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Background: Postsynaptic density (PSD) is an electron-dense structure that contains various scaffolding and signaling proteins. Shank1 is a master regulator of the synaptic scaffold located at glutamatergic synapses, and has been proposed to be involved in multiple neurological disorders. Methods: In this study, we investigated the role of shank1 in an in vitro Parkinson’s disease (PD) model mimicked by 6-OHDA treatment in neuronal SN4741 cells. The expression of related molecules was detected by western blot and immunostaining. Results: We found that 6-OHDA significantly increased the mRNA and protein levels of shank1 in SN4741 cells, but the subcellular distribution was not altered. Knockdown of shank1 via small interfering RNA (siRNA) protected against 6-OHDA treatment, as evidenced by reduced lactate dehydrogenase (LDH) release and decreased apoptosis. The results of RT-PCR and western blot showed that knockdown of shank1 markedly inhibited the activation of endoplasmic reticulum (ER) stress associated factors after 6-OHDA exposure. In addition, the downregulation of shank1 obviously increased the expression of PRDX3, which was accompanied by the preservation of mitochondrial function. Mechanically, downregulation of PRDX3 via siRNA partially prevented the shank1 knockdown-induced protection against 6-OHDA in SN4741 cells. Conclusion: In summary, the present study has provided the first evidence that the knockdown of shank1 protects against 6-OHDA-induced ER stress and mitochondrial dysfunction through activating the PRDX3 pathway. result: We found that 6-OHDA significantly increased the mRNA and protein levels of shank1 in SN4741 cells, but the subcellular distribution was not altered. Knockdown of shank1 via small interfering RNA (siRNA) protected against 6-OHDA treatment, as evidenced by reduced lactate dehydrogenase (LDH) release and decreased apoptosis. The results of RT-PCR and western blot showed that knockdown of shank1 markedly inhibited the activation of endoplasmic reticulum (ER) stress associated factors after 6-OHDA exposure. In addition, downregulation of shank1 obviously increased the expression of PRDX3, which was accompanied by preservation of mitochondrial function. Mechanically, downregulation of PRDX3 via siRNA partially prevented the shank1 knockdown-induced protection against 6-OHDA in SN4741 cells. conclusion: In summary, the present study has provided the first evidence that knockdown of shank1 protects against 6-OHDA-induced ER stress and mitochondrial dysfunction through activating PRDX3 pathway.

Chronic hydrocephalus after clipping aneurysmal subarachnoid hemorrhage (aSAH) often results in poor outcomes. This study was to establish and validate model to predict chronic hydrocephalus after aSAH by least absolute shrinkage and selection operator logistic regression. The model was constructed from a retrospectively analyzed. Two hundred forty-eight patients of aSAH were analyzed retrospectively in our hospital from January 2019 to December 2021, and the patients were divided into chronic hydrocephalus (CH) group (n=55) and non-CH group (n=193) according to whether occurred CH within 3 months. In summary, 16 candidate risk factors related to chronic hydrocephalus after aSAH were analyzed. Univariate analysis was performed to judging the risk factors for CH. The least absolute shrinkage and selection operator regression was used to filter risk factors. Subsequently, the nomogram was designed by the above variables. And area under the curve and calibration chart were used to detect the discrimination and goodness of fit of the nomogram, respectively. Finally, decision curve analysis was constructed to assess the practicability of the risk of chronic hydrocephalus by calculating the net benefits. Univariate analysis showed that age (60 y or older), aneurysm location, modified Fisher grade, Hunt-Hess grade, and the method for cerebrospinal fluid drainage, intracranial infections, and decompressive craniectomy were significantly related to CH (P0.05). Whereas 5 variables [age (60 y or older), posterior aneurysm, modified Fisher grade, Hunt-Hess grade, decompression craniectomy] from 16 candidate factors were filtered by LASSO logistic regression for further research. Area under the curve of this model was 0.892 (95% confidence interval: 0.799-0.981), indicating a good discrimination ability. Meanwhile, the result of calibration indicated a good fitting between the prediction probability and the actual probability. Finally, decision curve analysis showed a good clinical efficacy. In summary, this model could conveniently predict the occurrence of chronic hydrocephalus after aSAH. Meanwhile, it could help physicians to develop personalized treatment and close follow-up for these patients.

