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Background As one of the most important modified products of rosin, rosin glyceride was widely used in many aspects. However, the preparation of rosin glyceride is always unfriendly due to the use of liquid catalyst, such as H2SO4 and H3PO4. Methods The rosin glyceride with low acid value was synthesized in vacuum conditions using a novel Lewis acidic ionic liquid 1–butyl–3–methylimidazolium chloroscandinate[BuMeim][Sc2Cl7] as catalyst. The [BuMeim][Sc2Cl7] is of excellent catalytic activity and stability. The efficient catalytic activity was studied via the combined Density Functional Theory (DFT) and experimental conditions. Significant findings The DFT proved the free energy of the esterification could reach to 31.6 Kcal/mol, which illuminates that the excellent coordination of the anions and cations in the [BuMeim][Sc2Cl7] greatly reduces the reaction energy barrier and promotes the efficient progress of the reaction. As a result, [BuMeim][Sc2Cl7] is a good catalyst for the esterification of rosin and glycerol to prepare rosin glyceride. Furthermore, [BuMeim][Sc2Cl7] could be a potential catalysts for the other esterification.

OBJECTIVES This study was to explore the effects of teramethylpyrazine (TMP) administered in conjunction with neural stem cell transplantation on motor function, pathological lesions and the Janus kinase (JAK)2/signal transducer and activator of transcription 3 signal transduction pathway in rats following acute spinal cord injury (SCI). METHODS Female Sprague-Dawley rats were randomly divided into sham, model, neural stem cells (NSCs) and NSCs+TMP groups. Motor function was evaluated using the Basso, Beattie, Bresnahan scale. Spinal cord neuropathies and neuron apoptosis were observed by HE and TUNEL staining. The brain-derived neurotrophic factor (BDNF), Nogo-A, JAK2 and p-JAK2 protein levels were measured by western blot analysis. RESULTS NSCs+TMP significantly improved rat motor function, attenuated impaired spinal cords, and decreased cellular apoptosis, compared with NSCs therapy alone (P < 0.05). In addition, expression of BDNF protein was significantly higher in NSCs+TMP rats compared with other groups regardless of time postinjury (P < 0.05). The highest expression levels of Nogo-A protein were observed in the model group. The expression of p-JAK2 in the NSCs+TMP group was relatively lower than the model and NSCs groups (P < 0.05). CONCLUSIONS In rats with SCI, NSCs+TMP effectively improved motor function and offered spinal cord protection by increasing BDNF and decreasing Nogo-A levels, as well as inhibiting the JAK2/STAT3 signal transduction pathway, suggesting that TMP could be a useful agent in NSCs transplantation in the treatment of SCI.

Dysregulated long non-coding RNAs (lncRNAs) have been shown to contribute to the pathogenesis of ischemic stroke. However, the potential role of lncRNAs in post-stroke microglial activation remains largely unknown. Here, we uncovered that lncRNA-U90926 was significantly increased in microglia exposed to ischemia/reperfusion both in vivo and in vitro. In addition, adenovirus-associated virus (AAV)-mediated microglial U90926 silencing alleviated neurological deficits and reduced infarct volume in experimental stroke mice. Microglial U90926 knockdown could reduce the infiltration of neutrophils into ischemic lesion site, which might be attributed to the downregulation of C-X-C motif ligand 2 (CXCL2). Mechanistically, U90926 directly bound to malate dehydrogenase 2 (MDH2) and competitively inhibited the binding of MDH2 to the CXCL2 3' untranslated region (UTR), thus protecting against MDH2-mediated decay of CXCL2 mRNA. Taken together, our study demonstrated that microglial U90926 aggravated ischemic brain injury via facilitating neutrophil infiltration, suggesting that U90926 might be a potential biomarker and therapeutic target for ischemic stroke.

Background Circular RNAs (circRNAs) are important regulators that drive or inhibit cancer initiation and development. Here, we identified the expression and function of a circRNA, circ_KIAA1199, in colorectal cancer (CRC). Methods The expression levels of circ_KIAA1199, microRNA-34c-5p (miR-34c-5p) and Musashi RNA-binding protein 1 (MSI1) mRNA were detected by quantitative real-time PCR. Cell proliferative capacity was assessed by colony formation assay, EdU assay and MTT assay. Cell apoptosis was determined by flow cytometry assay. Cell migration and cell invasion were investigated by transwell assay. The expression of MSI1 protein and proliferation, migration-related markers was detected by western blot. The relationship between miR-34c-5p and circ_KIAA1199 or MSI1 was verified by dual-luciferase reporter assay. Animal models were constructed to ascertain the role of circ_KIAA1199 in vivo. Results The expression of circ_KIAA1199 was elevated in CRC. Circ_KIAA1199 downregulation suppressed CRC cell proliferation, survival, migration and invasion. MiR-34c-5p was a target of circ_KIAA1199. The effects of circ_KIAA1199 downregulation were reversed by miR-34c-5p deficiency. In addition, MSI1 was a target of circ_KIAA1199, and the inhibitory effects of miR-34c-5p restoration on CRC cell proliferation, survival, migration and invasion were reversed by MSI1 overexpression. Circ_KIAA1199 positively regulated MSI1 expression by targeting miR-34c-5p. Moreover, circ_KIAA1199 knockdown blocked tumor growth in animal models. Conclusion Circ_KIAA1199 functioned as an oncogene to drive the malignant development of CRC by activating MSI1 via competitively targeting miR-34c-5p.

Background The aim of this study was to identify important miRNAs and their target genes involved in cell apoptosis in intervertebral disc degeneration (IDD) patients. Methods The dataset, GSE63492, was obtained from the gene expression omnibus platform. After preprocessing, the differentially expressed miRNAs (DEMs) and their target genes were identified using the Limma package and miRWalk2.0 database, respectively. The clusterProfiler package in R was used to perform functional enrichment analysis of these target genes. Subsequently, protein-protein interaction (PPI) network and subnet clusters of the coregulated genes were conducted using the STRING database and MCODE, respectively. Further, the co-regulatory network of the key miRNAs and PPI networks were visualized using Cytoscape. Finally, cell apoptosis-related pathways and the genes enriched in these pathways were identified. Results The genes targeted by the upregulated (hsa-miR-302c-5p, hsa-miR-631, hsa-let-7f-1-3p, hsa-miR-3675-3p, and hsa-miR-585-3p) and downregulated miRNAs (hsa-miR-185-5p, hsa-miR-486-5p, hsa-miR-4306, and hsa-miR-4674) were interrelated with cell apoptosis-related pathways. MAPK1 and MAPK3 were targeted by hsa-miR-185-5p, while GSK3B was targeted hsa-miR-4306, hsa-miR-486-5p, hsa-miR-185-5p, hsa-let-7f-1-3p, and hsa-miR-631. Besides, MAPK3 and VEGFA were regulated by hsa-miR-3675-3p and hsa-miR-631, respectively. Conclusions The expression of GSK3B may be coregulated by miR-4306, miR-185-5p, miR-486-5p, hsa-let-7f-1-3p, and miR-631 and may affect IDD development. Besides, miR-185-5p and miR-3675-3p may control nucleus pulposus (NP) cell apoptosis through the MAPK signaling pathway in IDD patients. VEGFA expression may be regulated by miR-631, and help maintain NP cell survival in IDD patients. Our findings may help guide further research into the role of miRNAs in IDD progression.

