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Following the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 6 on p. 2898, the 'SAH' and 'SAH+NC' data panels contained an apparently overlapping section of data, such that these data appeared to have been derived from the same original source, even though they were intended to show the results from differently performed experiments. The authors have examined their original data, and realize that the 'SAH+NC' data panel had inadvertently been selected incorrectly for this figure. In addition, in response to a further query from the reader, the authors wished to point out that the standard deviations in their study were statistically analysed using GraphPad Prism software version 5.0a. The revised version of Fig. 6, now showing the correct data for the 'SAH+NC' experiment, is shown on the next page. The authors can confirm that the errors associated with this figure did not have any significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 42: 28912902, 2018; DOI: 10.3892/ijmm.2018.3858].
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Background and Objective: Re-vascularization is an effective treatment for moyamoya disease (MMD) patients, including direct re-vascularization, indirect re-vascularization and combined re-vascularization, in which combined re-vascularization is particularly widely used. At present, there are few reports on the analysis of epilepsy after combined re-vascularization surgery. To analysis the risk factors of epilepsy in adult MMD patients after combined re-vascularization. Material and Methods: Patients with MMD who underwent combined re-vascularization in the Department of Neurosurgery of the First People's Hospital of Yunnan Province from January 2015 to June 2020 were included. Their pre-operative and post-operative complication-related indicators were collected. Finally, logistic regression was used to analyze the clinical risk factors of epilepsy in MMD patients after operation. Results: The incidence of epilepsy after combined re-vascularization was 15.5%. Univariate analysis showed that pre-operative ischemic or hemorrhagic stroke, pre-operative epilepsy, pre-operative history of diabetes, the location of the bypass recipient artery (frontal or temporal lobe), post-operative new cerebral infarction, hyper-perfusion syndrome, and post-operative intra-cranial hemorrhage were the clinical risk factors of epilepsy in MMD patients (all P < 0.05). Multi-variate logistic regression analysis showed that pre-operative epilepsy, the location of the bypass recipient artery, new cerebral infarction, hyper-perfusion syndrome, and post-operative intra-cranial hemorrhage (all P < 0.05) were independent risk factors for post-operative epilepsy in MMD patients. Conclusions: Pre-operative epilepsy, the location of the bypass recipient artery, new cerebral infarction, hyper-perfusion syndrome, and intra-cranial hemorrhage may have a causal relationship with epilepsy in adult MMD patients. It is suggested that some risk factors could be intervened to reduce the incidence of post-operative epilepsy in MMD patients.
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Revascularización Cerebral , Epilepsia , Enfermedad de Moyamoya , Humanos , Adulto , Enfermedad de Moyamoya/complicaciones , Enfermedad de Moyamoya/cirugía , China/epidemiología , Infarto Cerebral , Hemorragias Intracraneales , Resultado del Tratamiento , Factores de Riesgo , Epilepsia/epidemiología , Epilepsia/etiología , Epilepsia/cirugía , Revascularización Cerebral/efectos adversos , Estudios RetrospectivosRESUMEN
Early brain injury (EBI) following subarachnoid hemorrhage (SAH) is an important cause of high mortality and poor prognosis in SAH. Bcell lymphoma 2associated X protein inhibitor1 (BI1) is an evolutionarily conserved antiapoptotic protein that is primarily located in the membranes of endoplasmic reticulum (ER). BI1 has been studied in certain nervous systemassociated diseases, but the role of this protein in SAH remains unclear. In the present study, the role of BI1 in EBI following SAH was investigated in rat models and its associated mechanisms were examined. The SAH rat model was generated by inserting nylon cords into the internal carotid artery from the external carotid artery. Samples were assessed using neurological scores, brain water content measurements, hematoxylin and eosin (H&E) staining, bloodbrain barrier (BBB) permeability, terminal deoxynucleotidyl transferasemediated dUTP nickend labeling and quantitative polymerase chain reaction assays, and western blot analyses. It was identified that the mRNA and protein levels of BI1 decreased markedly and were lowest at 24 h after SAH. BI1 overexpression and small hairpin RNA (shRNA)mediated silencing markedly suppressed or severely exacerbated EBI following SAH, respectively. BI1 overexpression in the SAH model improved neurological scores and decreased the brain water content, BBB permeability and levels of apoptosis compared with the control and sham groups following SAH. BI1 shRNA in the SAH model demonstrated contrary results. In addition, the mRNA or protein expression levels of ER stressassociated genes (glucose regulated protein, 78 kDa, C/EBP homologous protein, Serine/threonineprotein kinase/endoribonuclease IRE1, cJun N terminal kinases and apoptotic signaling kinase1) were markedly suppressed or increased following BI1 overexpression and shRNAmediated silencing, respectively. The present study suggested that BI1 serves a neuroprotective role in EBI following SAH by attenuating BBB disruption, brain edema and apoptosis mediated by ER stress.
