Underwater Oleophobic Electrospun Membrane with Spindle-Knotted Structured Fibers for Oil-in-Water Emulsion Separation.

The potential of spider silk as an intriguing biological prototype for collecting water from a humid environment has attracted wide attention, and various materials with suitable structures have been engineered. Here, inspired by this phenomenon, a kind of superwetting poly(vinylidene fluoride) (PVDF) membrane with spindle-knotted structured fibers was prepared by the electrospinning method followed by oxygen plasma etching treatment. The prepared membrane presented a satisfactory separation efficiency for various oil-in-water emulsions. The cooperative effect of the special wettability property and the spindle-knot structure stimulated the emulsified oil droplets to accumulate quickly on the membrane surface. A model that explains the accumulation of emulsified oil droplets has also been developed. Furthermore, an artificial fiber comprising a micron-sized spindle-knot structure was prepared by the dip-coating method to clearly illustrate the aggregation process of the emulsified oil droplets and to verify the theoretical explanation. We hope that this study will provide new inspiration for oil/water emulsion separation techniques.

Overexpressing SIRT6 can Attenuate the Injury of Intracerebral Hemorrhage by Down-Regulating NF-kB.

Sirtuin-6 (SIRT6), a member of the sirtuins family of NAD ( +) dependent deacetylases, has been shown to have beneficial effects in ischemic stroke. However, the role of SIRT6 in intracerebral haemorrhage (ICH) has not reported. We observed that SIRT6 expression was down-regulated in human ICH patients and down-regulated in ICH-induced rat cortical neurons. We subsequently found that SIRT6 overexpression reduced brain tissue damage and increased neuronal survival in the ICH model of rats and hemin-induced cortical neurons. Our further study found that overexpression of SIRT6 can reduce inflammatory response by down-regulating the expression of NF-kB and thus promote the recovery of neurological function in ICH animals. In conclusion, SIRT6 can inhibit the expression of NF-kB and plays a neuroprotective role in ICH by inhibiting the NF-kB-mediated inflammatory response.SIRT6 could be a novel therapeutic target for ICH.

Factors influencing mosaicism: a retrospective analysis.

RESEARCH QUESTION: What factors affect the incidence of mosaic embryos resulting from assisted reproductive technology? DESIGN: A retrospective analysis of data from preimplantation genetic testing for aneuploidies in 544 couples was conducted using data from an electronic medical record database. RESULTS: Of 1910 embryos studied, 127 (6.6%) were mosaic. In multivariable logistic regression analysis, mosaicism incidence increased in embryos from IVF versus intracytoplasmic sperm injection (ICSI) (odds ratio [OR] 4.560, 95% confidence interval [CI] 2.800-7.424, P < 0.001), and in embryos from abnormal versus normal semen (OR 3.496, 95% CI 2.455-4.979, P < 0.001). Embryos tested using SurePlex 24Sure had lower mosaicism percentages than those tested using MALBAC-NGS and PicoPLEX GenetiSure (OR 2.726, 95% CI 1.532-4.852, P = 0.001; OR 2.389, 95% CI 1.537-3.711, P < 0.001, respectively). CONCLUSIONS: Semen quality, fertilization method and detection system are independent factors associated with embryonic mosaicism.

Transcranial direct-current stimulation protects against cerebral ischemia-reperfusion injury through regulating Cezanne-dependent signaling.

Transcranial direct-current stimulation (tDCS) is proved safe and shows therapeutic effect in cerebral ischemic stroke in clinical trials. But the underlying molecular mechanisms remain unclear. Here we show that tDCS treatment reduces the infarct volume after rat cerebral ischemia-reperfusion (I/R) injury and results in functional improvement of stroke animals. At the cellular and molecular level, tDCS suppresses I/R-induced upregulation of Cezanne in the ischemic neurons. Cezanne inhibition confers neuroprotection after rat I/R and oxygen glucose deprivation (OGD) in the cortical neuronal cultures. Inhibiting Cezanne increases the level of SIRT6 that is downregulated in the ischemic neurons. Suppressing SIRT6 blocks Cezanne inhibition-induced neuroprotective effect and overexpressing SIRT6 attenuates OGD-induced neuronal death. We further show that downregulating Cezanne reduces DNA double-strand break (DSB) through upregulation of SIRT6 in OGD-insulted neurons. Together, this study suggests that Cezanne-dependent SIRT6-DNA DSB signaling pathway may mediate the neuroprotective effect of tDCS in ischemic neurons.

