Carotid massive intraplaque hemorrhage, lipid-rich necrotic core, and heavy circumferential calcification were associated with new ipsilateral ischemic cerebral lesions after carotid artery stenting: high-resolution magnetic resonance vessel wall imaging study.

Background: Following carotid artery stenting (CAS), new ipsilateral ischemic lesions (NIILs) in the brain are frequently seen using diffusion-weighted imaging (DWI). This study's goal was to identify the imaging characteristics associated with NIILs after CAS by high-resolution magnetic resonance vessel wall imaging (HR-VWI). Methods: This was a case-control study. 109 patients who received CAS for atherosclerotic carotid stenosis were retrospectively collected and categorized into NIILs positive and NIILs negative groups. Based on the existence or absence of stroke symptoms after CAS, the NIILs positive group was split into two subgroups: the NIILs symptomatic group and the NIILs asymptomatic group. Patients underwent preoperative HR-VWI and brain magnetic resonance imaging (MRI) within 7 days preoperatively and within 3 days postoperatively. Quantitatively assess carotid plaque burden and components using HR-VWI. The baseline and HR-VWI imaging characteristics of all patients were retrospectively analyzed. To ascertain the imaging characteristics connected with NIILs after CAS, logistic regression analysis was carried out. Results: Among 109 patients, 38 patients (34.9%) developed NIILs after CAS. Six patients (5.5%) developed symptomatic stroke with NIILs. The logistic regression analysis revealed that maximum wall thickness (Max WT) [odds ratio (OR), 1.53; 95% confidence interval (CI): 1.20-1.96; P=0.001], the maximum area percentage of lipid-rich necrotic core (LRNC) (OR, 1.05; 95% CI: 1.03-1.07; P<0.001), the volume of LRNC (OR, 1.004; 95% CI: 1.002-1.005; P<0.001), the maximum area percentage of intraplaque hemorrhage (IPH) (OR, 1.17; 95% CI: 1.11-1.24; P<0.001), the volume of IPH (OR, 1.06; 95% CI: 1.03-1.08; P<0.001), and maximum circumference score of calcification in a single slice (OR, 1.66; 95% CI: 1.04-2.63; P=0.03) were linked with NIILs following CAS. Conclusions: The massive IPH, LRNC, and heavy circumferential calcification were associated with NIILs after CAS. Preoperative quantitative assessment of carotid plaque using HR-VWI may be useful for predicting NIILs following CAS.

Epidemiology, Characteristic, and Prognostic Factors of Primary Sporadic Intradural Malignant Peripheral Nerve Sheath Tumor in the Spinal Canal: A Systematic Literature Review.

Purpose: Primary sporadic intradural malignant peripheral nerve sheath tumor (MPNST) in the spinal canal is a type of rare neoplasm with challenging diagnosis and therapy. The overall prognosis of this tumor is markedly different from that of the usual spinal intradural tumors. The purpose of this systematic review is to reduce the misdiagnosis and enhance the prognosis of the disease by reviewing the literature. Methods: PubMed, Medline, and Embase databases were searched for articles in English language published from 1980 to May 2021, yielding 500 potentially relevant articles. The keywords were as follows: "spinal", "malignant peripheral nerve sheath tumor", "neurosarcoma", "malignant schwannoma", and "malignant neurofibroma". Thirteen papers met the eligibility criteria, including 55 cases with spinal intradural primary sporadic MPNSTs, which were confirmed by post-operation pathology. We further analyzed the clinical manifestations, radiological manifestations, pathological features, comprehensive treatment strategies, and prognosis. Results: Fifty-five spinal intradural primary sporadic MPNSTs from 30 (54.5%) male and 25 (45.5%) female patients with an average age at diagnosis of 40 years (range, 3-70 years) were included in the study. The most common clinical manifestations were local or radicular pain and motor disturbance. All tumors had significant enhancement and heterogeneous enhancement was more common. Out of 18 lesions, 14 were diagnosed as high grade and the remaining 4 were diagnosed as low grade. The ki-67 labeling index ranged from 5% to 60%. The median recurrence and survival time were 36 and 72 months, respectively. The log-rank tests indicated that significant predictors of OS were patient age (≤30 vs. >30 years) at the time of diagnosis and the presence of metastatic disease, and similar analyses for RFS demonstrated that the presence of metastatic disease was the only significant predictor (60 vs. 10 months). The multivariate Cox proportional hazards regression analysis revealed that absence of metastasis was an independent factor for predicting a favorable prognosis. Conclusions: Spinal intradural primary sporadic MPNSTs are challenging malignant tumors without a systematic treatment plan. The factors affecting its prognosis are not clear. Even after surgical treatment and adjuvant treatment, the recurrence rate and mortality rate are still high. Clinicians should be alert to the possibility of this disease and achieve early detection and treatment.

