Ketogenic diet time-dependently prevents NAFLD through upregulating the expression of antioxidant protein metallothionein-2.

BACKGROUND & AIMS: The past few decades have witnessed a rapid growth in the prevalence of nonalcoholic fatty liver disease (NAFLD). While the ketogenic diet (KD) is considered for managing NAFLD, the safety and efficacy of the KD on NAFLD has been a controversial topic. Here, we aimed to investigate the effect of KD of different durations on metabolic endpoints in mice with NAFLD and explore the underlying mechanisms. METHODS: NAFLD mice were fed with KD for 1, 2, 4 and 6 weeks, respectively. The blood biochemical indexes (blood lipids, AST, ALT and etc.) and liver fat were measured. The LC-MS/MS based proteomic analysis was performed on liver tissues. Metallothionein-2 (MT2) was knocked down with adeno-associated virus (AAV) or small interfering RNA (siRNA) in NAFLD mice and AML-12 cells, respectively. H&E, BODIPY and ROS staining were performed to examine lipid deposition and oxidative stress. Furthermore, MT2 protein levels, nucleus/cytoplasm distribution and DNA binding activity of peroxisome proliferators-activated receptors α (PPARα) were evaluated. RESULTS: KD feeding for 2 weeks showed the best improvement on NAFLD phenotype. Proteomic analysis revealed that MT2 was a key candidate for different metabolic endpoints of NAFLD affected by different durations of KD feeding. MT2 knockdown in NAFLD mice blocked the effects of 2 weeks of KD feeding on HFD-induced steatosis. In mouse primary hepatocytes and AML-12 cells, MT2 protein levels were induced by ß-hydroxybutyric acid (ß-OHB). MT2 Knockdown blunted the effects of ß-OHB on alleviating PA-induced lipid deposition. Mechanistically, 2 weeks of KD or ß-OHB treatment reduced oxidative stress and upregulated the protein levels of MT2 in nucleus, which subsequently increased its DNA binding activity and PPARα protein expression. CONCLUSIONS: Collectively, these findings indicated that KD feeding prevented NAFLD in a time dependent manner and MT2 is a potential target contributing to KD improvement on steatosis.

Prevalence, characteristics, and risk factors of venous thromboembolism in patients with brain tumor undergoing craniotomy: a meta-analysis.

BACKGROUND: Brain tumor patients undergoing craniotomy are significantly associated with the development of venous thromboembolism (VTE), while the contributing factors remains controversial. Our study aimed to investigate the prevalence and risk factors for VTE in postoperational brain tumor patients. METHODS: We searched the PubMed, Embase, Web of Science, Medline, and Cochrane Library databases from their inception to July 2023. Article selection, data extraction, and study quality assessment were performed independently by two reviewers. Publication bias was assessed using Egger's and Begg's tests. Stata 15.0 software was used for data analysis. RESULTS: A total of 25 studies were considered, with a total of 49,620 brain tumor individuals. The pooled prevalence of VTE during hospitalization in postoperational brain tumor patients was 9% [95% CI: (0.08, 0.10)]. Moreover, our results demonstrated that patients with VTE were older than those without VTE [mean difference [MD] = 8.14, 95% CI: (4.97, 11.30)]. The following variables were significantly associated with VTE: prior history of VTE [OR = 7.81, 95% CI: (3.62, 16.88)], congestive heart failure [OR = 2.33, 95% CI: (1.08-5.05)], diabetes [OR = 1.87, 95% CI: (1.12-3.10)], hypertension [OR = 1.27, 95% CI: (1.07-1.50)], steroid use [OR = 1.63, 95% CI: (1.41, 1.88)], high white blood cells counts [MD = 0.32, 95% CI: (0.01, 0.63)], and high fibrinogen levels [MD = 0.19, 95% CI: (0.08, 0.30)]. CONCLUSION: This meta-analysis identified risk factors for postoperational VTE in patients with brain tumor, which can serve as a theoretical foundation for medical staff to manage and treat VTE. TRIAL REGISTRATION: CRD42023357459.

