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Background Placental infarction can result from the partial or complete obstruction of the uterine spiral artery, interrupting maternal blood flow and causing progressive villus tissue necrosis. This, in turn, can adversely impact placental transport, endocrine signaling, metabolic activity, and immune function, resulting in severe fetal growth restriction, fetal ischemic stroke, and even stillbirth. Prenatal magnetic resonance imaging (MRI) can allow clinicians to evaluate the fetus and the structure of the placenta to detect any morphological changes during pregnancy. The present case highlights the advantages of using MRI to diagnose placental and fetal cerebral ischemic lesions, providing clinical guidance to assist with the appropriate management of placental and fetal abnormalities. Case presentation: A 33-year-old female who was 26 weeks and 4 days pregnant presented with blood pressure that was elevated for 1 week detected during prenatal examination and was hospitalized for moderate preeclampsia and fetal distress. MRI examination in our hospital revealed placental infarction, fetal acute cerebral ischemic stroke, and intrauterine distress. Pathological examination confirmed the diagnosis of placental infarction, and a male stillbirth was induced by drug treatment/ Conclusion MRI scans can allow for the qualitative and quantitative diagnosis of circulatory and central nervous system abnormalities in the context of placental disease, providing guidance to support appropriate clinical decision-making and the termination of pregnancy following fetal ischemic stroke.

The homeodomain–leucine zipper(HD-ZIP) gene family is involved in a variety of physiological processes in plants and plays a number of roles in rice. However, the analysis of this gene family in rice (Oryza sativa L.) is not comprehensive. The genome-wide characterization of HD-ZIP family was explored by using high-quality rice genome sequence combined with transcriptome. The HD-ZIP superfamily has four subfamilies in rice, including 31 HOX gene members in subfamilies I, II, and III, and nine rice outermost cell-specific gene (ROC) members in subfamily IV. Four subfamily members can interact with many reproductive and developmental related proteins, and subfamily II is regulated by miR396 family. We explored the expression patterns of HD-ZIPs in different rice tissues and analysis of high temperature and low temperature stress by RT-PCR showed that HD-ZIPs played an important role in the early stage of stress. The transcriptome results of diploid and tetraploid grains at different development stages showed that most HD-ZIP members were highly expressed in the early stage of grain development, and the expression of some members in tetraploid glumes was significantly higher than that in diploid glumes. These findings indicate the evolutionary process, characteristics and expression profile of HD-ZIP gene family in rice, and reveal their role in rice development and response to abiotic stress.

Glioma is a common life-threatening tumor with high malignancy and high invasiveness. LncRNA ZFPM2 antisense RNA 1 (ZFPM2-AS1) was confirmed to be implicated in numerous tumors, while its biological function and mechanism have not been thoroughly understood in glioma. The gene expression was measured by RT-qPCR. Cell proliferation, cell cycle, and cell apoptosis of glioma cells were validated by CCK-8, colony formation, flow cytometry and TUNEL assays. The effect of ZFPM2-AS1 on tumor growth was verified by in vivo assay. The exploration on ZFPM2-AS1-mediated mechanism was carried out via ChIP, luciferase reporter, and RIP assays. In the present study, ZFPM2-AS1 was demonstrated as a highly-expressed lncRNA in glioma tissues and cells. ZFPM2-AS1 silencing suppressed cell proliferation and cell cycle, but facilitated cell apoptosis. In addition, the inhibitive effect of silenced ZFPM2-AS1 was also observed in tumor growth. Furthermore, we found that SP1 interacted with ZFPM2-AS1 promoter to transcriptionally activate ZFPM2-AS1 expression. Moreover, ZFPM2-AS1 was identified as a competing endogenous RNA (ceRNA) for miR-515-5p to target SOD2. Rescue assays verified that SOD2 overexpression partially abolished the suppressive impact of ZFPM2-AS1 silencing on glioma cell growth. In conclusion, this study corroborated the regulatory mechanism of SP1/ZFPM2-AS1/miR-515-5p/SOD2 axis in glioma, indicating that targeting ZFPM2-AS1 might be an effective way to treat glioma.

