We propose an in situ poling of vertically well-aligned piezoelectric nanowire arrays with preferential polarization orientation as highly sensitive self-powered sensors for monitoring vital signs.

Wide‐bandgap perovskites have great potential to enable high‐efficiency tandem photovoltaics by combining with the well‐established low‐bandgap absorbers. However, such wide‐bandgap perovskites are often necessarily constructed with a high Br content, and thus faced with issues of phase segregation–induced photoinstability and high defect density, severely hindering their photovoltaic performance. Herein, a remarkable boost of the stability and efficiency of wide‐bandgap perovskite solar cells (PSCs) is demonstrated by simply incorporating potassium ions. Experiments have shown the interstitial occupancy of potassium ions in the perovskite lattice and the formation of 2D K2PbI4 at the grain boundaries, both can reduce the trap density and inhibit ion migration, and thus suppress nonradiative recombination and photoinduced phase segregation. The average power conversion efficiency (PCE) of photovoltaic devices based on the perovskite with 40% Br is improved from 15.28% to 17.94%, among which the champion efficiency is 18.38% with an optimal 15% KI incorporation. Importantly, the champion open‐circuit voltage (Voc) remains unchanged (≈1.25 V) even when the bandgap reduces from 1.80 to 1.75 eV due to KI doping, effectively reducing the Voc deficit. In addition, the unencapsulated cells can sustain 94% of the initial PCE after 2000 h of storage in ambient atmosphere, affirming their outstanding stability.

Objective: To investigate the underlying mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in hypoxic-ischemic (HI)-induced neonatal cerebral palsy. Materials and methods: Neonatal rat model of HI injury was established to detect the motor function. LncRNA MIAT, miR-211, glial cell line-derived neurotrophic factor (GDNF) and caspase-3 expressions were measured by qRT-PCR or western blot. The apoptosis of Neuro2A cells was detected by flow cytometry. RNA immunoprecipitation (RIP) and RNA pull-down assays were performed to confirm the interaction between MIAT and miR-211. Results: Compared with control group, lncRNA MIAT and GDNF were downregulated in striatal tissues of neonatal rats in HI group and oxygen glucose deprivation (OGD)-induced ischemic injury of Neuro2A cells, whereas miR-211 was up-regulated in striatal tissues of HI group and OGDinduced ischemic injury of Neuro2A cells. LncRNA MIAT interacted with miR-211, and lncRNA MIAT overexpression reduced neuron apoptosis through miR-211. Besides, GDNF expression was positively regulated by lncRNA MIAT and negatively regulated by miR-211 in Neuro2A cells. In vivo experiment proved MIAT promoted motor function and relieved HI injury. Conclusion: MIAT overexpression reduced apoptosis of Neuro2A cells through miR-211/GDNF, which relieved HI injury of neonatal rats.

No abstract

Nonlinear holography has recently emerged as a novel tool to reconstruct the encoded information at a new wavelength, which has important applications in optical display and optical encryption. However, this scheme still struggles with low conversion efficiency and ineffective multiplexing. In this work, we demonstrate a quasi-phase-matching (QPM) -division multiplexing holography in a three-dimensional (3D) nonlinear photonic crystal (NPC). 3D NPC works as a nonlinear hologram, in which multiple images are distributed into different Ewald spheres in reciprocal space. The reciprocal vectors locating in a given Ewald sphere are capable of fulfilling the complete QPM conditions for the high-efficiency reconstruction of the target image at the second-harmonic (SH) wave. One can easily switch the reconstructed SH images by changing the QPM condition. The multiplexing capacity is scalable with the period number of 3D NPC. Our work provides a promising strategy to achieve highly efficient nonlinear multiplexing holography for high-security and high-density storage of optical information.

