Search

This study systematically analyzes the relationship of vitamin A on the neonatal respiratory diseases. An extensive literature search for relevant studies was conducted on PubMed, Web of Science, and so on. After screening in strict accordance with the inclusion and exclusion criteria, 12 articles on vitamin A deficiency and 12 articles on vitamin A supplementation were included. Stata 17.0 software was used to perform meta‐analysis, heterogeneity test, and sensitivity analysis, and the corresponding mathematical model was used to merge the data. The meta‐analysis results of the relationship between vitamin A deficiency and neonatal respiratory diseases indicated that compared with the neonates with normal vitamin A, the neonates with vitamin A deficiency had adverse health outcomes of neonatal respiratory diseases (OR = 4.86, 95% CI: 2.68–8.84), of which neonatal respiratory distress syndrome (NRDS) (OR = 4.10, 95% CI: 2.32–7.23) and neonatal pneumonia (OR = 3.22, 95% CI: 2.18–4.77) were analyzed by subgroup analysis. The meta‐analysis of the relationship between vitamin A supplementation therapy and neonatal respiratory diseases showed that vitamin A supplementation was an effective therapeutic measure for neonatal respiratory diseases (RR = 1.06, 95% CI: 1.04–1.07): NRDS (RR = 1.03, 95% CI: 1.02–1.05) and NBPD (RR = 1.08, 95% CI: 1.01–1.15). The funnel chart method results show that there was publication bias in studies on vitamin A deficiency induced to and vitamin A supplementation therapy for neonatal respiratory diseases. The sensitivity analysis results showed that excluding some special article had some effect on the final pooled effect. But generally speaking, the result of meta‐analysis was stable. There is a statistical correlation of vitamin A on the neonatal respiratory diseases from two aspects of etiological exploration and effect evaluation of treatment. [ABSTRACT FROM AUTHOR]

The global prevalence of gestational diabetes mellitus (GDM) is approximately 13. 4% and is expected to increase annually. However, the precise mechanism behind GDM remains to be established. Increasing evidence suggests that insulin resistance (IR) and β-cell impairment are key factors in the pathogenesis of GDM. Endoplasmic reticulum stress (ERS) is characterized by the activation of the unfolded protein response through three key endoplasmic reticulum transmembrane proteins: protein kinase RNA-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1α (IRE1α), and activating transcription factor 6 (ATF6). ERS is implicated in IR in adipose tissue, liver, skeletal muscle, and placenta, and also plays a crucial role in β-cell impairment through processes such as apopto-sis, pyroptosis, and autophagy. Therefore, targeting ERS could be a potential therapeutic approach for the prevention and treatment of GDM. This review explores the potential role of ERS in IR and β-cell dysfunction in GDM, and provides evidence for the preventive and intervention effects of bioactive compounds on GDM based on the ERS pathway. This aims to enhance our understanding of the molecular pathological basis of GDM and offer new strategies for its prevention and treatment. [ABSTRACT FROM AUTHOR]

Titanium dioxide nanoparticles (TiO2NPs) and cypermethrin (CPM) are widely used in various fields, and they can enter the environment in different ways. Combined exposure of TiO2NPs and CPM may increase the accumulation of pollutants in organisms and affect human health. This study was undertaken to evaluate the oxidative and inflammatory parameters associated with the combined exposure of TiO2NPs and CPM in rats. Twenty-four healthy male adult SD rats were randomly divided into four groups. The first group served as the control, while groups 2, 3, and 4 were treated with TiO2NPs (450 mg/m3); CPM (6.67 mg/m3) or combined exposure of TiO2NPs and CPM by inhalation for 90 days. We investigated the oxidative damage induced through combined exposure of TiO2NPs and CPM in rats by evaluating hematology of the rats and determining the blood biochemical index. Our results demonstrated that inhalation of TiO2NPs and CPM increased the levels of oxidative stress markers such as malondialdehyde and alkaline phosphatase in the serum of rats. These were accompanied by a decreased glutathione peroxidase and total superoxide dismutase levels. Furthermore, the level of glutathione peroxidase was further decreased while malondialdehyde was increased in the combined exposure of TiO2NPs and CPM. Interestingly, pathological sections showed that different degrees of tissue injury could be seen in the liver and lung tissues of each exposure group. In summary, the combined exposure of TiO2NPs and CPM can cause increased oxidative damage in rats and damage the tissue structure of the liver and lung. [ABSTRACT FROM AUTHOR]

Closing both the carbon and nitrogen loops is a critical venture to support the establishment of the circular, net‐zero carbon economy. Although single atom catalysts (SACs) have gained interest for the electrochemical reduction reactions of both carbon dioxide (CO2RR) and nitrate (NO3RR), the structure–activity relationship for Cu SAC coordination for these reactions remains unclear and should be explored such that a fundamental understanding is developed. To this end, the role of the Cu coordination structure is investigated in dictating the activity and selectivity for the CO2RR and NO3RR. In agreement with the density functional theory calculations, it is revealed that Cu‐N4 sites exhibit higher intrinsic activity toward the CO2RR, whilst both Cu‐N4 and Cu‐N4−x‐Cx sites are active toward the NO3RR. Leveraging these findings, CO2RR and NO3RR are coupled for the formation of urea on Cu SACs, revealing the importance of *COOH binding as a critical parameter determining the catalytic activity for urea production. To the best of the authors' knowledge, this is the first report employing SACs for electrochemical urea synthesis from CO2RR and NO3RR, which achieves a Faradaic efficiency of 28% for urea production with a current density of −27 mA cm–2 at −0.9 V versus the reversible hydrogen electrode. [ABSTRACT FROM AUTHOR]