Aim Renal injury induced by diabetes is reported to be associated with inflammation. Isomangiferin (ISO), a xanthone C-glucoside from the Cyclopia subfamily, exhibits many pharmacological properties. This study aimed to evaluate the protection of ISO against renal damage in diabetic mice. Methods Serum glucose, insulin, uric acid, creatinine, total cholesterol (TC), triglyceride (TG), and inflammatory cytokines in serum and the kidney of db/db diabetes model mice were detected. The components of high mobility group protein B1 (HMGB1)/NACHT leucine-rich repeat- and PYD-containing 3 (NLRP3)/nuclear factor kappa-B (NF-κB) pathway in the kidney were detected by Western blot and immunohistochemical analysis. Results ISO improved lipid profile and glucose tolerance, and inhibited the production of inflammatory cytokines in a db/db model mice. Moreover, ISO decreased biochemical indexes in the serum and inhibited the activation of HMGB1/NLRP3/NF-κB signaling in the kidney of db/db model mice. Conclusion ISO provides protection against renal injury via inhibiting HMGB1/NLRP3/NF-κB signaling in a diabetic mouse model.

Apigenin, a flavonoid found in many plants, has various biological properties. We aimed to investigate the anti-inflammatory and anti-oxidative activity of apigenin against carbon tetrachloride (CCl4)-induced acute liver injury in mice and hydrogen peroxide (H2O2)-induced oxidative stress in HepG2 cells and possible mechanism. In vivo, apigenin significantly reduced alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity in serum of mice challenged by CCl4 and markedly alleviated the lipid peroxidation as indicated by the increased level of superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidases (GSH-Px) and catalase (CAT), and the decreased malondialdehyde (MDA) in liver tissue. Apigenin also ameliorated inflammation by downregulating tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and upregulating IL-10. Consistently, the elevated ALT and AST level; the impaired balance between SOD, GSH activity, and excessive ROS; and the increased gene expression of TNF-α and IL-6 resulting from H2O2-induced oxidative stress were restored by apigenin. Moreover, the results from Western blot, real-time qPCR, and immunofluorescence assay indicated that apigenin enhanced the activity of TNF receptor-associated factor (TRAF) 2/3 and cellular inhibitor of apoptosis protein (c-IAP) 1, ameliorated NF-κB-inducing kinase (NIK), and mediated the nuclear translocation of NF-κB2, therefore had an inhibitory effect on the non-canonical NF-κB pathway which was activated in both models. siNIK canceled the protective effect of apigenin on H2O2-induced HepG2 cells. Altogether, our results demonstrated that apigenin mitigated liver injury by ameliorating inflammation and oxidative stress through suppression of the non-canonical NF-κB pathway, indicating the potential of apigenin for treatment of the liver injury.

There is no effective treatment for hemiplegia after hypertensive intracerebral hemorrhage. Considering that the branches of L4 nerve roots in the lumbar plexus root control the movement of the lower extremity anterior and posterior muscles, we investigated a potential method of nerve repair using the L4 nerve roots. Rat models of hindlimb hemiplegia after a hypertensive intracerebral hemorrhage were established by injecting autogenous blood into the posterior limb of internal capsule. The L4 nerve root on the healthy side of model rats was transferred and then anastomosed with the L4 nerve root on the affected side to drive the extensor and flexor muscles of the hindlimbs. We investigated whether this method can restore the flexible movement of the hindlimbs of paralyzed rats after hypertensive intracerebral hemorrhage. In a beam-walking test and ladder rung walking task, model rats exhibited an initial high number of slips, but improved in accuracy on the paretic side over time. At 17 weeks after surgery, rats gained approximately 58.2% accuracy from baseline performance and performed ankle motions on the paretic side. At 9 weeks after surgery, a retrograde tracing test showed a large number of fluoro-gold-labeled motoneurons in the left anterior horn of the spinal cord that supports the L4-to-L4 nerve roots. In addition, histological and ultramicrostructural findings showed axon regeneration of motoneurons in the anterior horn of the spinal cord. Electromyography and paw print analysis showed that denervated hindlimb muscles regained reliable innervation and walking coordination improved. These findings suggest that the L4-to-L4 nerve root transfer method for the treatment of hindlimb hemiplegia after hypertensive intracerebral hemorrhage can improve the locomotion of hindlimb major joints, particularly of the distal ankle. Findings from study support that the L4-to-L4 nerve root transfer method can effectively repair the hindlimb hemiplegia after hypertensive intracerebral hemorrhage. All animal experiments were approved by the Animal Ethics Committee of the First Affiliated Hospital of Nanjing Medical University (No. IACUC-1906009) in June 2019.