Chemokine receptor CXCR4 interacts with nuclear receptor Nur77 and promote glioma invasion and progression.

BACKGROUND: Glioma is the most common primary brain tumor. It is prone to progress and have high rate of mortality regardless of radiation or chemotherapy due to its invasive growth features. Chemokine and its receptor CXCL12 and CXCR4 play important roles in cancer metastasis. METHODS: In this study, we investigate the role of CXCR4 in the progression of glioma by various molecular technologies, including qRT-PCR, Western blotting, wound closure assay, transwell assay et al. RESULTS: It was found that CXCR4 was overexpressed in glioma tissues. The expression of CXCR4 was correlated with patients' overall survival. Wound closure assay and transwell invasion assay showed that inhibition of CXCR4 significantly reduced the expression of biomarkers related to the formation of invadopodium, leading to decrease the invasion and migration of glioma tumor cells. Knocking down the nuclear receptor Nur77 remarkably decreased CXCR4 expression and reduced glioma cell invasion and migration. The reduction of glioma cell invasion and migration were observed after Nur77 inhibitor treatment. CONCLUSION: Taken together, these results indicated that CXCR4 is critical in promoting glioma migration and invasion. Inhibition of Nur77 reduces CXCR4 related cancer progression.

An intrinsic polymer electrolyte via in situ cross-linked for solid lithium-based batteries with high performance.

Since the introduction of poly(ethylene oxide) (PEO)-based polymer electrolytes more than 50 years, few other real polymer electrolytes with commercial application have emerged. Due to the low ion conductivity at room temperature, the PEO-based electrolytes cannot meet the application requirements. Most of the polymer electrolytes reported in recent years are in fact colloidal/composite electrolytes with plasticizers and fillers, not genuine electrolytes. Herein, we designed and synthesized a cross-linked polymer with a three-dimensional (3D) mesh structure which can dissolve the Li bis(trifluoromethylsulfonyl)imide (LiTFSI) salt better than PEO due to its unique 3D structure and rich oxygen-containing chain segments, thus forming an intrinsic polymer electrolyte (IPE) with ionic conductivity of 0.49 mS cm-1 at room temperature. And it can hinder the migration of large anions (e.g. TFSI-) in the electrolyte and increase the energy barrier to their migration, achieving Li+ migration numbers (tLi+) of up to 0.85. At the same time, IPE has good compatibility with lithium metal cathode and LiFePO4 (LFP) cathode, with stable cycles of more than 2,000 and 700 h in Li//Li symmetric batteries at 0.2 and 0.5 mAh cm-2 current densities, respectively. In addition, the Li/IPE/LFP batteries show the capacity retention >90% after 300 cycles at 0.5 C current density. This polymer electrolyte will be a pragmatic way to achieve commercializing all-solid-state, lithium-based batteries.

Regulating SEI Components of Sodium Anode via Capturing Organic-Molecule Intermediates in Ester-Based Electrolyte.

Highly reversible sodium metal anodes are still regarded as a stubborn hurdle in ester-based electrolytes due to the issue of uncontrollable dendrites and incredibly unstable interphase. Evidently, a strong protective film on sodium is decisive, while the quality of the protective film is mainly determined by its components. However, it is challenging to actively adjust the expected components. This work can regulate the solid electrolyte interphase (SEI) components by introducing a functional electrolyte additive (2-chloro-1,3-dimethylimidazoline hexafluorophosphate (CDIH, namely CDI+ +PF6 - )) into FEC/PC ester-based electrolyte. Specifically, the chloride element in the CDI+ can easily react to form a NaF/NaCl-rich SEI together with the decomposition products of FEC; then the CDI+ without chlorine as a gripper to capture the organic-molecule intermediates generated during FEC decomposition to greatly reduce the content of unstable organic components in SEI, which can be confirmed by molecular dynamic simulation and experiment. Eventually, a highly reversible Na deposition behavior can be delivered. As expected, under the action of CDIH additives, the Na||Na symmetrical cell performs an excellent long-term cycling (>800 h, 0.5 mA cm-2 -0.5 mAh cm-2 ) and rate performance (0.5-4 mA cm-2 ). Furthermore, the Na||PB full cell exhibits the outstanding electrochemical performance with small polarization.

