Craniocervical decompression with duraplasty and cerebellar tonsillectomy as treatment for Chiari malformation-I complicated with syringomyelia.

This study aimed to investigate the therapeutic effects of craniocervical decompression with duraplasty and cerebellar tonsillectomy for the treatment of Chiari malformation-I with syringomyelia (CM I-SM). From January 2005 to December 2011, 127 patients with CM I-SM underwent craniocervical decompression with duraplasty and cerebellar tonsillectomy and the therapeutic effects of these surgeries were evaluated using Tator scores. No patient in this study died or showed disease deterioration after the surgery. Re-examination by magnetic resonance imaging (MRI) showed that the cisterna magna was obviously larger after the operation in all but one patient. Moreover, syringomyelia (SM) was reduced in 76 patients. CM I-SM symptoms disappeared or decreased in 112 patients after following discharge. Follow-up was conducted in 84 of the patients and 79 of these patients exhibited improved symptoms. A second MRI re-examination showed that the cisterna magna was successfully constructed in 44 patients; 42 of these patients showed further eliminated or obviously reduced SM. Craniocervical decompression with duraplasty and cerebellar tonsillectomy achieved favorable therapeutic effects. Thus, craniocervical decompression with duraplasty and cerebellar tonsillectomy is a rational surgical approach with beneficial clinical effects. The proposed approach may have useful applications in the treatment of CM I-SM.

Transplantation of Human umbilical cord mesenchymal stem cells promotes functional recovery after spinal cord injury by blocking the expression of IL-7.

OBJECTIVE: This research aimed to investigate the therapeutic effects of transplanted human umbilical cord mesenchymal stem cells (hUCMSCs) on spinal cord injury in mice and to explore its molecular mechanism. MATERIALS AND METHODS: Spinal cord injury model in C57BL/6J mice was established. On the 10th day of SCI, hUCMSCs were injected into the center of spinal cord injury area (hUCMSC), and control groups (Control) were injected with an equal amount of medium. Western blotting, Real Time-PCR, immunohistochemistry, and flow cytometry, were used to analyze the content of IL-7, inflammatory cytokines, and macrophages after spinal cord injury in different groups. Open field and Rota-Rod tests were used to determine the effect of hUCMSC transplantation on motor function recovery in SCI mice. RESULTS: Compared with the control mice, hUCMSC transplantation therapy significantly improved the motor function, myelin, and nerve cell survival in spinal cord injury site in SCI mice. It also reduced the expression of IL-7, IFN-γ, and TNF-α in injured sites but increased IL-4 and IL-13 expression and promoted the activation of M2 macrophages at the site of injury. CONCLUSIONS: Transplantation of hUCMSCs in SCI mice can promote the polarization of M2 macrophages by reducing the expression of IL-7 in the injured site, thereby weakening the inflammatory response at the injured site, promoting the repair of the injured site and improving the motor function.

Nrf2-ARE signaling pathway regulates the expressions of A1R and ENT1 in the brain of epileptic rats.

OBJECTIVE: To explore the behavioral changes and the expressions of the A1 receptor (A1R) and balanced nucleoside transporter-1 (ENT1) in the brain of epileptic rats after activating the NF-E2-related factor 2 (Nrf2)-ARE signaling pathway. MATERIALS AND METHODS: Adult male Sprague-Dawley (SD) rats were randomly divided into normal control group, epilepsy group, and t-butylhydroquinone (tBHQ) group, with 10 rats in each group. Lithium-pilocarpine induced epilepsy model in rats was established. The first epileptic latency and seizure frequency within 1 hour were observed in each group using the Racine scoring system. HE (Hematoxylin and Eosin) staining was used to observe the pathological lesions in the brain tissue of each group. The expressions of A1R, ENT1, and relative genes in Nrf2-ARE pathway in rat hippocampus was detected by immunohistochemistry and Western blot. RESULTS: Compared with rats in epileptic group, the first seizure latency was prolonged and the seizure frequency decreased in tBHQ group (p<0.05). The degree of brain lesions in tHBQ group was lighter than that of epilepsy group. ENT1 expression in rat hippocampus of epileptic group was significantly upregulated than that of normal control group and tBHQ group. Besides, the protein levels of A1R, Nrf2, HO-1, and ARE in rat hippocampus of epilepsy group markedly decreased compared with those of normal control group. However, protein expressions of A1R, Nrf2, HO-1, and ARE proteins in rat hippocampus of tBHQ group were markedly upregulated. CONCLUSIONS: Activation of the Nrf2-ARE signaling pathway can reduce the pathological damage of rat hippocampal neurons, prolong the latency of seizures, and reduce the degree of epileptic seizure in rats.

Effects of remote ischemic preconditioning on myocardial injury and endothelial function and prognosis after percutaneous coronary intervention in patients with acute coronary syndrome.

OBJECTIVE: To explore the effects of remote ischemic preconditioning on myocardial injury and prognosis after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome. PATIENTS AND METHODS: The study was a single center, prospective, randomized, controlled study. A total of 184 patients with unstable angina undergoing elective PCI were randomly assigned to remote ischemic preconditioning group (induced by four times of 5-min inflations of a blood pressure cuff to 200 mmHg around the upper arm, followed by 5-min intervals of reperfusion at 1 h before PCI therapy) or control group (an uninflated cuff around the arm). Successful completion of the PCI eventually included 130 cases of patients, including 72 cases in the remote ischemic preconditioning group and 58 cases in the control group. CK-MB, cTnI, sICAM-1, sVCAM-1 and Hs-CRP levels were measured at 6 am. of the day operating PCI and at 24 h after PCI in the two groups. Major adverse cardiac events were recorded of two groups of patients in the postoperative 6 months. (MACE, including recurrence of angina pectoris, myocardial infarction and death). RESULTS: There were no statistically significant differences in baseline indicators between the 2 groups. CK - MB, cTnI, sICAM-1, sVCAM-1 and Hs-CRP levels in patients with remote ischemic preconditioning group were significantly lower than those form the control group after PCI (p < 0.05), but there were no significant differences between the occurrence of MACE in the postoperative 6 months (p > 0.05). CONCLUSIONS: Remote ischemic preconditioning can reduce PCI related myocardial injury and protect vascular endothelial function.