HOXB13 exerts a close relation in several human cancers. This study explored the role of HOXB13 in glioblastoma (GBM), a brain tissue with the highest aggressive rate and mortality in adults. Through microarray and immunohistochemistry analyses, HOXB13 was highly expressed in GBM tissues. Furthermore, we showed that high-level expression of HOXB13 in GBM was associated with worse survival, suggesting that HOXB13 could be a prognostic marker for patients with GBM. GBM cells U87 and U251 overexpressing HOXB13 showed enhanced proliferation, migration, and invasion relative to the control cells, while knockdown of HOXB13 led to decreased cell proliferation, migration, and invasion abilities. In addition, dual-luciferase report assay, chromatin immunoprecipitation assay, and quantitative real-time polymerase chain reaction data showed that HOXB13 directly bound to HOXC-AS3 promoter. HOXC-AS3 was involved in HOXB13-induced proliferation, migration, and invasion of GBM cells. In summary, this study revealed the prognostic potential of HOXB13 in GBM. We believed that HOXB13/HOXC-AS3 signaling axis can be served as therapeutic targets for this highly aggressive cancer.

Background Hemiplegia after hypertensive intracerebral hemorrhage(HICH) is prevalent,devasta-ting,and currently unable to intervene satisfactorily.Established success in neurotization spurs our interest in restoring skilled lower-limb movement.Here,we explored whether contralesional L4 transfer to ipsilesional L4 root,featuring simultaneous invigoration of flexors and extensors,reanimated dexterous locomotion for the hemiplegic hindlimb after HICH.Methods We manufactured eligible rat models by injecting autologous vein blood into the left posterior limb of internal capsule (PLIC) and randomized thirty rats into three groups. We did not transect but expose bilateral L4 in group A (sham operation) after injection of saline,and infused equal blood followed by bilateral L4 transection and contralateral L4 transfer,in group B and group C,respectively.Behavioral,ultrastru-ctural,immunofluorescent,and electromyographic assessments were applied to efficacy analysis.MRI localized the PLIC impact.Results We could see marked reduction in movements and capture a denervated potential in the right hindlimb of model rats (P༞0.05).In the walking tests,group C exhibited an initially high slip,but,later, a larger increment in accuracy on the paretic side, compared to group B and group A(P༜0.001).Also,at Week 17,rats gained ∼58.2% accuracy and actuated ankle motions in group C(P༞0.05). In the retrograde tracing,at Week 9,fluoro-gold labeled motoneurons had been numerously present in the left anterior horn of the spinal cord from the L4-to-L4 root.Histological and ultra-microstructural assessments certified efficient axons regeneration.Electrom-yography and pawprint analysis implied the denervated muscles were reliably reinnervated,and myodynamia improvement(p>0.05).Conclusions Contralateral L4 transfer could render favorable outcomes for major joints,particularly for the ankle,therefore efficaciously repaired the hemiplegic hindlimb after HICH.

Background/Aims: Calcium-permeable ionotropic NMDAR-mediated hyperactivity is regarded as the critical factor in modulating the development of ischaemic stroke. Recently, there has been increasing interest in preventing post-stroke neuronal death by focusing on intervening in the function of subpopulations of NMDARs and their downstream signalling. Geniposide, an iridoid glycoside, has been found to have cytoprotective functions in various conditions. However, it is still unclear whether and how geniposide affects neuronal insult under experimental stroke. Methods: We demonstrate that dose-dependent geniposide significantly decreased the infarct volume in tMCAO models. Results: A medium level of geniposide improved anti-apoptotic functions and inhibited BBB leakage/haemorrhage via elevating GluN2A-containing NMDAR expression in tMCAO rats. Importantly, these effects could be eliminated by co-treatment of geniposide with the GluN2A antagonist NVP but not the GluN2B inhibitor ifenprodil. Moreover, geniposide’s protection was due to the enhancement of GluN2A-dependent survival signals, including pAKT, pERK and PSD-95. Conclusion: The results suggest that geniposide protects neurons against post-ischaemic neurovascular injury through the activation of GluN2A/AKT/ERK pathways. As a very promising natural agent, geniposide may be a future therapeutic for stroke patients.

