A Transparent Additive-Free Fibrous Facial Mask for Skin Moisturizing.

Most sheet facial masks for skincare are made of nonwovens and loaded with liquid active ingredients, which are usually opaque and require additives for long-term preservation. Herein, a Transparent Additive-Free Fibrous (TAFF) facial mask is reported for skin moisturizing. The TAFF facial mask consists of a bilayer fibrous membrane. The inner layer is fabricated by electrospinning functional components of gelatin (GE) and hyaluronic acid (HA) into a solid fibrous membrane to get rid of additives, the outer layer is an ultrathin PA6 fibrous membrane that is highly transparent, especially after absorbing water. The results indicate that the GE-HA membrane can quickly absorb water and become a transparent hydrogel film. By employing the hydrophobic PA6 membrane as the outer layer, directional water transport is achieved, which enables TAFF facial mask with excellent skin moisturizing effect. The skin moisture content is up to 84% ± 7% after placing the TAFF facial mask on the skin for 10 min. In addition, the relative transparency of the TAFF facial mask on the skin reaches 97.0% ± 1.9% when ultrathin PA6 membrane is used as the outer layer. The design of the transparent additive-free facial mask may serve as a guideline for developing new functional facial masks.

Down-Regulated microRNA-192-5p Protects Against Hypoxic-Ischemic Brain Damage via Regulation of YAP1-Mediated Hippo Signaling Pathway.

Hypoxic-ischemic brain damage (HIBD) is a familiar neurological disorder. Emerging reports manifest that microRNAs (miRs) are related to the progression of HIBD. The goal of this study is to explore the mechanism of miR-192-5p in HIBD via regulation of Yes-associated protein 1 (YAP1)-mediated Hippo signaling pathway. The miR-192-5p, YAP1, and Hippo pathway-related factors Phospho (p)-Triaminoguanidinium azide (TAZ) in hippocampal tissues and neurons were detected. The regulatory relationship between miR-192-5p and YAP1 was verified. Neonatal hypoxic ischemia and oxygen-glucose deprivation (OGD) were used to simulate HIBD in vivo and in vitro. The neurobehavioral impairment, neuronal damage and vascular endothelial growth factor (VEGF) expression of neonatal rats in each group were detected. The viability, apoptosis and VEGF expression of hippocampal neurons in each group were also examined. MiR-192-5p expression was elevated while YAP1 expression was reduced in hippocampal tissues of HIBD rats in vivo and OGD neurons in vitro. MiR-192-5p had a targeting relation with YAP1. Suppressed miR-192-5p or overexpressed YAP1 in HIBD rats alleviated neurobehavioral impairment and neuronal damage, and decreased the expression levels of p-TAZ and VEGF expression in vivo. Reduced miR-192-5p or augmented YAP1 decelerated the neuron apoptosis, decreased the p-TAZ level and VEGF level and promoted cell viability of OGD hippocampal neurons in vitro. The study highlights that inhibited miR-192-5p protects against HIBD via regulation of YAP1 and Hippo signaling pathway, which is beneficial for HIBD treatment.

Heart failure, metabolic acidosis, and postoperative multiple organ failure after anesthesia for cesarean section in a patient with Takayasu arteritis: a case report.

The incidence of Takayasu arteritis (TA) is approximately one in 200,000. The prevalence of this disease is higher among Asian women under the age of 30. Most pregnant women with mild TA receive spinal anesthesia for cesarean sections. Despite difficulties in measuring blood pressure, the entire surgical process, including the administering of anesthesia, is generally stable. Studies in this area are rare. The authors report a case of a pregnant woman with TA who received anesthesia for a cesarean section and then suffered for heart failure, metabolic acidosis, and postoperative multiple organ failure. The authors hope to contribute to the clinical studies on the subject of anesthesia for pregnant women with TA.

Comparing Electrochemical Passivation and Surface Film Chemistry of 654SMO Stainless Steel and C276 Alloy in Simulated Flue Gas Desulfurization Condensates.