Ultrafast and Ultralarge Lithium-Ion Storage Enabled by Fluorine-Nitrogen Co-Implanted Carbon Tubes.

As a holy grail in electrochemistry, both high-power and high-energy electrochemical energy storage system (EES) has always been a pursued dream. To simultaneously achieve the "both-high" EES, a rational design of structure and composition for storage materials with characteristics of battery-type and capacitor-type storage is crucial. Herein, fluorine-nitrogen co-implanted carbon tubes (FNCT) have been designed, in which plentiful active sites and expanded interlayer space have been created benefiting from the heteroatom engineering and the fluorine-nitrogen synergistic effect, thus the above two-type storage mechanism can get an optimal balance in the FNCT. The implanted fluorine heteroatoms can not only amplify interlayer spacing, but also induce the transformation of nitrogen configuration from pyrrole nitrogen to pyridine nitrogen, further promoting the activity of the carbon matrix. The extraordinary electrochemical performance as results can be witnessed for FNCT, which exhibit fast lithium-ion storage capability with a high energy density of 119.4 Wh kg-1 at an ultrahigh power density of 107.5 kW kg-1 .

Hederagenin suppresses glioma cell biological activities via Nur77 in vitro study.

The aim of this research was to discuss Hederagenin's antitumor effects on glioma by in vitro study. U251 and U87 cell lines were used as research target in our research. In the first step, the different Hed concentrations were treated to U251 and U87 cell lines, and the second step is Nur77 transfection in U251 and U87 with Hed treatment; measuring cell proliferation by MTT and EdU staining; evaluating cell invasion and migration abilities by transwell assay and relative gene and protein expressions by RT-qPCR and WB assay. Compared with NC group, U251 and U87 cell proliferation were significantly depressed with cell apoptosis significantly increasing, and cell invasion and migration abilities were significantly inhibited in Hed-treated groups (p < .05, respectively); however, with Nur77 transfection, the Hed's antitumor effects disappeared. Meanwhile, with Hed supplement, Nur77, PI3K, and AKT gene expressions were significantly downregulated (p < .05, respectively) in Hed-treated groups; and Nur77, p-PI3K, and p-AKT protein expressions were significantly decreased (p < .05, respectively) in Hed-treated groups. Hed had antitumor effects on glioma cell biological activities via Nur77/PI3K/AKT pathway in vitro study.

Chitinase-3 like-protein-1 promotes glioma progression via the NF-κB signaling pathway and tumor microenvironment reprogramming.

Background: Chitinase-3-like protein 1 (CHI3L1) is overexpressed in various types of tumors, especially in glioma, and contributes to tumor progression. However, the definite role of CHI3L1 and involved pathway in glioma progression are not completely understood. Methods: CHI3L1 expression in human gliomas and its association with patient survival was determined using enzyme-linked immunosorbent assay, western blot, immunohistochemistry, and public databases. Single-cell RNA-seq was used to characterize the landscape of tumor and myeloid cells. Human proteome microarray assay was applied to identify the binding partners of CHI3L1. Protein-protein interactions were analyzed by co-immunoprecipitation and cellular co-localization. The roles of CHI3L1 in glioma proliferation and invasion were investigated in tumor cell lines by gain- and loss- of function, as well as in vivo animal experiments. Results: CHI3L1 was up-regulated in all disease stages of glioma, which was closely related with tumor survival, growth, and invasion. CHI3L1 was primarily expressed in glioma cells, followed by neutrophils. Moreover, glioma cells with high expression of CHI3L1 were significantly enriched in NF-κB pathway. Pseudo-time trajectory analysis revealed a gradual transition from CHI3L1low to CHI3L1high glioma cells, along with the NF-κB pathway gradually reversed from inhibition to activation. Intriguingly, CHI3L1 binds to actinin alpha 4 (ACTN4) and NFKB1, and enhances the NF-κB signaling pathway by promoting the NF-κB subunit nuclear translocation in glioma cells. Further, CHI3L1 were released into the tumor microenvironment (TME) and interacted with CD44 expressed on tumor-associated macrophages to activate AKT pathway, thereby contributing to M2 macrophage polarization. In addition, CHI3L1 positively correlated to the expression of immune checkpoints, such as CD274 (PD-L1) and HAVCR2 (LAG3), which then remodeled the TME to an immunosuppressive phenotype. Conclusion: Our research revealed that CHI3L1 facilitated NF-κB pathway activation within glioma cells and reprogramed the TME, thereby serving as a promising therapeutic target for glioma.