The aggressiveness and recurrence of glioma are major obstacles for the treatment of this type of tumor. Further understanding of the molecular mechanisms of glioma is necessary to improve the efficacy of therapy. MicroRNAs have been widely studied in many human cancers. Here, we found that miR-940 was one of the primary downregulated miRNAs in clinical samples and glioma cell lines through bioinformatics analysis and qRT-PCR. Upregulating miR-940 expression significantly inhibited the proliferation and invasion and promoted apoptosis of U87 and U118 cells. In addition, experiments in vivo showed that upregulation of miR-940 expression inhibited xenograft growth. Methylenetetrahydrofolate dehydrogenase (MTHFD2), a dual-functional metabolic enzyme, is involved in the one-carbon metabolism of folate in mitochondria. We found MTHFD2 to be overexpressed in glioma tissues and our clinical samples by qRT-PCR and Western blot assays. Through TargetScan prediction and luciferase assays, we found that miR-940 directly targets MTHFD2. Upregulation of miR-940 expression inhibited the expression of MTHFD2 and led to intracellular one-carbon metabolism dysfunction. Furthermore, the antitumor effects of miR-940 could be attenuated by overexpression of MTHFD2. Together, the results of our study suggest that miR-940 may be a new therapeutic target for the treatment of glioma through targeting of MTHFD2.

A craniopharyngioma (CP) is a benign tumor commonly considered to originate from the pituitary stalk. However, it is still controversial as to whether the pituitary stalk should be maintained after microsurgery to resect the tumor despite its own physiological function of the pituitary stalk. In this study, meta-analysis was conducted to evaluate the influence of the pituitary stalk resection on endocrine function and tumor recurrence rate.The relevant publications were identified by searching databases including Pubmed, Embase, Medline, and Web of Science. The extracted data were used as the basis for the meta-analysis by the RevMan 5.2 software program.Seven articles were selected, including 420 clinical cases. The meta-analysis showed that retaining the pituitary stalk might reduce the occurrence rate of diabetes insipidus (OR=0.21, 95%CI=0.10, 0.46, P=0.0001) and the risk of potential impairment of anterior pituitary function (OR=0.04, 95%CI=0.01, 0.13, P0.0001). However, there was no significant relationship between craniopharyngioma recurrence and pituitary stalk treatment (i.e., preservation or resection) (OR=1.40, 95%CI=0.59, 3.34, P=0.45).The maintenance of the pituitary stalk may reduce the alterations in endocrine function and the occurrence of diabetes insipidus. However, it is not likely to enhance the recurrence rate of craniopharyngiomas.

Sodium alginate (SA) and tea polyphenols (TP) are natural preservatives commonly used in the food industry, including the production of fish products. The effect of SA coating infused with TP on the quality of fresh Japanese sea bass (Lateolabrax japonicas) fillets was evaluated over a 20-day period at 4 °C. SA (1.5%, w/v) or TP (0.5%, w/v) treatment alone, and the SA coating infused with TP (SA-TP) all reduced microbial counts, with the SA-TP providing the greatest effect. Fish fillet samples treated with SA-TP had significantly lower levels of total volatile basic nitrogen, lipid oxidation, and protein decomposition during the storage period, relative to the remaining treatments. The samples treated with SA-TP had the highest sensory quality rating as well. Collectively, sodium alginate coating infused with tea polyphenols may represent a promising treatment for preservation of Japanese sea bass fillets during cold storage.The sodium alginate-tea polyphenols composite coating has strong potential to be used as a new biopreservative for maintaining fish fillet quality.