This research examines the behavior of electrochemical passivation and the chemistry of surface films on 654SMO super austenitic stainless steel and C276 nickel-based alloy in simulated condensates from flue gas desulfurization in power plant chimneys. The findings indicate that the resistance to polarization of the protective film on both materials initially rises and then falls with either time spent in the solution or the potential of anodic polarization. Comparatively, 654SMO exhibits greater polarization resistance than C276, indicating its potential suitability as a chimney lining material. Mott-Schottky analysis demonstrates that the density of donors in the passive film formed on 654SMO exceeds that on C276, potentially due to the abundance of Fe oxide in the passive film, which exhibits the characteristics of an n-type semiconductor. The primary components of the passive films on both materials are Fe oxides and Cr oxides. The formation of a thin passive film on C276 in the simulated condensates is a result of the low Gibbs free energy of nickel oxide and low Cr content. The slower diffusion coefficient of point defects leads to the development of a thicker and more compact passive film on the surface of 654SMO.

Alzheimer's disease, a metabolic disorder: Clinical advances and basic model studies (Review).

Alzheimer's disease (AD) is a type of neurodegenerative disease characterized by cognitive impairment that is aggravated with age. The pathological manifestations include extracellular amyloid deposition, intracellular neurofibrillary tangles and loss of neurons. As the world population ages, the incidence of AD continues to increase, not only posing a significant threat to the well-being and health of individuals but also bringing a heavy burden to the social economy. There is epidemiological evidence suggesting a link between AD and metabolic diseases, which share pathological similarities. This potential link would deserve further consideration; however, the pathogenesis and therapeutic efficacy of AD remain to be further explored. The complex pathogenesis and pathological changes of AD pose a great challenge to the choice of experimental animal models. To understand the role of metabolic diseases in the development of AD and the potential use of drugs for metabolic diseases, the present article reviews the research progress of the comorbidity of AD with diabetes, obesity and hypercholesterolemia, and summarizes the different roles of animal models in the study of AD to provide references for researchers.

Block Copolymer Nanomicelle-Encapsulated Curcumin Attenuates Cerebral Ischemia Injury and Affects Stem Cell Marker Expression by Inhibiting lncRNA GAS5.

Stroke has become the most common cause of death among residents in China, among which ischemic stroke accounts for the vast majority reaching 70% to 80%. It is of great importance to actively investigate the protective mechanism of cerebral ischemia injury after IS (ischemic stroke). We constructed cerebral ischemia injury models in vivo MACO rat and in vitro (oxygen-glucose deprivation cell model) and set up different interference groups. RT-PCR (reverse transcription PCR) was conducted to detect the expression of lncRNA in neuronal cells, brain tissue, and plasma of different groups, and ELISA (enzyme-linked immunosorbent assay) and western blot were used to detect the expression of the protein in neuronal cells, brain tissue, and plasma of different groups. Cell activity was detected by the CCK-8 assay, while cell apoptosis was examined by TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) assay. In the rats' neuronal cells and brain tissue, curcumin can inhibit the expression of lncRNA GAS5 (long noncoding RNA growth arrest-specific 5). In oxygen-glucose-deprived neuronal cells in vitro, curcumin and low-expressed lncRNA GAS5 can enhance cell activity and decline cell apoptosis, but the addition of curcumin and overexpressed lncRNA GAS5 can make this phenomenon disappear. In neuronal cells, plasma, and brain tissue, curcumin and the low-expressed lncRNA GAS5 can inhibit the expression of IL-1ß (interleukin 1 beta), TNF-α (tumor necrosis factor alpha), IL-6 (interleukin 6), Sox2 (SRY-box transcription factor 2), Nanog, and Oct4 (octamer-binding transcription factor 4). However, overexpressed lncRNA GAS5 and curcumin made the inhibitory effect disappear. In conclusion, this study demonstrated that curcumin could inhibit the expression of lncRNA GAS5, thereby inhibiting the expression of inflammation-related factors IL-1ß, TNF-α, and IL-6, and ultimately achieve the purpose of attenuating cerebral ischemic cell damage. However, curcumin and lncRNA GAS5 may not alleviate cerebral ischemic cell damage by affecting stem cell differentiation.

