Treatment of Third Branch Trigeminal Neuralgia With a Balloon Inflated in the Foramen Ovale.

Objective: To investigate the efficacy of modified percutaneous balloon compression for simple third branch pain and its postoperative complications. Methods: Clinical data and surgical records of 132 patients with third branch pain treated with percutaneous balloon compression from March 2015 to May 2019 were retrospectively analyzed, of which 81 cases were in the modified group and 51 cases were in the classic group. The modified technique was to compress again at the foramen ovale to enhance the compression in V3 after compression of the Gasserian ganglion. Results: In the modified group, the overall therapeutic efficiency was 96.3%, with 77 patients (95.1%) having immediate postoperative pain relief and one patient (1.2%) having occasional pain without the need for medication. In the classic group, immediate postoperative pain relief was seen in 43 cases (84.3%), and two patients (3.9%) had occasional pain with no need for medication. The rate of complete pain relief was significantly higher in the modified group than in the classic group (P < 0.05). Postoperative follow-up ranged from 14 to 48 months. The pain-free rates were 77.8 and 54.9% in the modified and classic groups, respectively. The incidence of facial numbness in the region of the first branch was significantly lower than in the classic group (P < 0.001). Conclusion: The modified procedure has significant advantages over the classic procedure in improving surgical efficacy, reducing postoperative recurrence rate, and decreasing postoperative numbness in the region, and can be used to treat simple trigeminal neuralgia in the third branch.

Omi inhibition ameliorates neuron apoptosis and neurological deficit after subarachnoid hemorrhage in rats.

BACKGROUND: Subarachnoid hemorrhage (SAH) is a severe neurological emergency, resulting in cognitive impairments and threatening human's health. Currently, SAH has no effective treatment. It is urgent to search for an effective therapy for SAH. OBJECTIVE: To explore the expression of Omi protein after subarachnoid hemorrhage in rats. METHODS: SAH rat model was established by injecting blood into the prechiasmatic cistern. Neurological deficit was assessed by detecting neurological deficit scores and brain tissue water contents. Apoptotic cells were evaluated by TUNEL staining and IHC staining. Omi and Cleaved caspase 3 expressions in nerve cells were determined by double staining using IF. Apoptosis-related proteins were measured by Western blotting assay. RESULTS: SAH rat model was successfully established, showing more apoptotic cells and high neurological deficit scores in SAH rat. In SAH rat model, Omi expression in nerve cells was elevated and the upregulation of Omi mainly occurred in cytoplasm, accompanied by the degradation of XIAP and the increased cleaved caspase 3/9 and cleaved PARP. Once treated with UCF-101, a specific inhibitor of Omi, the increased cell apoptosis, left/right brain moisture contents and neurological deficits were notably reversed in SAH rat brain. Of note, SAH-induced the increases of apoptosis-related protein in nerve cells were also rescued by the administration of UCF-101. CONCLUSIONS: UCF-101-mediated Omi inhibition decreased the degradation of XIAP and subsequently inhibited the activation of apoptosis-related proteins, decreased nerve cell apoptosis, leading to the improvement on early brain injury in SAH rat. UCF-101-based Omi inhibition may be used to treat SAH with great potential application.

MerTK inhibits the activation of the NLRP3 inflammasome after subarachnoid hemorrhage by inducing autophagy.

The NLR family pyrin domain-containing 3 (NLRP3) multiprotein complex is associated with neuroinflammation and poor prognosis after subarachnoid hemorrhage (SAH). Accumulating evidence shows that Mer tyrosine kinase (MerTK) alleviates inflammatory responses via a negative feedback mechanism. However, the contribution and function of MerTK in SAH remain to be determined. In this study, we explored the role of MerTK during microglial NLRP3 inflammasome activation and evaluated its contribution to the outcome of SAH in mice. Activating MerTK with growth arrest-specific 6 (Gas6) alleviated brain edema, neuronal degeneration and neurological deficits after SAH by regulating neuroinflammation. Gas6 did not change the mRNA levels of Nlrp3 or Casp1 but decreased the protein expression of NLRP3, cleaved caspase1 (p20), interleukin-1ß and interleukin-18. Furthermore, Gas6 increased the expression of Beclin1, the ratio of LC3-II/LC3-I and the level of autophagic flux. Inhibiting autophagy with 3-MA reversed the inhibition of NLRP3 inflammasome activation and diminished the neuroprotective effects of Gas6. Thus, MerTK activation may exert protective effects by limiting neuroinflammation and promoting neurological recovery after SAH via autophagy induction.

Diagnostic and Prognostic Value of Neutrophil Extracellular Trap Levels in Patients With Acute Aortic Dissection.