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Proteínas Reguladoras de la Apoptosis/metabolismo , Lesiones Encefálicas/patología , Estrés del Retículo Endoplásmico , Proteínas de la Membrana/metabolismo , Hemorragia Subaracnoidea/patología , Animales , Apoptosis , Proteínas Reguladoras de la Apoptosis/análisis , Encéfalo/metabolismo , Encéfalo/patología , Edema Encefálico/etiología , Edema Encefálico/metabolismo , Edema Encefálico/patología , Lesiones Encefálicas/etiología , Lesiones Encefálicas/metabolismo , Masculino , Proteínas de la Membrana/análisis , Ratas , Ratas Sprague-Dawley , Hemorragia Subaracnoidea/complicaciones , Hemorragia Subaracnoidea/metabolismoRESUMEN
Objective To investigate the protective effect of lentivirus-mediated BI-1 overexpression on hippocampal neurons in rats with subarachnoid hemorrhage (SAH) and the relationship with endoplasmic reticulum IRE1-JNK signaling pathway. Methods The lentivirus solution of BI-1 over-expression was injected into the brain of rats 24 hours before SAH rat model was established by intravascular puncture method. At 24 hours after modeling, the brain water content and neurological score of the rats were measured. The apoptosis of hippocampal neurons was detected by TUNEL assay. Western blotting was used to detect the expressions of BI-1 protein and endoplasmic reticulum stress (ERS) marker proteins GRP78 and IRE1. ERS in hippocampal neurons of the rats with SAH was intervened by IRE1α-specific inhibitor KIRA6, and then the protein expressions of p-IRE1, p-JNK, Bax, Bcl2 and caspase-3 were detected by Western blotting. Results BI-1 over-expression improved neurobehavioral score, decreased brain water content and hippocampal neuron apoptosis rate, and also down-regulated GRP78 and IRE1 protein levels in the rats with SAH. Both the interference of KIRA6 and the over-expression of BI-1 inhibited the expressions of p-IRE1, p-JNK, Bax and caspase-3, and promoted the expression of anti-apoptotic protein Bcl2. Conclusion Over-expression of BI-1 can inhibit the apoptosis of hippocampal neurons in rats with SAH by inhibiting the activation of ERS-mediated IRE1-JNK signaling pathway, thus ultimately attenuating the early brain injury following SAH.
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Proteínas Reguladoras de la Apoptosis/genética , Apoptosis/genética , Endorribonucleasas/genética , Sistema de Señalización de MAP Quinasas/genética , Proteínas de la Membrana/genética , Complejos Multienzimáticos/genética , Neuronas/metabolismo , Proteínas Serina-Treonina Quinasas/genética , Hemorragia Subaracnoidea/genética , Animales , Proteínas Reguladoras de la Apoptosis/metabolismo , Retículo Endoplásmico/metabolismo , Chaperón BiP del Retículo Endoplásmico , Endorribonucleasas/metabolismo , Expresión Génica , Células HEK293 , Proteínas de Choque Térmico/genética , Proteínas de Choque Térmico/metabolismo , Hipocampo/citología , Humanos , Masculino , Proteínas de la Membrana/metabolismo , Complejos Multienzimáticos/metabolismo , Proteínas Serina-Treonina Quinasas/metabolismo , Ratas Sprague-Dawley , Hemorragia Subaracnoidea/metabolismoRESUMEN
In this study, we analyzed diffusion tensor imaging (DTI) results of brain white matter in rhesus macaques (Macaca mulatta) with four different parameter settings and found that the sequence A (b=1 000 s/mm(2), spatial resolution=1.25 mm×1.25 mm× 1.25 mm, numbers of direction=33, NSA=3) and B (b=800 s/mm(2), spatial resolution=1.25 mm×1.25 mm×1.25 mm, numbers of direction=33, NSA=3) could accurately track coarse fibers. The fractional anisotropy (FA) derived from sequence C (b=1 000s/mm(2), spatial resolution=0.55 mm×0.55 mm×2.5 mm, direction number=33, NSA=3) was too fuzzy to be used in tracking white matter fibers. By comparison, the high resolution and the FA with high contrast of gray matter and white matter derived from sequence D (b=800 s/mm(2), spatial resolution=1.0 mm×1.0 mm ×1.0 mm, numbers of direction=33, NSA=3) qualified in its application in tracking both thick and thin fibers, making it an optimal DTI setting for rhesus macaques.