Hepatic ischaemia/reperfusion (I/R) injury is a major clinical problem during liver surgical procedures, which usually lead to early transplantation failure and higher organ rejection rate, and current effective therapeutic strategies are still limited. Therefore, in‐depth exploring of the molecular mechanisms underlying liver I/R injury is key to the development of new therapeutic methods. β‐arrestins are multifunctional proteins serving as important signalling scaffolds in numerous physiopathological processes, including liver‐specific diseases. However, the role and underlying mechanism of β‐arrestins in hepatic I/R injury remain largely unknown. Here, we showed that only ARRB1, but not ARRB2, was down‐regulated during liver I/R injury. Hepatocyte‐specific overexpression of ARRB1 significantly ameliorated liver damage, as demonstrated by decreases in serum aminotransferases, hepatocellular necrosis and apoptosis, infiltrating inflammatory cells and secretion of pro‐inflammatory cytokines relative to control mice, whereas experiments with ARRB1 knockout mice gotten opposite effects. Mechanistically, ARRB1 directly interacts with ASK1 in hepatocytes and inhibits its TRAF6‐mediated Lysine 6‐linked polyubiquitination, which then prevents the activation of ASK1 and its downstream signalling pathway during hepatic I/R injury. In addition, inhibition of ASK1 remarkably abolished the disruptive effect result from ARRB1 deficiency in liver I/R injury in vivo, indicating that ASK1 was required for ARRB1 function in hepatic I/R injury. In conclusion, we proposed that ARRB1 is a novel protective regulator during liver I/R injury, and modulation of the regulatory axis between ARRB1 and ASK1 could be a novel therapeutic strategy to prevent this pathological process.

Background & Aims Non-alcoholic steatohepatitis (NASH) is associated with the dysregulation of lipid metabolism and hepatic inflammation. The causal mechanism underlying NASH is not fully elucidated. This study investigated the role of β-Arrestin1 (ARRB1) in the progression of NASH. Methods Liver tissue from patients with NASH and controls were obtained to evaluate ARRB1 expression. NASH models were established in Arrb1-knockout and wild-type mice fed either a high-fat diet (HFD) for 26 weeks or a methionine/choline-deficient (MCD) diet for 6 weeks. Results ARRB1 expression was reduced in liver samples from patients with NASH. Reduced Arrb1 levels were also detected in murine NASH models. Arrb1 deficiency accelerated steatohepatitis development in HFD-/MCD-fed mice (accompanied by the upregulation of lipogenic genes and downregulation of β-oxidative genes). Intriguingly, ARRB1 was found to interact with growth differentiation factor 15 (GDF15) and facilitated the transportation of GDF15 precursor (pro-GDF15) to the Golgi apparatus for cleavage and maturation. Treatment with recombinant GDF15 ablated the lipid accumulation in the presence of Arrb1 deletion both in vitro and in vivo. Re-expression of Arrb1 in the NASH models ameliorated the liver disease, and this effect was greater in the presence of pro-GDF15 overexpression. By contrast, the effect of pro-GDF15 overexpression alone was impaired in Arrb1-deficient mice. In addition, the severity of liver disease in patients with NASH was negatively correlated with ARRB1 expression. Conclusion ARRB1 acts as a vital regulator in the development of NASH by facilitating the translocation of GDF15 to the Golgi apparatus and its subsequent maturation. Thus, ARRB1 is a potential therapeutic target for the treatment of NASH. Lay summary Non-alcoholic steatohepatitis (NASH) is associated with the progressive dysfunction of lipid metabolism and a consequent inflammatory response. Decreased ARRB1 is observed in patients with NASH and murine NASH models. Re-expression of Arrb1 in the murine NASH model ameliorated liver disease, an effect which was more pronounced in the presence of pro-GDF15 overexpression, highlighting a promising strategy for NASH therapy.

Although many studies have focused on functional impairment after intracerebral hemorrhage, little is known about the relationship between secondary injuries to distal regions and neurological function. Our study aimed to evaluate the secondary injuries after intracerebral hemorrhage and explore their relationship to neurological functional outcome. Twenty-one patients with hemorrhages in supratentorial, deep locations and 10 healthy subjects were recruited. Longitudinal examinations of diffusion tensor imaging, hydrogen proton magnetic resonance spectroscopy imaging and neuropsychological assessment were performed after weeks 1 and 12 to elucidate the relationship between magnetic resonance imaging parameters and neurologic outcomes. By week 12, motor function had significantly improved, but cognitive function had deteriorated compared to week 1. Fractional anisotropy values for the ipsilateral cerebral peduncle correlated with motor function at week 1. No significant correlation between fractional anisotropy for the ipsilateral cerebral peduncle and the Fugl-Meyer Motor Scale was found at week 12. Fractional anisotropy values for the ipsilateral hippocampus were related to the Montreal Cognitive Assessment and Mini-Mental State Examination at weeks 1 and 12. Deep supratentorial hemorrhage may result in injury to distal regions, which correlate with impaired motor and cognitive function.

Neuroinflammation is a key factor that contributes to the secondary injury after cerebral ischemia/reperfusion (CI/R) injury. Chemokine receptor type 5(CCR5) has shown its pro-inflammatory effects during central nervous system (CNS) diseases. However, the role of CCR5 in CI/R injury is still unclear. In this study, we administered maraviroc (MVC,APEXBIO,UK-427857), a CCR5 antagonist, to the middle cerebral artery occlusion(MCAO) mice. In vivo studies showed that MVC was successively intraperitoneally (i.p.) with different doses (5, 20, or 50 mg/kg body weight) for 3 days after mice MCAO. MVC showed its neuroprotective effects in alleviating neurological deficits and infarct volumes after MCAO. The level of apoptosis and inflammation were remarkably decreased by MVC treatment after CI/R injury. Subsequently, primary microglia were stimulated with different doses of MVC (0.2, 2, 20 or 200nM) for 12h after oxygen-glucose deprivation/reoxygenation model (OGD/R) in vitro. MVC significantly increased the viability of primary microglia after (OGD/R). The expression of pro-inflammatory cytokines (IL-1β and IL-6) in microglia were down-regulated by MVC treatment. Mechanistically, MVC also inhibited the secretion of IL-1β and IL-6 by microglia after OGD stimulation. Furthermore, the key components of NF-κB pathway were measured in vivo and in vitro after MCAO and OGD. MVC significantly inhibited the activity of NF-κB pathway in the above pathological environments. Finally, our data indicated that MVC treatment decreased the activation of JNK signaling pathway after CI/R injury in vivo and in vitro. The JNK activator anisomycin (AN，Beyotime，SC0132-5mg) reversed the neuroprotective effects of MVC, indicating that the JNK pathway is involved in the anti-inflammatory and anti-apoptotic mechanisms of MVC in CI/R injury. Our data demonstrated that CCR5 inhibition exhibits neuroprotective effects after CI/R injury. MVC, which is widely used for HIV treatment by its anti-virus effect, is a potential drug for the treatment of ischemic stroke in the future clinical trials.

