BACKGROUND: The carcinogenesis of hepatocellular carcinoma (HCC) is a multi-factorial, multistep and complex process. Its prognosis is poor, and early diagnosis and monitoring metastasis of HCC is of the utmost import...BACKGROUND: The carcinogenesis of hepatocellular carcinoma (HCC) is a multi-factorial, multistep and complex process. Its prognosis is poor, and early diagnosis and monitoring metastasis of HCC is of the utmost importance. Circulating diagnostic and prognostic biomarkers could be used in proper postoperative treatment of patients at an early stage of HCC development. This review summarizes recent studies of the specific biomarkers in diagnosis and monitoring metastasis or postoperative recurrence of HCC. DATA SOURCES: An English-language literature search was conducted using MEDLINE (June 1998 to September 2006) on researches of some valuable specific biomarkers in diagnosis and monitoring metastasis or postoperative recurrence of HCC. RESULTS: Hepatoma tissues can synthesize various tumor-related proteins, polypeptides, and isoenzymes, such as alpha-fetoprotein (AFP), hepatoma-specific gamma-glutamyl transpeptidase (HS-GGT), etc, and then secrete into blood. The valuable early diagnostic and prognostic biomarkers could predict the development and metastases of HCC. Recent researches have confirmed that circulating hepatoma-specific AFP subfraction, transforming growth factor (TGF)-β1, HS-GGT, and free insulin-like growth factor (IGF)-Ⅱ may be more specific markers than total AFP level for early diagnosis for HCC. The circulating genetic markers such as AFP-mRNA, TGF-β1-mRNA, IGF-Ⅱ-mRNA, etc from peripheral blood mononuclear cells of HCC patients have been most extensively used in monitoring distal metastasis or postoperative recurrence of HCC. CONCLUSIONS: Hepatoma tissues synthesize and secrete valuable molecular markers into blood. The analyses of circulating hepatoma-specific biomarkers are usefulto early diagnosis of HCC or monitoring metastasis or postoperative recurrence of HCC.展开更多
BACKGROUND:The active form of nuclear factor-kappa B(NF- κB)is involved in the initiation,generation,and development of hepatocellular carcinoma(HCC),and is up-regulated in inflammation-associated malignancies.We inv...BACKGROUND:The active form of nuclear factor-kappa B(NF- κB)is involved in the initiation,generation,and development of hepatocellular carcinoma(HCC),and is up-regulated in inflammation-associated malignancies.We investigated the dynamic expression of NF-κB and its influences on the occurrence of HCC through antiangiogenic(thalidomide) intervention in NF-κB activation. METHODS:Hepatoma models were induced with 2-fluorenyl- acetamide(2-FAA,0.05%)in male Sprague-Dawley rats,and thalidomide(100 mg/kg body weight)was administered intragastrically to intervene in NF-κB activation.The pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining.NF-κB mRNA was amplified by RT-nested PCR.The alterations of NF-κB and vascular endothelial growth factor(VEGF)expression were analyzed by enzyme-linked immunosorbent assay,immunohistochemistry,and Western blotting. RESULTS:Rat hepatocytes showed denatured,precancerous,and cancerous stages in hepatocarcinogenesis,with an increasing tendency of hepatic NF-κB,NF-κB mRNA,and VEGF expression,and their values in the HCC group were higher than those in controls(P<0.001).In the thalidomide- treated group,the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages,and nodular hyperplasia or a little atypical hyperplasia at the final stages,with the expression of NF-κB (χ2=9.93,P<0.001)and VEGF(χ2=8.024,P<0.001)lower than that in the 2-FAA group. CONCLUSION:NF-κB is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-κB and VEGF,and delays the occurrence of HCC.展开更多
