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Zhu J.,Jinan Central Hospital Affiliated to Shandong UniversityJinan | Li H.,The Sixth Peoples Hospital of Jinan | Gu K.,Interventional Radiology | Zhao G.,Rehabilitation Medicine | And 2 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2016

Objective: To investigate the clinical characteristics of and prognostic factors for patients with glioma so as to provide a basis for improving its treatment and diagnosis. Methods: A retrospective analysis was made for the clinical characteristics and follow-up data of 216 patients with glioma admitted in the department of neurosurgery of our hospital from February 2009 to June 2014. A Cox proportional hazards regression model was used to investigate the prognostic factors for patients with glioma. Results: Among all included patients with glioma, 75.5% (163/216) patients had astrocytoma and their main symptoms included headache (77.8%, 164/216) and physical weakness (48.1%, 104/216) without specific clinical manifestations. The one-year and three-year survival rates of patients with glioma were 80.1% and 45.4% respectively and the median survival time was 30 months. Univariate analysis showed that the survival rates among patients with different age, tumor grade, tumor size, extent of tumor resection, KPS score and Ki-67 expression level were of statistically significant difference (P<0.05). Multivariate Cox regression showed that age >45 years (RR=1.75, 95% CI: 1.06-2.90) and pathological grading of III-IV (RR=3.39, 95% CI: 1.61-7.16) were independent prognostic factors and tumor total resection (RR=0.55, 95% CI: 0.37-0.84) and preoperative KPS score ≥70 points (RR=0.70, 95% CI: 0.51-0.95) protective prognostic factors (P<0.05). Conclusion: Patients with glioma have no specific clinical manifestation. Glioma patients with older age (>45 years), higher tumor grade, non-total resection and low preoperative KPS scores are more likely to undergo bad prognosis. © 2016, E-Century Publishing Corporation. All rights reserved.

Hao M.,Shandong University | Li X.,The Sixth Peoples Hospital of Jinan | Feng J.,Shandong University | Pan N.,Shandong University
Inflammation | Year: 2015

Inflammatory response plays an important role in the pathogenesis of ischemic stroke and anti-inflammatory agents may provide a choice of treatment. Triptolide is reported to be anti-inflammatory. In this study, we investigated the effects of triptolide on cultured neuronal cell line in vitro and experimental ischemic stroke in vivo. Oxygen–glucose deprivation (OGD) and tumor necrosis factor-α (TNF-α) stimulated SH-SY5Y cells were incubated with triptolide. In vivo, rats were subjected to middle cerebral artery occlusion (MCAO) for 1 h, followed by reperfusion for 23 h. Results of this study showed that triptolide treatment reduced the OGD-induced cytotoxicity and apoptosis and blocked TNF-α-induced activation of NF-κB and p38MAPK in SH-SY5Y cells. Intraperitoneal injection of triptolide showed significant neuroprotective actions in stroke rats. Triptolide attenuated neurological deficit, brain infarct volume, and brain water content, and inhibited activation of NF-κB and p38MAPK. These data show that triptolide protects rats against ischemic cerebral injury via inhibiting NF-κB and p38MAPK signaling pathways. © 2015, Springer Science+Business Media New York.

Wang J.,Shandong University of Traditional Chinese Medicine | Lu S.,Shandong University of Traditional Chinese Medicine | Zhao S.,The Sixth Peoples Hospital of Jinan
Pakistan Journal of Medical Sciences | Year: 2016

Objective: To compare the post-infectious irritable bowel syndrome (PI-IBS) and none post-infectious irritable bowel syndrome (NPI-IBS) clinically and experimentally. Methods: From May 2013 to January 2015, eighty-nine patients with irritable bowel syndrome (IBS)were recruited in the internal department of the affiliated hospital of Shandong University of Traditional Chinese Medicine. The clinical data were collected for all the patients, and a blood sample was collected to detect the level of C-reactive protein (CRP) and intestinal fatty acid binding protein (IFABP), an investigation questionnaire of gastrointestinal symptom rating scale (GSRS) and self-rating anxiety scale (SAS) were carried out to evaluate the gastrointestinal function and anxiety status. Results: In the study, forty-eight patients were included in PI-IBS group and 41 in Non-PI-IBS group. There was no significant difference in age, gender and GSRS between the two groups (p>0.05). In PI-IBS group 70.8% patients presented with the primary symptom of diarrhea and 60.4% presented with a SAS scores over 50, but in Non-PI-IBS group, the values were only 19% (p<0.05) and 34.1% (p<0.05). The level of IFABP and CRP were significantly higher in PI-IBS group than those in Non-PI-IBS group (p<0.05). Conclusion: The PI-IBS may be different from Non-PI-IBS in mechanism and should be treated using different strategies. © 2016, Professional Medical Publications. All rights reserved.

