CSF leukocyte, polykaryocyte, protein and glucose: Their cut-offs of judging whether post-neurosurgical bacterial meningitis has been cured.

OBJECT: This paper is aimed to explore a reasonable guideline for distinguishing whether post-neurosurgical bacterial meningitis has completely been cured, so as to avoid the deficient or excessive treatment for post-neurosurgical bacterial meningitis. PATIENTS AND METHODS: We conducted a retrospective analysis of 46 patients who attended General Hospital of Chinese People's Armed Police Force in Beijing, China, from January 1, 2014 to April 30, 2016. The CSF leukocyte, polykaryocyte, protein and glucose had been tested when their antibiotic treatments were empirically stopped. Between the non-relapse and relapse groups, Wilcoxon Rank Sum test was used to compare the differences of CSF leukocyte and polykaryocyte, and t-test was applied to contrast the distinctions of CSF protein and glucose, then, the thresholds of significant items were estimated by ROC curve. RESULTS: The CSF leukocyte counts in non-relapse group are 23.72 ± 14.12/mm3, which are statistically less than the relapse group's (47.00 ± 1.00/mm3, P = 0.014), so does the CSF polykaryocyte counts (1.74 ± 4.84/mm3 &4.67 ± 1.15/mm3, P = 0.012). Between the two groups, the AUCs of leucocyte and polykaryocyte are 0.926 (95% CI = 0.845-1.0, P = 0.014) and 0.884 (95%CI = 0.786-0.982, P = 0.028), respectively. Their critical values are 44/mm3 (sensitivity = 1, specificity = 0.907) and 3/mm3 (sensitivity = 1, specificity = 0.837). Conversely, CSF protein and glucose have no statistic differences between the two groups. CONCLUSION: Both CSF leukocyte and polykaryocyte can satisfactorily indicate whether the post-neurosurgical bacterial meningitis has completely been cured, 0-44/mm3 is recommended as the reference range of CSF leukocyte, and the CSF polykaryocyte' s is 0-3/mm3.

Increased Levels of Soluble Cluster of Differentiation 40 Ligand, Matrix Metalloproteinase 9, and Matrix Metalloproteinase 2 Are Associated with Carotid Plaque Vulnerability in Patients with Ischemic Cerebrovascular Disease.

OBJECTIVES: The objectives of this study were to examine the correlation between the level of serum inflammatory markers and the stability of carotid plaques in patients with ischemic cerebrovascular disease and to assess the ability of each inflammatory marker to identify vulnerable carotid plaques. METHODS: For the early identification of vulnerable carotid plaques, 65 patients with carotid plaques were divided into a stable plaque group (n = 21) and an unstable plaque group (n = 44) according to magnetic resonance imaging characteristics. The unstable plaque group was divided into an unstable unruptured plaque group (n = 29) and an unstable ruptured plaque group (n = 15) according to whether the fibrous cap was ruptured. The levels of serum soluble cluster of differentiation 40 ligand (sCD40L), matrix metalloproteinase (MMP)-9, and MMP-2 were measured by enzyme-linked immunosorbent assay. RESULTS: The levels of serum sCD40L and MMP-9 in the unstable plaque group, the unstable unruptured plaque group and the ruptured plaque group were significantly higher than those in the stable plaque group (P < 0.05). There was no significant difference in the MMP-2 level between the stable plaque group and unstable plaque group (P = 0.056). The MMP-2 levels in the stable plaque group, unstable unruptured plaque group, and ruptured plaque group were not different (P = 0.095). The carotid plaques and the positive rate of MMP-9 of ≥84.09 ng/mL were statistically significant, suggesting increased vulnerability. CONCLUSIONS: Serum levels of sCD40L and MMP-9 are associated with the stability of carotid plaques. Higher levels of serum sCD40L and MMP-9 may suggest that the plaques are vulnerable or have ruptured.

Saikosaponin a protects TBI rats after controlled cortical impact and the underlying mechanism.

The inflammatory response plays a significant role in neuronal cell death and functional deficits after Traumatic brain injury (TBI). Importantly, anti-inflammatory agents have neuroprotective effects. To date, however, no studies have investigated the neuroprotective effects of Saikosaponin a (SSa) after TBI. In the present study, rats with controlled cortical impact (CCI) were used to investigate the neuroprotective effects of SSa. The results showed that SSa reduced body weight loss, improved neurological functions andcognition, and reduced brain edema and blood brain barrier permeability after CCI. Moreover, SSa inhibited aquaporin-4 (AQP-4), matrix metalloprotein-9 (MMP-9), mitogen-activated protein kinase (MAPK), c-Jun N-terminal kinase (c-JNK), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). The reduction in the loss of occludin mediated by SSa may partially account for its neuroprotective effects. Together, our results suggest that SSa appears to counteract the inflammatory response and neurological function deficits after TBI and possibly via an anti-inflammatory response and inhibition of the MAPK signaling pathway.

