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1.
Neurosurgery ; 2024 Jun 07.
Artigo em Inglês | MEDLINE | ID: mdl-38847532

RESUMO

BACKGROUND AND OBJECTIVES: The current widely utilized clinical approach for severe intraventricular hemorrhage involves ventriculostomy with supportive drainage. The aim of our study was to evaluate the overall efficacy of neuroendoscopic hematoma removal combined with ventricular lavage as a treatment approach for severe intraventricular hemorrhage. METHODS: A prospective randomized controlled study was conducted, selecting a total of 98 patients with severe intraventricular hemorrhage at our hospital from February 2021 to November 2022. The patients were randomly distributed into 2 groups using a randomized number table method: the neuroendoscopic group (undergoing neuroendoscopic hematoma removal combined with ventricular lavage) and the control group (undergoing intraventricular trepanation and drainage), with 49 patients in each group. RESULTS: The neuroendoscopic group had significantly higher intraoperative blood loss than that of the control group (P = .037), while the drainage tube indwelling time and hospital stay in the neuroendoscopic group were significantly shorter (P < .001). At 6 hours (P = .021), 1 day (P = .002), 3 days (P < .001) and 7 days (P = .007) following surgery, the neuroendoscopic group exhibited evidently higher hematoma clearance rates compared with the control group. At 1 day and 3 days after surgery, the cerebrospinal fluid drainage volume in the neuroendoscopic group was significantly higher than that in the control group (P < .001), whereas at 7 days after surgery, it was significantly lower in the neuroendoscopic group compared with the control group (P < .001). Moreover, significantly lower incidence of intracranial infection (P = .045) and increased intracranial pressure (P = .008) was observed in the neuroendoscopic group compared with the control group. CONCLUSION: Neuroendoscopic hematoma removal combined with ventricle lavage emerged as an effective treatment strategy for severe intraventricular hemorrhage, yielding significant therapeutic benefits. Therefore, this approach holds promise for broader clinical application and promotion.

2.
Altern Ther Health Med ; 29(1): 238-244, 2023 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-36150015

RESUMO

Context: Pituitary adenoma is a clinical syndrome in which excessive production of pituitary corticotropin (ACTH). For ACTH tumor cells, researchers know little about the influence of the cell-cycle process on ACTH production and cell proliferation. Some research has shown that imatinib can induce apoptosis of tumor cells. Objective: The study intended to explore the effects and molecular mechanisms of imatinib combined with everolimus on AtT-20 cells in AtT-20 mouse pituitary tumors. Design: The research team performed a laboratory study using murine corticotropin tumor AtT-20 cells. Setting: The study took place at the Department of Neurosurgery at Renmin Hospital of the Hubei University of Medicine in Shiyan, Hubei, China. Intervention: The research team cultured the cells in AtT-20-cell-specific medium containing 100 µg/mL of streptomycin, 100 U/mL of penicillin, and 10% fetal bovine serum at 37°C and 5% CO2. The team divided the cells into a control group, a normal culture without the drug, and an intervention group, incubated for 24 hours with 1 µM of imatinib and 3 µM of everolimus when the cells grew to 40% confluence. Outcome Measures: The research team: (1) determined the effects of the combined drugs on cell viability using a methyl thiazolyl tetrazolium (MTT) assay; (2) detected the cell's mitochondrial membrane potential and LDH leakage using "sytox blue, 5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide," CBIC2(3) or JC-1, and lactate dehydrogenase (LDH) assay kits, respectively; (3) detected AtT-20 cell apoptosis using a "terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick-end labeling" (TUNEL) kit; (4) analyzed the expression of protein kinase B (p-Akt), cAMP-response element binding protein (p-CREB), p27, p53, and cyclin E using a Western blot test; (5) detected the mRNA expression of opioid melanin procorticotropin (POMC)), caspase-3, and pituitary tumor transforming gene 1 (PTTG1) using reverse transcription-polymerase chain reaction (RT-PCR); (6) measure the concentration of adreno-cortico-tropic-hormone (ACTH) in the supernatant using an enzyme-linked immunoassay (ELISA) kit; and (7) assessed the cell cycle distribution using flow cytometry. Results: No differences existed in cell viability between the groups at the baseline (0 h) of the culture period (P > .05). Compared to the control group, the intervention group's: (1) cell viability was significantly lower at 4, 8, and 12 hours and postintervention at 16 hours (P < .001); (2) LDH concentration was significantly higher (P < .001); (3) mitochondrial membrane potential was significantly lower (P < .001); (4) apoptosis rate of TUNEL was significantly higher (P < .001 ); (5) expression of p-Akt, p-CREB phosphorylation, and cyclin E was significantly lower (P < .001), (6) expression of p27 and p53 protein was significantly higher (P < .001); (7) mRNA expression of POMC and PTTG1 were significantly lower (P < .001); (8) mRNA expression of caspase-3 was significantly higher (P < .001); (9) concentration of ACTH was lower (P < .001); and (10) percentage of cells in the G0/G1 phase was significantly higher, while the percentage of cells in the S phase was significantly lower (P < .05). Conclusions: Imatinib combined with everolimus can affect the AtT-20 cell cycle through the signaling pathway of the phosphatidylin-ositol-3-kinase (PI3K)/Akt/ protein kinase A (PKA) system and can inhibit cell proliferation and induce cell apoptosis. Therefore, Imatinib and everolimus may be an effective combination of candidates for drugs for mouse pituitary tumor.


