A High Sensitivity Self-Powered Wind Speed Sensor Based on Triboelectric Nanogenerators (TENGs).

Triboelectric nanogenerators (TENGs) have excellent properties in harvesting tiny environmental energy and self-powered sensor systems with extensive application prospects. Here, we report a high sensitivity self-powered wind speed sensor based on triboelectric nanogenerators (TENGs). The sensor consists of the upper and lower two identical TENGs. The output electrical signal of each TENG can be used to detect wind speed so that we can make sure that the measurement is correct by two TENGs. We study the influence of different geometrical parameters on its sensitivity and then select a set of parameters with a relatively good output electrical signal. The sensitivity of the wind speed sensor with this set of parameters is 1.79 µA/(m/s) under a wind speed range from 15 m/s to 25 m/s. The sensor can light 50 LEDs at the wind speed of 15 m/s. This work not only advances the development of self-powered wind sensor systems but also promotes the application of wind speed sensing.

MST1R-targeted therapy in the battle against gallbladder cancer.

BACKGROUND: Gallbladder cancer (GBC) is characterized by high mortality rate. Our study sought therapeutic candidates for GBC. RESULTS: Bioinformatics analysis identified significant upregulation of MST1R in GBC. In vitro experiments demonstrated that the MST1R inhibitor MGCD-265 effectively restrained GBC cell proliferation at lower concentrations. Additionally, it induced cycle arrest and apoptosis in GBC cells in a dose-dependent manner. Mouse models exhibited that MGCD-265 treatment significantly diminished the proliferative capacity of GBC-SD cells. Transcriptomics sequencing revealed significant transcriptome alterations, with 200 transcripts upregulated and 883 downregulated. KEGG and GO analyses highlighted enrichment in processes like cell adhesion and pathways such as protein digestion and absorption. Downstream genes analysis identified JMJD6 upregulation post-MGCD-265 treatment. In vivo experiments confirmed that combining MGCD-265 with the JMJD6 inhibitor SKLB325 enhanced the anticancer effect against GBC. CONCLUSION: Overall, targeting MST1R and its downstream genes, particularly combining MGCD-265 with SKLB325, holds promise as a therapeutic strategy for GBC.

Efficient Production of Triacetic Acid Lactone from Lignocellulose Hydrolysate by Metabolically Engineered Yarrowia lipolytica.

Lignocellulose is a promising renewable feedstock for the bioproduction of high-value biochemicals. The poorly expressed xylose catabolic pathway was the bottleneck in the efficient utilization of the lignocellulose feedstock in yeast. Herein, multiple genetic and process engineering strategies were explored to debottleneck the conversion of xylose to the platform chemical triacetic acid lactone (TAL) in Yarrowia lipolytica. We identified that xylose assimilation generating more cofactor NADPH was favorable for the TAL synthesis. pH control improved the expression of acetyl-CoA carboxylase and generated more precursor malonyl-CoA. Combined with the suppression of the lipid synthesis pathway, 5.03 and 4.18 g/L TAL were produced from pure xylose and xylose-rich wheat straw hydrolysate, respectively. Our work removed the bottleneck of the xylose assimilation pathway and effectively upgraded wheat straw hydrolysate to TAL, which enabled us to build a sustainable oleaginous yeast cell factory to cost-efficiently produce green chemicals from low-cost lignocellulose by Y. lipolytica.

The clinical evaluation of preoperative abdominal aortic balloon occlusion for patients with placenta increta or percreta.

OBJECTIVE: To evaluate the efficacy and safety of abdominal aortic balloon for pregnant women with placenta increta or percreta (PIP). METHODS: Retrospective analysis of the parameters containing estimated blood loss, red cell suspension (RCS) transfusion volume, hysterectomy, surgery time, postoperative hospital days, neonatal status and complications between the two groups. RESULTS: The patients with preoperative abdominal aortic balloon occlusion (AABO) had significant reduction in blood loss volume, red cell suspension transfusion volume and plasma transfusion volume compared to patients without balloon. Similarly, the surgery time and hysterectomy were obviously reduced in the AABO group. However, there were no difference in the Apgar scores and neonatal complications between the two groups, indicating that the abdominal aortic balloon has little adverse effect on the newborns. CONCLUSION: AABO plays dramatic roles on reducing blood loss volume and blood transfusion volume and it is also a safe and effective technology providing new insight into the therapy of patient with PIP. SYNOPSIS: Preoperative abdominal aortic balloon occlusion (AABO), as a new intravascular interventional therapy, is safe and effective in patients with placenta increta or percreta.