Decompressive craniectomy for severe traumatic brain injury patients with fixed dilated pupils.

OBJECTIVE: The outcome of decompressive craniectomy (DC) for severe traumatic brain injury (sTBI) patients with fixed dilated pupils (FDPs) is not clear. The objective of this study was to validate the outcome of DC in sTBI patients with FDPs. PATIENTS: We retrospectively collected data from 207 sTBI patients with FDPs during the time period of May 4, 2003-October 22, 2013: DC group (n=166) and conservative care (CC) group (n=41). MEASUREMENTS: Outcomes that were used as indicators in this study were mortality and favorable outcome. The analysis was based on the Glasgow Outcome Scale recorded at 6 months after trauma. RESULTS: A total of 49.28% patients died (39.76% [DC group] vs 87.80% [CC group]). The mean increased intracranial pressure values after admission before operation were 36.20±7.55 mmHg in the DC group and 35.59±8.18 mmHg in the CC group. After performing DC, the mean ICP value was 14.38±2.60 mmHg. Approximately, 34.34% sTBI patients with FDPs in the DC group gained favorable scores and none of the patients in the CC group gained favorable scores. CONCLUSION: We found that DC plays a therapeutic role in sTBI patients with FDPs, and it is particularly important to reduce intracranial pressure as soon as possible after trauma. For the patients undergoing DC, favorable outcome and low mortality could be achieved.

CARMA3 is overexpressed in human glioma and promotes cell invasion through MMP9 regulation in A172 cell line.

Caspase recruitment domain-containing membrane-associated guanylate kinase protein 10 or CARMA3 (CARD10) is a recently characterized oncoprotein involved in the progression of several human malignancies. The present study aims to investigate the expression pattern and biological roles of CARMA3 protein in human glioma. CARMA3 expression was analyzed in 97 glioma specimens using immunohistochemistry. We observed negative staining in normal astrocytes and positive staining of CARMA3 in 25 out of 97 (25.8%) glioma samples. Overexpression of CARMA3 correlated with tumor grade (p < 0.001). Small interfering RNA knockdown was performed in A172 cell line with relatively high CARMA3 expression. Using colony formation assay and Matrigel invasion assay, we showed that CARMA3 depletion in A172 cell line inhibited cell proliferation and cell invasion. In addition, mRNA and protein levels of matrix metallopeptidase 9 (MMP9) were downregulated, indicating CARMA3 might regulate invasion through MMP9. In conclusion, CARMA3 serves as an oncoprotein in human glioma by regulating cell invasion, possibly through MMP9 regulation.

Glioma risks associate with genetic polymorphisms of XRCC1 gene in Chinese population.

Glioma is the most common type of primary brain tumors in adults. Previous evidence indicates that the X-ray repair cross-complementing group 1 gene (XRCC1) is an important candidate gene which influencing the pathogenesis of glioma. This study aims to assess the potential associations between glioma risks and genetic polymorphisms of XRCC1 gene. A total of 1,286 Chinese Han ethnic subjects consisting of 638 glioma patients and 648 controls were recruited in this case-control study. The genotyping of XRCC1 genetic polymorphisms (c.482C>T, c.1161G>A, and c.1804C>A) were conducted using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), created restriction site-PCR (CRS-PCR) and DNA sequencing methods. Our data indicated that the allelic and genotypic frequencies of these genetic polymorphisms in glioma patients were significantly different from those of controls. We detected that the alleles/genotypes were statistically associated with the increased risks of glioma (for c.482C>T, TT versus (vs.) CC: OR = 2.24, 95% CI = 1.48-3.39, P < 0.001; T vs. C: OR = 1.30, 95% CI = 1.09-1.53, P = 0.003; for c.1161G>A, AA vs. GG: OR = 1.62, 95% CI = 1.11-2.35, P = 0.012; A vs. G: OR = 1.19, 95% CI = 1.01-1.41, P = 0.040; for c.1804C>A, AA vs. CC: OR = 2.12, 95% CI = 1.45-3.11, P < 0.001; A vs. C: OR = 1.32, 95% CI = 1.12-1.56, P = 0.001). Our findings suggest that these genetic polymorphisms of XRCC1 gene may influence glioma risks in Chinese Han ethnic subjects, and might be potential molecular markers for evaluating glioma risks.