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Background: The mechanisms that underlie autophagy in cerebral ischemia remain poorly defined. Myeloid cell leukemia-1 (Mcl1), an anti-apoptotic member of the Bcl-2 family of proteins, regulates the balance between autophagy and apoptosis. However, little is known regarding its expression profile and contribution to cell fate in the brain following ischemic stroke. Results: In this study, we investigated the expression profile and cellular distribution of Mcl1 in brains from transient middle cerebral artery occlusion (MCAO) model rats. Brain slices from sham-operated control rats showed minimal immunoreactivity for Mcl1. Mcl1 was mainly produced in neurons. Immunoreactivity for Mcl1 increased as early as 4 hours after MCAO, peaked at 24 hours, and then declined, but still remained high, at 72 hours. Mcl1 positive cells never colocalized with either cleaved caspase-3 or terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cells. Both microtubule-associated protein 1 light chain 3 (LC3) and beclin-1 were evident in ischemic brain between 4 and 72 hours after MCAO. Most cells with strong LC3 staining were also labeled with beclin-1. Beclin-1 did colocalize with caspase-3 or Mcl1. Beclin-1/caspase-3 positive cells displayed the characteristic features of apoptosis including cell shrinkage and pyknotic nuclei, whereas beclin-1/Mcl1 positive cells had normal morphology. Pretreatment with 3-methyladenine attenuated autophagy without affecting the level of Mcl1 protein. Conclusions: These findings demonstrate that the expression of Mcl1 is involved in the survival of neuronal cells. In addition, the coexpression of Mcl1 with beclin-1 may attenuate beclin-1-dependent autophagy during ischemic stroke in rats. [ABSTRACT FROM AUTHOR]

Objective: To explore the effects of clinical indicators, particularly thymectomy on the development of juvenile myasthenia gravis (JMG) through the developmental status of bone age (BA) and height., Methods: A cross-sectional study of 80 JMG patients was recruited to examine whether JMG patients had the abnormalities of height and bone development according to the distribution of height standard deviation score (Ht SDS) and BA., Results: The mean BA was delayed by (0.15 ± 1.32) years compared with patient chronological age (CA). The mean Ht SDS (HtCA SDS -1.25 ± 1.03) was also lower than healthy controls. In multivariate analysis, the age at onset was negatively associated with delayed BA (P=0.007) whereas the cumulative intake of prednisone was negatively associated with HtCA SDS (P=0.043). No significant correlation existed between thymectomy and delayed BA or HtCA SDS. Delayed BA and slow growth existed in JMG patients. The age at onset of JMG was a correlative factor for delayed BA. And the intake of cumulative prednisone might be a determinant of height retardation. Thymectomy had no impact on the development of bone and height., Conclusion: We should pay more attention to monitoring BA and height in JMG patients to take appropriate therapeutic interventions.

Objective: To identify the recurrence-related factors in patients with myasthenia gravis (MG) after extended thymectomy., Methods: Followed up was conducted on 271 MG patients, 127 males and 146 females, aged 31 (4-57), who underwent extended thymectomy for 18-84 months. Post-operational pathological examination showed 32 cases of thymoma and 239 cases of diseases other than thymoma. After operation the patients were treated with pyridostigmine only or combined with adrenocortical hormone. The relevant factors of the 135 patients with relapse were evaluated: sex, Osserman classification, age while being operated on, duration of preoperative period, pathologic type of thymus, use of steroid before operation, infection after operation, whether only taking anticholinesterase drugs after operation, use of steroid immediately after operation, stopping medicine or decreasing the dose of medicine within 1-3 months after remission of symptoms., Results: COX univariate analysis revealed that failure to take steroid immediately after operation (OR = 2.914, P = 0.000), infection after operation (OR = 3.441, P = 0.000), only taking anticholinesterase drugs after operation (OR = 5.947, P = 0.000), and immediately stopping medicine use or decreasing the dose of medicine within 1-3 months after the remission of symptoms (OR = 2.242, P = 0.000) were prognostic factors for postoperative recurrence. On the other hand, multivariate logistic regression analysis revealed that infection after operation (OR = 47.63, P = 0.000), only taking anticholinesterase drugs after operation (OR = 62.38, P = 0.000), and stopping medicine or decreasing the dose of medicine 1-3 months after remission of symptoms (OR = 32.76, P = 0.000) were independent influencing factors of recurrence after operation., Conclusion: Post-operative infection, only taking pyridostigmine, and stopping medicine too early are independent factors of postoperative relapse. Regular treatment and timely use of adrenocortical hormone decrease the recurrence after operation.