In this work, Mo-MCM-41, Zr-MCM-41, Sn-MCM-41 and Ti-MCM-41 mesoporous molecular sieves were successfully synthesized via hydrothermal synthesis. An acidic group (SO42−, PTSA etc.) was introduced into the mesoporous molecular sieves to obtain modified mesoporous molecular sieve catalysts. The XRD, N2 absorption–desorption isotherms, FT-IR and Py-IR results reveal that PTSA/ZrO2/Mo-MCM-41 had a mesoporous molecular sieve structure containing a large number of acidic centers. The PTSA/ZrO2/Mo-MCM-41 catalyst illustrated superior catalytic performance for synthesis of rosin methyl ester and the esterification rate was 88.2% under the optimized conditions. At the same time, the PTSA/ZrO2/Mo-MCM-41 catalyst has excellent stability and can be recycled and reused with negligible loss in activity over six cycles.

Functional disruption of the neurovascular unit may lead to aggravation of ischemic cerebral injury. Connexin43 (Cx43)-dependent gap junctional channels (GJCs) are critical in maintaining brain homeostasis. However, excessive opening of hemichannels (HCs) after cerebral ischemia may cause apoptosis and finally lead to amplification of ischemic injury. Previous studies indicated that Cx43 mimetic peptides Gap26 and Gap27 may protect cerebral ischemic injury, but the latest studies showed they also inhibit the opening of GJCs, which are beneficial for neuroprotection. Recent studies showed that Gap19 is a new specific inhibitor of Cx43 HCs. We investigated the role of Gap19 on cerebral ischemia/reperfusion (I/R) injury in a mouse model of middle cerebral artery occlusion (MCAO). Ventricle-injected Gap19 significantly alleviated infarct volume, neuronal cell damage and neurological deficits after ischemia, the neuroprotective effect of Gap19 was significant stronger than Gap26. Post-treatment with TAT-Gap19 still provided neuroprotection when it was administered intraperitoneally at 4 h after reperfusion. In addition, we found that Gap19 decreased the levels of cleaved caspase-3 and Bax and increased the level of Bcl-2, suggesting the anti-apoptotic activity of specifically blocking the Cx43 HCs. Furthermore, our data indicate that Gap19 treatment increased the levels of phosphorylated JAK2 and STAT3 both in vivo and in vitro. Gap19 inhibited hemichannel activity assessed by dye uptake in astrocytes. And we detected that pSTAT3 co-localized with Cx43 together in astrocytes after oxygen glucose deprivation (OGD) injury. Finally, AG490, a blocker of the JAK2/STAT3 pathway, could reverse the neuroprotective effects of Gap19 both in vivo and in vitro. Our experiment investigated the anti-apoptotic activity of Gap19, the specific inhibitor of Cx43 HCs, and the potential mechanisms. Our results demonstrated that Gap19 plays an anti-apoptotic role via activating the JAK2/STAT3 pathway after cerebral I/R injury, indicating that specific blocking of Cx43 HCs is a potential target for ischemic stroke.

Phillyrin, a natural plant extract, has significant antioxidant and anti-apoptotic effects. However, its effect on intracerebral hemorrhage (ICH) remains unclear. In this study, we investigated a potential role for phillyrin in the regulation of the oxidative stress and apoptosis induced by ICH. A model of ICH was induced by collagenase IV (0.2 U in 1 μl sterile normal saline) in male C57BL/6J (B6) mice and different doses of phillyrin (5, 15, or 30 mg/kg) were intraperitoneally (i.p.) injected at 30 min, 6 h, and 22 h after modeling. We found that phillyrin significantly reduced neural function and lesion volume, improved injury of white and grey matter around the lesion, decreased apoptosis and oxidative stress, increased the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase 1(HO-1), NADPH quinone oxidoreductase 1 (NQO1) and Superoxide Dismutase-1(SOD-1) in vitro and in vivo, and protected neurons from the stimulation of hemin by promoting Nrf2 nuclear translocation. Treatment with ML385 (Nrf2 inhibitor) completely reversed the protective effects of phillyrin in vivo after ICH injury. Based on our findings, we conclude that phillyrin treatment alleviates ICH injury-induced apoptosis and oxidative stress via activation of the Nrf2 signaling pathway, highlighting a potential role for phillyrin as an ICH therapeutic.

Ankle sprain is a commonly recurring sports injury. This study aimed to compare the rehabilitation effects of resistance and balance training programs in patients with recurrent ankle sprain. Patients with recurrent lateral ankle sprain completed a home-based rehabilitation program comprising resistance training (RT; n = 27) or balance training (BT; n = 27). RT consisted of exercises using elastic tube bands, and BT consisted mainly of exercises performed using a variety of balance tools. Exercises were performed for 6 weeks, twice a day for 20 min, 5 days per week. Isokinetic eversion strength, Y-Balance test and hop tests, and foot and ankle outcome score (FAOS) were evaluated. Both RT and BT significantly improved strength and dynamic balance (p < 0.05). Compared to RT, BT also significantly improved the outcome of the crossover hop test (p = 0.008). The changes reflected group and time in pain (p = 0.022), sports (p = 0.027), and quality of life (p = 0.033) of FAOS were significantly greater in BT than RT.

MicroRNAs (miRNAs or miRs) serve essential roles in the pathogenic process of spinal cord injury (SCI). The present study investigated the role of miR-378-3p and autophagy-related 12 (ATG12) in SCI. RT-qPCR was used to detect the mRNA expression levels of miR-378-3p and ATG12. Cell viability and membrane integrity were evaluated using CCK-8 and LDH assays. For the analysis of the interaction between miR-378-3p and ATG12, a dual-luciferase reporter assay was conducted. The hindlimb function of rats was detected with the Basso, Beattie and Bresnahan score, and the motor deficit index score was used to evaluate nerve function. Using these approaches, it was identified that miR-378-3p expression was downregulated, while that of ATG12 was upregulated in SCI tissues and in cells exposed to hypoxia. Hypoxia repressed the expression of miR-378-3p via hypoxia-inducible factor 1-α. The overexpression of miR-378-3p exerted anti-apoptotic effects on nerve cells by directly repressing ATG12. The infusion of miR-378-3p improved hindlimb motor function and the neurological functions of rats with contusion SCI, which contributed to amelioration of functional deficits and the relief of contusion SCI. Therefore, it was concluded that upregulated expression of miR-378-3p in PC12 or N2A cells repressed the apoptosis of nerve cells, and the administration of miR-378-3p in model rats with contusion SCI improved neurological and motor functions.