Spontaneous subarachnoid hemorrhage (SAH) is an acute neurologic emergency with poor outcomes, and mitochondrial dysfunction is known as one of the key pathological mechanisms underlying the SAH-induced early brain injury (EBI). 1-{3-[2-(1-benzothiophen-5-yl)ethoxy]propyl} azetidin-3-ol maleate (T817MA) is a newly synthesized neurotrophic compound that has been demonstrated to exert protective effects against brain injury. Here, we investigated the effect of T817MA in neuronal injury following experimental SAH both in vitro and in vivo. Primary cultured cortical neurons were treated with oxyhemoglobin (OxyHb) to mimic SAH in vitro, and T817MA at concentrations higher than 0.1 µM reduced OxyHb-induced neuronal injury. T817MA treatment significantly inhibited lipid peroxidation, reduced neuronal apoptosis and attenuated mitochondrial fragmentation. The results of western blot showed that T817MA markedly reduced the expression of mitochondrial fission proteins, fission protein 1 (Fis-1) and dynamin-related GTPase-1 (Drp-1), but prolonged the expression of the postsynaptic protein activity-regulated cytoskeleton-associated protein (Arc). In addition, T817MA significantly increased the expression of sirtuin 1 (Sirt1), which was accompanied by preserved enzymatic of isocitrate dehydrogenase (IDH2) and superoxide dismutase (SOD). Knockdown of Sirt1 and Arc via small interfere RNA (siRNA) transfection partially prevented the T817MA-induced protection in cortical neurons. Furthermore, treatment with T817MA in vivo significantly reduced brain damage and preserved neurological function in rats. The decreased expression of Fis-1 and Drp-1, as well as the increased expression of Arc and Sirt1 were also observed in vivo. Taken together, these data indicate that the neuroprotective agent T817MA protects against SAH-induced brain injury via Sirt1- and Arc-mediated regulation of mitochondrial dynamics.

Introduction Perampanel is a highly selective and noncompetitive α‐amino‐3 ‐hydroxy‐5‐methyl‐4‐isoxazole propionate receptor (AMPAR) antagonist, which has been used as an orally administered antiepileptic drug in more than 55 countries. Recently, perampanel was shown to exert neuroprotective effects in hemorrhagic and ischemic stroke models via regulating blood–brain barrier (BBB) function. Aim Here, the protective effects of perampanel were investigated in an in vitro neurovascular unit (NVU) system established using a triple cell co‐culture model (neurons, astrocytes, and brain microvascular endothelial cells) and in an in vivo traumatic brain injury (TBI) model. Results Neurons in the NVU system exhibit a more mature morphological phenotype compared with neurons cultured alone, and the co‐culture system mimicked an impermeable barrier in vitro. Perampanel protects the NVU system against traumatic and excitotoxic injury, as evidenced by reduced lactate dehydrogenase (LDH) release and apoptotic rate. Treatment with perampanel attenuated lipid peroxidation and expression of inflammatory cytokines. In addition, perampanel increased Sirt3 protein expression, enhanced the activities of mitochondrial enzyme IDH2 and SOD2, and preserved BBB function in vitro. Knockdown of Sirt3 using specific siRNA (Si‐Sirt3) partially reserved the effects of perampanel on neuronal injury and BBB function. Treatment with perampanel in vivo attenuated brain edema, preserved neurological function, inhibited apoptosis and microglia activation after TBI. Furthermore, perampanel increased the expression of Sirt3 and preserved BBB function after TBI. The effect of perampanel on BBB function and brain edema was abolished by knockdown of Sirt3 in vivo. Conclusion Our results indicate that the noncompetitive AMPAR antagonist perampanel protects the NVU system and reduces brain damage after TBI via activating the Sirt3 cascades.

Background Forniceal deep brain stimulation (DBS) has been proposed as an alternative treatment for Alzheimer's disease (AD). Previous studies on mild to moderate AD patients demonstrated improvements in cognitive functions brought about by forniceal DBS. Here, we report our longitudinal findings in one severe AD patient for whom the activities of daily living (ADL) rather than cognitive function significantly improved after 3 mo of continuous stimulation. Case summary In 2011, a 62-year-old Chinese male with no previous history of brain injury or other neuropsychological diseases and no family history of dementia developed early symptoms of memory decline and cognitive impairment. Five years later, the symptoms had increased to the extent that they affected his daily living. He lost the ability to work as a businessman and to take care of himself. The patient was given a clinical diagnosis of probable AD and was prescribed donepezil and subsequently memantine, but no improvement in symptoms was observed. The patient then received DBS surgery. After 3 mo of continuous stimulation, the patient's ADL score decreased from 65 points to 47 points, indicating the quality of the patient's daily living improved distinctly. Other scores remained unchanged, suggesting no significant improvement in cognitive function. A follow-up positron emission tomography scan demonstrated perceivable increased glucose metabolism in the classical AD-related brain regions. Conclusion Based on this case we hypothesize that forniceal DBS may improve ADL through elevating regional glucose metabolism in the brain.