Lapatinib alleviates TOCP-induced axonal damage in the spinal cord of mouse.

Neuregulin-1 (NRG1), a family of EGF-like factors that activates ErbB receptors, can regulate the proliferation, migration, and myelinating of Schwann cells. We previously reported that NRG1/ErbB signal is responsible for organophosphate (OP)-induced delayed neuropathy (OPIDN) in hens, a susceptive animal model to neuropathic organophosphorous compounds. Our previous study discovered that a neuropathic OP, tri-o-cresyl phosphate (TOCP) activated NRG1/ErbB signaling pathway in both spinal cord and sciatic nerves of hens during the formation of OPIDN and lapatinib, a non-selective antagonist of ErbB1 and ErbB2 receptors, alleviated the toxicity. In this study, we intended to further look into the potential role of NRG1 in the pathogenesis of TOCP-induced axon damage in spinal cord and sciatic nerves and whether lapatinib could also rescue this damage in mice, an OPIDN-resistant animal model. The results revealed that no obvious toxic signs were observed after single TOCP exposure. However, slight histopathological wreck in lumbar spinal cord and sciatic nerves was found following TOCP intoxication, and the damage in sciatic nerves was characterized by axon degeneration of myelin sheath but not the loss of neural skeleton. Only histopathological damage induced by TOCP in spinal cord could be prevented by lapatinib. The translational expression of NRG1/ErbB signaling molecules was analyzed by both in vivo and in vitro studies. In general, NRG1/ErbB pathway was activated by TOCP while combined treatment with lapatinib attenuated TOCP-induced NRG1/ErbB signaling cascade. The results implied that NRG1/ErbB system may predominately play functional role in spinal cord (central nervous system) but not in sciatic nerves (peripheral nervous system) of mouse subjected to neurotoxic OP, which was confirmed by the study in vitro that lapatinib was not able to attenuate TOCP-induced neurotoxicity in rodent Schwann cell line RSC 96 cells.

The serratus anterior plane block for analgesia after thoracic surgery: A meta-analysis of randomized controlled trails.

BACKGROUND: The serratus anterior plane (SAP) block is a newer method that can be used in patients undergoing thoracic surgeries. The postoperative analgesia efficacy of SAP blocks for thoracic surgery remains controversial. We conduct a meta-analysis to evaluate the analgesia of SAP blocks after thoracic surgery. METHODS: We searched PubMed, Embase, EBSCO, the Cochrane Library, Web of Science, and CNKI for randomized controlled trials (RCTs) regarding the postoperative pain control of a SAP block on thoracic surgery. All of the dates were screened and evaluated by two researchers and meta-analysis was performed using RevMan5.3 software. RESULTS: A total of 8 RCTs involving 542 patients were included. The meta-analysis showed statistically significant differences between the two groups with respect to postoperative pain scores at 2 h (standardized mean difference [Std.MD] = -1.26; 95% confidence interval [CI] = -1.66 to -0.86; P < .0001); 6 h (SMD = -0.50; 95%CI = -0.88 to -0.11; P = .01); 12 h (SMD = -0.63; 95%CI = -1.10 to -0.16; P = .009); 24 h (SMD = -0.99; 95%CI = -1.44 to -0.51; P < .0001); postoperative opioid consumption at 24 h (SMD = -0.83; 95%CI = -1.10 to -0.56; P < .00001); and postoperative nausea and vomiting (PONV) rates (RR = 0.39; 95% CI = 0.21-0.73; P = .003). CONCLUSION: The SAP block can play an important role in the management of pain after thoracic surgery by reducing both pain scores and 24-h postoperative opioids consumption. In addition, there is fewer incidence of PONV in the SAP block group.