Cordycepin (3′-deoxyadenosine) is a naturally occurring adenosine analog and one of the bioactive constituents isolated from Cordyceps sinensis, species of the fungal genus Cordyceps. It has traditionally been a prized Chinese folk medicine for the human well-being. However, the actions of cordycepin against renal ischemia/reperfusion injury (I/R) are still unknown. In the present study, rats were subject to I/R and cordycepin was intragastrically administered for seven consecutive days before surgery to investigate the effects and mechanisms of cordycepin against renal I/R injury. The test results of kidney and peripheral blood samples of experimental animals showed that cordycepin significantly decreased serum blood urea nitrogen and creatinine levels and markedly attenuated cell injury. Mechanistic studies showed that cordycepin significantly regulated inflammation, apoptosis, and oxidative stress. These data provide new insights for investigating the natural product with the nephroprotective effect against I/R, which should be developed as a new therapeutic agent for the treatment of I/R in the future.

Through the roles of vitamin B1 and B12 in neuroprotection and in improving cerebral palsy symptoms have been previously noticed, the action mechanism is still unclear. This study aims to investigate the protective effect of vitamin B1 and B12 on neuron injury in cerebral palsy and to clarify the mechanism of vitamin B1 and B12 inhibiting neurons apoptosis, and to focus on the role of lncRNA MALAT1 in this process. In order to investigate the effect of vitamin B1 and B12 on neurons injury in vivo and on neuron apoptosis in vitro, we, respectively, introduced vitamin B1 and B12 into cerebral palsy rat and in apoptosis-induced N2A neurons by Oxygen Glucose Deprivation/reoxygenation (OGD/R). Our results demonstrated that vitamin B1 and B12 treatment improved the motor and memory functions and ameliorated the neurons injury in cerebral palsy rats. OGD/R treatment repressed the expression of MALAT1 and BDNF and the phosphorylation of PI3K and Akt, and enhanced the miR-1 expression, which were all reversed by vitamin B1 and B12 treatment in N2A neurons. Vitamin B1 and B12 inhibited miR-1 expression through MALAT1, promoted BDNF expression and activated PI3K/Akt signaling through the MALAT1/miR-1 axis. Vitamin B1 and B12 suppressed neuron apoptosis by up-regulating BDNF via MALAT1/miR-1 pathway. MALAT1 interference abolished the neuroprotective effect of vitamin B1 and B12 in cerebral palsy rats. Collectively, vitamin B1 and B12 up-regulates BDNF and its downstream PI3K/ Akt signaling through MALAT1/miR-1 axis, thus suppressing neuron apoptosis and mitigating nerve injury in cerebral palsy rats.

This study aimed to explore the correlation between red blood cell (RBC) transfusion volume and patient mortality in massive blood transfusion. A multicenter retrospective study was carried out on 1,601 surgical inpatients who received massive blood transfusion in 20 large comprehensive hospitals in China. According to RBC transfusion volume and duration, the patients were divided into groups as follows: 0–4, 5–9, 10–14, 15–19, 20–24, 25–29, 30–39 and ≥40 units within 24 or 72 h. Mortality in patients with different RBC transfusion volumes was analyzed. It was found that patient mortality increased with the increase in the volume of RBC transfusion when the total RBC transfusion volume was ≥10 units within 24 or 72 h. Survival analysis revealed significant differences in mortality according to the RBC transfusion volume (χ2=72.857, P<0.001). Logistic regression analysis revealed that RBC transfusion volume is an independent risk factor [odds ratio (OR) = 0.52; confidence interval (CI): 0.43–0.64; P<0.01] for the mortality of patients undergoing a massive blood transfusion. When RBCs were transfused at a volume of 5–9 units within 24 and 72 h, the mortality rate was the lowest, at 3.7 and 2.3% respectively. It is concluded that during massive blood transfusion in surgical inpatients, there is a correlation between RBC transfusion volume within 24 or 72 h and the mortality of the patients. Patient mortality increases with the increase in the volume of RBC transfusion. RBC transfusion volume, the length of stay at hospital and intensive care unit stay constitute the independent risk factors for patient mortality.