Interfacial Manipulation via In Situ Constructed Fast Ion Transport Channels toward an Ultrahigh Rate and Practical Li Metal Anode.

The successful substitution of Li metal for the conventional intercalation anode can promote a significant increase in the cell energy density. However, the practical application of the Li metal anode has long been fettered by the unstable solid electrolyte interface (SEI) layer on the Li metal surface and notorious dendritic Li growth. Herein, a stabilized SEI layer with in situ constructed fast ion transport channels has successfully been achieved by a robust In2S3-cemented poly(vinyl alcohol) coating. The modified Li metal demonstrates significantly enhanced Coulombic efficiency, high rate performance (10 mA cm-2), and ultralong life cycling stability (∼4900 cycles). The Li|LiCoO2 (LCO) cell presents an ultralong-term stable operation over 500 cycles at 1 C with an extremely low capacity decay rate (∼0.018% per cycle). And the Li|LCO full cell with the ultrahigh loading cathode (∼25 mg cm-2) and ultrathin Li foil (∼40 µm) also reveals a prolonged cycling performance under the low negative-to-positive capacity ratio of 2.2. Furthermore, the Li|LCO pouch cell with a commercial cathode and ultrathin Li foil still manifests excellent cycling performance even under the harsh conditions of limited Li metal and lean electrolyte. This work provides a cost-effective and scalable strategy toward high performance practical Li metal batteries.

Effects of Vestibular Damage on the Sleep and Expression Level of Orexin in the Hypothalamus of Rats and Its Correlation with Autophagy and Akt Tumor Signal Pathway.

The aim of this study was to investigate the effect of vestibular disruption on autophagy-related proteins and the tumour-associated pathway P13K/Akt in rat sleep and its hypothalamus tissue and to examine whether catechins trigger tumour autophagy. Healthy adult male rats were randomly selected and divided into the vestibular damage group, the sham operation group, and the control group, with 8 rats in each group. A vestibular damage model was established through penetrating the tympanic membrane of the external auditory canal by injecting sodium p-aminophenylarsonate. The electroencephalogram (EGG) activity was used to record the sleep-wakefulness cycle of rats, and the expression levels of hypothalamic orexin (orexin) mRNA and autophagy proteins were detected. Primary hippocampal neurons were intervened with orexin at different concentrations and at different times to detect cell viability and the expression of autophagy protein and P13K/Akt signal pathway protein. The results showed that compared with the control group and the sham operation group, NREM duration in the vestibular damage group decreased significantly (P < 0.05), while its W time increased significantly (P < 0.05). The expression level of orexin mRNA in the hypothalamus of the vestibular damage group was significantly higher than that of the other two groups (P < 0.05), the expression of autophagy microtubule-related proteins LC3B and Beclin-1 increased significantly (P < 0.05), and the protein expression level of p62 decreased significantly (P < 0.05). After orexin intervention, compared with the control group, the expression of Beclin-1 protein that positively correlated with autophagy decreased significantly (P < 0.05) and the expression of mTOR, PDK1, and Akt protein increased significantly (P < 0.05). Compared with the orexin intervention group, the expression of Beclin-1 and LC3B proteins in cells of the orexin receptor inhibitor (Almorexant) group, the autophagy activator (Rapamycin) group, the orexin + Almorexant group, and the orexin + Rapamycin group increased significantly (P < 0.05), and the expression of mTOR, PDK1, and Akt proteins decreased significantly (P < 0.05). Catechins trigger autophagy in part by regulating the p-Akt/p-mTOR and P13K pathways and by stimulating the MAPK pathway. Catechins initiate apoptosis in common tumour types of hepatocellular carcinoma cells by activating autophagy-related pathways. The conclusion is that vestibular damage can affect the sleep-wakefulness cycle of rats; the level of autophagy in hypothalamic tissue is upregulated and may affect cell proliferation and activity through mTOR-P13K/Akt, which has a certain reference value for tumor formation and provides a basis for the research of insomnia or sleep disorders caused by tumors. Autophagy activation is a key process by which catechins promote apoptosis in tumour cells, providing an avenue for more research on the use of catechins-rich diets for cardiovascular protection in the treatment of tumours.