Three-dimensional hierarchical Ni3Se2 nanorod array as binder/carbon-free electrode for high-areal-capacity Na storage.

A three-dimensional hierarchical Ni3Se2 nanorod array (NA) grown in situ on foam Ni is the first to act as a carbon/binder-free electrode of SIBs via a one-step reversible conversion reaction. By a special decomposition-fusion process, the morphology and composition of the NA are regulated to obtain ultrahigh areal capacity, which is three times greater than that reported for other metal selenides.

Activation of Neuregulin 1/ErbB Signaling Is Involved in the Development of TOCP-Induced Delayed Neuropathy.

Organophosphate-induced delayed neuropathy (OPIDN) is characterized by progressive axonal degeneration and demyelination of the spinal cord and sciatic nerves. The neuregulin 1/epidermal growth factor receptor (ErbB) signaling pathway is crucial for axonal myelination. In this study, we investigated whether the neuregulin 1/ErbB signaling pathway mediated the progression of OPIDN. Adult hens were given tri-o-cresyl phosphate (TOCP), a typical neuropathic organophosphorus compound, to induce OPIDN. The ErbB inhibitor lapatinib was administered to hens 4 h prior to and 4 days after TOCP exposure. The neuregulin 1/ErbB signaling pathway was examined for their role in maintaining spinal cord and sciatic nerve fiber integrity. Schwann cell line sNF96.2 was used as the in vitro cell model. The in vivo results showed that TOCP (750 mg/kg body weight, p.o.) induced prominent ataxia and significant axon degeneration in the spinal cord and sciatic nerves. Lapatinib (25 mg/kg body weight, p.o.) treatment attenuated OPIDN clinically and histopathlogically and partially prevented the TOCP-induced activation of neuregulin 1/ErbB signaling pathway. Lapatinib also prevented the TOCP-induced inhibition of neuropathy target esterase (NTE), a key enzyme during the development of OPIDN, and the disturbed metabolism of phosphatidylcholine in sciatic nerves. In addition, lapatinib was shown, in vitro, to protect sNF96.2 cells from TOCP-induced dedifferentiation through neuregulin 1/ErbB signaling. Our results suggest that neuregulin 1/ErbB, through regulation of NTE activity in the peripheral nervous system, mediates the progression of OPIDN. Thus, this signal may serve as a potential target for the treatment of OPIDN.

Serum expression level of miR-504 can differentiate between glioblastoma multiforme and solitary brain metastasis of non-small cell lung carcinoma.