BACKGROUND: Acute aortic dissection (AAD) is a fatal disease demanding prompt diagnosis and proper treatment. There is a lack of serum markers that can effectively assist diagnosis and predict prognosis of AAD patients. METHODS: Ninety-six AAD patients were enrolled in this study, and 249 patients with chest pain due to acute myocardial infarction, pulmonary embolism, intramural hematoma, angina or other causes and 80 healthy controls were included as control group and healthy control group. Demographics, biochemical and hematological data and risk factors were recorded as baseline characteristics. The 1-year follow-up data were collected and analyzed. The diagnostic performance and ability to predict disease severity and prognosis of NET components in serum and aortic tissue were evaluated. RESULTS: Circulating NET markers, citH3 (citrullination of histone 3), cell-free DNA (cfDNA) and nucleosomes, had good diagnostic value for AAD, with superior diagnostic performance to D-dimer in discriminating patients with chest pain due to other reasons in the emergency department. Circulating NET marker levels (i.e., citH3, cfDNA and nucleosomes) of AAD patients were significantly higher than that of control group and healthy control group. In addition, circulating NET markers levels were closely associated with the disease severity, in-hospital death and 1-year survival of AAD patients. Systolic blood pressure < 90 mmHg and serum citH3 levels were identified as independent risk factors for 1-year survival of AAD patients. Excessive NET components (i.e., neutrophil elastase and citH3) in the aortic tissue of AAD patient were significantly higher than that of healthy donor aortic tissue. The expression levels of granules and nuclear NET components were significantly higher in aortic tissue from AAD patients than controls. CONCLUSIONS: Circulating NET markers, citH3, cfDNA and nucleosomes, have significant diagnostic value and predictive value of disease severity and prognosis of AAD patients. The NETs components may constitute a useful diagnostic and prognostic marker in AAD patients.

The prognostic value of plasma thrombospondin-1 concentrations after aneurysmal subarachnoid hemorrhage.

BACKGROUND: Thrombospondin-1 is a homotrimeric glycoprotein with well known functions in hemostasis and angiogenesis. Its expression was increased after experimental intracerebral hemorrhage. We determined whether increased plasma thrombospondin-1 concentrations are predictive of clinical outcomes of aneurysmal subarachnoid hemorrhage (aSAH). METHODS: Plasma thrombospondin-1 concentrations of 118 aSAH patients and 118 age- and gender-matched healthy controls were determined using enzyme-linked immunosorbent assay. Patients were followed up until death or completion of 6months after aSAH. An unfavorable outcome was defined as Glasgow Outcome Scale score of 1-3. Multivariate analyses of significant variables of univariate analyses were performed to determine independent risk factors for the clinical outcomes. RESULTS: Plasma thrombospondin-1 concentrations were significantly higher in aSAH patients than in healthy controls; plasma thrombospondin-1 concentrations were independently associated with clinical severity reflected by the World Federation of Neurological Surgeons score and Fisher score; thrombospondin-1 was identified as an independent predictor of 6-month mortality and 6-month unfavorable outcome; thrombospondin-1 had similar predictive performance compared with the World Federation of Neurological Surgeons score and Fisher score according to receiver operating characteristic curve analysis. CONCLUSION: Higher plasma thrombospondin-1 concentrations are associated with clinical severity and long-term prognosis of aSAH patients.

A novel method for constructing a WIFI positioning system with efficient manpower.

With the rapid development of WIFI technology, WIFI-based indoor positioning technology has been widely studied for location-based services. To solve the problems related to the signal strength database adopted in the widely used fingerprint positioning technology, we first introduce a new system framework in this paper, which includes a modified AP firmware and some cheap self-made WIFI sensor anchors. The periodically scanned reports regarding the neighboring APs and sensor anchors are sent to the positioning server and serve as the calibration points. Besides the calculation of correlations between the target points and the neighboring calibration points, we take full advantage of the important but easily overlooked feature that the signal attenuation model varies in different regions in the regression algorithm to get more accurate results. Thus, a novel method called RSSI Geography Weighted Regression (RGWR) is proposed to solve the fingerprint database construction problem. The average error of all the calibration points' self-localization results will help to make the final decision of whether the database is the latest or has to be updated automatically. The effects of anchors on system performance are further researched to conclude that the anchors should be deployed at the locations that stand for the features of RSSI distributions. The proposed system is convenient for the establishment of practical positioning system and extensive experiments have been performed to validate that the proposed method is robust and manpower efficient.

Plasma 8-iso-Prostaglandin F2α concentrations and outcomes after acute intracerebral hemorrhage.

