Objective To propose two different types of information encoding methods for the information encoding mode of neuronal networks based on Hodgkin-Huxley(HH)model.Methods The biological neuronal networks with different topologies were built with numerical simulations using HH model and chemical synapses.The specificities of two information encoding methods,namely average frequency encoding and interspike interval encoding,under the stimulus of sinusoidal signals and random audio signals were investigated,and the information encoding mode of neuronal networks stimulated by different signals was also analyzed.Results The information encoding mode of the neuronal networks was correlated with the stimulus signal type.When being stimulated by a continuous periodic signal,the neuronal network would generate a discharge sequence with periodicity corresponding to the stimulus signal.When the stimulus signal was a random signal,the discharge rate of the neuronal network would change with the stimulus signal intensity,and the higher the stimulus signal intensity was,the higher the action potential discharge rate was.Under the same stimulus signal,the temporal structure of the neuronal network discharge sequence was affected by the topology of the neuronal network.Conclusion The information encoding mode of neuronal networks is correlated with the stimulus signal,and the temporal structure of the discharge sequence of neuronal networks with different topologies is different.Interspike interval encoding has higher accuracy and contains more information,and the combination with the average frequency encoding can effectively express the dynamic change of the information encoding mode of neuronal networks under the stimulus.

OBJECTIVETyrosine kinase inhibitors (TKIs) of the epidermal growth factor receptor (EGFR) have been reported to be effective in the treatment of esophageal and esophagogastric junction cancers. The aim of this study was to detect the frequency of EGFR mutation and expression in Chinese patients with esophageal, esophagogastric junction and gastric cancers, and to clarify the value of EGFR mutation and expression in predicting the efficacy of TKI in the treatment of these tumors.

METHODSIn this study, 180 tumor samples with histologically confirmed esophageal cancer (39 cases), cancer of the esophagogastric junction (92 cases) and gastric cancer (49 cases) were collected. Twenty-nine different EGFR mutations in exons 18-21 were assessed by real-time PCR-optimized oligonucleotide probe method. EGFR protein expression was evaluated by immunohistochemistry (IHC) in 89 tumor samples.

RESULTSThe mutation analysis for EGFR (exons 18-21) showed no mutations in any of the hotspots of the gene in the 180 tumor samples analyzed. EGFR expression was negative in 12 tumor samples, 1+ in 31 tumor samples, 2+ in 24 tumor samples, and 3+ in 22 tumor samples. EGFR expression was 2+ or 3+ in 12 (92.3%) of the 13 esophageal squamous cell carcinomas, 29 (47.5%) of the 61 esophagogastric junction cancers, and 5 (33.3%) of the 15 gastric adenocarcinomas.

CONCLUSIONSOur results indicate that EGFR mutation in exons 18-21 is absent in the examined samples of esophageal, esophagogastric junction and gastric cancers. More studies are warranted to explore the predictive biological markers for the therapeutic response to EGFR TKI.

Adenocarcinoma ; genetics ; metabolism ; Adult ; Aged ; Carcinoma, Adenosquamous ; genetics ; metabolism ; Carcinoma, Squamous Cell ; genetics ; metabolism ; Esophageal Neoplasms ; genetics ; metabolism ; Esophagogastric Junction ; metabolism ; pathology ; Exons ; Female ; Humans ; Male ; Middle Aged ; Mutation ; Receptor, Epidermal Growth Factor ; genetics ; metabolism ; Stomach Neoplasms ; genetics ; metabolism ; Young Adult

Objective:This study aims to determine the efficacy of chemotherapy and to identify potential chemotherapy agents for advanced primary duodenal carcinoma (PDC). Methods:Fifty-six patients with advanced PDC, who did and did not receive chemo-therapy, were involved in this study. Response rates (RR), disease control rates (DCR), progression-free survival (PFS), and overall sur-vival (OS) were analyzed. Results:The overall RR and DCR of 43 patients were 19.04%and 71.42%, respectively. The patients who re-ceived chemotherapy agents fluorourzcil and oxaliplatin exhibited higher RR compared with patients who received other chemotherapy combinations (35.29%vs. 7.69%, P=0.010 9). Palliative chemotherapy improved the OS of patients with advanced PDC compared with patients who did not receive chemotherapy (13.35 months vs. 5.65 months, HR=0.203, 95%CI:0.083 to 0.497, P=0.000 5). Compared with the use of other chemotherapy regimens, treatment with a fluorourzcil-based chemotherapy agent resulted in a longer PFS (5.08 months vs. 1.08 months, HR=0.004, 95%CI:0.000 to 0.315, P=0.013 2). Multivariate analysis indicated mucinous histology and lymph mode metastasis as factors predictive of poor prognosis in patients with advanced PDC. Conclusion:Palliative chemotherapy may im-prove the OS of patients with advanced PDC.