Purpose This research aims to analyze the diagnostic contribution of different discriminative regions of the breast ultrasound image and develop a more effective diagnosis method taking advantage of the discriminative regions' complementarity. Methods First, the discriminative regions of the original breast ultrasound image as the inner region of the lesion, the marginal zone of the lesion, and the posterior echo region of the lesion were defined. The pretrained Inception-V3 network was used to analyze the diagnostic contribution of these discriminative regions. Then, the network was applied to extract the deep features of the original image and the other three discriminative region images. Since there are many features, principal components analysis (PCA) was used to reduce the dimensionality of the extracted deep features. The selected deep features from different discriminative regions were fused to original image features and sent to the stacking ensemble learning classifier for classification experiments. In this study, 479 cases of breast ultrasound images, including 356 benign lesions and 123 malignant ones, were collected retrospectively and randomly divided into the training and validation set. Results Experimental results show that by using Inception-V3, the diagnostic performance of each discriminative region is different, and the diagnostic accuracy and the area under the ROC curve (AUC) of the lesion marginal zone image (78.3%, 0.798) are higher than those of the lesion inner region image (73.3%, 0.763) and the posterior echo region image (71.7%, 0.688), but lower than those of the original image (80.0%, 0.817). Furthermore, the best classification performance was obtained when all the four types of deep features (from the original image and three discriminative region images) were fused, and the ensemble learning for classification evaluation was employed. Compared with the original image, the classification accuracy and AUC increased from 80.83%, 0.818 to 85.00%, 0.872, and the classification sensitivity and specificity varied from 0.710, 0.798 to 0.871, 0.787. Conclusions The inner region of the lesion, the marginal zone of the lesion, and the posterior echo region of the lesion play significant roles in the diagnosis of the breast ultrasound image. Deep feature fusion of these three kinds of images and the original image can effectively improve the accuracy of diagnosis.

Background: To investigate the risk factors for open fractures in children and adolescents (≤18 years old) presenting with traumatic fractures.Methods: We retrospectively reviewed the records of 2418 children and adolescents who presented with traumatic fractures and were admitted to our university-affiliated hospitals, among which 206 patients (8.5%) presented with open fractures.Results: This study enrolled 1789 males (74.0%) and 629 females (26.0%) with an average age of 11.2±5.0 years. There were 206 patients (8.5%) who presented with open fractures. The five most common fracture sites were the tibia (31.1%, 64/206), fibula (20.9%, 43/206), phalanx (15.5%, 32/206), humerus (11.2%, 23/206) and ulna (9.7%, 20/206). Univariate logistic regression analysis showed that the aetiology (P﹤0.001) and fracture site (P﹤0.001) were risk factors for open fracture. Multivariate logistic regression analysis indicated that mechanical trauma (OR=64.229, P﹤0.001), being hurt/cut by others (OR=26.757, P﹤0.001), and being struck by an object (OR=15.345, P﹤0.001) were stronger risk factors for open fracture than were low falls; additionally, lower limb fractures (OR=5.970, P﹤0.001), upper limb fractures (OR=5.865, P﹤0.001) and multiple fractures (OR=5.414, P﹤0.001) were stronger risk factors than craniofacial fractures for open fractures.Conclusions: Aetiology (especially being injured by a machine or being hurt/cut by others) and the fracture site (including lower limb fractures, upper limb fractures and multiple fractures) were independent risk factors for open fractures.

Pedicle screw fixation of the cervical spine allows superior, simultaneous stabilization of all three columns of the cervical spine. However, pedicle screw fixation has the risk of neurovascular injury from penetration of the small cervical pedicle. The chapter introduces the anatomic parameters of the cervical pedicle and describes screw entry points, angles, and depth in details. At the same time, the procedure of inserting C4 pedicle screw in the cadaver is shown as a step-by-step example. Pearls and pitfalls of cervical pedicle screw fixation are summarized at the end of the chapter.

Objective To discuss how the sequence of spinal surgery and hip replacement is determined for patients with both degenerative scoliosis and hip disease. Methods Twenty-six patients treated for both degenerative scoliosis and hip disease from June 2012 to June 2015 were retrospectively studied. Eleven patients underwent hip replacement followed by lumbar surgery (Group A), and 15 patients underwent lumbar surgery followed by hip replacement (Group B). The average follow-up duration was 1.5 years. Related indicators were assessed preoperatively and postoperatively. Results The parameters showing significant differences between Groups A and B after surgery were acetabular anteversion, the Oswestry functional disability score, and the Harris hip score. Postoperatively, five patients in Group A had unequal shoulder heights and inclination of the trunk to one side. After lumbar surgery and before total hip arthroplasty in Group B, eight patients could not walk, and the limitation was more severe than that preoperatively. Conclusion Spinal surgery may be performed first to resolve lumbar nerve symptoms and restore sagittal balance of the spine; hip replacement may then be performed to simplify hip replacement difficulties and resolve the imbalance after spinal surgery. Severely limited range of motion exists after lumbar surgery and before total hip arthroplasty.

Background In the central nervous system (CNS), connexin 43 (Cx43) is mainly expressed in astrocytes and regulates astrocytic network homeostasis. Similar to Cx43 overexpression, abnormal excessive opening of Cx43 hemichannels (Cx43Hcs) on reactive astrocytes aggravates the inflammatory response and cell death in CNS pathologies. However, the role of excessive Cx43Hc opening in intracerebral hemorrhage (ICH) injury is not clear. Methods Hemin stimulation in primary cells and collagenase IV injection in C57BL/6J (B6) mice were used as ICH models in vitro and in vivo. After ICH injury, the Cx43 mimetic peptide Gap19 was used for treatment. Ethidium bromide (EtBr) uptake assays were used to measure the opening of Cx43Hcs. Western blotting and immunofluorescence were used to measure protein expression. qRT-PCR and ELISA were used to determine the levels of cytokines. Coimmunoprecipitation (Co-IP) and the Duolink in situ proximity ligation assay (PLA) were applied to measure the association between proteins. Results In this study, Cx43 expression upregulation and excessive Cx43Hc opening was observed in mice after ICH injury. Delayed treatment with Gap19 significantly alleviated hematoma volume and neurological deficits after ICH injury. In addition, Gap19 decreased inflammatory cytokine levels in the tissue surrounding the hematoma and decreased reactive astrogliosis after ICH injury in vitro and in vivo. Intriguingly, Cx43 transcriptional activity and expression in astrocytes were significantly increased after hemin stimulation in culture. However, Gap19 treatment downregulated astrocytic Cx43 expression through the ubiquitin-proteasome pathway without affecting Cx43 transcription. Additionally, our data showed that Gap19 increased Yes-associated protein (YAP) nuclear translocation. This subsequently upregulated SOCS1 and SOCS3 expression and then inhibited the TLR4-NFκB and JAK2-STAT3 pathways in hemin-stimulated astrocytes. Finally, the YAP inhibitor, verteporfin (VP), reversed the anti-inflammatory effect of Gap19 in vitro and almost completely blocked its protective effects in vivo after ICH injury. Conclusions This study provides new insight into potential treatment strategies for ICH injury involving astroglial Cx43 and Cx43Hcs. Suppression of abnormal astroglial Cx43 expression and Cx43Hc opening by Gap19 has anti-inflammatory and neuroprotective effects after ICH injury.

