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AIM: The objective is to investigate the prognostic factors associated with gliomas and to develop and assess a predictive nomogram model connected to survival that may serve as an additional resource for the clinical management of glioma patients. METHOD: From 2010 to 2015, participants included in the study were chosen from the Surveillance Epidemiology and End Results (SEER) database. Gliomas were definitively diagnosed in each of them. They were divided into the training group and the validation cohort at random (7/3 ratio) using a random number table. To identify the independent predictive markers for overall survival (OS), Cox regression analysis was utilized. Subsequently, the training cohort's survival-related nomogram predictive model for OS was created by incorporating the fundamental patient attributes. Following that, the training cohort's model underwent internal validation. The nomogram model's authenticity and reliability were assessed through the computation of receiver operating characteristic (ROC) curves and concordance index (C-index). To evaluate the degree of agreement between the observed and predicted values in the training and validation cohorts, calibration plots were created. RESULT: Age, primary site, histological type, surgery, chemotherapy, marital status, and grade were the independent predictive factors for OS in the training cohort, according to Cox regression analysis. Moreover, the nomogram model for predicting 1-year, 3-year, and 5-year OS was built using these variables. The C-indexes of OS for glioma patients in the training cohort and internal validation cohort were found to be 0.779 (95% CI=0.769-0.789) and 0.776 (95% CI=0.760-0.792), respectively, according to the results. The ROC curves also demonstrated good discrimination. Additionally, calibration plots demonstrated a fair amount of agreement. CONCLUSIONS: In summary, the nomogram prediction model of OS demonstrated a moderate level of reliability in its predictive performance, offering valuable reference data to enable doctors to quickly and easily determine the survival likelihood of patients with gliomas.
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Neoplasias Encefálicas , Glioma , Nomogramas , Programa de VERF , Humanos , Glioma/mortalidad , Glioma/terapia , Femenino , Masculino , Persona de Mediana Edad , Neoplasias Encefálicas/mortalidad , Neoplasias Encefálicas/terapia , Anciano , Adulto , Pronóstico , Reproducibilidad de los Resultados , Curva ROC , Modelos de Riesgos ProporcionalesRESUMEN
Objective: The primary purpose of our study is to systemically evaluate the effect of repetitive transcranial magnetic stimulation (rTMS) on recovery of dysphagia after stroke. Search Methods: We searched randomized controlled trials (RCTs) and non-RCTs published by PubMed, the Cochrane Library, ScienceDirect, MEDLINE, and Web of Science from inception until April 24, 2021. Language is limited to English. After screening and extracting the data, and evaluating the quality of the selected literature, we carried out the meta-analysis with software RevMan 5.3 and summarized available evidence from non-RCTs. Results: Among 205 potentially relevant articles, 189 participants (from 10 RCTs) were recruited in the meta-analysis, and six non-RCTs were qualitatively described. The random-effects model analysis revealed a pooled effect size of SMD = 0.65 (95% CI = 0.04-1.26, p = 0.04), which indicated that rTMS therapy has a better effect than conventional therapy. However, the subgroup analysis showed that there was no significant difference between low-frequency and high-frequency groups. Even more surprisingly, there were no statistically significant differences between the two groups and the conventional training group in the subgroup analysis, but the combined effect was positive. Conclusion: Our study suggests that rTMS might be effective in treating patients with dysphagia after stroke.
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Baicalein, a typical flavonoid compound, has neuroprotective properties in several neurological disorders. Autophagy plays a central role in maintaining the cellular homeostasis, and is involved in the pathogenesis of Parkinson's disease (PD). Recently, baicalein has been reported to induce autophagy. Therefore, the current study was designed to investigate whether baicalein could protect against rotenone-induced neurotoxicity via induction of autophagy both in SH-SY5Y cells and in a mouse model. A chronic PD mouse model was established by continuous intragastric administration of rotenone for 12 weeks. Baicalein was administrated from 7 to 12 week. Our results showed that baicalein prevented rotenone-induced behavioral deficits, dopaminergic neuronal loss, apoptosis and mitochondrial dysfunction. Furthermore, baicalein restored rotenone-impaired autophagy, and blocking the baicalein-induced autophagy using 3-methyladenine inhibited the neuroprotective effects of bacalein. Baicalein increased cell viability and restored mitochondrial function in SH-SY5Y cells. The beneficial effect of baicalein was abrogated by 3-methyladenine treatment. Furthermore, rapamycin increased autopahgy and reduced the rotenone-induced neurotoxicity in SH-SY5Y cells. Collectively, these results suggest that baicalein could prevent rotenone-induced neurotoxicity via restoring autophagy.