The exact effect of glycine pre-treatment on brain ischemic tolerance (IT) remains quite controversial. The objective of this study was to investigate the potential effects of glycine on IT. We used rat models of both in vitro ischemia (oxygen and glucose deprivation) and in vivo ischemia (transient middle cerebral artery occlusion). Low doses of glycine (L-Gly) significantly decreased hippocampal ischemic LTP (i-LTP), infarct volume, and neurological deficit scores which were administered before ischemia was induced in rats, whereas high doses of glycine exerted deteriorative effects under the same condition. These findings suggested that exogenous glycine may induce IT in a dose-dependent manner. Furthermore, L-Gly-dependent neuronal protection was inversed by L689, a selective NMDAR glycine site antagonist both in vitro (abolished i-LTP depression) and in vivo (increased infarct size reduction), but not glycine receptor (GlyR) inhibitor strychnine. Importantly, L-Gly-induced IT was achieved by NR2A-dependent cAMP-response element binding protein phosphorylation. These data imply that glycine pre-treatment may represent a novel strategy for inducing IT based on synaptic NMDAR-dependent neuronal transmission. A model of glycine induced dose-dependent bidirectional regulations in ischemic tolerance. (a) Under low dose of Gly pre-treatment, glycine induces NMDAR potentiation and CREB-dependent neuroprotection through the NMDAR co-agonist binding site. (b) Under high dose of Gly pre-treatment, the excessive glycine in synaptic cleft can activate neighboring extrasynaptic sites and combine to the GlyRs. Then, the deteriorative effects would be triggered after NMDAR endocytosis and synaptic depression. AMPAR, α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor; CREB, cAMP response element-binding protein; Gly, glycine; GlyR, glycine receptor; GlyT1, gycine transportor 1; NMDAR, N-methyl-d-aspartate receptor.

Vanishing lung syndrome, also known as idiopathic giant bullous emphysema, is a rare disease characterized by giant emphysematous bullae. The disease is diagnosed by radiological findings of giant bullae in one, or both, of the upper lobes of the lung, occupying at least one-third of the hemithorax. There have been several reports of vanishing lung syndrome, however it remains to be determined whether genetic inheritance is associated with the disease. In the present study, five patients within one family, with vanishing lung syndrome, were reported during a follow-up period of ~ 20 years. All of the patients were diagnosed by radiological findings, which showed diffuse bullae in the lungs, which were of varying size and asymmetrical distribution, and the occurrence of pneumothorax or emphysema. The Medical Ethics Committee of the People's Hospital of Zhangye Municipality (Zhangye, China) approved this study, and all subjects gave their informed consent During the follow-up period of 20 years, bullae in these patients were shown to progressively increase, and no other pulmonary diseases, including lung cancer, tuberculosis, pneumoconiosis and chronic bronchitis were observed. Autosomal dominant inheritance was observed in five cases, and autosomal recessive inheritance was observed in one case. The present study suggests that vanishing lung syndrome may be associated with autosomal dominant and recessive genetic inheritance.

The association between ALOX5AP SG13S114 polymorphism and ischemic stroke (IS) susceptibility has extensively been investigated, especially in white populations; however, the results were inconclusive. Here, we perform a meta-analysis to clarify the effect of SG13S114 variant on the IS risk in Europeans. The Web of Science, PubMed, EMBASE, and Medline were searched up to August 1st, 2016. Data were extracted and the odd ratios (ORs) and 95% confidence intervals (CIs) were calculated by a fixed-effects or random-effects model. In total, 8 case control studies involved 8062 subjects were finally included in this meta-analysis. We observed a significantly decreased IS risk in persons carrying an A allele at the SG13S114 polymorphism compared with those with a T allele (A vs T, OR = 0.856, 95% CI = 0.797–0.919, p < 0.001). In addition, the results of sensitivity and cumulative meta-analysis indicated the robustness of our results. In addition, the publication bias was not detected using the funnel plot and Egger’s tests. In summary, the present meta-analysis suggested that the A allele at the ALOX5AP SG13S114 polymorphism is a protective factor for the IS in the Europeans. In addition, further studies with large sample size are needed to validate the association, as well as in other ethnic groups.