Cerebral ischaemia/reperfusion (CI/R) injury is a major challenge due to the lack of effective neuroprotective drugs. Hederagenin (HE) is the aglycone part of saponins extracted from Hedera helix Linné that has exhibited anti-apoptotic and anti-inflammatory effects; however, the role of HE in CI/R has not been elucidated. In this study, mice were intraperitoneally (i.p.) injected with HE (26.5, 53, or 106 μmol/kg body weight) for 3 days after middle cerebral artery occlusion (MCAO). Neural function and brain infarct volume were evaluated. HE treatment attenuated CI/R-induced apoptosis and inflammatory cytokine expression within the infarcted areas. HE treatment also decreased the activation of the MLK3 signalling pathway, which potentiates CI/R damage via the MAPK and NFκB pathways. Due to HE’s safety profile, it has potential to be used for the clinical treatment of ischaemic stroke.

Clubroot disease, a major plant root disease caused byPlasmodiophora brassicae, has become one of the most destructive diseases among cultivated cruciferous vegetables. However, clubroot-resistantBrassica oleraceamaterials are rare. A few clubroot-resistant cabbage varieties are available on the market, but all are Ogura cytoplasmic male sterile (CMS) types. Therefore, in this study, to reutilize the clubroot-resistant Ogura CMS germplasm of cabbage, a new fertility-restored Ogura CMS material, 16Q2-11, was used as a bridge to transfer the clubroot resistance (CR) gene from the Ogura CMS cytoplasm to the normal cytoplasm by a two-step method (a fertility restoration and cytoplasm replacement method). In the first cross for fertility restoration of Ogura CMS clubroot-resistant cabbage (FRCRC), 16Q2-11 was used as a restorer to cross with Ogura CMS materials containing the CR geneCRb2. ElevenRfo-positive progenies were generated, of which four containedCRb2: F8-514, F8-620, F8-732 and F8-839. After inoculation with race 4 ofP. brassicae, these fourCRb2-positive individuals showed resistance. Furthermore, F8-514 and F8-839 were then used as male parents in the second cross of FRCRC to cross with cabbage inbred lines, resulting in the successful introgression of theCRb2gene into the inbred lines. All offspring produced from this step of cross, which had a normal cytoplasm, showed a high resistance to race 4 ofP. brassicaeand could be utilized for the breeding of clubroot-resistant cabbage varieties in the future. This is the first time that the Ogura CMS restorer has been used to restore the fertility of Ogura CMS clubroot-resistant cabbages, which could improve germplasm diversity in cabbage and provide a reference method for using CMS germplasm inBrassicacrops.

BACKGROUND: Echinocystic acid (EA), a natural extract from plants of Gleditsia sinensis Lam, exhibits anti-inflammatory, antioxidant and analgesic activities in different diseases. In this study, we explored the pharmacological effects of EA on intracerebral haemorrhage (ICH) in a collagenase-induced ICH mouse model. METHODS: EA (50 mg/kg, i.p. q.d) was injected after the establishment of ICH, and we measured the amount of degraded neurons in brain tissue with Fluoro-Jade C staining and the haemorrhagic injury volume with Luxol fast blue staining on day 3 after ICH. We also assessed animal behaviour by rotarod test, claw force test and modified neurological severity score (mNSS) score. The expression of apoptosis-related proteins such as Bcl-2, Bax and cleaved caspase-3 was analysed by Western blot. RESULTS: EA reduced both the death of neurons and the volume of haemorrhagic injury after ICH. The haemorrhage infarct volume of the ICH+EA group was 9.84%±3.32% lower than that in the ICH group of mice (P

A new and environmental friendly route has been developed to hydrogenate α-pinene to cis-pinane. The α-pinene was hydrogenated using ruthenium (Ru) nanoparticles that were stabilized by modified carboxymethyl cellulose in aqueous medium. The conversion of α-pinene reached 96.6% and the selectivity of cis-pinane was 98.4%. Ru nanoparticles could be recycled 18 times. Ru nanoparticles and micelles were characterized by transmission electron microscopy (TEM), confocal laser scanning microscopy (CLSM), dynamic light scattering (DLS), X-ray diffraction (XRD), and other detection techniques. Ru nanoparticles (3.2 nm) had a good stability and uniform distribution, the reaction was divided into micelles that appeared to act as “microreactors”, and the micelle size was increased in the absence of sodium carbonate. The good stability of the Ru nanoparticles could be attributed to electrostatic and steric stabilization.

Fe3O4@C supported ultrasmall and highly monodisperse ruthenium (Ru) nanoparticles (Ru/Fe3O4@C) were prepared as novel nanocatalysts for hydrogenation reactions. The catalysts displayed high activity for the hydrogenation of rosin to form hydrogenated rosin with extraordinary selectivity. The role of controlled carbon size on the catalytic properties of the catalysts was studied. The Ru/Fe3O4@C catalyst can be easily separated from the organic solvent by applying an external magnetic field and the separated Ru/Fe3O4@C can simply and efficiently used in ten consecutive runs without significant decrease in activity. Significantly, Ru/Fe3O4@C nanocatalysts showed a wide substrate scope for hydrogenation reactions under mild conditions.

Background and purpose A higher Totaled Health Risks in Vascular Events (THRIVE) score has been shown to predict poor functional outcome in patients with acute ischemic stroke (AIS) and anterior circulation large vessel occlusions undergoing thrombectomy treatment. We attempted to evaluate the value of the THRIVE score in predicting the outcome of thrombectomy treatment in AIS patients with basilar artery occlusion (BAO). Methods A total of 68 AIS patients with BAO who underwent thrombectomy treatment from May 2014 to August 2018 were included in the present study. Multivariable logistic regression was performed to determine the predictive value of the THRIVE score for poor functional outcome (defined as modified Rankin Scale score ≥ 3), all‐cause mortality, and hemorrhage transformation (HT) at 3 months. Results A total of 42 (61.8%) participants experienced poor functional outcomes, 25 (36.8%) patients died from all causes, and 21 (30.9%) patients had HT during the 3‐month follow‐up. Multivariable logistic regression showed that a higher THRIVE score was significantly associated with poor functional outcome (odds ratio [OR] 5.86, 95% confidence interval [CI], 2.28–14.91, p 5; sensitivity, 88.5%; specificity, 83.3%, p = .007) and all‐cause mortality (AUC = 0.768; cutoff > 5; sensitivity, 92.0%; specificity, 65.1%, p = .018). Conclusions A high THRIVE score was independently associated with an increased risk of poor functional outcome and all‐cause mortality in AIS patients with BAO who underwent thrombectomy treatment. Moreover, the THRIVE score appeared to be a better predictor of clinical outcome than the NIHSS score., A high THRIVE score was independently associated with an increased risk of poor functional outcomes and all‐cause mortality in AIS patients with basilar artery occlusion who underwent thrombectomy treatment. Moreover, the THRIVE score appeared to be a better predictor of clinical outcome than NIHSS score.