Biological functions of miR-363-3p/BTG2 in the metastasis of bladder cancer.

PURPOSE: This study aimed to detect the differential expression of microRNA-363-3p (miR-363-3p) in bladder cancer (BC) samples and to explore its influence on metastasis of BC cells. METHODS: Expression level of miR-363-3p in 70 cases of BC tissues and paracancerous tissues was detected. After establishing miR-363-3p overexpression model in 253j and RT4 cells, their migratory ability was assessed by Transwell and wound healing assay. The interaction between miR-363-3p and its downstream gene was predicted online and further confirmed by luciferase assay. Their involvement in regulating metastasis of BC cells was finally explored. RESULTS: MiR-363-3p was downregulated in BC tissues compared with that in the paracancerous tissues. Overexpression of miR-363-3p markedly weakened migratory ability in BC cells. BTG2 was the downstream gene binding miR-363-3p. In addition, overexpression of BTG2 reversed the inhibitory effect of miR-363-3p on BC cell migration. CONCLUSIONS: MiR-363-3p is lowly expressed in BC samples. It weakens in vitro migratory ability in BC cells through downregulating BTG2.

Triblock Copolymer Nanomicelles Loaded with Curcumin Attenuates Inflammation via Inhibiting the NF-κB Pathway in the Rat Model of Cerebral Ischemia.

AIM: Cerebral ischemic injury is one of the debilitating diseases showing that inflammation plays an important role in worsening ischemic damage. Therefore, studying the effects of some potential anti-inflammatory compounds can be very important in the treatment of cerebral ischemic injury. METHODS: This study investigated anti-inflammatory effects of triblock copolymer nanomicelles loaded with curcumin (abbreviated as NC) in the brain of rats following transient cerebral ischemia/reperfusion (I/R) injury in stroke. After preparation of NC, their protective effects against bilateral common carotid artery occlusion (BCCAO) were explored by different techniques. Concentrations of free curcumin (C) and NC in liver, kidney, brain, and heart organs, as well as in plasma, were measured using a spectrofluorometer. Western blot analysis was then used to measure NF-κB-p65 protein expression levels. Also, ELISA assay was used to examine the level of cytokines IL-1ß, IL-6, and TNF-α. Lipid peroxidation levels were assessed using MDA assay and H&E staining was used for histopathological examination of the hippocampus tissue sections. RESULTS: The results showed a higher level of NC compared to C in plasma and organs including the brain, heart, and kidneys. Significant upregulation of NF-κB, IL-1ß, IL-6, and TNF-α expressions compared to control was observed in rats after induction of I/R, which leads to an increase in inflammation. However, NC was able to downregulate significantly the level of these inflammatory cytokines compared to C. Also, the level of lipid peroxidation in pre-treated rats with 80mg/kg NC was significantly reduced. CONCLUSION: Our findings in the current study demonstrate a therapeutic effect of NC in an animal model of cerebral ischemia/reperfusion (I/R) injury in stroke through the downregulation of NF-κB-p65 protein and inflammatory cytokines.

A risk score staging system based on the expression of seven genes predicts the outcome of bladder cancer.