Improving the Quality of Frozen Lamb by Microencapsulated Apple Polyphenols: Effects on Cathepsin Activity, Texture, and Protein Oxidation Stability.

This study aimed to evaluate the efficiency of microencapsulated apple polyphenols (MAP) in controlling cathepsin activity and texture, as well as inhibiting protein oxidation and metmyoglobin formation in lamb meat during frozen storage at -18 °C for 40 weeks. The effects of degradation in vitro on cathepsin and the microstructure in lamb were also evaluated. Results indicated that relative to the control group, the lamb treated with MAP exhibited increased cathepsin activity and inhibited metmyoglobin production. Textural characteristics, such as hardness and springiness, significantly changed (p < 0.05). Treatment with 0.2-1.6 mg/mL of MAP effectively reduced the mean particle size, increasing the zeta potential, delaying the conversion of α-helices to random coils, and maintaining the integrity of the tissue structure. However, treatment with 3.2 mg/mL of MAP damaged the protein structure. Degradation in vitro indicated that protein oxidation hindered the effect of cathepsin and was a dominant factor affecting protein during the frozen storage. These results demonstrated that microencapsulation can potentially be used for meat preservation and replace chemical antioxidants in the meat industry.

Application of iTRAQ Technology to Identify Differentially Expressed Proteins of Sauce Lamb Tripe with Different Secondary Pasteurization Treatments.

Vacuum-packed sauce lamb tripe was subjected to secondary pasteurization by high-pressure processing (HPP) and heat treatment (HT), and iTRAQ technology was applied to investigate the differentially expressed proteins (DEPs). The analysis revealed 484 and 398 DEPs in the HPP and HT samples, respectively, compared with no treatment. These DEPs were sorted by texture results, and it was revealed that these DEPs acted in different biological processes with many structural proteins and protein subunits related to lamb tripe texture. The results verified by Western blot were consistent with the protein expression changes observed by proteomics. The bioinformatics analysis showed that the hardness and gumminess of the sauce lamb tripe after HT might be related to changes in the expression of CNN1 and FN1. The changes in the expression of TMP, FN1, YWHAG, TTN, collagen isoforms, and ARPC3 might be related to the improved springiness and chewiness of lamb tripe after HPP.

Short-Term Effects of Low-Level Ambient Air NO2 on the Risk of Incident Stroke in Enshi City, China.

Previous studies found that exposure to ambient nitrogen dioxide (NO2) was associated with an increased risk of incident stroke, but few studies have been conducted for relatively low NO2 pollution areas. In this study, the short-term effects of NO2 on the risk of incident stroke in a relatively low-pollution area, Enshi city of Hubei Province, China, were investigated through time-series analysis. Daily air-pollution data, meteorological data, and stroke incidence data of residents in Enshi city from 1 January 2015 to 31 December 2018 were collected. A time-series analysis using a generalised additive model (GAM) based on Poisson distribution was applied to explore the short-term effects of low-level NO2 exposure on the risk of incident stroke and stroke subtypes, as well as possible age, sex, and seasonal differences behind the effects. In the GAM model, potential confounding factors, such as public holidays, day of the week, long-term trends, and meteorological factors (temperature and relative humidity), were controlled. A total of 9122 stroke incident cases were included during the study period. We found that NO2 had statistically significant effects on the incidence of stroke and ischemic stroke, estimated by excess risk (ER) of 0.37% (95% CI: 0.04-0.70%) and 0.58% (95% CI: 0.18-0.98%), respectively. For the cumulative lag effects, the NO2 still had a statistically significant effect on incident ischemic stroke, estimated by ER of 0.61% (95% CI: 0.01-1.21%). The two-pollutant model showed that the effects of NO2 on incident total stroke were still statistically significant after adjusting for other air pollutants (PM2.5, PM10, SO2, CO, and O3). In addition, the effects of NO2 exposure on incident stroke were statistically significant in elderly (ER = 0.75%; 95% CI: 0.11-1.40%), males (ER = 0.47%; 95% CI: 0.05-0.89%) and cold season (ER = 0.83%; 95% CI: 0.15-1.51%) subgroups. Our study showed that, as commonly observed in high-pollution areas, short-term exposure to low-level NO2 was associated with an increased risk of incident stroke, including ischemic stroke. Males and elderly people were more vulnerable to the effects of NO2, and the adverse effects might be promoted in the cold season.