Striatal asymmetry is a common feature in Parkinson's disease (PD), which changes with the progression of the disease. However, the correlation between the striatal asymmetry and severity of PD remains unclear. The present study aimed to investigate the characteristics of asymmetry in PD, and analyze the correlation between the striatal asymmetry index (SAI) and disease severity.This retrospective study enrolled 63 patients with idiopathic PD. The severity of PD was classified according to the HoehnYahr (HY) staging system. The SAI in the subregions of the striatum was measured usingThere was a significant difference in the SAI of the posterior putamen among the three groups (HY stage I, HY stage II, and HY stage III-IV; p = 0.001). However, there was no difference in the SAI of the anterior putamen (p = 0.340) or SAI of the caudate nucleus (p = 0.342) among the three groups. The SAI of the posterior putamen in patients with PD was significantly higher than that in patients with multiple system atrophy or progressive supranuclear palsy (p = 0.008).The SAI of the posterior putamen is associated with the severity of PD, and may be correlated to the loss of dopamine cells in the pars compacta of the ventrolateral substantia nigra projecting to the posterior putamen. The SAI may be a potential indicator for evaluating the severity of PD, and distinguishing PD from other degenerative diseases.

It was demonstrated that the electrochemical performance enhancements in KOH-activated carbon materials should be mainly due to the created polar oxygen-containing functional groups (OFGs, such as such as C–O, C O, –OH, and O–C O), while the role of each OFGs on the electrochemical enhancements is still unclear. In this work, KOH activation treatments were systematically conducted on carbon nanotubes (CNTs) to explore the role of each OFG on the performance enhancements of Li–S batteries (LSBs). Results showed that the capacity of activated-CNT-sulfur (a-CNT-S) cathodes is 33% higher than that of the pristine CNT-S cathodes, and their rate capability and cycling stability are also enhanced. And the electrochemical analysis combining with Fourier transform infrared spectroscopy indicated that the formed C–O bonds are the real factor for the enhanced electrochemical performances of a-CNT-S cathodes. Furthermore, the optimal activation conditions on CNT-based cathodes for LSBs were optimized to be 10 min at 700 °C.

Spinal cord ischemia-reperfusion injury (SCIRI) can cause dramatic neuron loss and lead to paraplegia in patients. In this research, the role of mGluR5, a member of the metabotropic glutamate receptors (mGluRs) family, was investigated both in vitro and in vivo to explore a possible method to treat this complication. In vitro experiment, after activating mGluR5 via pretreating cells with (RS)-2-Chloro-5-hydroxyphenylglycine (CHPG) and 3-cyano-N-(1,3-diphenyl-1H-pyrazol-5-yl) benzamide (CDPPB), excitotoxicity induced by glutamate (Glu) was attenuated in primary spinal cord neurons, evidenced by higher neuron viability, decreased lactate dehydrogenase (LDH) release and less detected TUNEL-positive cells. According to Western Blot (WB) results, Glu treatment resulted in a high level of large-conductance Ca2+- and voltage-activated K+ (BK) channels, with activation relying on the mGluR5-IP3R (inositol triphosphate) pathway. In vivo part, a rat model of SCIRI was built to further investigate the role of mGluR5. After pretreating them with CHPG and CDPPB, the rats showed markedly lower spinal water content, attenuated motor neuron injury in the spinal cord of L4 segments, and better neurological function. This effect could be partially reversed by paxilline, a blocker of BK channels. In addition, activating BK channels alone using specific openers: NS1619 or NS11021 can protect spinal cord neurons from injury induced by either SCIRI or Glu. In conclusion, in this research, we proved that mGluR5 exerts a protective role in SCIRI, and this effect partially works via IP

Dysfunction of ionotropic glutamate receptors (iGluRs) is a key molecular mechanism of excitotoxic neuronal injury following traumatic brain injury (TBI). Edonerpic maleate is a low molecular-weight compound that was screened as a candidate neuroprotective agent. In this study, we investigated its effects on TBI and GluRs signaling. Traumatic neuronal injury (TNI) induced by scratch followed by glutamate treatment was performed to mimic TBI in vitro. Edonerpic maleate at 1 and 10 μM exerted protective activity when it was added within 2 h following injury. The protective activities were also confirmed by the reduction of lipid peroxidation and oxidative stress. In addition, edonerpic maleate inhibited the expression of surface NR2B, total GluR1, and surface GluR1, and mitigated the intracellular Ca2+ responses following injury in vitro. Western blot analysis showed that edonerpic maleate reduced the cleavage of collapsing response mediator protein 2 (CRMP2), but increased the expression of postsynaptic protein Arc. By using gene overexpression and silencing technologies, CRMP2 was overexpressed and Arc was knockdown in cortical neurons. The results showed that the effect of edonerpic maleate on NMDA receptor expression was mediated by CRMP2, whereas the edonerpic maleate-induced AMPA receptor regulation was dependent on Arc activation. In in vivo TBI model, 30 mg/kg edonerpic maleate alleviated the TBI-induced brain edema, neuronal loss, and microglial activation, with no effect on locomotor function at 24 h. However, edonerpic maleate improves long-term neurological function after TBI. Furthermore, edonerpic maleate inhibited CRMP2 cleavage but increased Arc activation in vivo. In summary, our results identify edonerpic maleate as a clinically potent small compound with which to attenuate TBI-related brain damage through regulating GluRs signaling.