The track is mainly composed of track shoes, track pins and rubber bushing elements. In order to suppress the transversal vibration of the upper track during the smooth running process of the tracked vehicle, it is necessary to study the important factors affecting the frequency characteristics of the kinematic chain and their interaction. Unlike the conventional chain drive system, the track in the natural state has a bending rigidity due to the action of the rubber bushing. Based on the dynamic theory of axially moving beam, the differential equation of transversal vibration of a beam element is established. The entire upper track is assumed to be a continuous multi-span axially moving Euler-Bernoulli beam with an axial tension. Based on the Transfer Matrix Method of Multibody System, the transfer equation is obtained. According to the boundary conditions, the natural frequency of the system is solved. The correctness of the beam model hypothesis is verified by experiments. The results show that the first-order natural frequency of the upper track increases with the increase of the tension and the decrease of the vehicle speed. Through frequency analysis, the main excitation source for the transversal vibration of the track is the polygon effect produced by the meshing of the track and the sprocket. This study provides a theoretical basis for the vibration analysis and stability control of the upper track on the tracked vehicle.

Background and aims Liver cancer stem cells (CSCs) exist in the tumor environment and are critically involved in the initiation and progression of hepatocellular carcinoma (HCC). However, the underlying molecular mechanisms of self-renewal and maintenance of liver CSCs remain poorly understood. Approach and results We identified that xanthine oxidoreductase (XOR), which was expressed at low levels in human HCC samples and liver CSCs, restrained HCC formation and chemoresistance by attenuating liver CSC propagation. Mechanistically, XOR physically interacts with ubiquitin-specific peptidase 15 (USP15), thereby promoting deubiquitination of Kelch-like ECH associated protein 1 (KEAP1) to stabilize its expression, which leads to degradation of Nrf2 (nuclear factor erythroid 2-related factor 2) through ubiquitination and subsequently reactive oxygen species accumulation in liver CSCs. Finally, our data reveal that XOR promotes USP15-mediated Nrf2-KEAP1 signaling to block liver CSCs and tumor propagation. Conclusion We identified that XOR may represent a potential therapeutic target for clinical intervention in HCC driven by liver CSCs.

Purpose. Fractures are common among all types of paediatric injuries, with differences in incidence over time. Here, we present the epidemiologic features of traumatic fractures in a population of youth ≤ 18 years of age who were admitted to our university-affiliated hospitals from 2002 to 2010. Methods. We retrospectively reviewed 2450 children and adolescents who had traumatic fractures. The data include variables such as age, sex, date of injury, and the mechanism of injury. For the period of 2002-2010, there were 2450 injury events that resulted in at least 1 fracture. Results. Low falls (1042, 42.5%) and upper limb fractures (1068, 43.6%) were the most common aetiologies and fracture sites. With increasing age, the proportion of injuries due to motor vehicle collisions (MVCs) decreased and the injuries due to being hit by others and due to sprains increased. With increasing age, the proportion of craniofacial fractures (CFFs) decreased, and lower limb fractures (LLFs), spinal fractures (SFs), and fractures of ribs and the sternum (RSFs) increased. Over time, the proportion of injuries due to MVCs and mechanical injury decreased. Male patients presented with a significantly higher proportion of injuries due to low falls, being struck by an object, being hit by others, and due to sprains. There were a significantly lower proportion of injuries due to MVCs in female patients. Male patients presented with a significantly higher proportion of ULFs in the ≤6-year-old age group and a significantly lower proportion of LLFs and SFs in the 12-18-year-old age group than did female patients. Conclusions. Low falls and upper limb fractures were the leading cause and fracture sites. To further improve the prevention and treatment of traumatic fractures in children and adolescents, policy makers should pay attention to these characteristics.

The recovery of spinal cord injury (SCI) involves multiple factors, of which miRNAs take an important part. In this study, we evaluated the function of microRNA-211-5p (miR-211-5p) on SCI in a rat model. SCI model was established using modified Allen's weight-drop method and Basso-Bcattie-Bresnahan score was applied to assess the locomotor function. MiR-211-5p agomir was utilized to increase miR-211-5p expression and endoplasmic reticulum (ER) stress inhibitor, 4-PBA (4-phenylbutyric acid), was utilized to suppress ER stress. Neuron apoptosis and the expressions of miR-211-5p, activating transcription factor 6 (ATF6), apoptosis-related proteins, pro-inflammatory cytokines and endoplasmic reticulum stress-related proteins were detected. Dual luciferase reporter gene assay was performed to verify the binding between miR-211-5p and ATF6. The results showed that miR-211-5p directly targeted ATF6. MiR-211-5p was down-regulated and ATF6 was up-regulated in SCI rats. Both interferences with miR-211-5p agomir and 4-PBA effectively attenuated neuron apoptosis and reversed the expressions of apoptosis, inflammation and endoplasmic reticulum stress-related molecules post SCI in rats. These findings demonstrated that miR-211-5p could effectively alleviate SCI-induced neuron apoptosis and inflammation via directly targeting ATF-6 and regulating ER stress.

Background Based on accumulating evidence, excessive activation of microglia-mediated inflammatory responses plays an essential role in ischemic stroke. Poncirin (Pon) exerts anti-hyperalgesic, anti-osteoporotic and anti-tumor effects on various diseases. However, the roles of Pon in microglial activation and the underlying mechanism have not been elucidated. This study aimed to explore whether Pon inhibits lipopolysaccharide (LPS)-induced microglial neuroinflammation and protects against brain ischemic injury in experimental stroke in mice. Methods Primary microglia cells were prepared from the cerebral cortices of 1- to 2-day-old C57BL/6J mice. Murine BV2 cells and primary microglia were stimulated with LPS and the effects of a non-cytotoxic concentration of Pon on LPS-stimulated pro-inflammatory factors were measured using real-time PCR and enzyme-linked immunosorbent assays (ELISAs). Western blot analyses were used for mechanistic studies. In an in vivo study, 8-week-old male C57BL/6J mice were subjected to focal cerebral ischemia through middle cerebral artery occlusion (MCAO). Pon (30 mg/kg, i.p.) or the same volume of saline was administered after the MCAO model was established, and the infarct volume was evaluated using 2,3,5-triphenyltetrazolium chloride (TTC) staining. We also evaluated animal behaviours, the expression of pro-inflammatory cytokines and microglial activation in the ischemic hemisphere. Results Pon prevented the release of nitric oxide (NO), prostaglandin E2 (PGE2), interleukin (IL)-1β, IL-6 and tumor necrosis factor-alpha (TNF-α) in both BV2 cells and primary microglia stimulated with LPS. The inhibitory effects of Pon were associated with the regulation of the ERK1/2, JNK and nuclear factor kappa B (NF-κB) signaling pathways. In mice that underwent MCAO, Pon administration decreased the lesion size and improved neurological deficits. Furthermore, Pon attenuated the production of inflammatory cytokines mainly by restraining microglial activation after ischemic stroke. Conclusions Based on the findings from the present study, Pon provides neuroprotection through its anti-inflammatory effects on microglia and it may be a useful treatment for ischemic stroke.

