ObjectiveChildhood absence epilepsy (CAE) is a common syndrome of idiopathic generalized epilepsy.However, little is known about the brain structural changes in this type of epilepsy, especially in the default mode network (DMN) regions.Diffusion tensor imaging (DTI) is a noninvasive techniques that can be used to quantitatively explore structural characteristics of brain.This study aims at using the DTI technique to quantify structural abnormalities of DMN nodes in CAE patients.MethodDTI data were obtained in 14 CAE patients and 13 age-and gender-matched healthy controls.The data were analyzed using voxel-based analysis (VBA) and statistically compared between patients and controls.For the regions with significant difference in group comparison, their DTI metrics were further analyzed with clinical symptoms using Pearson's correlation.ResultsPatients showed significant increase of apparent diffusion coefficient (ADC) in left medial prefrontal cortex (MPFC) (P=0.042), while fractional anisotropy (FA) value was significantly decreased in left precuneus (P=0.010).In correlation analysis, ADC value from left MPFC was positively associated with duration of epilepsy.Neither the disease duration nor the seizure frequency showed significant correlation with FA values.ConclusionThe findings indicate that structural impairments exist in DMN regions in children suffering from absence epilepsy.This may contribute to understanding the pathological mechanisms and chronic neurological deficits of this disorder.
Objective To evaluate the role of topotecan in the treatment of small cell lung cancer (SCLC). Methods Up to 2006, we searched The Cochrane Library, MEDLINE, EMbase, Cancerlit, CBM, CNKI and VIP. Handsearch and additional search were also conducted. The quality of included studies was evaluated and meta-analyses were performed for the results of homogeneous studies by RevMan 4.2.8 software. Results Fourteen studies involving 2 099 participants with SCLC were included. All included studies were adequate in reporting randomization, while inadequate in allocation concealment and blinding. Meta-analyses showed that the response rate of TP (topotecan + cisplatin) regimen had no significant difference compared with EP regimen (etoposide + cisplatin) with OR 0.83 and 95%CI 0.63 to 1.09, but myelo-suppression such as leucopenia and thrombopenia was more severe with TP regimen; the response rate of monotherapy with topotecan was similar with that of CE (carboplatin + etoposide) regimen with OR 0.59 and 95%CI 0.22 to 1.60; the response rate of TEP (topotecan + etoposide + cisplatin) regimen was comparable with that of EP regimen with OR 1.37 and 95%CI 0.82 to –2.28, but myelosuppression and anemia were more severe with TEP regimen; the response rate with OR 0.97 and 95％CI 0.60 to –1.57, median time to progression with WMD –2.32 and 95％CI –5.72 to 1.09 and median survival time with WMD –1.65 and 95％CI –7.13 to 3.83 of IV topotecan were similar to those of oral topotecan, while neutropenia was more severe with IV topotecan. Forty-five treatment-related deaths were reported in all included studies. Conclusions Topotecan is an effective agent for SCLC when used as monotherapy or in combined treatment, but myelosuppression such as leucopenia and thrombopenia was relatively severe. Although it has been recommended as a second-line agent for recurrence of sensitive SCLC, more clinical trials are needed to define its role in first-line treatment. Due to a high risk of selection bias and detection bias in included studies, the evidence is insufficient to determine the effect of topotecan. Further large-scale trials are required to define the role of topotecan in the treatment of SCLC.