Neuronal injury following subarachnoid hemorrhage (SAH) has been shown to be associated with mitochondrial dysfunction and oxidative stress. βIIPKC, a subtype of protein kinase C (PKC), accumulates on the mitochondrial outer membrane and phosphorylates mitofusin 1 (Mfn1) at serine 86. Here, we investigated the role of Mfn1-βIIPKC interaction in brain damage and neurological function in both in vivo and in vitro experimental SAH models. The expression of βIIPKC protein and the interaction of Mfn1-βIIPKC were found to be increased after OxyHb treatment in primary cultured cortical neurons and were also observed in the brain following SAH in rats. Treatment with the βIIPKC inhibitor βIIV5-3 or SAMβA, a peptide that selectively antagonizes Mfn1-βIIPKC association, significantly attenuated the OxyHb-induced neuronal injury and apoptosis. These protective effects were accompanied by inhibited mitochondrial dysfunction and preserved mitochondrial biogenesis. The results of western blot showed that βIIV5-3 or SAMβA markedly increased the expression of Sirt3 and enhanced the activities of its downstream mitochondrial antioxidant enzymes in OxyHb-treated neurons. Knockdown of Sirt3 via specific targeted small interfering RNA (siRNA) partially prevented the βIIV5-3- or SAMβA-induced protection and antioxidative effects. In addition, treatment with βIIV5-3 or SAMβA in vivo was found to obviously reduce brain edema, alleviate neuroinflammation, and preserve neurological function after experimental SAH in rats. In congruent with in vitro data, the protection induced by βIIV5-3 or SAMβA was reduced by Sirt3 knockdown in vivo. In summary, our present results showed that blocking Mfn1-βIIPKC interaction protects against brain damage and mitochondrial dysfunction via Sirt3 following experimental SAH.

Carbon nanotubes (CNTs) and their related hybrids grown by chemical vapor deposition (CVD) method have been frequently used as energy-storage electrode materials. In most cases, the tips of CNTs are almost well closed, which often limits the utilization efficiency of their tubular structure in storage of charges. In this work, the authors have designed a type of tip-open CNT/CNF hierarchical hybrids via KOH activation on the CVD-grown Al/Fe-catalyzed CNT/CNF precursors. Results showed that the CNT hierarchies' tips can be fully opened via KOH activation at 700–750 °C for 90 min. As expected, the tip-open CNT-CNF hybrids show a highly improved specific capacitance, which increases by 3.3 times that of the pristine ones. Moreover, sweep analysis indicated that the diffusion-type capacitance increases by 3.7 times while the Helmholtz-type capacitance increases only by 1.5 times, indicating that the tip-open CNTs contribute to ∼30% of the increase in double-layer capacitance. Further optimization on activation time and temperature indicated that activation at 700 °C for 90 min is suitable for opening the tips of CNT hierarchies and protecting the CNTs’ tubular structure. This research would give some useful advice for the preparation of high-performance CNT-related electrode materials for energy storage.

Based on coupled mode theory, electro-optic modulation theory, and microring resonance theory, a structural model was proposed for a polymer parallel channel microring resonator (MRR) electro-optic switch array, and in the meantime, with a resonance wavelength of 1550 nm, optimization design and simulation analysis were conducted on a eight microrings and nine channels switch array. According to the results of numerical simulation, the free spectral range (FSR) was about 17.71 nm and the 3-dB bandwidth of the output spectrum was about 0.18 nm when the cross-section size of the waveguide core was 1.5 × 1.5 μm2, the confining layer between the waveguide core and the electrode was 2.0 μm thick, the metal electrode was 0.05 μm thick, the coupling gap between the microring and the channel was 0.1 μm, and the microring radius was 12.76 μm. When the voltage of 7 V was applied on microring i of the device in turn, the output optical power Pi of horizontal channel i was the largest, and the output optical power of all the other channels became very small, which meant that the switching function of horizontal channel i was fulfilled. The insertion loss of the device was within a range of 1.39–8.17 dB, and the crosstalk was smaller than −4.8 dB.

