Objective To investigate the effects of multiple doses of propofol or/and monosialotetrahexosyl ganglioside (GM1) on cognitive function and caspase-3 expression in immature rats.Methods Seventy-seven immature SD rats,17-18-day old and weighted 33-40g,were randomly divided into 7 groups (11 each):control group (NS),propofol 50mg/kg group (P50),propofol 100mg/kg group (P_ 100 ),propofol 200mg/kg group (P_ 200 ),GM1 10mg/kg group (G),propofol 100mg/kg and GM1 10mg/kg group (P_ 100 G),and propofol 200mg/kg and GM1 10mg/kg group (P_ 200 G).Each group received normal saline,propofol 50mg/(kg?d),100 mg/(kg?d),200mg/(kg?d),GM1 10mg/(kg?d),propofol 100mg/(kg?d) and GM1 10mg/(kg?d),or propofol 200 mg/(kg?d) and GM1 10mg/(kg?d) intraperitoneally in a bolus or divided doses,respectively,for 6 consecutive days.The tests of learning and memory were performed in Morris water maze everyday at the 3rd hour after the rats waked up from anesthesia.The animals were sacrificed on the 6th day after the Morris water maze test to obtain the brain specimen,and the expression of caspase-3 was detected by immunohistochemistry and Western blotting.Results Latency period of water maze test was significantly longer in groups P_ 100,P_ 200 and P_ 200 G than in group NS,and the frequency of crossing platform were fewer in P_ 100,P_ 200 and P_ 200 G groups (P

Objective This study was to investigate the lymph node metastasis pattern in thoracic esophageal squamous cell carcinoma (ESCC),and analyze the risk factors to provide reference for the delineation of radiotherapy target.Methods A total of 319 patients with thoracic ESCC who underwent surgical treatment at the second hospital of Dalian medical university were analyzed retrospectively.The lymph nodes around esophageal were divided into 20 groups according to the mapping scheme of the American Thoracic Society (ATS) modified by Casson et al.Analyzed the pattern of lymph node metastasis and its relationship with tumor location,tumor length,depth of invasion,pathological grade,and vessel invasion.Results The lymph node metastatic rate was 48.90％ (156/319),while the metastatic ratio of lymph node (LMR) was 15.70％ (562/3 581).The lymph node metastatic rates had gradually increasing trend with tumor sites descending (upper ESCC 35.48％,middle ESCC 47.06％ and lower ESCC 56.43％),but no statistically significance (P ＞ 0.05) was observed.In the whole 20 groups,the higher node metastasis stations of upper thoracic ESCC LMR were 1,2,4,5,7,9 (x2 =27.38,P ＜ 0.05),while the middle thoracic ESCC LMR were 2,4,5,7,8M (x2 =57.77,P ＜ 0.05),and the lower thoracic ESCC LMR were 4,5,7,8L,16,17,20 (x2 =28.88,P ＜ 0.05),with statistically significance.So the main lymph node metastasis stations were paraesophageal nodes,tracheobronchial nodes,paratracheal nodes,aroticopumonary nodes,left gastric nodes,subcarinalnodes and celiac nodes.The univariate analysis revealed that lymph node metastasis was correlated with the tumor length,depth of invasion,pathological grade,and presence of vascular invasion (x2 =6.82,26.04,36.26,4.56respectivcly,P ＜ 0.05).The muhi-variate regression analysis showed that tumor length and depth of tumor invasion were independent risk factors for lymph node metastasis (OR =2.212,2.123,P ＜ 0.05).Conclusions The factors influencing lymph node metastasis in thoracic ESCC include tumor length,depth of invasion,pathological grade,and presence of vascular invasion,which should be carefully considered during the target delineation of radiotherapy for esophageal carcinoma.

Even though mutations in LMNA have been reported in patients with typical dilated cardiomyopathy (DCM) and atrioventricular block (AVB) previously, the purpose of this study was to disclose this novel genetic abnormality in one Chinese family with the atypical phenotype of progressive AVB followed by DCM with normal QRS interval. Genome-wide linkage analysis mapped the AVB gene in this family to a marker at chromosome 1q21.2, where the LMNA gene was located. Direct DNA sequence analysis revealed a heterozygous G to A transition at nucleotide 244 in exon 1 of LMNA, which resulted in an E82K mutation. The E82K mutation co-segregated with all affected individuals in the family, and was not present in 200 normal controls. Further clinical evaluation of mutation carriers showed that 5 of 6 AVB patients exhibited mild DCM with a late onset of age in the fourth and fifth decades. Ejection fractions were documented in 5 patients with DCM, but 4 showed a normal value of [Symbol: see text]50%. Echocardiography showed that atrial dilatation occurred earlier than ventricular dilatation in the patients. This study suggests that progressive AVB with normal QRS interval and accompanying DCM at later stages may represent a distinct type of DCM. The molecular mechanism by which the E82K mutation causes AVB as the prominent phenotype in DCM may be a focus of future studies.

Even though mutations in LMNA have been reported in patients with typical dilated cardio-myopathy(DCM)and atrioventricular block(AVB)previously,the purpose of this study was to disclose this novel genetic abnormality in one Chinese family with the atypical phenotype of progressive AVB followed by DCM with normal QRS interval.Genome-wide linkage analysis mapped the AVB gene in this family to a marker at chromosome 1q21.2,where the LMNA gene was located.Direct DNA sequence analysis revealed a heterozygous G to A transition at nucleotide 244 in exon 1 of LMNA,which resulted in an E82K mutation.The E82K mutation co-segregated with all affected individuals in the family,and was not present in 200 normal controls.Further clinical evaluation of mutation carriers showed that 5 of 6 AVB patients exhibited mild DCM with a late onset of age in the fourth and fifth decades.Ejection fractions were documented in 5 patients with DCM,but 4 showed a normal value of ≥50%.Echocardiography showed that atrial dilatation occurred earlier than ventricular dilatation in the patients.This study suggests that progressive AVB with normal QRS interval and accompanying DCM at later stages may represent a distinct type of DCM.The molecular mechanism by which the E82K mutation causes AVB as the prominent phenotype in DCM may be a focus of future studies.