Causal association between adiponectin and risk of trigeminal neuralgia: A Mendelian randomization study.

OBJECTIVE: To determine whether adiponectin levels and the risk of trigeminal neuralgia (TN) were causally related, a two-sample Mendelian Randomization (MR) study design was used. METHODS: We obtained data regarding adiponectin from the UK Biobank genome wide association studies (GWAS) (n = 39,883) as the exposure and TN, using GWAS summary statistics generated from FinnGen, (total n = 195 847 159; case = 800, control = 195 047) as the outcome. We conducted a two-sample Mendelian randomization analysis employing inverse variance-weighted (IVW), MR-Egger regression, weighted median, and weighted mode analyses. RESULTS: We selected 14 single nucleotide polymorphisms (SNPs) with genome-wide significance from the GWAS on adiponectin as instrumental variables. Based on the IVW method, a causal association between adiponectin levels and TN was evidenced (OR= 0.577, 95 %CI: 0.393-0.847). MR-Egger regression revealed that directional pleiotropy was unlikely to be biasing the result (intercept = -0.01; P = 0.663), but it showed no causal association between adiponectin and TN (OR=0.627, 95 %CI: 0.369-1.067). However, the weighted median (OR=0.569, 95 %CI: 0.353-0.917) and Weighted mode (OR= 0.586, 95 %CI: 0.376-0.916) approach yielded evidence of a causal association between adiponectin and TN. Cochran's Q-statistics and funnel plots indicated no evidence of heterogeneity or asymmetry, indicating no directional pleiotropy. CONCLUSION: The results of the MR analysis suggested that adiponectin may be causally associated with an increased TN risk.

Hemorrhagic meningioma with pulmonary metastasis: Case report and literature review.

Meningiomas are extra-axial neoplasms that originate from the arachnoid cap cells located on the inner surface of the meninges. Approximately 36% of central nervous system tumors are meningiomas. Based on earlier findings to be benign in most cases, they are categorized as slow-growing tumors that form gradually over time. Meningiomas are usually asymptomatic and discovered inadvertently. They rarely present with immediate clinical symptoms or abrupt hemorrhagic strokes. However, tumor hemorrhage can be fatal in high-grade meningiomas, particularly those with vascularization. We describe a 58-year-old man who was hospitalized after experiencing an unexpectedly acute headache. The right cerebellar hemisphere and vermis cerebellar hemorrhage were detected on computed tomography (CT), and the cerebellar hemorrhage was explained by a diagnosis of hypertension. When additional analysis of the patient's chest CT indicated lung mass lesions, we assumed that the lung cancer had spread to the brain. However, the pathological outcomes of a guided definite pulmonary aspiration biopsy, in conjunction with resection of the cerebellar tumor, suggested a subtentorial meningioma with ruptured hemorrhage and pulmonary meningioma metastasis. The patient was transferred to a hospital closer to home for ongoing follow-up and, after 2 months, he had recovered well.

Endoscopic Third Ventriculostomy vs. Ventriculoperitoneal Shunt for Obstructive Hydrocephalus: A Meta-Analysis of Randomized Controlled Trials.

AIM: To conduct a meta-analysis for investigating the safety and efficacy of endoscopic third ventriculostomy (ETV) and extracranial shunting for patients with obstructive hydrocephalus. MATERIAL AND METHODS: Randomized controlled trials (RCTs) of ETV and ventriculoperitoneal shunting (VPS) for obstructive hydrocephalus were analyzed systematically by using MEDLINE, EMBASE, and the Cochrane Controlled Trials Register. The reference lists of the retrieved studies were also perused. Postoperative infection, postoperative cerebrospinal fluid (CSF) leakage, mortality and surgical success were the main outcomes of the analysis. RESULTS: Among 841 selected studies, 6 RCTs evaluated ETV and VPS. Compared to VPS, ETV had lower postoperative infection incidence (risk ratio [RR]: 0.19, 95% confidence interval [CI]: 0.08-0.43, p=0.0001), postoperative CSF leakage (RR: 5.10, 95% CI: 1.19-21.89, p=0.03) VPS. VPS had no mortality as compared to ETV (RR 0.64, 95% CI: 0.26-1.56, p=0.32). CONCLUSION: While VPS had no mortality in comparison to ETV, the latter showed lower incidences of major complications, such as postoperative infection and CSF leakage, than those of the former for patients with obstructive hydrocephalus.

Unilateral thalamic infarction onset with lethargy: A case report and literature review.