Sequential interval micro-droplet loading in closed hemi-straw carrier system: A convenient and efficient method for ultra-rapid cryopreservation in extreme oligozoospermia.

Cryopreservation of human spermatozoa with low concentration while maintaining adequate post-thawing motility remains a major challenge for male fertility preservation. A convenient and efficient ultra-rapid freezing method for small amounts of human spermatozoa in a closed Hemi-Straw carrier system (CHS) was developed. Spermatozoa from 60 healthy men were involved in a parameter refining test and another 15 extreme oligozoospermic specimens were assigned to a verification test. A commercialized sperm freezing medium, Quinn's Advantage® Sperm Freeze medium (glycerol and sucrose as the cryoprotective agent) was used in the study. The results showed that the highest recovery rates would be obtained via the method of 2 µl single droplet sequential interval loading, by placing the straw at 1 cm above the liquid nitrogen (LN2) surface for 60 s during freezing and 2 cm above the LN2 for 2 min during thawing. This method was applied in cryopreservation for the normozoospermic specimens and compared with a conventional slow freezing method. The results were better than those in the control group in the total motility recovery rate (77.8 ± 11.2% vs 56.6 ± 11.9%, P < 0.01), progressive motility recovery rate (77.6 ± 13.2% vs 47.7 ± 14.6%, P < 0.01), 24 h survival index (60.9 ± 13.4% vs 42.1 ± 14.1%, P < 0.01) and the sperm DNA fragment index (4.2 ± 3.7% vs 5.8 ± 3.7%, P = 0.126). This method was applied to the oligozoospermic specimens. Motile spermatozoa could be found in 12 of 15 cases in the ultra-rapid freezing group, while only in 7 cases in control group. The results indicated that this freezing method was simple, convenient and bio-safe for cryopreservation of severe oligozoospermic specimens.

Integrin alpha 7 correlates with poor clinical outcomes, and it regulates cell proliferation, apoptosis and stemness via PTK2-PI3K-Akt signaling pathway in hepatocellular carcinoma.

This study aimed to evaluate the correlation of integrin alpha 7 (ITGA7) with clinical outcomes and its effect on cell activities as well as stemness in hepatocellular carcinoma (HCC). HCC tumor tissues and paired adjacent tissues from 90 HCC patients were obtained and ITGA7 expression was detected using immunohistochemistry assay. Cellular experiments were conducted to examine the effect of ITGA7 on cell activities, astemness via ITGA7 ShRNA transfection, and compensation experiments were further performed to test whether ITGA7 functioned via regulating PTK2-PI3K-AKT signaling pathway. ITGA7 was overexpressed in tumor tissues compared with paired adjacent tissues and its high expression was correlated with larger tumor size, vein invasion and advanced Barcelona Clinic Liver Cancer stage, and it also independently predicted worse overall survival in HCC patients. In cellular experiments, ITGA7 was upregulated in SMMC-7721, Hep G2, HuH-7 and BEL-7404 cell lines compared with normal human liver cells HL-7702. ITGA7 knockdown suppressed cell proliferation but promoted apoptosis, and it also downregulated CSCs markers (CD44, CD133 and OCT-4) as well as PTK2, PI3K and AKT expressions in SMMC-7721 and Hep G2 cell lines. ITGA7 overexpression promoted cell proliferation but inhibited apoptosis, and it also upregulated CSCs markers in HL-7702 cells. Further compensation experiments verified that ITGA7 regulated cell proliferation, apoptosis and CSCs markers via PTK2-PI3K-Akt signaling pathway. ITGA7 negatively associates with clinical outcomes in HCC patients, and it regulates cell proliferation, apoptosis and CSCs markers via PTK2-PI3K-Akt signaling pathway.

RIP3 deficiency protects against traumatic brain injury (TBI) through suppressing oxidative stress, inflammation and apoptosis: Dependent on AMPK pathway.