A Plasmid With Conserved Phage Genes Helps Klebsiella pneumoniae Defend Against the Invasion of Transferable DNA Elements at the Cost of Reduced Virulence.

Klebsiella pneumoniae exhibits extensive phenotypic and genetic diversity. Higher plasmid loads in the cell were supposed to play an key role in its genome diversity. Although some plasmids are widely distributed in Kp populations, they are poorly recognized. A plasmid named p2 in strain Kp1604 was predicted to be an intact prophage like Salmonella phage SSU5. However, our study showed that p2 was specifically packaged into membrane vesicles (MVs) rather than phage particles triggered by mitomycin C and subinhibitory concentrations of antibiotics. p2-minus mutant Kp1604Δp2 did not affect MV production. Compared with Kp1604, the capacity of plasmid uptake and the amount of phage burst of Kp1604Δp2 were improved. Moreover, virulence of Kp1604Δp2 also increased. Our results indicated that p2 could contribute to the host defense against the invasion of transferable DNA elements at the cost of reduced virulence. Further study on the mechanism will help us understand how it provides adaptive phenotypes to host evolution.

The efficacy of enoxaparin for recurrent abortion: a meta-analysis of randomized controlled studies.

Introduction: The efficacy of enoxaparin for recurrent abortion remains controversial. We conduct a systematic review and meta-analysis to explore the influence of enoxaparin versus placebo on recurrent abortion.Methods: We search PubMed, Embase, Web of Science, EBSCO, and Cochrane Library databases through February 2019 for randomized controlled trials (RCTs) assessing the effect of enoxaparin versus placebo on recurrent abortion. This meta-analysis is performed using the fixed or random-effect model when appropriate.Results: Six RCTs involving 1034 patients are included in the meta-analysis. Overall, compared with control group for patients with recurrent abortion, enoxaparin has no obvious impact on live births (RR = 1.06; 95% CI = 0.97-1.16; p = .17), abortion rate (RR = 0.71; 95% CI = 0.45-1.10; p = .13), birth weight (std. MD = 0.38; 95% CI = -0.21-0.96; p = .21), preterm delivery (RR = 0.55; 95% CI = 0.30-1.00; p = .05), preeclampsia (RR = 1.52; 95% CI = 0.42-5.51; p = .52), and postpartum hemorrhage (RR = 1.17; 95% CI = 0.69-1.99; p = .55).Conclusions: Enoxaparin may provide no significant benefits to patients with recurrent abortion.

Knockdown of activated Cdc42-associated kinase inhibits human extravillous trophoblast migration and invasion and decreases protein expression of pho-Akt and matrix metalloproteinase.

Introduction: The sufficient invasion and migration of human extravillous trophoblast (EVTs) cells are crucial for placentation. Inadequate invasion of trophoblasts may correlate with the development of preeclampsia. Many studies have suggested that activated Cdc42-associated kinase (ACK1) is associated with tumor metastasis and invasion. This study investigated the ACK1 expression and its function in trophoblasts during placental development.Methods: ACK1 expression in human placentas was determined through immunofluorescence. We investigated the migration/invasion of the immortalized human first-trimester EVT cell line HTR8/SVneo. Hypoxia-reoxygenation (H/R) conditions were applied to mimic preeclampsia model in vitro. Lentiviral vector-based short-hairpin RNA directed against the sequence of ACK1 (ACK1 shRNA) was used to knock down ACK1 expression in HTR8/SVneo cells. Cell apoptosis and proliferation were determined through flow cytometry and cell counting Kit-8 (CCK-8) assays, respectively. The expression of matrix metalloproteinase (MMP) 2/9 and tissue inhibitors of metalloproteinase (TIMP) 1/2 was measured by western blotting.Results: ACK1 localized within trophoblasts of human placental villi, decidual cells in the maternal decidua. ACK1 levels in preeclampsia (PE) placentas were significantly lower than those in controls. ACK1 shRNA significantly inhibited HTR8/SVneo cells migration and invasion but did not affect their apoptosis and proliferation. ACK1 knockdown decreased MMP2/9 and increased TIMP1/2 expression, as well as downregulated the phosphorylation of AKt (p-Akt). In addition, ACK1 and MMP2/9 were downregulated following treatment with LY294002, whereas ACK1 shRNA had no effect on phosphorylation of PI3K(p-PI3K). After exposed in H/R condition, ACK1 expression, MMP2/9 protein, and p-Akt were also significantly decreased.Discussion and conclusions: ACK1 expression is lowered in preeclamptic placentas and promotes trophoblast cell invasion, migration. H/R conditions decrease ACK1 expression and appear to decouple the positive relationship between ACK1 expression and Akt activation.

