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Objective To investigate the effects and mechanisms of median nerve electrical stimulation on synaptic plasticity in ischemic stroke rats.Methods 18 healthy male SD rats were randomly divided into Sham group(n = 6),ischemic stroke group(MCAO group,n = 6)and median nerve electrical stimulation group(MNES group,n = 6).The left middle cerebral artery occlusion model of rats was established by thread plug method.Thread plug was not inserted in sham group.The median nerve electrical stimulation group was given median nerve electrical stimulation intervention on the 3rd day after modeling,and intervention on the next day.After intervention for 7 times,behavioral detection,HE staining was used to detect median nerve injury.Nissl staining was used to detect cerebral infarction volume.Western blot was used for detection of the expression level of proteins related to synaptic plasticity,and electron microscopy was performed.Results HE staining showed that median nerve electrical stimulation did not cause damage to the median nerve in stroke rats,and the median nerve membrane was intact without obvious inflammatory cells.Compared with MCAO group,the neural function,motor function and coordination of the injured forelimb in MNES group were significantly improved(P<0.01).Compared with MCAO group,cerebral infarction volume in MNES group was significantly reduced(P<0.05),the pyknosis of Nissl bodies in ischemic penumbra decreased.Compared with MCAO group,the expression levels of synaptic plastication-related proteins PSD95 and synI in the cortex of MNES group were significantly up-regulated after median nerve electrical stimulation(P<0.05),the number of synapses in the ischemic cortex increased significantly(P<0.01).Conclusion Median nerve electrical stimulation is a safe and effective therapeutic measure to improve nerve function after stroke,and its mechanism is related to promoting synaptic plasticity.
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After ischemic stroke, the key to reduce the mortality and disability rate is to restore the blood supply of brain tissue as soon as possible. However, the cerebral ischemia-reperfusion injury (CIRI) caused by blood flow restoration is also an important cause of brain tissue structural damage and dysfunction. Studies in recent years have shown that the activation of mitophagy at CIRI stage can reduce the volume of cerebral infarction and protect neurons from CIRI, while excessive or insufficient mitophagy can aggravate CIRI. This suggests that inducing moderate mitophagy may be a potential therapeutic target for neuroprotection after stroke. However, the neuroprotective mechanism of mitophagy has not yet been fully elucidated. This article reviews the neuroprotective mechanism and potential application of mitophagy in stroke, and discusses some problems of mitophagy as a therapeutic target for stroke.
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Objective To evaluate the relationship between the early incidence of postoperative complications and renal pelvic pressure during minimally invasive percutaneous nephrolithotomy. Methods 133 renal calculi patients were monitored during MPCNL. Then the patients were separated into two groups according to the renal pelvic pressure,and the postoperative fever,the perirenal fluid and impairment of renal function were analyzed. Results The average body temperature was higher in high pelvic pressure group than that in low pelvic pressure group from the first day to the fourth day after operation(P<0. 05). The urinary protein of all patients raised obviously after the op-eration while it decreased gradually afterward. The urinary protein of the high pelvic pressure group was much higher than that of the low pel-vic pressure group in same day with a significant difference (P<0. 05). The incidence of perirenal fluid was much higher in high pelvic pres-sure group than that in low pelvic pressure group (P<0. 05). Conclusion The incidence of early postoperative complications was related to renal pelvic pressure during MPCNL.
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<p><b>BACKGROUND</b>Laparoscopic cholecystectomy has been widely used in clinical practice during the recent decades; however, the effects of pneumoperitoneum and the surgery on the coagulation system are largely unknown. This clinical study aimed to observe any possible effects of pneumoperitoneum and the surgery on the coagulation system of patients.</p><p><b>METHODS</b>This was a prospective observational study. The inclusion criteria included (1) patients with chronic cholecystitis and/or cholecystic polyps and (2) patients in the relief stage of acute cholecystitis. The exclusion criteria included (1) patients in the episodic stage of acute cholecystitis and those complicated with cholangiolithiasis; (2) patients with concomitant hematologic diseases, damages to the liver function, malignant tumors or immune system diseases, or patients complicated with thrombotic or hemorrhagic disorders; and (3) patients who had taken anticoagulant medication within a week before surgery. Fifty patients who were hospitalized into our department for elective laparoscopic cholecystectomy between November 2011 and February 2013 were eligible and enrolled into this study. Of the 50 patients, 22 were male and 28 female. The age of the patients ranged from 29 to 78 (mean 56.7±11.5) years. The surgery for each of the 50 patients was performed with the same equipment and conditions. The surgeries for all the patients were performed under general anesthesia with the patients in a 30-degree head-up tilted posture, and the pressure of pneumoperitoneum was maintained at 13 mmHg. Venous blood specimens were taken from each patient before and at the end of pneumoperitoneum (i.e., 0 hour after surgery) and at 8 hours after surgery for determination of prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (Fib), thrombin time (TT), and D-dimer (DD). The results of the determinations of these parameters were compared.</p><p><b>RESULTS</b>(1) All the patients recovered well without any complications. (2) The pre-pneumoperitoneum values of the parameters of coagulation had normalized. (3) The PT values slightly increased (P > 0.05) at the end of pneumoperitoneum (i.e., 0 hour after surgery) and decreased by 0.5 seconds at 8 hours after surgery as compared to the pre-pneumoperitoneum values (P < 0.05). (4) APTT at 0 and 8 hours decreased by 1.4 seconds (P > 0.05) and 3.7 seconds (P < 0.05) respectively as compared to pre-pneumoperitoneum values, while the difference between the APTT values at 0 and 8 hours after surgery was not statistically significant (P > 0.05). (5) FIB determined at 0 hour post-operation increased by 0.1 g/L as compared to pre-pneumoperitoneum values (P > 0.05); however, the FIB values at 8 hours after operation increased by 1.2 g/L as compared to the pre-pneumoperitoneum values (P < 0.05), and increased by 1.1 g/L as compared to 0 hour post-operation (P < 0.05). (6) The TT values obtained at 0 and 8 hours post-operation were not significantly different as compared to the pre-pneumoperitoneum values (P > 0.05). (7) The DD values gradually increased after operation; as compared to pre-pneumoperitoneum values, DD at 0 and 8 hours after operation increased by 210.8 ng/ml and 525.9 ng/ml respectively (P < 0.05) and DD at 8 hours after operation increased by 315.1 ng/ml as compared to 0 hour post-operation (P < 0.05).</p><p><b>CONCLUSIONS</b>The pneumoperitoneum for laparoscopic cholecycstectomy may lead to postoperative hypercoagulation in the patients, and thereby may increase the risks for development of postoperative thrombosis; Patients may have risks for occurrence of thrombosis within 8 hours after the operation, to which attention should be paid in favor of preventing thrombosis.</p>