Background/Aims: Glycine is a strychnine-sensitive inhibitory neurotransmitter in the central nervous system (CNS), especially in the spinal cord, brainstem, and retina. The objective of the present study was to investigate the potential neuroprotective effects of GlyT1 inhibitor N [3-(4'-fluorophenyl)-3-(4'-phenylphenoxy) propyl] sarcosine (NFPS) in the rat model of experimental stroke. Methods: In vivo ischaemia was induced by transient middle cerebral artery occlusion (tMCAO). The methods of Western Blotting, Nissl Staining and Morris water maze methods were applied to analyze the anti-ischaemia mechanism. Results: The results showed that high dose of NFPS (H-NFPS) significantly reduced infarct volume, neuronal injury and the expression of cleaved caspase-3, enhanced Bcl-2/Bax, and improved spatial learning deficits which were administered three hours after transient middle cerebral artery occlusion (tMCAO) induction in rats, while, low dose of NFPS (L-NFPS) exacerbated the injury of ischaemia. These findings suggested that low and high dose of NFPS produced opposite effects. Importantly, it was demonstrated that H-NFPS-dependent neuronal protection was inverted by salicylate (Sal), a specific GlyR ɑ1 antagonist. Such effects could probably be attributed to the enhanced glycine level in both synaptic and extrasynaptic clefts and the subsequently altered extrasynaptic GlyRs and their subtypes. Conclusions: These data imply that GlyT1 inhibitor NFPS may be a novel target for clinical treatment of transient focal cerebral ischaemia and reperfusion which are associated with altered GlyR alpha 1 subunits.

Background We hypothesized that isoflurane has a greater potency to induce neurodegeneration than sevoflurane in the developing brains of neonatal mice based on our previous studies in cell culture. Methods We treated 7-day-old mice with either 0.75% isoflurane or 1.1% sevoflurane ( approximately 0.5 minimum alveolar concentration) for 6 h and then obtained blood and brain samples at 2 h after the anesthesia treatment for determination of neuroapoptosis in different brain regions and the neurodegenerative biomarker S100beta in the blood. The mechanisms of neurodegeneration induced by isoflurane or sevoflurane were also compared by determining protein expressions of the cell cycle and apoptosis-related proteins. In separate groups, memory and learning ability were evaluated through the use of Morris Water Maze testing in mice at postnatal day 42 after anesthesia treatment at postnatal day 7. Results Isoflurane but not sevoflurane significantly increased the neurodegenerative biomarker S100beta in the blood. Isoflurane treatments significantly increased apoptosis indicated by the activation of caspase-3 and elevation of poly-(ADP-ribose) polymerase in different brain regions. An equipotent exposure of sevoflurane tended to increase apoptosis in hippocampal and cortex areas but was significantly less potent than isoflurane. Neither isoflurane nor sevoflurane significantly changed protein levels of glyceraldehyde-3-phosphate dehydrogenase, beta-site amyloid beta-precursor protein-cleaving enzyme, and cell cycle regulatory proteins (CDK4, cyclin D1). Isoflurane and sevoflurane at the selected exposures did not significantly alter memory and learning ability. Conclusion At equipotent exposures, isoflurane has a greater potency than sevoflurane to cause neurodegeneration in the developing brains of neonatal mice.

The great civilizations are created both in ancient China and India, but they differ considerably in the forms in which the culture achieves expression. This article puts in order the different forms from the aspects of language, linguistics, the philosophy of linguistics, the relation between language and literature, etc., which keep alive the cultural traditions of the two countries. The article explores the underlying causes and explains how the Indian Buddhism makes the direct connection with the ancient Chinese culture, and plays the complementary and supplementary role in the development of the ancient Chinese linguistics and literature.

Device-to-Device (D2D) communication technology has emerged as an interesting and important area nowadays. In D2D system, Synchronization is a key technology which can ensure effective discovery. There has been extensive research on synchronization method in the context of ad hoc networks during the last few years. However, few of them seems suitable for the D2D communication since they perform badly when there are massive devices. Therefore, a cluster-based timing synchro-nization method for D2D communication with infrastructure is proposed in this paper. The method, which utilize the random access process used in LTE system and build synchronization cluster according to UEs' transmission power and battery level, can achieve timing synchronization quickly and easily without complex operation. From the simulation results, we verified that the proposed method can reduce the heavy burden of eNodeB in massive devices scenario compare with classic timing synchro-nization methods. In the meantime, the D2D devices in RRC_idle state can get timing synchronization easily using the proposed method.