Objective To investigate clinical efficacy of and optimal therapeutic strategy for ventricular intracranial pressure monitoring (V-ICPM) in patients with traumatic bifrontal contusions (TBCs). Methods From 8760 patients with traumatic brain injury treated between January 2010 and January 2016, a retrospective analysis was performed on 105 patients with TBCs who underwent V-ICPM and 282 patients with TBCs who did not. All patients underwent treatment at the 101st Hospital of PLA, Wuxi, China. Rates of successful conservative treatment, decompressive craniectomy, and bifrontal craniotomy; incidence of neurologic dysfunction; length of stay; and medical expenses were compared between groups. Results Glasgow Outcome Scale was used to assess all patients during follow-up (range, 6 months to 5.5 years). There were no significant differences in prognosis between the 2 groups (P = 0.100). Compared with the patients who did not undergo V-ICPM, the V-ICPM group had a significantly better successful conservative treatment rate (64.8% vs. 47.2%, P = 0.002), decompressive craniectomy rate (8.1% vs. 22.1%, P = 0.008), and bifrontal craniotomy rate (5.7% vs. 15.6%, P = 0.01); shorter length of stay (P = 0.000); and lower medical expenses (P = 0.004). Conclusions Patients with TBCs should be strictly, closely, and dynamically observed by neurosurgery intensive care unit physicians and nurses. Patients should undergo ventricular intracranial pressure probe implantation in a timely manner. V-ICPM can help optimize treatment. Although V-ICPM did not significantly improve the prognosis of patients, it had many other advantages. V-ICPM warrants further clinical research and may be beneficial for patients with TBCs.

Background and objectives: Previous studies have shown that deep brain stimulation can improve clinical symptoms in patients with mild Alzheimer’s disease, but the therapeutic effect in patients with moderate-to-severe Alzheimer’s disease remains unclear. Therefore, we intend to assess the therapeutic effect of deep brain stimulation on moderate-to-severe Alzheimer’s disease through a 24-month follow-up visit. Design: A prospective single-center, self-controlled study. Methods: This trial will be performed at the 101st Hospital of PLA, Wuxi, China. We will include 20 patients with moderate-to-severe Alzheimer’s disease who will be given bilateral deep brain stimulation via an implant located beside the fornical column. Outcome measures: The primary outcome measure is the percent of patients whose scores on the Mini Mental State Examination have improved after 24 months. The secondary outcome measures include the percent of patients whose scores on the Mini Mental State Examination Scale have improved at other visits, their Montreal Cognitive Assessment-Basic score, Rey-Osterrieth Complex Figure Test score, score on the delayed recall of the Rey-Osterrieth Complex Figure Test, trail making test score, Hamilton Rating Scale for Depression score, functional magnetic resonance imaging results, functional PET imaging results at each visit point, and the incidence of adverse events. Discussion: This trial will provide feasible, objective, and quantifiable evidence for deep brain stimulation in the clinical treatment of moderate-to-severe Alzheimer’s disease. Ethics and dissemination: This study protocol was approved by the Institution Review Board of the 101st Hospital of PLA in China (approval No. L2017002) in December 2016. Design of the study was finished in October 2016, and registered in August 2017. Participant recruitment was started at October 2017, and was expected to be finished within 12 months. Data analysis will be completed until October 2020. The results of the study will be disseminated through presentations at peer-reviewed publications. Trial registration: This trial was registered in the Chinese Clinical Trial Registry with registration No. ChiCTR-ONC-17012311 (version 2.0).

The aim of the present study was to assess the therapeutic effects of atorvastatin on cerebral vessel autoregulation and to explore the underlying mechanisms in a rabbit model of subarachnoid hemorrhage (SAH). A total of 48 healthy male New Zealand rabbits (weight, 2‑2.5 kg) were randomly allocated into SAH, Sham or SAH + atorvastatin groups (n=16/group). The Sham group received 20 mg/kg/d saline solution, whereas 20 mg/kg/d atorvastatin was administered to rabbits in the SAH + atorvastatin group following SAH induction. Changes in diameter, perimeter and basilar artery (BA) area were assessed and expression levels of the vasoactive molecules endothelin‑1 (ET‑1), von Willebrand factor (vWF) and thrombomodulin (TM) were measured. Neuronal apoptosis was analyzed 72 h following SAH by terminal deoxynucleotidyl-transferase‑mediated dUTP nick‑end labeling (TUNEL) staining. The mortality rate in the SAH group was 18.75, 25% in the SAH + atorvastatin treated group and 0% in the Sham group (n=16/group). The neurological score in the SAH + atorvastatin group was 1.75±0.68, which was significantly higher compared with the Sham group (0.38±0.49; P