Miao G.,Shandong University | Liu Z.,Shandong University | Wei S.,The Sixth Peoples Hospital of Jinan | Luo J.,Shandong University | And 2 more authors.
Neuroscience | Year: 2015

Inflammatory response induced by protrused nucleus pulposus (NP) has been shown to play a crucial role in the process of radicular pain. Lipoxins represent a unique class of lipid mediators that have anti-inflammatory and pro-resolving action. The present study was undertaken to investigate if intrathecal lipoxin A4 (LXA4) could alleviate mechanical allodynia in the rat models of application of NP to the L5 dorsal root ganglion (DRG). Non-compressive models of application of NP to L5 DRG were established and intrathecal catheterization for drug administration was performed in rats. Daily intrathecal injection of vehicle or LXA4 (10ng or 100ng) was performed for three successive days post-operation. Mechanical thresholds were tested and the ipsilateral lumbar (L4-L6) segment of spinal dorsal horns were removed for the determination of tumor necrosis factor-α (TNF-α), IL-1β, transforming growth factor-β1 (TGF-β1) and IL-10 expression and NF-κB/p65, extracellular signal-regulated kinase (ERK), C-Jun N-terminal kinase (JNK) and P38 expression. Application of NP to DRG in rats induced mechanical allodynia, increased the expression of pro-inflammatory factors (TNF-α and IL-1β), NF-κB/p65, the phosphorylated-ERK (p-ERK), -JNK (p-JNK) and -P38 (p-p38) and decreased the expression of anti-inflammatory cytokines (TGF-β1 and IL-10) in the ipsilateral lumbar (L4-L6) segment of spinal dorsal horns. Intrathecal injection of LXA4 alleviated the development of neuropathic pain, inhibited the upregulation of pro-inflammatory cytokines (TNF-α and IL-1β), upregulated the expression of anti-inflammatory cytokines (TGF-β1 and IL-10) and attenuated the activation of NF-κB/p65, p-ERK, p-JNK, but not p-p38, in a dose-dependent manner.In this study, we have demonstrated that LXA4 potently alleviate radicular pain in a rat model of non-compressive lumbar disc herniation. The anti-inflammatory and pro-resolution properties of LXA4 have shown a great promise for the management of radicular pain caused by intervertebral disc herniation. © 2015 IBRO.

Wang X.,The Sixth Peoples Hospital of Jinan | Jia L.,The Sixth Peoples Hospital of Jinan | Jin X.,The Sixth Peoples Hospital of Jinan | Liu Q.,The Sixth Peoples Hospital of Jinan | And 4 more authors.
Oncology Letters | Year: 2015

Glioblastoma multiforme (GBM) demonstrates an unsatisfactory clinical prognosis due to the intrinsic or acquired resistance to temozolomide (TMZ) exhibited by the tumors. One possible cause of TMZ resistance in GBM is the overexpression of O6‑methylguanine‑DNA methyltransferase (MGMT), which can repair the TMZ‑induced guanine damage in DNA. Additionally, excessive activated NF‑κB is reported to be a component of the major inflammatory transcription pathway that is associated with TMZ resistance in GBM. However, the association between the NF‑κB pathway and MGMT expression in GBM cells is unknown. Therefore, in the present study, the TMZ resistant (TR) U251 cell line (TR/U251) was successfully constructed to detect how the TR/U251 cell line and the parental U251 cell line each interact with TMZ in vitro. The TR/U251 cells were approximately five times more resistant to TMZ compared with the parental cells. Furthermore, it was found that the NF‑κB inhibitor BAY 11‑7082 suppressed the expression of MGMT in TR/U251 cells and enhanced TMZ‑induced cytotoxicity and apoptosis, thereby indicating that the NF‑κB pathway and MGMT interact to promote TMZ resistance. The inhibition of NF‑κB may be a promising strategy to reverse drug resistance in TR glioma cells. The present results propose a potential mechanism for using the NF‑κB inhibitor BAY 11‑7082 as a potential therapy for the treatment of TR glioma. Although BAY 11‑7082 is a well‑known NF‑ κB inhibitor, the present study further investigated its underlying mechanisms through a series of new experiments. © 2015, Spandidos Publications. All Rights Reserved.

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