PURPOSE: Gliomas are the most common primary intracranial tumors of the central nervous system (CNS), accounting for about one third of all brain tumors. Glioblastoma multiforme (GBM) is the aggressive grade IV glioma with survival as low as 2-5% in the second year post-diagnosis, hence necessitating efficient diagnostic markers. More than 50% of the non-small cell lung cancer (NSCLC) brain metastases are solitary lesions, often difficult to differentiate from gliomas by conventional imaging diagnostics. Here, we explored the utility of measuring serum expression levels of Micro-RNAs (miRs) 221, 608 and 504 as biomarkers for differentiating primary GBMs from solitary metastatic lesions of NSCLC. METHODS: Serum expression level of miRs 221, 608 and 504 were determined in 49 GBM, 27 NSCLC brain metastasis patients, and 30 cancer-free normal controls by real time PCR using commercially available miR specific primers. Mann-Whitney U test was used to compare the expression of each miR between each group. Receiver operating characteristics (ROC) curve analysis was also carried out to determine the feasibility of using miR expression as differential diagnosis test. RESULTS: Our results indicated that serum expression of mir-221 was upregulated in GBM as well as in metastatic NSCLC patients. Although both miR-608 and 504 were specifically downregulated only in the GBM patient group, ROC curve analysis showed that only miR-504 serum expression can be utilized as reliable differential diagnosis marker (sensitivity and specificity; 100 and 88.89% respectively). CONCLUSIONS: Serum expression level of miR-504 is a reliable biomarker to be used for differentiating primary GBM from solitary brain metastasis of NSCLC.

Erratum: Effect of granatin B on the glioma cancer by inducing apoptosis.

[This corrects the article on p. 3970 in vol. 8, PMID: 27725877.].

Autophagy in Tri-o-cresyl Phosphate-Induced Delayed Neurotoxicity.

The widely used organophosphorus compound tri-o-cresyl phosphate (TOCP) elicits delayed neurotoxicity characterized by progressive axonal degeneration in the spinal cord and peripheral nerves. However, the precise mechanisms of TOCP-induced delayed neurotoxicity are not clear. Because autophagy has been linked to the pathogenesis of neurodegenerative diseases, we aimed to characterize autophagy in the progression of TOCP-induced delayed neurotoxicity. In vivo experiments using the adult hen animal model showed that autophagy in spinal cord axons and in sciatic nerves was markedly induced at the early preclinical stage of TOCP-induced delayed neurotoxicity; it was decreased as the delayed neurotoxicity progressed to the overt neuropathy stage. In cultured human neuroblastoma SH-SY5Y cells, TOCP reduced cell growth, and induced prominent autophagy. The autophagy inhibitor 3-methyladenine could attenuate TOCP-induced cytotoxicity, indicating that the autophagy is accountable for TOCP-induced neurotoxicity. In addition, we found that TOCP-induced Parkin translocation to mitochondria in SH-SY5Y cells, suggesting that autophagy may function to degrade mitochondria after TOCP exposure. These results suggest that autophagy may play an important role in the initiation and progression of axonal damage during TOCP-induced neurotoxicity.

Effect of granatin B on the glioma cancer by inducing apoptosis.

Glioblastoma is a highly malignant cancer of glioma cells. Present study investigates the anti proliferative activity of granatin B on glioma cell by inducing apoptosis. In this study Glioma cell (U87) was used on which anti proliferative activity of granatin B (0, 20, 40 & 80 µM) assessed by 3-(4, 5-dimethylthylthiazol-2-yl)-2,5 diphenyltetrazolium bromide (MTT) assay. Thereafter Apoptosis of glioma cell was assessed by apoptosis detection kit suing flow cytometer, DAPI staining and by estimating the activity of caspase 3 & 9 using caspase 3 & 9 kit. Expression of MMP9 protein was determined through gelatin zymography. Possible mechanism of apoptosis induction was proved by estimating the effect of granatin B with MMP9 agonist on cell proliferation, caspase 3 activity & MMP9 expression on glioblastoma cell. Result of the study suggested that granatin B significantly decreases the cell proliferation of glioma cell compared to 0 µM treated group. It was also observed that treatment with granatin B significantly induces apoptosis and increases the activity of caspase 3 & 9 protein compared to 0 µM treated group. Expression of MMP9 protein was also decreases with granatin B treatment of glima cell. MMP9 agonist significantly reverses the effect of granatin B on cell proliferation, caspase 3 and expression of MMP9 protein in glima cell. Present study concludes the anticancer activity of granatin B on glioblastoma cell by inducing apoptosis.

Metabolomics analysis and biomarker identification for brains of rats exposed subchronically to the mixtures of low-dose cadmium and chlorpyrifos.

