Long non-coding RNA HCG11 silencing protects against cerebral ischemia/reperfusion injury through microRNA miR-381-3p to regulate tumour protein p53.

INTRODUCTION: Long non-coding RNA (LncRNA) plays a critical role in cerebral ischemia-reperfusion (CI/R) injury. The purpose of the current research was to investigate the regulatory role of the LncRNA human leukocyte antigen complex group 11 (HCG11) in CI/R injury and explore its potential mechanism. MATERIAL AND METHODS: The rat middle cerebral artery occlusion (MCAO) model was established to simulate CI/R injury in vivo. mRNA levels of HCG11, microRNA (miR)-381-3p, tumour protein p53, and neuro-inflammatory factors were detected by quantitative reverse transcription PCR (RT-qPCR). Bederson score and Longa score were assessed for neurological deficits. Triphenyl tetrazolium chloride (TTC) staining was used to examine the cerebral infarct volume. What is more, oxidative stress was evaluated by the commercial kit. Finally, the relationship between HCG11, miR-381-3p, and p53 was verified by a dual-luciferase reporter assay. RESULTS: HCG11 was elevated in MCAO rats. And it competitively bound miR-381-3p and down-regulated the expression of p53. Inhibition of HCG11 inhibited cerebral infarct volume and neurological deficits in MCAO rats, and inhibited the secretion of neuro-inflammation and the over-activation of oxidative stress, exerting the protective effect of CI/R injury. However, inhibition of miR-381-3p in rats significantly weakened the protective effect of depression of HCG11 in MCAO rats, resulting in increased cerebral infarction volume and neurological deficits, elevated neuro-inflammatory secretion, and oxidative stress activation. CONCLUSIONS: The present research shows that LncRNA HCG11 silencing protects against cerebral ischemia/reperfusion injury through miR-381-3p to regulate p53.

Effect of temozolomide on survival in elderly patients with glioblastoma and impaired performance status: a propensity score-matching analysis.

OBJECTIVE: At present, there is no consensus regarding the standard treatment for glioblastoma (GBM) in elderly patients with impaired Karnofsky performance status (KPS) scores. This study aimed to determine the effects of temozolomide (TMZ) versus best supportive care (BSC) in this population. MATERIALS AND METHODS: We conducted a retrospective observational study of patients aged ≥65 years with histologically confirmed GBM and KPS scores ≤70 who were treated at our institution between January 2006 and July 2014. Demographic data, treatments, and outcomes were evaluated. Univariate and multivariate analyses were performed to identify the independent prognostic factors of overall survival (OS) and progression-free survival (PFS). The impact of TMZ on survival was analyzed by the application of propensity score matching of clinicopathological factors among patients who received TMZ vs BSC. RESULTS: There were 153 patients (86 men, 56.2%) in this study. The median patient age was 70 years (range: 65-83 years). The median KPS score was 60 (range: 30-70). Seventy-eight patients (51.0%) received TMZ, whereas 75 (49.0%) received BSC. Median OS and PFS were 6.0 and 4.5 months, respectively. Compared with BSC, TMZ was associated with improved OS (hazard ratio [HR]: 0.38, 95% CI: 0.17-0.70; P=0.002) and PFS (HR: 0.41, 95% CI: 0.21-0.76; P=0.003) after propensity score matching. Factors independently associated with OS were KPS score (HR: 2.11, 95% CI: 1.48-7.67; P=0.016), extent of resection (HR: 1.98, 95% CI: 1.45-5.14; P=0.026), and treatment group (HR: 0.49, 95% CI: 0.23-0.87; P=0.019). The most frequent toxicity in the TMZ group was myelosuppression. CONCLUSION: Compared with BSC, TMZ increased survival with acceptable toxicity in elderly GBM patients with KPS scores ≤70.

Mucin 1 and poly I:C activates dendritic cells and effectively eradicates pituitary tumors as a prophylactic vaccine.

Pituitary tumors are the most common type of cancer within the central nervous system. In the present study, the expression levels of mucin 1 (Muc1) were examined in invasive and non­invasive pituitary tumor samples, and the results of immunohistochemical staining and Western blot analysis demonstrated marked positive expression of Muc1. In addition, Muc1 + polyinosinic:polycytidylic acid (poly I:C) was found to stimulate the expression levels of the surface molecules cluster of differentiation (CD)40, CD83 and CD80, and HLA­DRm and decreased the expression of CD14 in the dendritic cells, determined using fluorescence­activated cell sorting. The secretions of interleukin (IL)­6, tumor necrosis factor­α and IL­1ß cytokines were also significantly induced, in a dose­dependent manner. In in vivo experiments, a higher percentage of CD3+CD4+ T lymphocytes was detected, and the levels of interferon­Î³ and IL­2 in the splenocytes were also upregulated. Furthermore, the combination treatment of Muc1 with poly I:C increased anti­Muc1 IgM and anti­Muc1 IgG titers, and altered the balance of IgG2a and IgG1, all of which increased the T helper (Th)1 polarized immune response. Thus, the tumor antigen, Muc1, with poly I:C may produce potent protective effects, which polarize immune responses towards Th1, and elicit antitumor immunity to inhibit the progression of pituitary tumors.

[CLINICAL RESEARCH AND DISCUSSION OF MODIFIED CRANIOPLASTY].

OBJECTIVE: To study and design a modified cranioplasty, and to explore the effectiveness so as to reduce the incidence rate of operative complications. METHODS: A total of 68 patients with craniocerebral trauma or hypertensive cerebral hemorrhage between August 2012 and March 2014 were selected and randomly divided into 2 groups. The standard decompress craniectomy and under-temporal cranioplasty were performed in 32 cases (group A), and several small bone chips were placed under-tempus during decompress craniectomy and then the shape of temporal muscle was designed and the temporal muscle was reconstructed at the attachment sites during cranioplasty in 36 cases (group B). No significant difference was found in gender, age, side of operation, cause of injury, time between injury and decompress craniectomy, and time between postoperation and cranioplasty between 2 groups (P > 0.05). Then the postoperative complications were compared between the 2 groups. RESULTS: Primary healing of incision was obtained in all patients. The patients were followed up 12 months on average (range, 6-16 months) in 2 groups. The follow complications occurred in group A: 4 cases of asymmetric appearance (12.50%), 12 cases of temporal muscle atrophy (37.50%), 6 cases of temporal pain and masticatory atonia (18.75%), 2 cases of epilepsy (6.25%), 9 cases of leakage of cerebrospinal fluid (28.13%), 1 case of cerebral contusion and laceration (3.13%), and 1 case of cerebral hemorrhage (3.13%); temporal muscle atrophy was observed in 2 cases (5.56%) and the rate of complication was significantly lower than that in group A (P < 0.05). The symmetrical appearance of the skull and good function were achieved in the other patients having no complication. CONCLUSION: New technique of setting bone chip markers during decompress craniectomy and reconstructing temporal muscle during cranioplasty can reduce the incidence of complications and thus it is an effective surgical procedure.