ISG15 enhances glioma cell stemness by promoting Oct4 protein stability.

The effects of ISG15 or ISGylation on tumor progression have been widely revealed; however, its roles in glioma progression are largely unknown. This study aims to explore the roles and underlying mechanisms of ISG15 in glioma progression. Here, ISG15 level was found to be upregulated in glioma tissues compared to the paired/unpaired normal tissues, and positively correlated with the level of stemness markers in glioma tissues. Loss of functional experiments indicated that ISG15 positively regulated glioma cell stemness, as evident by the increase of sphere formation ability, ALDH activity, stemness marker expression, and tumor-initiating ability. Further mechanistic studies revealed that ISG15 directly interacted with Oct4 protein, a critical stemness promoter, induced the ISGylation of Oct4 protein, and thus enhanced Oct4 protein stability. Additionally, it was found that Oct4 was ISGylated at lysine 284 (K284), which has been confirmed to be the ubiquitination site of Oct4 protein, and ISG15 knockdown did not degrade K284R mutant Oct4. Furthermore, ISG15 knockdown-induced downregulation of glioma cell stemness was rescued by Oct4 overexpression, but not by K284R mutant Oct4. Altogether, we suggest that ISG15-induced ISGylation of Oct4 protein is essential for glioma cell stemness.

Characteristics of TP53 germline variants and their correlations with Li-Fraumeni syndrome or Li-Fraumeni-like syndrome in Chinese tumor patients.

Li-Fraumeni syndrome (LFS), a rare autosomal-dominant inheritance condition, is associated with a family cancer history as well as pathogenic/likely-pathogenic TP53 germline variants (P/LP TP53 GV). The current clinical methods for detecting LFS are limited. Here, we retrospectively investigate P/LP TP53 GV among Chinese cancer patients by next-generation sequencing and evaluate its relationship with a family cancer history. A total of 270 out of 19,226 cancer patients have TP53 GV, including 53 patients with P/LP TP53 GV. Patients with P/LP TP53 GV are mainly found in male with glioma, lung cancer or sarcoma. The median age of diagnosis for P/LP TP53 GV patients is significantly lower than that of non-P/LP TP53 GV patients (31-years vs. 53-years; P < 0.01). One LFS patient and 3 Li-Fraumeni-like syndrome (LFL) patients are among the 26 followed-up P/LP TP53 GV patients. Among 25 types of P/LP TP53 GV, the highest variant frequencies occurred at codon 175 and 248. p.M237I, p.R158H, p.C238Y and p.C275R, are firstly identified among the Chinese LFS/LFL patients. This study reports the (P/LP) TP53 GV characteristics of Chinese pan-cancer patients. These findings suggest analyzing the P/LP TP53 GV in cancer patients is an effective strategy for identifying cancer predisposition syndrome.

Intracranial solitary fibrous tumor mimicking meningioma: A case report.