Hypoxia-induced Downregulation of SRC-3 Suppresses Trophoblastic Invasion and Migration Through Inhibition of the AKT/mTOR Pathway: Implications for the Pathogenesis of Preeclampsia.

Preeclampsia (PE) is characterized by poor placentation, consequent on aberrant extravillous trophoblast (EVT) cell function during placental development. The SRC family of proteins is important during pregnancy, especially SRC-3, which regulates placental morphogenesis and embryo survival. Although SRC-3 expression in mouse trophoblast giant cells has been documented, its role in the functional regulation of extravillous trophoblasts and the development of PE remains unknown. This study found that SRC-3 expression was significantly lower in placentas from PE pregnancies as compared to uncomplicated pregnancies. Additionally, both CoCl2-mimicked hypoxia and suppression of endogenous SRC-3 expression by lentivirus short hairpin RNA attenuated the migration and invasion abilities of HTR-8/SVneo cells. Moreover, we demonstrated that SRC-3 physically interacts with AKT to regulate the migration and invasion of HTR-8 cells, via the AKT/mTOR pathway. We also found that the inhibition of HTR-8 cell migration and invasion by CoCl2-mimicked hypoxia was through the SRC-3/AKT/mTOR axis. Our findings indicate that, in early gestation, accumulation of HIF-1α inhibits the expression of SRC-3, which impairs extravillous trophoblastic invasion and migration by directly interacting with AKT. This potentially leads to insufficient uterine spiral artery remodeling and placental hypoperfusion, and thus the development of PE.

SRC-3 Plays a Critical Role in Human Umbilical Vein Endothelial Cells by Regulating the PI3K/Akt/mTOR Pathway in Preeclampsia.

Preeclampsia (PE) is currently thought to be characterized by oxidative stress which may lead to endothelial dysfunction. The normal function of vascular endothelium is essential to vascular homeostasis. Previous studies have shown that steroid receptor coactivator 3 (SRC-3) interacts with estrogen receptors (ERs) which are involved in the vasoprotective effects of estrogen and is also associated with cell migration, invasion, and inflammation; however, its role in PE remains unclear. The main purpose of this study is to identify the role of SRC-3 in the function of human umbilical vein endothelial cells (HUVECs) during the development of PE. Our study demonstrated that the expression of SRC-3 was significantly decreased in PE placentas compared to normal placentas. Additionally, lentivirus short hairpin RNA against SRC-3 and hypoxia/reoxygenation treatments attenuated migration and tube formation abilities and enhanced HUVEC apoptosis. Furthermore, we detected possible downstream in the PI3K/Akt/mammalian target of rapamycin (mTOR) signal pathway activity, which is involved in SRC-3-mediated HUVEC function. Our data suggest that oxidative stress plays a crucial role in controlling SRC-3 expression, which influences the migration and tube formation abilities of endothelial cells through the PI3K/Akt/mTOR signaling pathways. This action may then result in PE pathogenesis.

[Effect of TTRAP expression on apoptosis induced by hydroquinone in HL-60 cells in vitro.].

OBJECTIVE: To study the effect of TTRAP expression on apoptosis induced by hydroquinone in HL-60 cells in vitro, and explore the relationship between TTRAP expression and the apoptosis. METHODS: Apoptotic and necrotic rate was examined by flow cytometer with Anti-AnnexinV/FITC Plus PI staining. The mRNA expression of TTRAP was detected by RT-PCR. The differences in different treated groups were compared. RESULTS: After different concentrations of hydroquinone to the cells for 0, 4, 8, 12 h culture, were added, the cell apoptotic rate in different concentrations of hydroquinone groups was significantly higher than that in blank control groups. The optimal concentration of hydroquinone was 200 micromol/L, lasting for 8 h. When it was 250 micromol/L, the necrotic rate increased significantly. The apoptosis induced by hydroquinone was associated with the culture time at the concentration of 200 micromol/L, and the peak apoptotic time was 8 h. Then the apoptotic rate decreased and necrotic rate increased. Furthermore, with the concentrations of hydroquinone increased and time lasted for 8 h, the apoptotic rate of cells increased, the amount of TTRAP expression in the mRNA level also increased accordingly. When the concentrations of hydroquinone was above 250 micromol/L, necrotic rate increased sharply, and the amount of TTRAP expression decreased. CONCLUSION: Hydroquinone could induce apoptosis of HL-60 cells. The up-regulation of TTRAP expression may promote hydroquinone to induce HL-60 cells to go into apoptosis in vitro with dose-effect and time-effect relationship.

