cell activities, and keratinocyte proliferation and angiogenesis. Data from multiple previous studies warrant consideration of proanthocyanidins as a promising strategy for the treatment of psoriasis.