Bladder cancer (BLCA) is among the most malignant types of cancer. At present, the prognostic tools available for this disease are insufficient. In the present study, the transcriptome of 1,049 BLCA samples from four datasets from the Gene Expression Omnibus and The Cancer Genome Atlas (TCGA) were analyzed. By utilizing the RNA-seq data provided by TCGA, a risk score staging system model was built to predict the outcome of patients with BLCA using random forest variable hunting and Cox multivariate regression. A total of 7 genes, including zinc finger protein 230, Bcl2-like 14, AHNAK, transmembrane protein 109, apolipoprotein L2, advanced glycation end-product specific receptor and amine oxidase, copper containing 2 were identified as predicting the survival time of patients with BLCA. The patients with a low risk score had a significantly higher survival rate than those with a high-risk score both in the training and validation datasets. Association analyses between risk score and other clinical information were additionally performed; it was demonstrated that the risk score was significantly associated with pathological stage. A nomogram was plotted to compare risk score and other clinical information. The risk score spanned the greatest range of points, indicating the relative accuracy of risk score. In summary, the risk staging model based on the expression of 7 genes is robust and performs more effectively than other clinical information in predicting a prognosis.

Regionspecific survival and differentiation of mouse embryonic stem cell-derived implants in the adult rat brain.

Totipotent and regionally non-specified embryonic stem (ES) cells provide a powerful tool to understand mechanisms controlling stem cell differentiation in different regions of the adult brain. As the development capacity of ES cells in the adult brain is still largely unknown, we grafted small amounts of mouse ES (mES) cells into adult rat brains to explore the survival and differentiation of implanted mES cells in different rat brain regions. We transplanted the green fluorescent protein (GFP)-positive mES cells into the hippocampus, septal area, cortex and caudate nucleus in rat brains. Then the rats were sacrificed 5, 14 and 28 d later. Of all the brain regions, the survival rate of the transplanted cells and their progeny were the highest in the hippocampus and the lowest in the septal area (P<0.01). The grafted ES cells could differentiate into nestin-positive neural stem cells. Nestin-positive/GFP-positive cells were observed in all brain regions with the highest frequency of nestin-positive cells in the hippocampus and the lowest in the medial septal area (P<0.01). mES cells differentiated into end cells such as neurons and glial cells in all transplantation sites in recipient brains. In the hippocampus, the ES cells differentiated into neurons in large amounts. These results demonstrate that only some brain regions permit survival of mES cells and their progeny, and form instructive environments for neuronal differentiation of mES cells. Thus, because of region specific presence of microenvironmental cues and their environmental fields, the characteristics of the recipient tissue were considerably important in formulating cell replacement strategies for neural disorders.

[Study on distribution of neural stem cells in the brain of Alzheimer disease transgenic mice through caudal vein transplantation].

OBJECTIVE: To observe whether neural stem cells (NSCs) can successfully permeate into the brain through the blood-brain barrier (BBB) of Alzheimer disease (AD) transgenic mice and explore the methods of distribution and migration. METHODS: NSCs were isolated from 12-day-old fetal mice, cultured, labeled with enhanced green fluorescent protein (eGFP) and then transplanted into 10 AD transgenic mice and normal mice as controls through caudal vein. The mice were killed 48 h, 1 w, 2 w, and 4 w after transplantation respectively. The brains of the mice were made into continual frozen sections, the distribution and migration of the eGFP-labeled NSCs were studied under fluorescence microscope. RESULTS: At different time points after transplantation the eGFP-labeled NSCs were diffusely distributed in the brain: distributed around the blood vessels in the first 48 h, and then migrated gradually towards the hippocampus and cortex until 4 weeks later. There were no obvious abnormal complications occurring after transplantation. CONCLUSION: NSCs can successfully permeate into the brain through the BBB of AD transgenic mice, and migrate into the brain parenchyma gradually.

Statistical Analysis for Collision-free Boson Sampling.

Boson sampling is strongly believed to be intractable for classical computers but solvable with photons in linear optics, which raises widespread concern as a rapid way to demonstrate the quantum supremacy. However, due to its solution is mathematically unverifiable, how to certify the experimental results becomes a major difficulty in the boson sampling experiment. Here, we develop a statistical analysis scheme to experimentally certify the collision-free boson sampling. Numerical simulations are performed to show the feasibility and practicability of our scheme, and the effects of realistic experimental conditions are also considered, demonstrating that our proposed scheme is experimentally friendly. Moreover, our broad approach is expected to be generally applied to investigate multi-particle coherent dynamics beyond the boson sampling.