Therapy using acellular spinal cord (ASC) scaffolds seeded with bone marrow stromal cells (BMSCs) has previously been shown to restore function of the damaged spinal cord and improve functional recovery in a rat model of acute hemisected spinal cord injury (SCI). The aim of the present study was to determine whether BMSCs and ASC scaffolds promote the functional recovery of the damaged spinal cord in a rat SCI model through regulation of apoptosis and immune responses. Whether this strategy regulates secondary inflammation, which is characterized by the infiltration of immune cells and inflammatory mediators to the lesion site, in SCI repair was investigated. Basso, Beattie, and Bresnahan scores revealed that treatment with BMSCs seeded into an ASC scaffold led to a significant improvement in motor function recovery compared with treatment with an ASC scaffold alone or untreated controls at 2 and 8 weeks after surgery (P0.05). The results of this study demonstrated that BMSCs seeded into ASC scaffolds for repair of spinal cord hemisection defects promoted functional recovery through the early regulation of inflammatory cell recruitment with inhibition of apoptosis and secondary inflammation.

Wave shapes that induce velocity skewness and acceleration asymmetry are usually responsible for onshore sediment transport, whereas undertow and bottom slope effect normally contribute to offshore sediment transport. By incorporating these counteracting driving forces in a phase-averaged manner, the theoretically-based quasi-steady formula of Wang (2007) is modified to predict the magnitude and direction of net cross-shore total load transport under the coaction of wave and current. The predictions show an excellent agreement with the measurement data on medium and fine sand collected by Dohmen-Janssen and Hanes (2002) and Schretlen (2012) in a full-scale wave flume at the Coastal Research Centre in Hannover, Germany. The modified formula can predict the net onshore transport of fine sand in sheet flows. In particular, it can predict the net offshore transport of medium sand in rippled beds through enlarged bed roughness, as well as the net offshore transport of fine-to-coarse sand in sheet flows with the aid of a new criterion to judge the occurrence of net offshore transport.

To report treatment experiences with titanium mesh cranioplasty infection at a single institution over the last 5 years.We retrospectively reviewed 11 consecutive patients who were diagnosed with infection under the skin flap after titanium mesh cranioplasty and received our new treatment between Feb 2008 and Feb 2013. We performed a 2- to 6-year follow-up to evaluate prognosis and security.All 11 patients were cured and discharged, and all saved their infected bone flap (titanium mesh) completely. There was no recurrence of infection after follow-up for 2-6 years.Sensitive antibiotics combined with enclosed continuous irrigation and drainage is a safe, easy, economical and effective treatment for infection after titanium mesh cranioplasty that can save the infected bone flap.

Background Therapeutic hypothermia may need prolonged duration for the patients with severe traumatic brain injury (sTBI). Methods The Long-Term Hypothermia trial was a prospective, multicenter, randomized, controlled clinical trial to examine the safety and efficacy in adults with sTBI. Eligible patients were 18–65, Glasgow Coma Scale score at 4 to 8, and initial intracranial pressure (ICP) ≥ 25 mm Hg, randomly assigned to the long-term mild hypothermia group (34–35 °C for 5 days) or normothermia group at 37 °C. The primary outcome was the Glasgow outcome scale (GOS) at 6 months. Secondary outcomes included ICP control, complications and laboratory findings, the length of ICU and hospital stay, and GOS at 6 months in patients with initial ICP ≥ 30 mm Hg. This trial is registered with ClinicalTrials.gov, NCT01886222. Findings 302 patients were enrolled from June 25, 2013, to December 31, 2018, with 6 months follow-up in 14 hospitals, 156 in hypothermia group and 146 in normothermia group. There was no difference in favorable outcome (OR 1·55, 95%CI 0·91–2·64; P = 0·105) and in mortality (P = 0·111) between groups. In patients with an initial ICP ≥ 30 mm Hg, hypothermic treatment significantly increased favorable outcome over normothermia group (60·82%, 42·71%, respectively; OR 1·861, 95%CI 1·031–3·361; P = 0·039). Long-term mild hypothermia did not increase the incidences of complications. Interpretation Long-term mild hypothermia did not improve the neurological outcomes. However, it may be a potential option in sTBI patients with initial ICP ≥ 30 mm Hg. Funding : Shanghai municipal government and Shanghai Jiao Tong University/School of Medicine.