Cadmium (Cd) and chlorpyrifos (CPF) are widespread harmful environmental pollutants with neurotoxicity to mammals. Although the exposure to Cd and CPF at the same time may pose a significant risk to human health, the subchronic combined neurotoxicity of these two chemicals at low levels in the brain is poorly understood. In this study, we treated rats with three doses (low, middle, and high) of Cd, CPF, or their mixture for 90 days. No obvious symptom was observed in the treated animals except those treated with high-dose CPF. Histological results showed that middle and high doses of the chemicals caused neuronal cell damage in brains. GC-MS-based metabonomics analysis revealed that energy and amino acid metabolism were disturbed in the brains of rats exposed to the two chemicals and their combinations even at low doses. We further identified the unique brain metabolite biomarkers for rats treated with Cd, CPF, or both. Two amino acids, tyrosine and l-leucine, were identified as the biomarkers for Cd and CPF treatment, respectively. In addition, a set of five unique biomarkers (1,2-propanediol-1-phosphate, d-gluconic acid, 9H-purine, serine, and 2-ketoisovaleric acid) was identified for the mixtures of Cd and CPF. Therefore, the metabolomics analysis is more sensitive than regular clinical observation and pathological examination for detecting the neurotoxicity of the individual and combined Cd and CPF at low levels. Overall, these results identified the unique biomarkers for Cd and CPF exposure, which provide new insights into the mechanism of their joint toxicity.

Enhanced waveguide-type ultraviolet electroluminescence from ZnO/MgZnO core/shell nanorod array light-emitting diodes via coupling with Ag nanoparticles localized surface plasmons.

Localized surface plasmon (LSP) enhanced waveguide-type ultraviolet light-emitting diodes (LEDs) were fabricated by sputtering Ag nanoparticles (Ag-NPs) onto ZnO/MgZnO core/shell nanorod array (CS-NRA)/p-GaN heterostructures. A ∼9-fold enhancement of ZnO ultraviolet electroluminescence (EL) was demonstrated by the Ag-NPs decorated LED compared with the device without Ag-NPs. Angle-dependent EL measurements, as well as finite-difference time-domain simulations of the EL intensity spatial distribution, confirmed the waveguide-type EL transmission mode along the NR's axial direction. The increased spontaneous emission rate observed in time-resolved spectroscopy suggested that the ZnO EL enhancement was attributed to LSP-exciton/polariton coupling. However, a direct coupling is very difficult to achieve between Ag-LSPs and electron-hole pairs in the active region due to their "remote" separation. Thereby, two possible models involving the dynamic process of interactions among excitons, photons, and LSPs, were established to understand the selective enhancement of ZnO EL.

Vitreoscilla hemoglobin promotes Salecan production by Agrobacterium sp. ZX09.

Salecan is a novel exopolysaccharide produced by the strain Agrobacterium sp. ZX09, and it is composed of only glucose monomers. The unique chemical composition and excellent physicochemical properties make Salecan a promising material for applications in coagulation, lubrication, protection against acute liver injury, and alleviating constipation. In this study, we cloned the Vitreoscilla hemoglobin gene into a broad-host-range plasmid pCM158. Without antibiotic selection, there was negligible loss of the plasmid in the host Agrobacterium sp. ZX09 after one passage of cultivation. The expression of Vitreoscilla hemoglobin was demonstrated by carbon monoxide (CO) difference spectrum. The engineered strain Agrobacterium sp. ZX09 increased Salecan yield by 30%. The other physiological changes included its elevated respiration rate and cellular invertase activity.

Enhanced ultraviolet emission and improved spatial distribution uniformity of ZnO nanorod array light-emitting diodes via Ag nanoparticles decoration.