Assuntos
Neoplasias Hipofisárias , Camundongos , Animais , Proteínas Proto-Oncogênicas c-akt/metabolismo , Proteínas Proto-Oncogênicas c-akt/farmacologia , Everolimo/farmacologia , Mesilato de Imatinib/farmacologia , Proteína Supressora de Tumor p53/metabolismo , Proteína Supressora de Tumor p53/farmacologia , Caspase 3/metabolismo , Caspase 3/farmacologia , Ciclina E/metabolismo , Ciclina E/farmacologia , Pró-Opiomelanocortina/genética , Pró-Opiomelanocortina/metabolismo , Linhagem Celular Tumoral , Hormônio Adrenocorticotrópico/metabolismo , Apoptose , RNA Mensageiro/farmacologia , Proliferação de Células
3.
J Investig Med ; 70(5): 1273-1279, 2022 06.
Artigo em Inglês | MEDLINE | ID: mdl-35338094

RESUMO

This study aims to evaluate the efficacy and safety of endovascular therapy versus neurosurgical clipping carried out for patients with unruptured middle cerebral artery bifurcation aneurysms (MCABAs). Patients diagnosed with MCABAs were enrolled in this prospective study according to the inclusion and exclusion standard. Enrolled patients were divided into a study group (endovascular therapy) and a control group (neurosurgical clipping), with 65 cases in each group. In terms of efficacy, we found that the proportion of Glasgow Outcome Scale (GOS) grade 1 after treatment in the study group was significantly higher than in the control group (p<0.001), while the proportion of GOS grades 2, 3, and 4 after treatment was significantly lower in the study group than in the control group (p<0.05). The postoperative brain injury indicators neuron-specific enolase and S100ß in the study group were significantly lower than in the control group (p<0.001), and the postoperative life activity score of patients in the study group was significantly higher than in the control group (p<0.001). In terms of safety, the postoperative hospital stay of patients in the study group was significantly shorter than in the control group (p<0.001), and the incidence rate of postoperative pulmonary and intracranial infections in the study group was significantly lower than in the control group (p<0.05). Endovascular therapy for patients with unruptured MCABAs may be effective in improving outcomes and has better safety profile compared with neurosurgical clipping, but may increase the risk of postoperative recurrence.


Assuntos
Procedimentos Endovasculares , Aneurisma Intracraniano , Humanos , Aneurisma Intracraniano/cirurgia , Artéria Cerebral Média/cirurgia , Estudos Prospectivos , Estudos Retrospectivos , Resultado do Tratamento
4.
Biomed Pharmacother ; 92: 33-38, 2017 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-28528183

RESUMO

Quercetin is a flavonoid that has been shown to have anti-oxidation, anti-inflammation, anti-allergic, anti-viral, and anti-cancer activities. Here, we examined the effects of quercetin on cell viability, cell cycle progression, and migration in U251 cells, a human glioblastoma cell line. We found that quercetin inhibited cell proliferation after treating cells for 24 (IC50 of 113.65µg/ml) or 48h (IC50 of 48.61µg/ml). Quercetin treatment also induced apoptosis via deregulating the expression of apoptotic genes, including Bax and Bcl-2, and arrested cell cycle at G2/M phases. We further found that quercetin impaired cell migration and invasion via downregulating the expression of matrix metallopeptidases MMP9 and MMP2. Our results provide evidences that quercetin has inhibitory effects on glioblastoma cell proliferation and invasion, and suggest a potential clinical application for glioblastoma.


Assuntos
Antineoplásicos Fitogênicos/farmacologia , Antioxidantes/farmacologia , Apoptose/efeitos dos fármacos , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Glioblastoma/tratamento farmacológico , Neurônios/efeitos dos fármacos , Quercetina/farmacologia , Linhagem Celular Tumoral , Movimento Celular/efeitos dos fármacos , Proliferação de Células/efeitos dos fármacos , Sobrevivência Celular/efeitos dos fármacos , Fase G2/efeitos dos fármacos , Glioblastoma/metabolismo , Glioblastoma/patologia , Humanos , Metaloproteinase 2 da Matriz/química , Metaloproteinase 2 da Matriz/genética , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/química , Metaloproteinase 9 da Matriz/genética , Metaloproteinase 9 da Matriz/metabolismo , Invasividade Neoplásica , Proteínas de Neoplasias/antagonistas & inibidores , Proteínas de Neoplasias/genética , Proteínas de Neoplasias/metabolismo , Proteínas do Tecido Nervoso/antagonistas & inibidores , Proteínas do Tecido Nervoso/genética , Proteínas do Tecido Nervoso/metabolismo , Neurônios/metabolismo , Neurônios/patologia , Proteínas Proto-Oncogênicas c-bcl-2/antagonistas & inibidores , Proteínas Proto-Oncogênicas c-bcl-2/genética , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Proteína X Associada a bcl-2/antagonistas & inibidores , Proteína X Associada a bcl-2/genética , Proteína X Associada a bcl-2/metabolismo
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