Post-grown hierarchical pseudocapacitive nanostructures often suffer from their bad long-term cycling stability. In this work, a type of hierarchical partially-embedded MnO nanocube/electrospun carbon nanofiber composites (pe-MnO/ECNFs) was designed. Results show the MnO nanocubes are partially embedded into the ECNFs skeletons, showing a strong joint between them. The pe-MnO/ECNFs electrodes exhibit a high specific capacitance of 146 F g−1 (to the whole electrode mass) at scan rate of 5 mV s−1, and an ultralow decay rate of 0.004‰ per cycle for 20,000 cycles at 10 A g−1, which is much better than those of the MnO2/ECNF ones (96 F g−1, decay rate of 0.015‰ per cycle). Furthermore, the assembled flexible symmetric supercapacitors show an high energy density of 6.8 W h kg−1, a high dynamic bending stability, and a robust long cycling stability (low decay rate of 0.003‰ per cycle for 6000 cycles at 1 A g−1).

Arteriovenous malformations (AVMs) associated with aneurysm have rarely been reported in the literature. The present study reports the case of a 21-year-old pregnant female patient who presented with a subarachnoid hemorrhage and an intracranial hematoma located in the anterior end of the corpus callosum. Furthermore, an anterior cerebral aneurysm and an AVM were identified by digital subtraction angiography and magnetic resonance angiography. The aneurysm was clipped and the AVM was successfully removed by microsurgery. The diagnosis of AVM associated with an aneurysm was confirmed via intraoperative and postoperative pathological examinations. By performing a review of the current literature, issues and surgical considerations associated with AVM associated with aneurysm were analyzed.

We proposed a 1×N-channel cross-grid microring resonator array (MRRA) model according to the coupled mode theory (CMT), electro-optic (EO) modulation theory, and microring resonance theory. This model integrates wavelength division multiplexing and switching functions. When this model is subjected to an operating voltage, the horizontal channel outputs a new resonance wave. As an example, the 1×8-channel cross-grid MRRA with 1550-nm central wavelength and 0.8-nm wavelength spacing is used to analyze its transmission characteristics. The simulation results show that the resonant wavelength in the horizontal channels shifts when the sectional size of the waveguide core, the buffer layer thickness between the waveguide core and electrode, electrode thickness, and coupling gap between the microring and channel are 1.5 × 1.5 μ m 2 , 2.0 μm, 0.05 μm, and 0.1μm, respectively; this shift also occurs when the switching voltage changes from 0 to 21.3V. Thus, resonance wavelength conversion with 0.8-nm wavelength spacing can be achieved in the same horizontal channel.

Many heterostructures containing two types of strong polar bonds were often designed to synergistically increase the chemical confining for soluble lithium polysulfide in lithium-sulfur batteries (LSBs). To make maximum use of the two chemical interactions on confining the polysulfides, a novel structure of 2D hexagonal WS2-rimmed Co9S8 heterostructure nanoflakes was designed on the surface of carbon nanofiber (CNF) skeletons via a simple technique. The composite nanoflakes are ~50 nm in diameter and ~5 nm in thickness, and comprised of a ~40-nm Co9S8 core and a 3–4 WS2 edge. In this design, the Co9S8 core and WS2 edge can confine the polysulfides and catalyze the electrochemical progresses at the same time. Electrochemical tests indicated that the CNF@WS2@Co9S8-S cathodes show a high capacity (1175 mAh g−1 at 0.1 C), an excellent rate capability (keep 77.85% at 2.0 C), and a superior cycling stability (a low decay rate of 0.061% per cycle at 2.0 C, even lower at 7.0 C and 12.0 C).

Herein, a cross-grid microring resonator electro-optic switching array model is proposed on the basis of the coupled mode theory, electro-optic modulation theory, and microring resonance theory. The proposed device has N+1 horizontal channels, N vertical channels, and 2N microrings with equal radii. By applying an operating voltage to the microrings in the array unit in various ways, the switching function of the N+1 horizontal channel can be realized. Taking the structure of 9 × 8 channels as an example, the output spectrum, insertion loss, crosstalk, extinction ratio, and other characteristics of this switching array device under a resonant wavelength of 1550 nm are simulated and analyzed.