BACKGROUND:Chemokines and their receptors play key roles in the pathogenesis of acute pancreatitis.This study aimed to establish a rat model of severe acute pancreatitis(SAP) for investigating monocyte chemotactic pro...BACKGROUND:Chemokines and their receptors play key roles in the pathogenesis of acute pancreatitis.This study aimed to establish a rat model of severe acute pancreatitis(SAP) for investigating monocyte chemotactic protein-1(MCP-1) expression in the pathogenesis of the disease.We assessed the effects of the inhibitor of MCP-1,Bindarit,on SAP and explored the mechanisms underlying SAP. METHODS:Seventy-two Sprague-Dawley rats were randomly divided into a saline control group(group S),an SAP group (group P),and a Bindarit group(group T).The SAP model was induced by retrograde infusion of 4%sodium taurocholate into the bilio-pancreatic duct.Based on the SAP model,Bindarit was injected intraperitoneally in group T,and 0.5% methyl cellulose was injected intraperitoneally in groups S and P.In group S,saline was retrogradely infused into the bili- pancreatic duct.Serum amylase levels and the histological changes in the pancreas were assessed at different time- points in each group.Expression of MCP-1 in serum was measured by enzyme-linked immunoadsorbent assay(ELISA). MCP-1 protein and mRNA expression levels were detected by immunohistochemistry,Western blotting,and semi- quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS:Serum amylase levels in groups P and T were higher than those in group S.Serum amylase levels were significantly lower in group T than in group P at 6 and 12 hours after operation.The levels of MCP-1 in serum at 6 and 12 hours after operation in group P were significantly higher than in group S,and significantly lower in group T than in group P at 6 and 12 hours after operation.The pathological damage in the pancreas was milder in group T than in group P.MCP-1 protein and mRNA expression levels in the pancreas were higher in groups P and T than in group S.These expression levels were positively correlated with the pathological damage of pancreatic tissues.The activity of MCP-1 in group T was significantly lower than in group P.CONCLUSION:MCP-1 may play important roles in the pathogenesis of SAP.The data suggest that Bindarit ameliorates SAP by inhibiting the activity of MCP-1 in vivo.展开更多
BACKGROUND:Hepatocellular carcinoma(HCC)is one of the most common malignant tumors.We analyzed the expression of nuclear-transcription factor-kappa B(NF-κB) during hepatocarcinogenesis in order to evaluate its dynami...BACKGROUND:Hepatocellular carcinoma(HCC)is one of the most common malignant tumors.We analyzed the expression of nuclear-transcription factor-kappa B(NF-κB) during hepatocarcinogenesis in order to evaluate its dynamic expression and its clinical value in the development and diagnosis of HCC. METHODS:Hepatoma models were induced by oral administration of 2-acetamidoflurene(2-FAA)to male Sprague-Dawley rats.Morphological changes were observed after hematoxylin and eosin staining.The cellular distribution of NF-κB expression during different stages of cancer development was investigated by immunohistochemistry, and the level of NF-κB expression in liver tissues was quantitatively analyzed by ELISA.The gene fragments of hepatic NF-κB were amplified by nested-polymerase chain reaction assay. RESULTS:Hepatocytes showed vacuole-like degeneration during the early stages,then had a hyperplastic nodal appearance during the middle stages,and finally progressed to tubercles of cancerous nests with high differentiation. The NF-κB-positive material was buff-colored,fine particles localized in the nucleus,and the incidence of NF-κB-positive cells was 81.8%in degeneration,83.3%in precancerous lesions,and 100%in cancerous tissues.All of these values were higher than those in controls(P<0.01). Hepatic NF-κB expression and hepatic NF-κB-mRNA were also higher during the course of HCC development(P<0.01).CONCLUSION:The NF-κB signal transduction pathway is activated during the early stages of HCC development, and its abnormal expression may be associated with the occurrence of HCC.展开更多
BACKGROUND:Pancreatic cancer is one of the most common malignant tumors.Early diagnosis of pancreatic cancer is difficult because of the latent onset and lack of good biomarkers.This study aimed to look for and identi...BACKGROUND:Pancreatic cancer is one of the most common malignant tumors.Early diagnosis of pancreatic cancer is difficult because of the latent onset and lack of good biomarkers.This study aimed to look for and identify differentially expressed proteins in tissues of pancreatic cancer and adjacent noncancerous tissues by proteomic approaches so as to provide information about possible pancreatic cancer markers and therapeutic targets.METHODS:Proteins extracted from 3 paired adjacent noncancerous and cancerous