RATIONALE: Solitary fibrous tumor is a rare mesenchymal tumor. This case report describes the diagnosis and treatment of this tumor. PATIENT CONCERNS: A 31-year-old patient presented with epileptic seizure and headache 1 day prior to the visit and showed transient right limb hemiplegia for 6 hours that was resolved after intravenous infusion of mannitol. DIAGNOSES: Based on imaging, the provisional diagnosis was meningioma. Postsurgical histopathological diagnosis confirmed solitary fibrous tumor. INTERVENTIONS: The lesion was totally excised. The patient improved remarkably after the operation, without any signs of associated limb movement disorder. No epileptic seizure was observed or reported after the operation. OUTCOMES: Postoperation computed tomography (CT) scans showed no obvious residual tumor. The patient was followed up every 3 months for a total of 1 year following the operation, during which time the patient did not complain of headache or seizure. LESSONS: The manifestation of solitary fibrous tumor (SFT) through imaging methods has certain specific findings,butimmunohistochemistry is still very important for confirming the diagnosis.

Expression of nuclear factor erythroid 2-related factor 2 following traumatic brain injury in the human brain.

Secondary brain injury imposes great effects on the prognosis of patients following traumatic brain injury (TBI). Accumulating evidence suggests that nuclear factor erythroid 2-related factor 2 (Nrf2) could play a neuroprotective role in experimental TBI models by regulating the expression of numerous antioxidant, anti-inflammatory, and neuroprotective proteins. However, whether Nrf2 is activated in patients following TBI is still unknown. In this study, human brain tissues were obtained during surgery from patients suffering from TBI. The purpose of this study was to investigate the expression of Nrf2 and Nrf2-regulated gene products, NAD(P)H quinine oxidoreductase 1, and glutathione S-transferase in human injured brain tissue after TBI. Our results revealed that the nuclear level of Nrf2 was significantly increased in injured brain tissues, whereas the cytoplasmic level of Nrf2 was markedly decreased. In addition, the expression of NAD(P)H quinine oxidoreductase 1 and glutathione S-transferase was significantly upregulated. Nrf2 may be activated and confer neuroprotection against secondary brain injury following TBI. Therefore, Nrf2 could serve as a promising molecular target for the treatment of TBI.

Nur77 is a promoting factor in traumatic brain injury-induced nerve cell apoptosis.

Traumatic brain injury (TBI) poses a serious threat to human health. TBI has a high mortality rate, resulting in a great burden on the affected individual's family as well as society as a whole. The incidence of craniocerebral fractures continues to rise as both the economy and transportation options grow, making it imperative that the mortality and disability rate of craniocerebral trauma be reduced. Nur77 is a transcription factor of the nuclear receptor superfamily. Following stimulation of extracellular apoptosis, Nur77 is involved in a variety of diseases as a powerful pro-apoptotic molecule. Here, we determined the effect and mechanism of Nur77 in TBI-induced nerve cell apoptosis in vitro and in vivo. We found that Nur77 and Bcl-2 protein expression increased as nerve cell apoptosis increased in TBI tissues. Furthermore, inhibition of Nur77 improved nerve cell injury by regulation of Bcl-2 and downstream pathways in vitro and in vivo.

Expression of the long non-coding RNA H19 and MALAT-1 in growth hormone-secreting pituitary adenomas and its relationship to tumor behavior.

Aggressive growth hormone-secreting pituitary adenomas (GHPAs) represent an important clinical problem in patients with acromegaly. Surgical therapy, although often the mainstay of treatment for GHPAs, is less effective in aggressive GHPAs due to their invasive and destructive growth patterns, and their proclivity for infrasellar invasion. LncRNAs are important players in cancer development and emerging in various fundamental biological processes. In the present study, qRT-PCR was performed to examine the expression of lncRNA H19 and MALAT-1 in invasive and non-invasive GHPAs. Our results revealed that the expression of lncRNA H19 was remarkably higher in invasive GHPAs, however, there was no significant differences between the expression of lncRNA MALAT-1 in invasive GHPAs and non-invasive GHPAs, suggesting that lncRNA H19 may play an important role in GHPA invasion. LncRNA H19 might be a target for the study of GHPAs invasion, and a potential index for the diagnosis or prognosis of GHPAs.