Localized surface plasmon (LSP) enhanced ultraviolet (UV) light-emitting diodes (LEDs) were fabricated by embedding a ZnO nanorod array/p-GaN film heterostructure into a Ag-nanoparticles/PMMA composite. By optimizing the concentration of Ag nanoparticles in PMMA, two distinct changes in electroluminescence (EL) spectra were observed: (1) the UV EL component from ZnO excitons was selectively enhanced more than 13-fold and the entire spectral lineshape was changed and (2) the spatial uniformity of the output photon intensity was improved and the linewidth of an angular distribution curve was increased by ∼2 times. These observations can be attributed to near-field optical coupling between Ag LSPs and ZnO excitons. Time-resolved luminescence measurements and a model calculation reveal that the optical coupling results in the increase of the spontaneous emission rate and internal quantum efficiency of Ag-nanoparticles-decorated ZnO nanorod arrays. Moreover, the LSP-exciton interaction allows the device's EL to be coupled out of the nanorod waveguide and to be isotropically scattered into every direction, thus broadening the angular distribution of the EL intensity.

Role of mitochondrial function in the protective effects of ischaemic postconditioning on ischaemia/reperfusion cerebral damage.

OBJECTIVE: To investigate the effects of ischaemic postconditioning on brain injury and mitochondria in focal ischaemia and reperfusion, in rats. METHODS: Adult male Wistar rats (n = 15 per group) underwent sham surgery, ischaemia (2-h middle cerebral artery occlusion), or ischaemia followed by ischaemic postconditioning (three cycles of 30 s reperfusion/30 s reocclusion). Brain infarction size, neurological function, mitochondrial reactive oxygen species (ROS) production, mitochondrial membrane potential and mitochondrial swelling were evaluated 24 h postsurgery. RESULTS: Infarct size was significantly smaller, and neurological function was significantly better, in the ischaemic postconditioning group than in the ischaemia group. Ischaemia resulted in significant increases in mitochondrial ROS production and swelling, and a reduction in mitochondrial membrane potential, all of which were significantly reversed by postconditioning. CONCLUSIONS: The protective role of ischaemic postconditioning in focal ischaemia/reperfusion may be due to decreased mitochondrial ROS production, reduced mitochondrial membrane potential and suppressed mitochondria swelling. Mitochondria are potential targets for new therapies to prevent brain damage caused by ischaemia and reperfusion.

[Effect of electroacupuncture on the expression of corticotropin releasing hormone (CRH) and CRHR 1 mRNA in paraventricular nucleus of hypothalamus in stress-induced anxiety rats].

OBJECTIVE: To investigate the effects of electroacupuncture (EA) on the expression of corticotropin releasing hormone (CRH) and CRHR 1 mRNA in paraventricular nucleus (PVN) of hypothalamus, to explore its mechanism in anti-anxiety. METHODS: Thirty-three male SD rats were randomly divided into control, model and EA groups. Chronic emotional stress anxiety model was established by using chronic unpredictable emotional stress stimulation for 21 days. EA (15/25 Hz, 1-2 mA) was applied to "Baihui" (GV 20) and "Sanyinjiao" (SP 6) for 15 min/d and 21 days. The expression of CRH and CRHR 1 mRNA in hypothalamic PVN was measured by immunohistochemistry and in situ hybridization techniques separately. RESULTS: Compared with control group, the values of open-arms entries (OE%) and open-arms time (OT%) in model group were decreased significantly (P<0.01). In comparison with model group, OE% and OT% in EA group were increased obviously (P<0.05, P<0.01). Compared with control group, the optical density values of CRH immuno-reaction positive products and CRHR 1 mRNA expressed neurons of hypothalamic PVN in model group were increased obviously (P<0.05, P<0.01); while in comparison with model group, those of CRH and CRHR 1 mRNA in EA group were significantly decreased (P<0.05, P<0.01). CONCLUSION: EA can effectively relieve chronic stress stimulation induced anxiety in the rat, which is closely related to its effect in down regulating both CRH and CRHR 1 mRNA expression in PVN of hypothalamus.