Carbon nanomaterials have been frequently used to physically inhibit the lithium polysulfide's shuttle in lithium–sulfur batteries, especially those crumpled structure of graphene. Here, a type of reduced graphene oxide fiber enwrapped nano-sulfur (rGOF@nano-S) hybrids were synthesized by a simple sulfur-containing-ion assisted microwave (MW) synthesis method and then utilized as a sulfur host for lithium–sulfur batteries. The synergistic reactions of MW treatments and sulfur-containing-ion force on the precursor GO nanosheets (NSs) have induced a well-crumpled fibrous structure, and simultaneously uniformly wrapped the nano-S particles in them, which would make the resultant cathodes achieve improved electrochemical performances. The rGOF@nano-S hybrid cathodes showed a high reversible capacity (886 mA h g−1 at 0.1 C rate), a high rate capability (remaining 61% at 2 C rate), and an excellent cycling stability (with a minimal decay rate of 0.04% per cycle over 800 cycles at 1 C), which are highly improved compared to those of the hybrids without MW treatments. In addition, the optimal MW treatment time on rGOF@nano-S hybrid cathodes were also explored to be 2.4 min under 700-W power. This work suggests that MW treatments would be a useful strategy for the preparation of high-performance cathodes for Li–S batteries.

Summary China has more patients with traumatic brain injury (TBI) than most other countries in the world, making this condition a major public health concern. Population-based mortality of TBI in China is estimated to be approximately 13 cases per 100 000 people, which is similar to the rates reported in other countries. The implementation of various measures, such as safety legislation for road traffic, establishment of specialised neurosurgical intensive care units, and the development of evidence-based guidelines, have contributed to advancing prevention and care of patients with TBI in China. However, many challenges remain, which are augmented further by regional differences in TBI care. High-level care, such as intracranial pressure monitoring, is not universally available yet. In the past 30 years, the quality of TBI research in China has substantially improved, as evidenced by an increasing number of clinical trials done. The large number of patients with TBI and specialised trauma centres offer unique opportunities for TBI research in China. Furthermore, the formation and development of research collaborations between China and international groups are considered essential to advancing the quality of TBI care and research in China, and to improve quality of life in patients with this condition.

Traumatic brain injury (TBI) is a prominent public health issue that has a significant negative impact on patients and their family members. It is the leading cause of mortality and disability among young (below 50 years old) individuals. Intracranial hypertension (ICH) remains the single most difficult therapeutic challenge for the management of severe TBI. Therapeutic hypothermia may reduce intracranial hypertension and improve patient outcomes; however, the use of hypothermia is controversial. It has been reported that therapeutic hypothermia elicits no therapeutic benefit for patients with TBI. The present study presents two patients with severe(s) TBI who were admitted to 101st Hospital of the People's Liberation Army Between June 2017 to October 2017. Multimodal brain monitoring measurements of intracranial pressure, cerebral perfusion pressure (CPP) and bispectral index (BIS) were used during assisted hypothermia for management of patients with sTBI. The duration, degree of hypothermia treatment and speed of re-warming were assessed.

Aim To report treatment experiences with titanium mesh cranioplasty infection at a single institution over the last 5 years. Material and methods We retrospectively reviewed 11 consecutive patients who were diagnosed with infection under the skin flap after titanium mesh cranioplasty and received our new treatment between Feb 2008 and Feb 2013. We performed a 2- to 6-year follow-up to evaluate prognosis and security. Results All 11 patients were cured and discharged, and all saved their infected bone flap (titanium mesh) completely. There was no recurrence of infection after follow-up for 2-6 years. Conclusion Sensitive antibiotics combined with enclosed continuous irrigation and drainage is a safe, easy, economical and effective treatment for infection after titanium mesh cranioplasty that can save the infected bone flap.

By solving the rate equations and the propagation equations based on the energy transfer process of Er3+ and Yb3+ ions, the effects of the cooperative upconversion (UC) on the gain and noise characteristics of the Er3+ doped and Er3+/Yb3+ co-doped waveguide amplifiers are analyzed. Comparisons are performed between the amplifiers on waveguide length, pump power, Er3+ ion concentration and ion concentration ratio NYb/NEr, respectively. Results show that it is very necessary to consider the UC in the optimization design and analysis of waveguide amplifiers.

A modified coaxial electrospinning process is developed for producing medicated nanofiber membranes of shellac. With pure ethanol as a sheath fluid, high quality borneol-loaded shellac nanofibers have been successfully fabricated using the modified coaxial process. Electron scanning microscopic observations demonstrated that the nanofibers had better quality than those fabricated using a single fluid electrospinning in terms of nanofiber diameters and their distributions. The former had an average diameter of 570 ± 80 nm under a sheath-to-core flow rate ratio of 0.25, whereas the later was 940 ± 230 nm. X-ray diffraction results verified that borneol existed in the shellac matrix in an amorphous state. The medicated nanofiber membranes could significantly improved the physical stability of borneol due to the favorable hydrogen bonding between the drug and the polymer matrix, as demonstrated by the weight loss experiments. The modified coaxial electrospinning process described here expands the capability of electrospinning process in generating high quality functional membranes.