Traumatic brain injury (TBI) is a leading cause of disability and mortality in young adults worldwide. The pathophysiology is not fully understood. Programmed necrosis (necroptosis) is a newly identified mechanism of cell death combining features of both apoptosis and necrosis. Receptor-interacting protein 3 (RIP3) plays an important role in programmed necrosis. However, the effect of RIP3-related pathway in TBI is little to be known. We attempted to explore the significance of RIP3 in regulating TBI in vivo. Significantly, TBI induced over-expression of RIP3 in the hippocampus of mice, as well as RIP1 and phosphorylated mixed lineage kinase domain-like protein (MLKL). Mice after TBI exhibited cognitive dysfunction and activation of glia cells, which were significantly attenuated by RIP3-knockout (KO). Moreover, inflammation and oxidative stress in hippocampus were markedly induced by TBI in wild type (WT) mice. Of note, the reduction of pro-inflammatory cytokines and oxidants was observed in RIP3-deficient mice, which was linked to the blockage of NLR pyrin domain containing 3 (NLRP3)/apoptosis-associated speck-like protein containing a CARD (ASC)/Caspase-1 and kelch-like ECH-associated protein 1 (Keap 1) pathways. Further, TBI induced hippocampus apoptosis, evidenced by the increase of cleaved Caspase-8/-3 and poly (ADP)-ribose polymerase (PARP) in WT mice, whereas being decreased by RIP3-knockout. In addition, RIP3 knockout led to phosphorylation of AMP-activated protein kinase α (AMPKα) in hippocampus of mice after TBI. And of note, the in vitro findings indicated that RIP3-ablation attenuated oxidative stress, inflammation and apoptosis in astrocytes, which was dependent on AMPKα activation. Together, suppressing RIP3 might be served as a therapeutic target against brain injury through inhibiting inflammation, oxidative stress and apoptosis.

D-dimer may predict poor outcomes in patients with aneurysmal subarachnoid hemorrhage: a retrospective study.

Serum biomarkers may play a reliable role in predicting the outcomes of patients with aneurysmal subarachnoid hemorrhage. This study retrospectively analyzed the relationship between serum biomarkers on admission and outcomes in patients with aneurysmal subarachnoid hemorrhage. We recruited 146 patients with aneurysmal subarachnoid hemorrhage who were treated in Renmin Hospital of Wuhan University of China between 1 May 2014 and 30 March 2016. There were 57 males and 89 females included and average age of included patients was 57.03 years old. Serum samples were taken immediately on admission (within 48 hours after initial hemorrhage) and the levels of serum biomarkers were detected. Baseline information, complications, and outcomes at 6 months were recorded. Univariate and multivariate logistic regression analyses were used to explore the relationship between biomarkers and clinical outcomes. Receiver operating characteristic curves were obtained to investigate the possibility of the biomarkers predicting prognosis. Of the 146 patients, 102 patients achieved good outcomes and 44 patients had poor outcomes. Univariate and multivariate analyses showed that high World Federation of Neurosurgical Societies grade, high serum D-dimer levels, and high neurological complications were significantly associated with poor outcomes. Receiver operating characteristic curves verified that D-dimer levels were associated with poor outcomes. D-dimer levels strongly correlated with neurological complications. In conclusion, we suggest that D-dimer levels are a good independent prognostic factor for poor outcomes in patients with aneurysmal subarachnoid hemorrhage.

Magnetic Resonance Imaging of Plaque Burden in Vascular Walls of the Middle Cerebral Artery Correlates with Cerebral Infarction.

Intracranial atherosclerosis may be related to the risk of ischemic stroke. High-resolution magnetic resonance imaging (H-R MRI) makes it possible to measure the intracranial atheroma in vivo. The aim of this study was to evaluate the plaque burden of the middle cerebral artery (MCA) using H-R MRI, and to determine its relationship with both cerebral infarction size and plaque burden in the carotid artery (CA). 54 patients with MCA territory infarction were enrolled and HR-MRI was performed within 7 days following stroke onset. The lumen area (LA), wall area (WA), total vessel area (TVA), and the normalized wall index (NWI) of MCA and CA were measured. We analyzed the status of MCA and CA atheroma, and the size of cerebral infarction, in the corresponding vascular territory. We observed a significant positive correlation between the NWI of the index artery and the volume of the ipsilateral ischemic lesions. In addition, the mean NWI of MCA was significantly correlated with that of the ipsilateral CA (left, r = 0.88, P.0.001; right, r = 0.79, P.0.001), and the plaque burden of the M1 segment of MCA was significantly higher than that of the ipsilateral CA (P < 0.05). There was no significant correlation between the TVA and WA of MCA and that of CA. Our findings suggest that MCA atherosclerosis is significantly correlated with cerebral infarction. In ischemic stroke patients, the plaque burden of M1 segment of MCA is more significant than that of CA.