Comparison of Clinical and Radiographic Outcomes for Posterior Fossa Decompression with and without Duraplasty for Treatment of Pediatric Chiari I Malformation: A Prospective Study.

OBJECTIVE: The aim of this study was to prospectively compare the radiographic and clinical outcomes between the posterior fossa decompression (PFD) and PFD with duraplasty (PFDD) procedures in adolescent patients with Chiari malformation type I (CMI). METHODS: Ninety adolescent patients with CMI were randomly assigned to undergo either PFDD or PFD. In both groups, a dissection from the occipital bone was performed. The dura was not opened in the PFD group, and the outer layer of dura was resected. However, in the PFDD group, the dura mater was opened and expanded. Data were analyzed for clinical outcome, complications, and syrinx resolution. RESULTS: The age, gender, and preoperative neurologic status were similar between the 2 groups. Compared with the PFD group, patients undergoing PFDD had significantly longer operation time, longer postoperative drainage time, and higher drainage volume. At the latest follow-up, no statistically significant difference was found between the 2 groups in terms of syrinx resolution. The clinical outcomes were similar in the PFDD and PFD group. Compared with the PFD group, patients in the PFDD group had a higher incidence of cerebrospinal fluid leak. CONCLUSIONS: Compared with the more aggressive decompression with duraplasty, PFD without duraplasty produces comparable radiologic and clinical outcomes and is associated with a lower risk of complications.

Inhibition of myeloid differentiation primary response protein 88 provides neuroprotection in early brain injury following experimental subarachnoid hemorrhage.

Accumulating of evidence suggests that activation of nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs) exacerbates early brain injury (EBI) following subarachnoid hemorrhage (SAH) by provoking pro-inflammatory and pro-apoptotic signaling. Myeloid differentiation primary response protein 88 (MyD88) is an endogenous adaptor protein in the toll-like receptors (TLRs) and interleukin (IL) -1ß family signaling pathways and acts as a bottle neck in the NF-κB and MAPK pathways. Here, we used ST2825, a selective inhibitor of MyD88, to clarify whether inhibiting MyD88 could provide neuroprotection in EBI following SAH. Our results showed that the expression of MyD88 was markedly increased at 24 h post SAH. Intracerebroventricular injection of ST2825 significantly reduced the expression of MyD88 at 24 h post SAH. Involvement of MAPKs and NF-κB signaling pathways was revealed that ST2825 inhibited SAH-induced phosphorylation of TAK1, p38 and JNK, the nuclear translocation of NF-κB p65, and degradation of IκBα. Further, ST2825 administration diminished the SAH-induced inflammatory response and apoptosis. As a result, SAH-induced EBI was alleviated and neurological deficits caused by SAH were reversed. Our findings suggest that MyD88 inhibition confers marked neuroprotection against EBI following SAH. Therefore, MyD88 might be a promising new molecular target for the treatment of SAH.

Surgical overreduction and hyperlordotic fusion of C1-C2 joint are associated with cervical sagittal malalignment.

