Construction of Low-Cost Z-Scheme Heterojunction Cu2O/PCN-250 Photocatalysts Simultaneously for the Enhanced Photoreduction of CO2 to Alcohols and Photooxidation of Water.

Solar-driven high-efficiency conversion of CO2 with water vapor into high-value-added alcohols is a promising approach for reducing CO2 emissions and achieving carbon neutrality. However, the rapid recombination of photogenerated carriers and low CO2 adsorption capacity of photocatalysts are usually the factors that limit their applicability. Herein, a series of low-cost Z-scheme heterostructures Cu2O/PCN-250-x are constructed by in situ growth of ultrasmall Cu2O nanoparticles on PCN-250. A systematic investigation revealed that there is a strong interaction between Cu2O nanoparticles and PCN-250. The resulting Cu2O/PCN-250-2 exhibits excellent photogenerated carrier separation efficiency and CO2 adsorption capacity, which dramatically promote the conversion of CO2 into alcohols. Notably, the total yield of 268 µmol gcat-1 for the production of CH3OH and CH3H2OH is superior to that of isolated PCN-250 and Cu2O. This study provides a new perspective for the design of a Cu2O nanoparticle/metal-organic framework Z-scheme heterojunction for the reduction of CO2 to alcohols with water vapor.

Oxidative stress: Roles in skeletal muscle atrophy.

Oxidative stress, inflammation, mitochondrial dysfunction, reduced protein synthesis, and increased proteolysis are all critical factors in the process of muscle atrophy. In particular, oxidative stress is the key factor that triggers skeletal muscle atrophy. It is activated in the early stages of muscle atrophy and can be regulated by various factors. The mechanisms of oxidative stress in the development of muscle atrophy have not been completely elucidated. This review provides an overview of the sources of oxidative stress in skeletal muscle and the correlation of oxidative stress with inflammation, mitochondrial dysfunction, autophagy, protein synthesis, proteolysis, and muscle regeneration in muscle atrophy. Additionally, the role of oxidative stress in skeletal muscle atrophy caused by several pathological conditions, including denervation, unloading, chronic inflammatory diseases (diabetes mellitus, chronic kidney disease, chronic heart failure, and chronic obstructive pulmonary disease), sarcopenia, hereditary neuromuscular diseases (spinal muscular atrophy, amyotrophic lateral sclerosis, and Duchenne muscular dystrophy), and cancer cachexia, have been discussed. Finally, this review proposes the alleviation oxidative stress using antioxidants, Chinese herbal extracts, stem cell and extracellular vesicles as a promising therapeutic strategy for muscle atrophy. This review will aid in the development of novel therapeutic strategies and drugs for muscle atrophy.

Chronic kidney disease-induced muscle atrophy: Molecular mechanisms and promising therapies.

Chronic kidney disease (CKD) is a high-risk chronic catabolic disease due to its high morbidity and mortality. CKD is accompanied by many complications, leading to a poor quality of life, and serious complications may even threaten the life of CKD patients. Muscle atrophy is a common complication of CKD. Muscle atrophy and sarcopenia in CKD patients have complex pathways that are related to multiple mechanisms and related factors. This review not only discusses the mechanisms by which inflammation, oxidative stress, mitochondrial dysfunction promote CKD-induced muscle atrophy but also explores other CKD-related complications, such as metabolic acidosis, vitamin D deficiency, anorexia, and excess angiotensin II, as well as other related factors that play a role in CKD muscle atrophy, such as insulin resistance, hormones, hemodialysis, uremic toxins, intestinal flora imbalance, and miRNA. We highlight potential treatments and drugs that can effectively treat CKD-induced muscle atrophy in terms of complication treatment, nutritional supplementation, physical exercise, and drug intervention, thereby helping to improve the prognosis and quality of life of CKD patients.

Diabetic Muscular Atrophy: Molecular Mechanisms and Promising Therapies.

Diabetes mellitus (DM) is a typical chronic disease that can be divided into 2 types, dependent on insulin deficiency or insulin resistance. Incidences of diabetic complications gradually increase as the disease progresses. Studies in diabetes complications have mostly focused on kidney and cardiovascular diseases, as well as neuropathy. However, DM can also cause skeletal muscle atrophy. Diabetic muscular atrophy is an unrecognized diabetic complication that can lead to quadriplegia in severe cases, seriously impacting patients' quality of life. In this review, we first identify the main molecular mechanisms of muscle atrophy from the aspects of protein degradation and synthesis signaling pathways. Then, we discuss the molecular regulatory mechanisms of diabetic muscular atrophy, and outline potential drugs and treatments in terms of insulin resistance, insulin deficiency, inflammation, oxidative stress, glucocorticoids, and other factors. It is worth noting that inflammation and oxidative stress are closely related to insulin resistance and insulin deficiency in diabetic muscular atrophy. Regulating inflammation and oxidative stress may represent another very important way to treat diabetic muscular atrophy, in addition to controlling insulin signaling. Understanding the molecular regulatory mechanism of diabetic muscular atrophy could help to reveal new treatment strategies.

The effect of HES130/0.4 sodium chloride solution on kidney function following early fluid resuscitation in shock patients.

BACKGROUND: Doctors often use a small dose of hydroxyethyl starch (HES) 130/0.4 sodium chloride solution in the emergency room; however, its effect on kidney function remains controversial. This study aimed to evaluate the effect of a small dose of HES130/0.4 sodium chloride solution on kidney function in shock patients during early fluid resuscitation. METHODS: This cohort study retrospectively analyzed the data of 129 shock patients requiring fluid resuscitation who had been admitted to the Emergency Department of the Affiliated Hospital of Nantong University from January 2019 to December 2020. Patients were divided into the observation group (n=40) and control group (n=89) according to the type of fluid resuscitation. In relation to the fluid resuscitation treatment, the observation group was treated with crystalloid solution, while the control group was treated with crystalloid and HES130/0.4 sodium chloride solution. To further explore the effect of a small dose of HES130/0.4 sodium chloride solution, the patients were further divided into the following 4 groups based on the specific fluid administered: (I) the HES(+), lactated Ringer's (LR)(+) group (n=85); (II) the HES(+), LR(-) group (n=4); (III) the HES(-), LR(+) group (n=31); and (IV) the HES(-), LR(-) group (n=9). The outcomes were in-hospital mortality and changes in creatinine (CR) level after fluid resuscitation. RESULTS: There were no significant differences in the in-hospital mortality rates between the observation and control groups (P=0.343). The CR levels of patients in the control and HES(+), LR(+) groups were reduced after fluid resuscitation (P=0.034; P=0.028). There was no significant change in patients' CR levels in the HES(+), LR(-) group after fluid resuscitation (P=0.999). CONCLUSIONS: Administering a small dose of HES 130/0.4 sodium chloride in patients with shock does not appear to affect kidney function and in-hospital mortality; however, these findings should be considered exploratory, and further studies should be conducted to confirm these results.