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Autofagia/efectos de los fármacos , Flavanonas/uso terapéutico , Fármacos Neuroprotectores/uso terapéutico , Síndromes de Neurotoxicidad/prevención & control , Fitoterapia , Rotenona/toxicidad , Scutellaria baicalensis/química , Adenina/análogos & derivados , Adenina/farmacología , Animales , Apoptosis/efectos de los fármacos , Línea Celular Tumoral , Supervivencia Celular , Modelos Animales de Enfermedad , Dopamina/metabolismo , Flavanonas/farmacología , Homeostasis , Humanos , Insecticidas/toxicidad , Masculino , Ratones Endogámicos C57BL , Mitocondrias/efectos de los fármacos , Mitocondrias/fisiología , Fármacos Neuroprotectores/farmacología , Síndromes de Neurotoxicidad/metabolismo , Síndromes de Neurotoxicidad/fisiopatología , Enfermedad de Parkinson/metabolismo , Enfermedad de Parkinson/fisiopatología , Enfermedad de Parkinson/prevención & control , Extractos Vegetales/farmacología , Extractos Vegetales/uso terapéutico , Especies Reactivas de Oxígeno/metabolismoRESUMEN
Neuropathic pain is a long-lasting clinical problem that is often refractory to medical management. Gene transfer of specific genes for therapeutic benefit offers a novel approach to the treatment of neuropathic pain. In this study, we tested whether the transfer of the glutamic acid decarboxylase (GAD) gene to dorsal root ganglion (DRG) cells would attenuate below-injury level central neuropathic pain after spinal cord injury (SCI) by using a novel human foamy virus (HFV) vector to achieve release of gamma-aminobutyric acid (GABA). Subcutaneous inoculation of a replication-defective HFV vector, which expresses GAD (vector rdvGAD67) for 7days after T13 spinal cord hemisection, reversed mechanical allodynia and thermal hyperalgesia evoked by SCI. The antiallodynic effect lasted 6 weeks and was reestablished by reinoculation. We also found that subcutaneous inoculation of rdvGAD67 resulted in enhanced production of GAD and tonical GABA release from transduced DRG neurons. These results suggest that HFV-mediated gene transfer to DRG could be employed to treat below-injury level central neuropathic pain after incomplete SCI.
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Terapia Genética/métodos , Glutamato Descarboxilasa/genética , Neuralgia/terapia , Traumatismos de la Médula Espinal/complicaciones , Spumavirus/genética , Animales , Conducta Animal , Ganglios Espinales/fisiología , Técnicas de Transferencia de Gen , Hiperalgesia/etiología , Hiperalgesia/terapia , Inyecciones Subcutáneas , Masculino , Neuralgia/etiología , Ratas , Ratas Sprague-Dawley , Ácido gamma-Aminobutírico/fisiologíaRESUMEN
Human foamy virus (HFV), with its nonpathogenic nature and several unique features for gene transfer, is a promising vector system for neurological disorders gene therapy. The question of whether HFV vectors can be developed for the expression of therapeutic genes in primary astrocytes of the brain may be of interest. First, efficient expression for foreign genes, which is critical for the potentials of HFV-derived vector in gene therapy, was successfully demonstrated in rat-cultured astrocytes by the enhanced green fluorescent protein (EGFP) transduction through an HFV vector bearing an EGFP expression cassette. Second, HFV vectors containing human glutamic acid decarboxylase (GAD) complementary DNA, which encodes an inhibitory neurotransmitter gamma-aminobutyric acid (GABA)-producing enzyme, were used to examine the function of GAD on GABA synthesis in cultured astrocytes. We found that the transduction of GAD vector resulted in isoform-specific expression of GAD, synthesis of a significant amount of GABA and tonical GABA release, and behavioral recovery in rat Parkinson's disease (PD) models. These results suggested that HFV vector had the ability to transduce astrocytes and HFV vector-derived GAD expression in astrocytes provided a potential strategy for the treatment of neurological disorders associated with hyperexcitable or diminished inhibitory activity.