In recent years, the study of oxidative stress (OS) has become increasingly popular. In particular, the role of OS on female fertility is very important and has been focused on closely. The occurrence of OS is due to the excessive production of reactive oxygen species (ROS). ROS are a double-edged sword; they not only play an important role as secondary messengers in many intracellular signaling cascades, but they also exert indispensable effects on pathological processes involving the female genital tract. ROS and antioxidants join in the regulation of reproductive processes in both animals and humans. Imbalances between pro-oxidants and antioxidants could lead to a number of female reproductive diseases. This review focuses on the mechanism of OS and a series of female reproductive processes, explaining the role of OS in female reproduction and female reproductive diseases caused by OS, including polycystic ovary syndrome (PCOS), endometriosis, preeclampsia and so on. Many signaling pathways involved in female reproduction, including the Keap1-Nrf2, NF-κB, FOXO and MAPK pathways, which are affected by OS, are described, providing new ideas for the mechanism of reproductive diseases.

Intestinal diseases caused by sleep deprivation (SD) are severe public health threats worldwide. This study focuses on the effect of melatonin on intestinal mucosal injury and microbiota dysbiosis in sleep‐deprived mice. Mice subjected to SD had significantly elevated norepinephrine levels and decreased melatonin content in plasma. Consistent with the decrease in melatonin levels, we observed a decrease of antioxidant ability, down‐regulation of anti‐inflammatory cytokines and up‐regulation of pro‐inflammatory cytokines in sleep‐deprived mice, which resulted in colonic mucosal injury, including a reduced number of goblet cells, proliferating cell nuclear antigen‐positive cells, expression of MUC2 and tight junction proteins and elevated expression of ATG5, Beclin1, p‐P65 and p‐IκB. High‐throughput pyrosequencing of 16S rRNA demonstrated that the diversity and richness of the colonic microbiota were decreased in sleep‐deprived mice, especially in probiotics, including Akkermansia, Bacteroides and Faecalibacterium. However, the pathogen Aeromonas was markedly increased. By contrast, supplementation with 20 and 40 mg/kg melatonin reversed these SD‐induced changes and improved the mucosal injury and dysbiosis of the microbiota in the colon. Our results suggest that the effect of SD on intestinal barrier dysfunction might be an outcome of melatonin suppression rather than a loss of sleep per se. SD‐induced intestinal barrier dysfunction involved the suppression of melatonin production and activation of the NF‐κB pathway by oxidative stress.

Hypoxia, a ubiquitously aberrant phenomenon implicated in tumor growth, causes severe tumor resistance to therapeutic interventions. Instead of the currently prevalent solution through intratumoral oxygen supply, we put forward an “O2-economizer” concept by inhibiting the O2 consumption of cell respiration to spare endogenous O2 and overcome the hypoxia barrier. A nitric oxide (NO) donor responsible for respiration inhibition and a photosensitizer for photodynamic therapy (PDT) are co-loaded into poly­(d,l-lactide-co-glycolide) nanovesicles to provide a PDT-specific O2 economizer. Once accumulating in tumors and subsequently responding to the locally reductive environment, the carried NO donor undergoes breakdown to produce NO for inhibiting cellular respiration, allowing more O2 in tumor cells to support the profound enhancement of PDT. Depending on the biochemical reallocation of cellular oxygen resource, this O2-economizer concept offers a way to address the important issue of hypoxia-induced tumor resistance to therapeutic interventions, including but not limited to PDT.

Hydrogels, consisting of hydrophilic polymers, can be used as films, scaffolds, nanoparticles and drug carriers. They are one of the hot research topics in material science and tissue engineering and are widely used in the field of biomedical and biological sciences. Researchers are seeking for a type of material that is similar to human tissues and can partially replace human tissues or organs. The hydrogel has brought possibility to solve this problem. It has good biocompatibility and biodegradability. After entering the body, it does not cause immune and toxic reactions. The degradation time can be controlled, and the degradation products are nontoxic and nonimmunogenic; the final metabolites can be excreted outside the body. Owing to the lack of blood vessels and poor migration ability of chondrocytes, the self-healing ability of damaged cartilage is limited. Tissue engineering has brought a new direction for the regeneration of cartilage. Drug carriers and scaffolds made of hydrogels are widely used in cartilage tissue engineering. The present review introduces the natural hydrogels, which are often used for cartilage tissue engineering with respect to synthesis, modification and application methods. The translational potential of this article This review introduces the natural hydrogels that are often used in cartilage tissue engineering with respect to synthesis, modification and application methods. Furthermore, the essential concepts and recent discoveries were demonstrated to illustrate the achievable goals and the current limitations. In addition, we propose the putative challenges and directions for the use of natural hydrogels in cartilage regeneration.

The ever-increasing consumption of fossil fuels and resultant environmental issues, such as global warming, ozone layer depletion and acid rains, necessitate searching for clean energy sources. [1] Hydrogen is considered to be a promising alternative to fossil fuels by virtue of its high energy density and environmental-friendliness. [2] Renewable energy (such as electricity produced from photovoltaics and wind farms) powered water splitting provides an attractive method for sustainable production of hydrogen. [3] However, the two half electrochemical reactions involved in a water splitting process, namely, the oxygen evolution reaction (OER) and hydrogen evolution reaction (HER), are kinetically sluggish, leading to significant electrode overpotentials, and thus requires efficient electrocatalysts to improve energy efficiency. [3] Currently, precious-metal based electrocatalysts, such as Ir/Ru for OER and Pt for HER, could realize low overpotentials for water splitting. Unfortunately, the scarcity and high cost of these precious metals greatly prohibit their widespread applications.To this end, efforts have been devoted to searching for low-cost alternatives [4][5][6][7][8] and numerous Received: ((will be filled in by the editorial staff))Revised: ((will be filled in by the editorial staff))

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To investigate the effects of various monochromatic lights on early posthatch changes in satellite cell mitotic activity of pectoral muscle, a total of 416 newly hatched broilers were exposed to blue light (BL), green light (GL), red light (RL), and white light (WL) by light emitting diode system for 3 weeks, respectively. Both, in culture and in vivo studies showed that after hatching, the relative number of satellite cells altered in correlation. The enhancement of satellite cell mitotic activity peaked at post-hatching day (P) 3 and then declined with age concomitantly with the rise in satellite cell differentiation and reduction of satellite cell proliferation. These alterations became more obvious in GL than in RL. The data suggested that early posthatch changes in satellite cell population of broilers occurred through the two different processes, i.e., cellular generation (before P3) and cellular degeneration (after P3). GL promoted significantly the broiler satellite cells to proliferate before P3 and to differentiate after P3. In addition, the circulating insulin-like growth factor-I (IGF-I) levels were higher in GL and BL groups versus WL and RL groups at P3 and P5 indicating that IGF-I plays a central role for GL illumination promoting broiler satellite cell myogenic processes during early posthatch stages. Anat Rec, 293:1315Rec, 293: -1324

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