INTRODUCTION: Infarct-induced lethargy is a common disabling symptom that lacks a consensual definition and a standardized method of care. Identifying the causes of the infarct in the thalamic reticular nucleus (TRN) induced lethargy is crucial in stroke patients. CASE PRESENTATION: A 68-year-old female patient was admitted to the hospital with lethargy and weakness in the right limb. A computed tomography (CT) scan performed at the presentation showed no bleeding. She was given intravenous thrombolysis. A head computed tomography (CT) scan clearly showed that the infarct was located in the TRN. After 1 hour of treatment, the weakness in the patient's limb was relieved. However, she was still lethargic, but her lethargy symptoms improved after 3 days. DISCUSSION AND CONCLUSIONS: Our case highlights that despite the small size of the infarct, the patient was unconscious, which makes it difficult for physicians to understand and treat the condition, resulting in trouble managing the case. We performed a literature review and proposed that the infarction located in the TRN causes lethargy. However, further clinical and pathophysiological research is still needed to improve patient care.

Nursing Value Analysis and Risk Assessment of Acute Gastrointestinal Bleeding Using Multiagent Reinforcement Learning Algorithm.

Gastrointestinal bleeding (GIB) indicates an issue in the digestive system. Blood can be found in feces or vomiting; however, it is not always visible, even if it makes the stool appear darkish or muddy. The bleeding can range in harshness from light to severe and can be dangerous. It is advised that nursing value analysis and risk assessment of patients with GIB is essential, but existing risk assessment techniques function inconsistently. Machine learning (ML) has the potential to increase risk evaluation. For evaluating risk in patients with GIB, scoring techniques are ineffective; a machine learning method would help. As a result, we present а unique machine learning-based nursing value analysis and risk assessment framework in this research to construct a model to evaluate the risk of hospital-based interventions or mortality in individuals with GIB and make a comparison to that of other rating systems. Initially, the dataset is collected, and preprocessing is done. Feature extraction is done using local binary patterns (LBP). Classification is performed using a fuzzy support vector machine (FSVM) classifier. For risk assessment and nursing value analysis, machine learning-based prediction using a multiagent reinforcement algorithm is employed. For improving the performance of the proposed system, we use spider monkey optimization (SMO) algorithm. The performance metrics like classification accuracy, area under the receiver-operating characteristic curve (AUROC), area under the curve (AUC), sensitivity, specificity, and precision are analyzed and compared with the traditional approaches. In individuals with GIB, the suggested technique had a good-excellent prognostic efficacy, and it outperformed other traditional models.

HO-1 protects the nerves of rats with cerebral hemorrhage by regulating the PI3K/AKT signaling pathway.

Objective: This study aimed to investigate the neuroprotective effect of heme oxygenase-1 (HO-1) on the PI3K/AKT signaling pathway in rats with cerebral hemorrhage. Materials and methods: Adult male Sprague-Dawley rats were randomly divided into: a sham group, a model group and an HO-1 inhibitor group (ZnPP group). Functional defects after surgery were scored according to the Longa5 standard. Hemotoxylin and eosin staining was used to detect whether the model was constructed successfully. Superoxide dismutase (SOD) vitality and malondialdehyde (MDA) content were calculated by the xanthine oxidase method and thiobarbituric acid method, respectively. Blood-brain barrier permeability was measured by Evans Blue. Apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. The expression of Bcl-2 and BAX was evaluated by immunohistochemistry and the expression of PI3K, p-PI3K, AKT and p-AKT was tested by Western blotting. Results: The rat intracerebral hemorrhage model was successfully constructed. Compared with the model group, the bleeding in the ZnPP group was more serious, the cell edema and deformation were aggravated, and the neurological deficit score in the rat was significantly increased. In addition, the content of Evans blue, MDA, the number of apoptotic cells, the water content of brain tissue and the expression of BAX were significantly increased, while the SOD activity and the expressions of Bcl-2, p-PI3K and p-AKT protein were decreased. Conclusion: HO-1 could protect the nerves of rats with cerebral hemorrhage by regulating the PI3K/AKT signaling pathway.

Dexmedetomidine Improves Cerebral Ischemia-Reperfusion Injury in Rats via Extracellular Signal-Regulated Kinase/Cyclic Adenosine Monophosphate Response Element Binding Protein Signaling Pathway.