The three-component couplings of α-oxy-aldehydes, alkynes, and amines in water were investigated by using gold, silver and copper catalysts. Gold(I) was found to be the most effective catalyst in this reaction to afford propargylamines in good yields and moderate diastereoselectivities. On the other hand, silver catalysts show the best catalytic activities on non-coordinating α-alkyl-substituted aldehydes.

Based on the step-stress accelerated life test and the laser strap-down inertial navigation system, this paper studies the accelerated life model and the test method, provides the likelihood function, the likelihood equation and the two-order derivative when the stress level is k, evaluates the effectiveness of the method with the simulation test model established by MATLAB, applies the research findings in the storage reliability study of the XX laser strap-down inertial navigation system, and puts forward an effective evaluation method of the storage life of the inertial navigation system.

Early decompressive craniectomy (DC) has been shown to reduce mortality in malignant middle cerebral artery (MCA) infarction, whereas efficacy of DC on functional outcome is inconclusive. Here, we performed a meta-analysis to estimate the effects of DC on malignant MCA infarction and investigated whether age of patients and timing of surgery influenced the efficacy. We systematically searched PubMed, Medline, Embase, Cochrane library, Web of Science update to June 2014. Finally, A total of 14 studies involved 747 patients were included, of which 8 were RCTs (341 patients). The results demonstrated that early DC (within 48 h after stroke onset) decreased mortality (OR = 0.14, 95%CI = 0.08, 0.25, p3) (OR = 0.38, 95%CI = 0.20, 0.73, p = 0.004) for 12 months follow-up. In the subgroup analysis stratified by age, early DC improved outcome both in younger and older patients. However, later DC (after 48h after stroke onset) might not have a benefit effect on lowering mortality or improving outcome in patients with malignant infarction. Together, this study suggested that decompressive surgery undertaken within 48 h reduced mortality and increased the number of patients with a favourable outcome in patients with malignant MCA infarction.

Background Ceramide accumulation is considered a contributing factor to neuronal dysfunction and damage. However, the underlying mechanisms that occur following ischemic insult are still unclear. Methods In the present study, we established cerebral ischemia models using four-vessel occlusion and oxygen-glucose deprivation methods. The hippocampus neural cells were subjected to immunohistochemistry and immunofluorescence staining for ceramide and neutral sphingomyelinase 2 (nSMase2) levels; immunoprecipitation and immunoblot analysis for nSMase2, receptor for activated C kinase 1 (RACK1), embryonic ectoderm development (EED), p38 mitogen-activated protein kinase (p38MAPK) and phosphorylated p38MAPK expression; SMase assay for nSMase and acid sphingomyelinase (aSMase) activity; real-time reverse transcription polymerase chain reaction for cytokine expression; and Nissl, microtubule-associated protein 2 and terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick-end labeling staining. Results We found considerable production of ceramide in astrocytes, but not in neurons, during early cerebral ischemia. This was accompanied by the induction of nSMase (but not aSMase) activity in the rat hippocampi. The inhibition of nSMase2 activity effectively reduced ceramide accumulation in astrocytes and alleviated neuronal damage to some extent. Meanwhile, the expression levels of proinflammatory cytokines, including tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and IL-6, were found to be upregulated, which may have played an import role in neuronal damage mediated by the nSMase2/ceramide pathway. Although enhanced binding of nSMase2 with RACK1 and EED were also observed after cerebral ischemia, nSMase2 activity was not blocked by the TNF-α receptor inhibitor through RACK1/EED signaling. p38MAPK, but not protein kinase Cζ or protein phosphatase 2B, was able to induce nSMase2 activation after ischemia. p38MAPK can be induced by A2B adenosine receptor (A2BAR) activity. Conclusions These results indicate that the inhibition of ceramide production in astrocytes by targeting A2BAR/p38MAPK/nSMase2 signaling may represent a viable approach for attenuating inflammatory responses and neuronal damage after cerebral ischemia.

The three-component couplings of α-oxy-aldehydes, alkynes, and amines in water were investigated by using gold, silver and copper catalysts. Gold(I) was found to be the most effective catalyst in this reaction to afford propargylamines in good yields and moderate diastereoselectivities. On the other hand, silver catalysts show the best catalytic activities on non-coordinating α-alkyl-substituted aldehydes.