pancreatic tissue specimens were separated by two-dimensional gel electrophoresis(2-DE).The protein spots exhibiting statistical alternations between the two groups through computerized image analysis were then identified by matrix-assisted laser desorption ionization time-of-flight mass spectrometry(MALDI-TOF-MS).In addition,Western blotting and immunohistochemistry were performed to verify the expression of certain candidate proteins.RESULTS:Twelve proteins were significantly upregulated and 4 were downregulated between cancerous and paired adjacent noncancerous pancreatic tissues.Several proteins(S100A11,Ig gamma-1 chain C region,GSTO1 and peroxiredoxin 4) were found for the first time to be associated with pancreatic cancer.Differential expression of some identified proteins was further confirmed by Western blotting analysis and/or immunohistochemical analysis.CONCLUSIONS:Comparative proteomic analysis using 2-DE and MALDI-TOF-MS is an effective method for identifying differentially expressed proteins that may be the potential diagnostic biomarkers and therapeutic targets for pancreatic cancer.展开更多
BACKGROUND: Hepatocellular carcinoma (HCC) is characterized by multicause, obvious multistage and multifocal processes of tumor progression. The development of HCC is related intimately to overexpression and signal tr...BACKGROUND: Hepatocellular carcinoma (HCC) is characterized by multicause, obvious multistage and multifocal processes of tumor progression. The development of HCC is related intimately to overexpression and signal transduction of many cellular factors. This study was undertaken to investigate the dynamic expression and alteration of heat shock protein (HSP) gp96 along with its gene during HCC development. METHODS: A rat model of hepatoma induced with 2-fluorenylacetamide (2-FAA, 0.05%) was established in male Sprague-Dawley rats. Total RNA and pathological changes were observed during hepatocarcinogenesis. Total RNAs were transcribed into cDNA by reverse transcription and the gene fragment of gp96 was amplified by nested RT-PCR. The gp96 expression in rat liver tissues was semi-quantitatively analyzed by immunohistochemistry. RESULTS: Histological examination suggested that hepato-cytes in rats fed with 2-FAA showed vacuole-like denaturation at the early stages, then dysplastic nodules appeared at the middle stage, and finally progressed to tubercles of cancerous nests. A tendency of increasing liver gp96 protein level was found from normal liver to precancerous to cancerous tissues during hepatoma development (P<0.01), and was in accordance with the changes in gp96 mRNA (P<0.05).CONCLUSION: HSP gp96 is involved in HCC development and its overexpression may be a useful marker for early diagnosis.展开更多
BACKGROUND:Telomerase activity is reported to be specific and frequent in human pancreatic cancer.We conducted this study to assess the usefulness of monitoring telomerase activity in exfoliated cells obtained by panc...BACKGROUND:Telomerase activity is reported to be specific and frequent in human pancreatic cancer.We conducted this study to assess the usefulness of monitoring telomerase activity in exfoliated cells obtained by pancreatic duct brushing during endoscopic retrograde cholangiopancreatography(ERCP)for the diagnosis of pancreatic cancer. METHODS:Exfoliated cells obtained by pancreatic duct brushing during ERCP from 21 patients(18 with pancreatic cancer,3 with chronic pancreatitis) were examined.Telomerase activity was detected by polymerase chain reaction and telomeric repeat amplification protocol assay(PCR-TRAP-ELISA). RESULTS:D450 values of telomerase activity were 0.446± 0.2700 in pancreatic cancer and 0.041±0.0111 in chronic pancreatitis.77.8%(14/18)of patients with pancreatic cancer had cells with telomerase activity.None of the samples from patients with chronic pancreatitis showed telomerase activity,when the cutoff value of telomerase activity was set at 2.0.Cytological examination showed cancer cells in 66.7%(12/18)of the patients. CONCLUSIONS:Telomerase activity may be an early malignant event in pancreatic cancer development Cytology and telomerase activity in cells obtained bypancreatic duct brushing may complement each other for the diagnosis of pancreatic cancer.展开更多