Connexin 43 (Cx43) widely exists in all components of the neurovascular unit (NVU) and is a constituent of gap junctions and hemichannels. In physiological states, gap junctions are open for regular intercellular communication, and the hemichannels present low open probability in astrocytes. After cerebral ischemia, a large number of hemichannels are unusually opened, leading to cell swelling and even death. Most known hemichannel blockers also inhibit gap junctions and sequentially obstruct normal electrical cell-cell communication. In this study, we tested the hypothesis that Gap19, a selective Cx43-hemichannel inhibitor, exhibited neuroprotective effects on cerebral ischemia/reperfusion (I/R). An obvious improvement in neurological scores and infarct volume reduction were observed in Gap19-treated mice after brain ischemia induced by middle cerebral artery occlusion (MCAO). Gap19 treatment attenuated white matter damage. Moreover, Gap19 treatment suppressed the expression of Cx43 and Toll-like receptor 4 (TLR4) pathway-relevant proteins and prevented the overexpression of tumour necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). To further explore downstream signaling, we established an in vitro model-oxygen glucose deprivation (OGD) to simulate ischemic conditions. Immunofluorescence staining showed that Cx43 co-existed with TLR4 in astrocytes. The hemichannel activity was increased after OGD and Gap19 could inhibit this effect on astrocytes. Gap19 substantially improved relative cell vitality and decreased the expression of Cx43, TLR4 and inflammatory cytokines in vitro. In addition, in the lipopolysaccharide (LPS) stimulation OGD model, Gap19 also exhibited a protective effect via inhibiting TLR4 pathway activation. In summary, our results showed that Gap19 exerted a neuroprotective effect after stroke via inhibition of the TLR4-mediated signaling pathway.

The present study aimed to investigate whether ginsenoside Rb1 (G-Rb1) attenuates spinal cord injury-associated oxidative stress in rats by regulating the endothelial nitric oxide synthase eNOS/nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase (HO)-1 signaling pathway. Sprague Dawley rats were randomly divided into the sham operation group (S group), spinal cord injury group (SCI group), G-Rb1 treatment group (G-Rb1 group) and SCI+G-Rb1+Inhibitor L-name group (L-name group). The posterior limb function was evaluated via the Basso, Beattie and Bresnahan scoring method. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT) and glutathione (GSH) in serum were measured by ELISA. The pathological changes in the spinal cord were observed by H&E staining. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were used to detect eNOS, phosphorylated (p)-eNOS, heat shock protein (HSP)90, Nrf2 and NAD(P)H quinone dehydrogenase 1 (Nqo1) at the mRNA and protein level. Immunohistochemistry was used to detect the expression of Nrf2 and p-eNOS. Compared with the S group, the scores of spinal cord function in the SCI group were significantly lower, and the levels of MDA were significantly increased, while the levels of SOD, CAT and GSH protein in spinal cord were significantly decreased (P

Lateral radiographs are commonly used to assess cervical sagittal alignment. Three assessment methods have been described and are commonly utilized in clinical practice. These methods are described for perfect lateral cervical radiographs, however in everyday practice radiograph quality varies. The aim of this study was to compare the reliability and reproducibility of 3 cervical lordosis (CL) measurement methods.Forty-four standing lateral radiographs were randomly chosen from a lateral long-cassette radiograph database. Measurements of CL were performed with: Cobb method C2-C7 (CM), C2-C7 posterior tangent method (PTM), sum of posterior tangent method for each segment (SPTM). Three independent orthopaedic surgeons measured CL using the three methods on 44 lateral radiographs. One researcher used the three methods to measured CL three times at 4-week time intervals. Agreement between the methods as well as their intra- and interobserver reliability were tested and quantified by intraclass correlation coefficient (ICC) and median error for a single measurement (SEM). ICC of 0.75 or more reflected an excellent agreement/reliability. The results were compared with repeated ANOVA test, with p 0.05 considered as significant.All methods revealed excellent intra- and interobserver reliability. Agreement (ICC, SEM) between three methods was (0.89°, 3.44°), between CM and SPTM was (0.82°, 4.42°), between CM and PTM was (0.80°, 4.80°) and between PTM and SPTM was (0.99°, 1.10°). Mean values CL for a CM, PTM, SPTM were 10.5° ± 13.9°, 17.5° ± 15.6° and 17.7° ± 15.9° (p 0.0001), respectively. The significant difference was between CM vs PTM (p 0.0001) and CM vs SPTM (p 0.0001), but not between PTM vs SPTM (p 0.05).All three methods appeared to be highly reliable. Although, high agreement between all measurement methods was shown, we do not recommend using Cobb measurement method interchangeably with PTM or SPTM within a single study as this could lead to error, whereas, such a comparison between tangent methods can be considered.

To determine the safety and short-term curative effects of internal fixation using a dynamic neutralization system (Dynesys) for multi-segmental lumbar disc herniation (ms-LDH) with the control group treated by posterior lumbar interbody fusion (PLIF). Forty-five patients with ms-LDH were selected as study group treated with Dynesys and 40 patients as control group with PLIF. The surgical efficacy was evaluated by comparing the visual analogue scale (VAS) scores, the Oswestry Disability Index (ODI) scores and the ROMs of the adjacent segment before and after surgery. The postoperative complications related to the implants were identified. All patients were followed up for an average duration of over 30 months. Dynesys stabilization resulted in significantly higher preservation of motion at the index level (p

Painful diabetic neuropathy is a common complication of diabetes mellitus, which often makes the patients suffer from severe hyperalgesia and allodynia. Thus far, the treatment of painful diabetic neuropathy remains unsatisfactory. Metformin, which is the first-line drug for type-2 diabetes, has been proved to attenuate hyperexcitability in sensory neurons linked to chemotherapy-induced neuropathic pain, highlighting its potential in alleviating pain related with painful diabetic neuropathy. The present study was designed to investigate the potential beneficial effect of metformin on hyperalgesia and allodynia in diabetic rats. The mechanical sensitivity, heat nociception, and cold allodynia were examined. The levels of malondialdehyde, superoxide dismutase, and advanced glycation end-products in the blood were measured. The expression of adenosine monophosphate-activated protein kinase (AMPK) phosphorylation and AMPK target genes were examined in the sciatic nerves of the animals. It was found that metformin was capable of attenuating diabetes-induced mechanical hyperalgesia, heat hyperalgesia and cold allodynia. In addition, metformin was capable of decreasing malondialdehyde and glycation end-products levels in blood, as well as increasing superoxide dismutas activity, indicating the inhibitory effect of metformin against diabetes-induced oxidative stress. Further studies showed that metformin could activate AMPK and increase the AMPK target genes in sciatic nerves in diabetic rats. In conclusion, metformin is able to attenuate diabetes-induced hyperalgesia and allodynia, which might be associated its anti-oxidative effect through AMPK pathway. Metformin might be used as an effective drug, especially with fewer side effects, for abnormal sensation in painful diabetic neuropathy.