Objective Tyrosine kinase inhibitors ( TKIs) of the epidermal growth factor receptor ( EGFR) have been reported to be effective in the treatment of esophageal and esophagogastric junction cancers.The aim of this study was to detect the frequency of EGFR mutation and expression in Chinese patients with esophageal , esophagogastric junction and gastric cancers , and to clarify the value of EGFR mutation and expression in predicting the efficacy of TKI in the treatment of these tumors .Methods In this study, 180 tumor samples with histologically confirmed esophageal cancer (39 cases), cancer of the esophagogastric junction ( 92 cases ) and gastric cancer ( 49 cases ) were collected .Twenty-nine different EGFR mutations in exons 18-21 were assessed by real-time PCR-optimized oligonucleotide probe method. EGFR protein expression was evaluated by immunohistochemistry ( IHC) in 89 tumor samples.Results The mutation analysis for EGFR ( exons 18-21) showed no mutations in any of the hotspots of the gene in the 180 tumor samples analyzed .EGFR expression was negative in 12 tumor samples, 1+in 31 tumor samples, 2+in 24 tumor samples,and 3+in 22 tumor samples.EGFR expression was 2+or 3+in 12 (92.3%)of the 13 esophageal squamous cell carcinomas , 29 (47.5%) of the 61 esophagogastric junction cancers , and 5 (33.3%) of the 15 gastric adenocarcinomas .Conclusions Our results indicate that EGFR mutation in exons 18-21 is absent in the examined samples of esophageal , esophagogastric junction and gastric cancers . More studies are warranted to explore the predictive biological markers for the therapeutic response to EGFR TKI.

Objective Tyrosine kinase inhibitors ( TKIs) of the epidermal growth factor receptor ( EGFR) have been reported to be effective in the treatment of esophageal and esophagogastric junction cancers.The aim of this study was to detect the frequency of EGFR mutation and expression in Chinese patients with esophageal , esophagogastric junction and gastric cancers , and to clarify the value of EGFR mutation and expression in predicting the efficacy of TKI in the treatment of these tumors .Methods In this study, 180 tumor samples with histologically confirmed esophageal cancer (39 cases), cancer of the esophagogastric junction ( 92 cases ) and gastric cancer ( 49 cases ) were collected .Twenty-nine different EGFR mutations in exons 18-21 were assessed by real-time PCR-optimized oligonucleotide probe method. EGFR protein expression was evaluated by immunohistochemistry ( IHC) in 89 tumor samples.Results The mutation analysis for EGFR ( exons 18-21) showed no mutations in any of the hotspots of the gene in the 180 tumor samples analyzed .EGFR expression was negative in 12 tumor samples, 1+in 31 tumor samples, 2+in 24 tumor samples,and 3+in 22 tumor samples.EGFR expression was 2+or 3+in 12 (92.3%)of the 13 esophageal squamous cell carcinomas , 29 (47.5%) of the 61 esophagogastric junction cancers , and 5 (33.3%) of the 15 gastric adenocarcinomas .Conclusions Our results indicate that EGFR mutation in exons 18-21 is absent in the examined samples of esophageal , esophagogastric junction and gastric cancers . More studies are warranted to explore the predictive biological markers for the therapeutic response to EGFR TKI.

BACKGROUNDEndostar™ (rh-endostatin, YH-16) is a new recombinant human endostatin developed by Medgenn Bioengineering Co. Ltd., Yantai, Shandong, P.R.China. Pre-clinical study indicated that YH-16 could inhibit tumor endothelial cell proliferation, angiogenesis and tumor growth. Phase I and phase II studies revealed that YH-16 was effective as single agent with good tolerance in clinical use.The current study was to compare the response rate , median ti me to progression (TTP) ,clinical benefit andsafety in patients with advanced non-small cell lung cancer ( NSCLC) , who were treated with YH-16 plus vi-norelbine and cisplatin (NP) or placebo plus NP.

METHODSFour hundred and ninety-three histologically or cy-tologically confirmed stage IIIB and IV NSCLC patients , withlife expectancy > 3 months and ECOG perform-ance status 0-2 , were enrolledin a randomized ,double-blind ,placebo-controlled , multicenter trial ,either trialgroup : NP plus YH-16 (vinorelbine 25 mg/m² on day 1 and day 5 ,cisplatin 30mg/m² on days 2 to 4 , YH-167.5mg/m² on days 1 to 14) or control group : NP plus placebo (vinorelbine 25 mg/m² on day 1 and day 5 ,cis-platin 30 mg/m² on days 2 to 4 ,0.9% sodium-chloride 3 .75 ml on days 1 to 14) every 3 weeks for 2-6 cycles .The trial endpoints included response rate ,clinical benefit rate ,time to progression,quality of life and safety .

RESULTSOf 486 assessable patients , overall response rate was 35.4% in trial group and 19.5% in controlgroup (P=0 .0003) . The median TTP was 6 .3 months and 3 .6 months for trial group and control group respectively (P < 0 .001) . The clinical benefit rate was 73 .3 %in trial group and 64.0% in control group (P=0 .035) .In untreated patients of trial group and control group ,the response rate was 40 .0% and 23.9%(P=0 .003) ,the clinical benefit rate was 76 .5 % and 65 .0 % (P=0 .023) ,the median TTP was 6 .6 and 3 .7months (P=0 .0000) ,respectively .In pretreated patients of trial group and control group ,the response ratewas 23.9% and 8.5%(P=0 .034) ,the clinical benefit rate was 65.2% and 61.7%(P=0 .68) ,the median TTP was 5 .7 and 3 .2 months (P=0 .0002) ,respectively . The relief rate of clinical symptoms in trial groupwas higher than that of those in control group ,but no significance existed (P > 0 .05) . The score of quality oflife in trial group was significantly higher than that in control group (P=0 .0155) after treatment . There were no significant differences in incidence of hematologic and non-hematologic toxicity , moderate and severe sideeffects betweentrial group and control group .

CONCLUSIONSThe addition of YH-16 to NP regimen results in significantly and clinically meaningful improvement in response rate , median time to tumor progression,and clinical benefit rate compared with NP alone in advanced NSCLC patients . YH-16 in combination with chemotherapy shows a synergic activity and a favorable toxic profile in advanced cancer patients .