To suppress the interference in the ultra-wideband (AI-UWB) system is a challenging problem. An anti-interference multiband orthogonal frequency-division multiplexing ultra-wideband (AI-UWB) system, based on spreading...To suppress the interference in the ultra-wideband (AI-UWB) system is a challenging problem. An anti-interference multiband orthogonal frequency-division multiplexing ultra-wideband (AI-UWB) system, based on spreading and interleaving is addressed. It will exploit the frequency diversity across the subcarriers and provide the robustness to narrow-band interference, by spreading the coded bit streams within each sub-band and interleaving across all sub-bands. Simulating results show that the spreading and interleaving provide about 5 dB to 10 dB advantages over the conventional multiband orthogonal frequency-division multiplexing ultra-wideband system in signal-to-interference ratio. Spreading and interleaving is an effective cure for enhancing the robustness to narrow-band interference,展开更多
Skeletal muscle atrophy inevitably occurs in denervated skeletal muscle,and cell apoptosis plays an important role in skeletal muscle atrophy and degeneration.The present study established rat models of simple nerve i...Skeletal muscle atrophy inevitably occurs in denervated skeletal muscle,and cell apoptosis plays an important role in skeletal muscle atrophy and degeneration.The present study established rat models of simple nerve injury by transecting the ventral or dorsal spinal nerve root and observed rat skeletal muscle cell apoptosis following simple motor nerve injury versus simple sensory nerve injury.Following skeletal muscle denervation for 10 weeks,cell apoptosis was detected in skeletal muscle,which was accompanied by obvious changes in rat behavior and electrophysiological responses.In addition,changes in cross-sectional area and average gray-scale of motor endplates of the gastrocnemius muscle were analyzed following sciatic nerve injury and motor nerve injury.Cell nuclei in denervated skeletal muscle tissue were more densely arranged than in normal skeletal muscle tissue.Cell nuclei were most dense in the sciatic nerve injury group,followed by the motor nerve injury group and the sensory nerve injury group.Fas/FasL expression and the number of apoptotic cells increased in denervated skeletal muscle,and apoptosis-related changes were observed.These findings suggested that motor and sensory nerves provided trophic actions following skeletal muscle and motor nerve injury,resulting in a greater influence on skeletal muscle atrophy than sensory nerve injury.Therefore,reconstruction of motor nerves should be preferentially considered for treating denervation-induced skeletal muscle atrophy.展开更多
AIM: To find evidences about whether NOD1/CARD4 insertion/deletion polymorphism is associated with inflammatory bowel disease by meta-analysis. METHODS: We surveyed the studies on the association of NOD1/CARD4 inserti...AIM: To find evidences about whether NOD1/CARD4 insertion/deletion polymorphism is associated with inflammatory bowel disease by meta-analysis. METHODS: We surveyed the studies on the association of NOD1/CARD4 insertion/deletion polymorphism with inflammatory bowel disease in PubMed. Meta-analysis was performed for genotypes GG/T vs T/T, GG/GG vs T/T, GG/T + GG/GG vs T/T, GG/GG vs T/T + GG/T, and GG allele vs T allele in a fixed/random effect model. RESULTS: We identified 8 studies (6439 cases and 4798 controls) in Caucasian populations using PubMed search. We found no association between NOD1/CARD4 insertion/deletion polymorphism and inflammatory bowel disease, Crohn's disease, and ulcerative colitis. Stratification of cases by age showed that NOD1/CARD4 insertion/deletion polymorphism was associated with inflammatory bowel disease in younger age group at onset (< 40 years) (GG vs T: OR = 0.68, 95% CI: 0.50-0.93, P = 0.02; GG/T + GG/GG vs T/T: OR = 0.71, 95% CI: 0.59-0.85, P = 0.0003). CONCLUSION: This meta-analysis demonstrates an association between NOD1/CARD4 insertion/deletion polymorphism and inflammatory bowel disease in the younger age group at onset (< 40 years) in Caucasian populations.展开更多
基金This study was supported by grants from the Key Project of Medical Science from Jiangsu Province (RC2003100)the Project of Medical Science from Department of Health, Jiangsu Province (H200523), China.
