Endoscopic treatment of suprasellar cysts without hydrocephalus.

OBJECTIVE At present, endoscopic treatment is advised as the first procedure in cases of suprasellar arachnoid cysts (SSCs) with hydrocephalus. However, the appropriate therapy for SSCs without hydrocephalus has not been fully determined yet because such cases are very rare and because it is usually difficult to perform the neuroendoscopic procedure in patients without ventriculomegaly given difficulties with ventricular cannulation and the narrow foramen of Monro. The purpose of this study was to find out the value of navigation-guided neuroendoscopic ventriculocystocisternostomy (VCC) for SSCs without lateral ventriculomegaly. METHODS Five consecutive patients with SSC without hydrocephalus were surgically treated using endoscopic fenestration (VCC) guided by navigation between March 2014 and November 2015. The surgical technique, success rate, and patient outcomes were assessed and compared with those from hydrocephalic patients managed in a similar fashion. RESULTS The small ventricles were successfully cannulated using navigational tracking, and the VCC was accomplished in all patients. There were no operative complications related to the endoscopic procedure. In all patients the SSC decreased in size and symptoms improved postoperatively (mean follow-up 10.4 months). CONCLUSIONS Endoscopic VCC can be performed as an effective, safe, and simple treatment option by using intraoperative image-based neuronavigation in SSC patients without hydrocephalus. The image-guided neuroendoscopic procedure improved the accuracy of the endoscopic approach and minimized brain trauma. The absence of hydrocephalus in patients with SSC may not be a contraindication to endoscopic treatment.

PCSK9 regulates apoptosis in human neuroglioma u251 cells via mitochondrial signaling pathways.

Proprotein convertase subtilisin/kexin type 9 (PCSK9), belongs to a family of proprotein convertases (PCs), encodes a neural apoptosis-regulated convertase 1. However, the precise role of PCSK9 during glioma cells apoptosis has not been reported. Therefore, we examined the effects of knockdown and overexpression of PCSK9 on apoptosis of human neuroglioma U251 cells, and investigated the underlying mechanisms of apoptosis. We found that PCSK9 regulated cells proliferation as determined by CCK-8 and Hoechst staining analysis. In addition, western blot results showed that PCSK9 siRNA promote apoptosis via activation of caspase-3 and down-regulation of the anti-apoptotic proteins, XIAP and p-Akt, while PCSK9 overexpression inhibited apoptosis. Moreover, PCSK9 siRNA improved the ratio of Bax/Bcl-2 which leads to the release of cytochrome c, while PCSK9 overexpression decreased it. Taken together, these data demonstrate that PCSK9 may regulate apoptosis through mitochondrial pathway and is expected to be a promising therapeutic strategy for the malignant glioma.

Loss of 15-hydroxyprostaglandin dehydrogenase indicates a tumor suppressor role in pituitary adenomas.

15-hydroxyprostaglandin dehydrogenase (15-PGDH) may function as a tumor suppressor that antagonizes the action of the cyclooxygenase-2 (COX-2) oncogene in several types of tumors. However, it is unknown if it has a role in the pituitary. Recently, our group found that 15-PGDH expression was low in prolactin (PRL) secreting adenomas (prolactinomas) and growth hormone (GH) secreting adenomas (GHomas) using fiber-optic BeadArray technology. In this study, we examined the relative expression of 15-PGDH and COX-2 mRNA in clinical specimens and examined the effects of 15-PGDH on GH3 rat pituitary tumor cell proliferation, apoptosis and hormone secretion. 15-PGDH expression was lower and COX-2 expression was higher in prolactinomas and GHomas compared with normal controls. Overexpressed 15-PGDH inhibited tumor cell proliferation and induced apoptosis. It had a significant suppressive effect on mRNA levels and on the secretion of PRL and GH in GH3 cells. The inhibition of cell proliferation was accompanied by the decreased expression of cox-2, matrix metalloproteinase-9 (MMP-9) and B cell leukemia/lymphoma-2 (Bcl-2). These data are suggestive of a previously unrecognized pathway in pituitary tumorigenesis, and this novel observation may shed light on therapeutic strategies for pituitary tumors.

[Regulation of MAVS-mediated pathway by p21].

AIM: To study the interaction between MAVS and p21 regulates MAVS-mediated pathway. METHODS: Firstly, we cloned full-length p21 gene by PCR. And then the interaction between MAVS and p21 was further demonstrated by co-immunoprecipitation. The regulation of MAVS-mediated pathway by p21 was analyzed by luciferase reporter assays. RESULTS: There are interaction between p21 and MAVS in 293T cells. p21 downregulates activity of MAVS. CONCLUSION: It is shown that p21 inhibits MAVS-mediated activation of NF-κB and IFN-ß by Luciferase reporter assays. Overall, these results laid the foundation for further investigating the function of p21 in MAVS-mediated pathway.

[Lethal anaphylactic shock model induced by human mixed serum in guinea pigs].

OBJECTIVE: To establish an anaphylactic shock model induced by human mixed serum in guinea pigs. METHODS: Eighteen guinea pigs were divided into two groups: sensitized and control, The sensitized group were immunized intracutaneously with human mixed serum and then induced by endocardiac injection after 3 weeks. RESULTS: Symptoms of anaphylactic shock appeared in the sensitized group. The level of serum IgE were increased in the sensitized group significantly. CONCLUSIONS: An animal model of anaphylactic shock wer established successfully. It provide a tool for both forensic study and anaphylactic shock therapy.