OBJECTIVE: To investigate the mechanism of dexmedetomidine (Dex) in improving brain damage induced by cerebral ischemia-reperfusion injury in rats. METHODS: Rats were randomly divided into a sham operation group, ischemia-reperfusion group, Dex group, piracetam group, and yohimbine + Dex group, with 12 rats per group. 2,3,5-Triphenyltetrazolium chloride staining was used to analyze cerebral infarct size. Hematoxylin-eosin staining and immunohistochemistry were used to observe brain damage caused by ischemia-reperfusion. Cognitive and memory functions was detected by Morris water maze test, and the expression of phosphorylated extracellular signal-regulated kinases 1 and 2 (ERK1/2) and phosphorylated cyclic adenosine monophosphate response element binding protein (CREB) were measured by Western blot. RESULTS: Cognitive dysfunction was improved in the Dex group and the piracetam group compared with the ischemia-reperfusion group. Compared with the ischemia-reperfusion group, infarct size and neuronal cell death rates were decreased in the Dex group and the piracetam group. The expression of phosphorylated ERK1/2 and phosphorylated CREB in the Dex group was increased, whereas the expression of phosphorylated ERK1/2 and phosphorylated CREB in the yohimbine + Dex group was lower than in the Dex group (P < 0.05). CONCLUSIONS: Dex improved ischemic brain damage by promoting signal transduction of the ERK/CREB pathway, which may provide new ways for clinical treatment of cerebral ischemia-reperfusion injury.

miR-7-5p inhibits cell migration and invasion in glioblastoma through targeting SATB1.

MicroRNAs (miRNAs/miRs) have been revealed to influence the development and progression of glioblastoma. Although a number of miRNAs are abnormally expressed in glioblastoma it is not clear whether they are a factor associated with glioblastoma pathogenesis. In the present study, miR-7-5p was identified as being aberrantly downregulated in glioblastoma tissues and cell lines. miR-7-5p overexpression significantly decreased the migratory and invasive capacity of the cells, while miR-7-5p silencing had the opposite effect. In addition, a luciferase assay confirmed that special AT rich sequence binding protein 1 (SATB1) was a direct target gene of miR-7-5p in glioblastoma. The overexpression of SATB1 in glioblastoma was revealed to promote cell migration and invasion. In addition, SATB1 overexpression may weaken the inhibitory effect of miR-7-5p on cell migration and invasion. miR-7-5p overexpression reversed the effects of SATB1 on cell migration and invasion in glioblastoma cells. In conclusion, miR-7-5p may be a useful therapeutic target for the diagnosis and treatment of patients with glioblastoma.

MicroRNA-153 suppresses cell invasion by targeting SNAI1 and predicts patient prognosis in glioma.

Glioma is the most common and rapidly progressive type of malignant primary brain tumor in adults. miR-153 plays a major role in many malignancies; nevertheless, few studies have been conducted on glioma. The aim of the present study was to explore the role of miR-153 and SNAI1 on invasion in glioma. Reverse transcription-quantitative PCR was employed to measure the expression levels of miR-153 and SNAI1 mRNA. Transwell assay was utilized to calculate the capacity of invasion. Luciferase report assay was applied to detect whether SNAI1 was a target of miR-153. miR-153 was downregulated in glioma tissues and cells versus paracancerous tissues and normal immortalized gliocyte HEB cells. Transwell assay was used to measure whether a low expression of miR-153 in glioma indicated inhibition of cell invasion. We verified that SNAI1 was a target of miR-153 and had a negative association with miR-153 detected by luciferase reporter assay. Additionally, miR-153 suppressed cell invasive ability by regulating SNAI1 expression, whose partial function was reversed by SNAI1. miR-153 suppressed cell invasion of glioma by directly targeting SNAI1. Thus, miR-153/SNAI1 axis may be a novel target for cervical cancer treatment.

Down-Regulation of Mir-145 Improves Learning and Memory Abilities in Epileptic Rats by Regulating Hippocampal Neuron Apoptosis.

OBJECTIVES: To investigate effect of miR-145 on learning and memory ability in rats with epilepsy. METHODS: Rats with epilepsy were induced by lithium chloride-pilocarpine. miR-145 antagomir and antagomir-control were injected into epileptic brains by the stereotactic technique, respectively. Then, rats were divided into a normal group (N), epilepsy group (Ep), miR-145 antagomir group (A) and antagomir-control group (C). After 1 and 7 days of treatment, the expression of miR-145 and Caspase-9 were detected, and the apoptosis of hippocampal neurons in CA1 of hippocampus was detected. After 7 days of treatment, the learning and memory abilities of rats was measured by using the Morris water maze test. RESULTS: The rat epilepsy model was successfully constructed. Compared with the N group, the target quadrant time and platform crossing times were reduced and the expression of miR-145 and Caspase-9 was increased in the epilepsy groups (P < 0.05). Compared with the Ep and C groups, the target quadrant time and platform crossing times were increased and the expression of miR-145 and Caspase-9 was down-regulated in the A group (P < 0.05). The number of apoptotic hippocampal neurons in the hippocampal CAl area of the Ep group was more than that in the N group and in the A group was less than that in the C group at 1 and 7 days after modeling respectively (P < 0.05). CONCLUSIONS: Down-regulated miR-145 improved the apoptosis of hippocampal neurons by reducing the Caspase-9 expression in hippocampus and further affected learning and memory abilities of rats with epilepsy.