IL-1ß-induced NF-κB activation down-regulates miR-506 expression to promotes osteosarcoma cell growth through JAG1.

Nowadays, the role of miRNA in tumorigenesis has been largely reported. It was found that miR-506 might be associated with tumorigenesis of various cancers. The present study was aimed to investigate the character of miR-506 and some related factors in human osteosarcoma (OS) carcinogenesis. The expression level of miR-506 was downregulated in OS compared with the normal control group by RT-PCR, both in vivo and in vitro. In addition, IL-1ß stimulation decreased the expression of miR-506. MiR-506 interfered with JAG1 gene transcription throughmiR-506 binding to the 3'-UTR region of JAG1 gene. Further siRNA strategy suggested that IL-1ß may regulate miR-506 level via NF-κB, and then alter the JAG1 expression. Besides, the suppression of JAG1 by miR-506 inhibited OS cell proliferation. Taken together, our data indicate a process of NF-κB-induced miR-506 suppression and JAG1 upregulation upon IL-1ß induction, which can be regarded as a new pathway for modulating cell proliferation via miR-506. It may be of clinical value in treating OS in the future.

The Role of MGAT5 in Human Umbilical Vein Endothelial Cells.

Preeclampsia (PE) is associated with shallow invasion of the trophoblast and insufficient remodeling of the uterine spiral artery. Glycosylation reactions are catalyzed by glycosyltransferases including N-acetylglucosaminyltransferase V (MGAT5) and accumulating evidence suggests that MGAT5 is correlated with the migration, proliferation, and survival of various cell types. Our previous study confirmed that MGAT5 is a negative regulator of trophoblast migration and invasion via the direct or indirect inhibition of matrix metalloproteinase 2/9 activity. The primary purpose of this study is to investigate the role of MGAT5 in the function of human umbilical vein endothelial cells (HUVECs) during the development of PE. We observed that MGAT5 was specifically localized within the decidual cells and endothelial cells in maternal decidual tissues. The expression of MGAT5 was elevated in PE placentas compared with the normal control placentas. Moreover, the expression of MGAT5 was increased in hypoxia-reoxygenation (H/R)-treated HUVECs. The knockdown of MGAT5 and PD98059 treatment significantly enhanced cell migration in vitro, promoted tube formation capacity, and inhibited apoptosis in H/R-exposed HUVECs. Our data suggest that oxidative stress induces the overexpression of MGAT5 via the regulation of the focal adhesion kinase-extracellular signal-regulated kinase signaling pathway, which, in turn, affects the function of endothelial cells, which then participates in the pathogenesis of PE.

Targeting chemotherapy-induced PTX3 in tumor stroma to prevent the progression of drug-resistant cancers.

The tumor microenvironment has been suggested to participate in tumorigenesis, but the nature of the communication between cancer cells and the microenvironment, especially in response to anticancer drugs, remains obscure. We determined that activation of the CCAAT/enhancer binding protein delta (CEBPD) response to Cisplatin and 5-Fluorouracil in cancer-associated macrophages and fibroblasts contributed to the metastasis, invasion, acquired chemoresistance and stemness of cancer cells by in vitro and in vivo assays. Specifically, reporter and in vivo DNA binding assays were used to determine that Pentraxin 3 (PTX3) is a CEBPD responsive gene and serves a protumor role upon anticancer drug treatment. Finally, a PTX3 peptide inhibitor RI37 was developed and assessed the antitumor effects by in vivo assays. RI37 could function as a promising inhibitor for preventing cancer progression and the metastasis, invasion and progression of drug-resistant cancers. The identification of PTX3 provided a new insight in the interaction between host and tumor and the RI37 peptide showed a great opportunity to largely reduce the risk of invasion and metastasis of cancer and drug-resistant cancers.