Theoretical study of piezoelectric and light absorption properties, and carrier mobilities of Janus TiPX (X = F, Cl, and Br) monolayers.

Janus TiPX (X = F, Cl, and Br) monolayers were systematically investigated through first-principles calculations. The Janus TiPX monolayers exhibit mechanical and dynamic stability. Two monolayers are indirect bandgap semiconductors, except the TiPBr monolayer, which has the features of a quasi-direct bandgap semiconductor.

3D Printing Graphene Oxide Soft Robotics.

We propose a universal strategy to 3D printing the graphene oxide (GO) complex structure with GO highly aligned and densely compacted, by the combination of direct ink writing and constrained drying. The constraints not only allow the generation of a huge capillary force accompanied by water evaporation at nanoscale, which induces the high compaction and alignment of GO, but also limit the shrinkage of the extruded filaments only along the wall thickness direction, therefore, successfully maintaining the uniformity of the structure at macroscale. We discover that the shrinkage stress gradually increased during the drying process, with the maximum exceeding ∼0.

miR-6769b-5p targets CCND-1 to regulate proliferation in cadmium-treated placental trophoblasts: Association with the impairment of fetal growth.

Environmental cadmium (Cd) is positively associated with placental impairment and fetal growth retardation. Nevertheless, its potential mechanisms remain unclear. microRNAs (miRNAs) are known to influence placental development and fetal growth.

Environmental cadmium impairs blood-testis barrier via activating HRI-responsive mitochondrial stress in mice.

Cadmium (Cd) is a well-known testicular toxicant. Blood-testis barrier (BTB), a vital part of testes, which has been reported to be damaged upon Cd exposure. However, the detailed mechanism about Cd-mediated disruption of BTB remains unclear.

Gestational exposure to environmental cadmium induces placental apoptosis and fetal growth restriction via Parkin-modulated MCL-1 degradation.

Heavy metal cadmium (Cd), a classical environmental pollutant, causes placental apoptosis and fetal growth restriction (FGR), whereby the mechanism remains unclear. Here, our human case-control study firstly showed that there was a positive association of Parkin mitochondrial translocation, MCL-1 reduction, placental apoptosis, and all-cause FGR. Subsequently, Cd was administered to establish in vitro and in vivo models of placental apoptosis or FGR.

Gestational cadmium exposure impairs placental angiogenesis via activating GC/GR signaling.

Gestational exposure to environmental Cd caused placental angiogenesis impairment and fetal growth restriction (FGR). However, its mechanism remained unclear. This study was to investigate the effects of Cd exposure during pregnancy on placental angiogenesis and its mechanism.

Environmental cadmium exposure during pregnancy causes diabetes-like phenotypes in mouse offspring: Association with oxidative stress in the fetal liver.

Cadmium (Cd), a noxious heavy metal, is widespread in the living environment. Gestational exposure to Cd at environmental dose has been shown to cause fetal growth restriction (FGR). However, the long-term effects and the mechanisms underlying environmental Cd exposure on glucose metabolism in offspring remain unclear.

Melatonin protects against environmental stress-induced fetal growth restriction via suppressing ROS-mediated GCN2/ATF4/BNIP3-dependent mitophagy in placental trophoblasts.

Gestational exposure to environmental stress induces fetal growth restriction (FGR), and thereby increasing the risk of infant death and chronic noncommunicable diseases in adults. However, the mechanism by which environmental stress induces FGR remains unclear. Based on case-control study, we found that the reduced level of melatonin (MT), a major secretory product from the pineal gland, was observed in placentae of FGR.

Environmental cadmium exposure induces fetal growth restriction via triggering PERK-regulated mitophagy in placental trophoblasts.

Cadmium (Cd), an environmental toxicant, is positively associated with fetal growth restriction (FGR). However, the mechanism by which gestational exposure to Cd induces FGR remains unclear. This study designed in vitro and in vivo experiments to explore the role of placental mitophagy in Cd-impaired fetal growth.

Autophagy in Sertoli cell protects against environmental cadmium-induced germ cell apoptosis in mouse testes.

Cadmium (Cd) was an environmental pollutant, which could result in germ cell apoptosis in testes. Sertoli-germ cell communication was vital for germ cell development and maturity. However, little was known about the effect of Sertoli cell autophagy on Cd-induced germ cell apoptosis.

Cadmium down-regulates 11β-HSD2 expression and elevates active glucocorticoid level via PERK/p-eIF2α pathway in placental trophoblasts.

Fetal overexposure to active glucocorticoid (GC) is the major cause for fetal growth restriction (FGR). This study investigated the influences of cadmium (Cd) exposure on active GC and its mechanism in placental trophoblasts. Pregnant mice were exposed to CdCl (4.

[Observation on therapeutic effects of electroacupuncture at Neiguan (PC 6) on silent myocardial ischemia].

Objective: To observe the therapeutic effects of acupuncture at Neiguan (PC 6) on silent myocardial ischemia (SMI).

Methods: Forty patients with SMI were randomly divided into an electroacupuncture group and a medicine group, 20 cases in each group. The Electroacupuncture group was treated with electroacupuncture and Neiguan (PC 6) was selected as the main acupoint, and the other acupoints were selected by syndrome differentiation.