INTRODUCTION: Previous studies have shown that hyperlordotic C1-C2 fusion was related to postoperative subaxial kyphosis. However, most of the patients in these studies were complicated with rheumatoid arthritis (RA). Moreover, no studies have specifically evaluated the relationship between C1-C2 fusion angle and cervical sagittal vertical axis (cSVA), T1 slope or cranial tilt (CRT) after posterior C1-C2 fusion. This study aimed to investigate the cervical sagittal alignment in non-RA patients following posterior C1-C2 fusion and the correlation between C1-C2 fusion angle and postoperative cervical sagittal alignment. MATERIALS AND METHODS: From August 2004 to December 2015, twenty-eight consecutive patients with an average age of 39.2 years (range 6-70 years) who underwent posterior C1-C2 fusion from a single institution were enrolled. The mean follow-up period was 30.7 months (range 12-77 months). Angles of Oc-C1, C1-C2, C2-C3 and C2-C7, cSVA, T1 slope and CRT were measured in lateral cervical radiographs in neutral position before surgery and at the final follow-up. RESULTS: C1-C2 angle significantly increased from 13.6° ± 12.4° to 22.0° ± 8.1° at the final follow-up (P < 0.001). A significant decrease was found both in Oc-C1 and C2-C7 angles from pre-operation to the final follow-up (P < 0.001 and P = 0.011, respectively). Moreover, cSVA and CRT dramatically increased from pre-operation to the final follow-up (P < 0.001). C1-C2 fusion angle was significantly associated with Oc-C1, C2-C7 angle, cSVA and CRT at the final follow-up. A significant correlation was also observed between postoperative change of C1-C2 angle and that of Oc-C1, C2-C7 angle, cSVA and CRT. CONCLUSIONS: Apart from decreased subaxial lordosis, posterior C1-C2 fusion in hyperextension may also lead to kyphotic change of atlanto-occipital alignment and increased tilting forward of the cervical spine. Therefore, intraoperative overreduction of C1-C2 angle and hyperlordotic C1-C2 fusion should be avoided to maintain the physiologic cervical sagittal alignment.

The Promotion of Neural Regeneration in A Rat Facial Nerve Crush Injury Model Using Collagen-Binding NT-3.

Traumatic facial nerve injury, an important cause of facial paralysis, has a number of adverse effects, including facial muscle dysfunction and facial asymmetry. It has been demonstrated in our previous work that native human NT-3 fused with a collagen-binding domain (CBD-NT-3) could bind to collagen, specifically to exert neurotrophic effects, promoting axonal regeneration. To evaluate the effect of CBD-NT-3 in inducing facial nerve regeneration and functional recovery, the differing effects of CBD-NT-3 and native neurotrophin-3 (NAT-NT-3) were observed using the results of facial nerve functional recovery, electrophysiological testing, and axonal and myelin changes in a rat model of facial nerve crush injury. The rats were injected in the epineurium in crushed fibers of the facial nerve with CBD-NT-3, NAT-NT-3, and PBS respectively. After 4 weeks, the CBD-NT-3 group demonstrated significantly more ordered growth of axons and nerve functional recovery than the NAT-NT-3 group. The results suggest that CBD-NT-3 considerably enhances facial nerve regeneration and functional recovery.

[Characterization of ibeB gene of meningitic Escherichia coli strains in calves from Xinjiang].

Objective: To understand the molecular biology information of ibeB gene of meningitic Escherichia coli isolates in calves. Methods: The strain used was isolated from the brain and liver tissue of calves died from Meningitis. It was identified to be an O161-K99-STa pathogenic Escherichia coli strain and named as bovine-EN and bovine-EG. Based on the sequence of ibeB gene of meningitic Escherichia coli K1 RS218 strain in GenBank, a pair of primers was designed and the ibeB gene was cloned from isolates by PCR. Part molecular biology information of ibeB among different strains was compared. Results: The sequence length of isolates ibeB gene was 1500 bp, containing a 1371 bp open reading frame (ORF) encoding 457 amino acids. Bioinformatics analysis showed that the nucleotide and amino acid homology of ibeB gene of bovine-EN strain shared 90.5% and 96.9% identity with Escherichia coli K1 RS218 ibeB gene, respectively, while bovine-EG strain shared 99.4% and 100.0% identity with Escherichia coli K12 respectively. The ibeB gene of bovine-E strains encoded water-soluble protein whose molecular weight was 50.26 kDa and isoelectric point was 6.05. This protein contained a signal peptide A but no transmembrane domain. Subcellular localization of ibeB belonged to the secreted protein, which secretory signal path site (SP) proportion was 0.939. Conclusion: The ibeB gene was cloned from meningitic E. coli isolates and had higher homology and similar biological characteristics with meningitis E. coli K1 RS218ibeB, which belongs to extraintestinal pathogenic Escherichia coli.