We report on a method for the determination of the herbicide atrazine in tap water samples using melamine-modified gold nanoparticles (Mel-AuNPs). If a solution containing atrazine is added to a solution of such NPs, a color change occurs from wine-red to blue. This is due to a transition from monodisperse to aggregated Mel-AuNPs and caused by strong hydrogen bonding between atrazine and melamine. The color change can be monitored by a UV–vis spectrophotometer or with bare eyes. The ratio of the absorbances at 640 and 523 nm is linearly related to the logarithm of the atrazine concentration in the 0.165 to 16.5 μM range, and (with different slope) in the 16.5 μM to 330 μM range. The detection limit of atrazine is as low as 16.5 nM (S/N = 3). The method was successfully applied to the determination of atrazine in spiked tap water and gave recoveries that ranged from 72.5 % to 102.3 %.

Connexin43 (Cx43) is one of the most abundant gap junction proteins in the central nervous system. Abnormal opening of Cx43 hemichannels after ischemic insults causes apoptotic cell death. In this study, we found persistently increased expression of Cx43 8 h to 7 d after hypoxia/ischemia (HI) injury in neonatal rats. Pre-treatment with Gap26 and Gap27, two Cx43 mimetic peptides, significantly reduced cerebral infarct volume. Gap26 treatment at 24 h after ischemia improved functional recovery on muscle strength, motor coordination, and spatial memory abilities. Further, Gap26 inhibited Cx43 expression and reduced active astrogliosis. Gap26 interacted and co-localized with Cx43 together in brain tissues and cultured astrocytes. After oxygen glucose deprivation, Gap26 treatment reduced the total Cx43 level in cultured astrocytes; but Cx43 level in the plasma membrane was increased. Degradation of Cx43 in the cytoplasm was mainly via the ubiquitin proteasome pathway. Concurrently, phosphorylated Akt, which phosphorylates Cx43 on Serine(373) and facilitates the forward transport of Cx43 to the plasma membrane, was increased by Gap26 treatment. Microdialysis showed that increased membranous Cx43 causes glutamate release by opening Cx43 hemichannels. Extracellular glutamate concentration was significantly decreased by Gap26 treatment in vivo. Finally, we found that cleaved caspase-3, an apoptosis marker, was attenuated after HI injury by Gap26 treatment. Effects of Gap27 were analogous to those of Gap26. In summary, our findings demonstrate that modulation of Cx43 expression and astroglial function is a potential therapeutic strategy for ischemic brain injury.

The aim of this study is to investigate the incidence and pattern of traumatic fractures (TFs) as a result of falls in a population of children and adolescents (≤18 years old) in China. This was a cross-sectional study. We retrospectively reviewed 1412 patients who were children and adolescents with TFs as a result of falls admitted to our university-affiliated hospitals in China from 2001 to 2010. Etiologies included high fall (height ≥2) and low fall (height

Ischemic stroke often results in severe injury to white matter structures including the axons, oligodendroglia, and other glial cells. Immature stages of oligodendroglia, such as oligodendrocyte precursor cells (OPCs) and premature oligodendroglia, are more vulnerable to ischemia than mature oligodendroglia. Extensive studies have been performed on the necroptosis of neurons following cerebral ischemia. The present study aimed to investigate the effect of necrostatin-1 (Nec-1), a necroptosis inhibitor, on the survival of OPCs and long-term functional recovery following transient cerebral ischemia. Male adult ICR mice (25–30 g) were subjected to 60-min middle cerebral artery occlusion (MCAO) and 24 h of reperfusion. Nec-1 (0.04 mg/kg) was injected intracerebroventricularly 1 h before the onset of MCAO. Cognitive functions were evaluated ≤30 days after MCAO. Necroptosis-related proteins, receptor-interacting protein kinase 1 (RIPK1), RIPK3, MLKL, and P-MLKL, were assessed by western blot analyses. The cultured primary mouse OPCs were used to confirm the effects of Nec-1 on the viability of OPCs following oxygen-glucose deprivation (OGD). This study demonstrated that pretreatment with Nec-1 significantly promoted OPCs survival, alleviated white matter injury, and improved cognitive function after transient cerebral ischemia. Nec-1 also inhibited the activation of RIPK1, RIPK3, MLKL, and P-MLKL in the subventricular zone (SVZ) and corpus callosum regions after MCAO. OPCs’ culture experiments confirmed that Nec-1 significantly reduced the necroptosis of OPCs, perhaps by inhibiting the expression of RIPK1, RIPK3, MLKL, and P-MLKL. Nec-1, an inhibitor of RIPK1, may reduce ischemic white matter damage and improve recovery of long-term neurological function following cerebral ischemia.

Ogura cytoplasmic male sterility (Ogu-CMS) is widely used in the production of commercial hybrids of Brassica oleracea. However, the widespread application of the Ogu-CMS system in B. oleracea has hindered the germplasm innovation of Ogu-CMS resources due to the lack of a natural restorer line. Previously, the Ogu-CMS fertility-restored interspecific hybrids between rapeseed 15Y403 (2n = 38, AACC) and Chinese kale JL1 (2n = 18, CC) have been successfully produced. However, these progenies, which still contained a large proportion of rapeseed genomic components, showed poor fertility and a low seed setting rate under natural pollination. To improve fertility and seed setting, a successive backcross with JL1 was performed to produce BC2 progenies. Screening with the Rfo-specific marker, five individuals harboring the Rfo gene were identified among 98 BC2 progenies. These five individuals underwent background marker screening and an evaluation of agronomic traits and fertility. One individual (code: 15Q23) was identified with higher pollen viability, better seed setting under natural pollination, and a closer genetic background to the parent Chinese kale JL1. Many morphological traits showed no significant differences (P

We experimentally demonstrate cascaded Raman scattering continuum generation at 1.0–1.3 μm with pulse energy of 47 nJ by utilizing a commercially available all-normal-dispersion single-mode fiber (SMF) with a low threshold pump power. We achieve passively mode-locked all-fiber lasing by nonlinear polarization rotation technique. Continuous Raman gain is obtained by the same SMF in every roundtrip because of the ring-cavity configuration, which makes it possible to achieve high-order Raman Stokes waves by a short fiber length. Limited by the pump power, the maximum output average power and peak power are 87.4 and 339 mW, but it has great potential to be improved. These make it an ideal continuum source for many applications, such as optical coherence tomography.