BACKGROUND: Higher plasma 8-iso-Prostaglandin F2α concentrations have been associated with poor outcome of severe traumatic brain injury. We further investigated the relationships between plasma 8-iso-Prostaglandin F2α concentrations and clinical outcomes in patients with acute intracerebral hemorrhage. METHODS: Plasma 8-iso-Prostaglandin F2α concentrations of 128 consecutive patients and 128 sex- and gender-matched healthy subjects were measured by enzyme-linked immunosorbent assay. We assessed their relationships with disease severity and clinical outcomes including 1-week mortality, 6-month mortality and unfavorable outcome (modified Rankin Scale score>2). RESULTS: Plasma 8-iso-Prostaglandin F2α concentrations were substantially higher in patients than in healthy controls. Plasma 8-iso-Prostaglandin F2α concentrations were positively associated with National Institutes of Health Stroke Scale (NIHSS) scores and hematoma volume using a multivariate linear regression. It emerged as an independent predictor for clinical outcomes of patients using a forward stepwise logistic regression. ROC curves identified the predictive values of plasma 8-iso-Prostaglandin F2α concentrations, and found its predictive value was similar to NIHSS scores and hematoma volumes. However, it just numerically added the predictive values of NIHSS score and hematoma volume. CONCLUSIONS: Increased plasma 8-iso-Prostaglandin F2α concentrations are associated with disease severity and clinical outcome after acute intracerebral hemorrhage.

Comparison of the performances of copeptin and multiple biomarkers in long-term prognosis of severe traumatic brain injury.

Enhanced blood levels of copeptin correlate with poor clinical outcomes after acute critical illness. This study aimed to compare the prognostic performances of plasma concentrations of copeptin and other biomarkers like myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, Tau and ubiquitin carboxyl-terminal hydrolase L1 in severe traumatic brain injury. We recruited 102 healthy controls and 102 acute patients with severe traumatic brain injury. Plasma concentrations of these biomarkers were determined using enzyme-linked immunosorbent assay. Their prognostic predictive performances of 6-month mortality and unfavorable outcome (Glasgow Outcome Scale score of 1-3) were compared. Plasma concentrations of these biomarkers were statistically significantly higher in all patients than in healthy controls, in non-survivors than in survivors and in patients with unfavorable outcome than with favorable outcome. Areas under receiver operating characteristic curves of plasma concentrations of these biomarkers were similar to those of Glasgow Coma Scale score for prognostic prediction. Except plasma copeptin concentration, other biomarkers concentrations in plasma did not statistically significantly improve prognostic predictive value of Glasgow Coma Scale score. Copeptin levels may be a useful tool to predict long-term clinical outcomes after severe traumatic brain injury and have a potential to assist clinicians.

Plasma copeptin level predicts acute traumatic coagulopathy and progressive hemorrhagic injury after traumatic brain injury.

Higher plasma copeptin levels correlate with poor clinical outcomes after traumatic brain injury. Nevertheless, their links with acute traumatic coagulopathy and progressive hemorrhagic injury are unknown. Therefore, we aimed to investigate the relationship between plasma copeptin levels, acute traumatic coagulopathy and progressive hemorrhagic injury in patients with severe traumatic brain injury. We prospectively studied 100 consecutive patients presenting within 6h from head trauma. Progressive hemorrhagic injury was present when the follow-up computerized tomography scan reported any increase in size or number of the hemorrhagic lesion, including newly developed ones. Acute traumatic coagulopathy was defined as an activated partial thromboplastic time greater than 40s and/or international normalized ratio greater than 1.2 and/or a platelet count less than 120×10(9)/L. We measured plasma copeptin levels on admission using an enzyme-linked immunosorbent assay in a blinded fashion. In multivariate logistic regression analysis, plasma copeptin level emerged as an independent predictor of progressive hemorrhagic injury and acute traumatic coagulopathy. Using receiver operating characteristic curves, we calculated areas under the curve for progressive hemorrhagic injury and acute traumatic coagulopathy. The predictive performance of copeptin was similar to that of Glasgow Coma Scale score. However, copeptin did not obviously improve the predictive value of Glasgow Coma Scale score. Thus, copeptin may help in the prediction of progressive hemorrhagic injury and acute traumatic coagulopathy after traumatic brain injury.

Prognostic significance of plasma copeptin detection compared with multiple biomarkers in intracerebral hemorrhage.

BACKGROUND: Higher plasma copeptin concentrations have been associated with poor clinical outcomes after intracerebral hemorrhage. This study was designed to compare plasma concentrations of copeptin and other biomarkers like myelin basic protein, glial fibrillary astrocyte protein, S100B, neuron-specific enolase, phosphorylated axonal neurofilament subunit H, tau and ubiquitin carboxyl-terminal hydrolase L1 for analysis of their prognostic prediction. METHODS: We measured plasma concentrations of these biomarkers in 118 healthy controls and in 118 acute patients with a comparison analysis for their prediction of 6-month mortality and unfavorable outcome (modified Rankin Scale score>2). RESULTS: Plasma concentrations of these biomarkers were statistically significantly higher in all patients than in healthy controls, in non-survivors than in survivors and in patients with unfavorable outcome than with favorable outcome. Areas under receiver operating characteristic curves of plasma concentrations of these biomarkers were similar to those of the National Institute of Health Stroke Scale score for prognostic prediction. Plasma copeptin concentration statistically significantly improved the prognostic predictive value of the National Institute of Health Stroke Scale score, but other biomarkers did not. CONCLUSIONS: Copeptin may help in the prediction of long-term clinical outcomes after intracerebral hemorrhage.