文摘BACKGROUND: The carcinogenesis of hepatocellular carcinoma (HCC) is a multi-factorial, multistep and complex process. Its prognosis is poor, and early diagnosis and monitoring metastasis of HCC is of the utmost importance. Circulating diagnostic and prognostic biomarkers could be used in proper postoperative treatment of patients at an early stage of HCC development. This review summarizes recent studies of the specific biomarkers in diagnosis and monitoring metastasis or postoperative recurrence of HCC. DATA SOURCES: An English-language literature search was conducted using MEDLINE (June 1998 to September 2006) on researches of some valuable specific biomarkers in diagnosis and monitoring metastasis or postoperative recurrence of HCC. RESULTS: Hepatoma tissues can synthesize various tumor-related proteins, polypeptides, and isoenzymes, such as alpha-fetoprotein (AFP), hepatoma-specific gamma-glutamyl transpeptidase (HS-GGT), etc, and then secrete into blood. The valuable early diagnostic and prognostic biomarkers could predict the development and metastases of HCC. Recent researches have confirmed that circulating hepatoma-specific AFP subfraction, transforming growth factor (TGF)-β1, HS-GGT, and free insulin-like growth factor (IGF)-Ⅱ may be more specific markers than total AFP level for early diagnosis for HCC. The circulating genetic markers such as AFP-mRNA, TGF-β1-mRNA, IGF-Ⅱ-mRNA, etc from peripheral blood mononuclear cells of HCC patients have been most extensively used in monitoring distal metastasis or postoperative recurrence of HCC. CONCLUSIONS: Hepatoma tissues synthesize and secrete valuable molecular markers into blood. The analyses of circulating hepatoma-specific biomarkers are usefulto early diagnosis of HCC or monitoring metastasis or postoperative recurrence of HCC.
基金supported by grants from the Project of Elitist Peak in Six Fields(No.2006-B-063)the Project of Medical Sciences(H200727),the Bureau of Health,Jiangsu Province,China
文摘BACKGROUND:The active form of nuclear factor-kappa B(NF- κB)is involved in the initiation,generation,and development of hepatocellular carcinoma(HCC),and is up-regulated in inflammation-associated malignancies.We investigated the dynamic expression of NF-κB and its influences on the occurrence of HCC through antiangiogenic(thalidomide) intervention in NF-κB activation. METHODS:Hepatoma models were induced with 2-fluorenyl- acetamide(2-FAA,0.05%)in male Sprague-Dawley rats,and thalidomide(100 mg/kg body weight)was administered intragastrically to intervene in NF-κB activation.The pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining.NF-κB mRNA was amplified by RT-nested PCR.The alterations of NF-κB and vascular endothelial growth factor(VEGF)expression were analyzed by enzyme-linked immunosorbent assay,immunohistochemistry,and Western blotting. RESULTS:Rat hepatocytes showed denatured,precancerous,and cancerous stages in hepatocarcinogenesis,with an increasing tendency of hepatic NF-κB,NF-κB mRNA,and VEGF expression,and their values in the HCC group were higher than those in controls(P<0.001).In the thalidomide- treated group,the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages,and nodular hyperplasia or a little atypical hyperplasia at the final stages,with the expression of NF-κB (χ2=9.93,P<0.001)and VEGF(χ2=8.024,P<0.001)lower than that in the 2-FAA group. CONCLUSION:NF-κB is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-κB and VEGF,and delays the occurrence of HCC.
基金supported by grants from the social Burteall Foundation of Nantong(S5054)
文摘BACKGROUND:Chemokines and their receptors play key roles in the pathogenesis of acute pancreatitis.This study aimed to establish a rat model of severe acute pancreatitis(SAP) for investigating monocyte chemotactic protein-1(MCP-1) expression in the pathogenesis of the disease.We assessed the effects of the inhibitor of MCP-1,Bindarit,on SAP and explored the mechanisms underlying SAP. METHODS:Seventy-two Sprague-Dawley rats were randomly divided into a saline control group(group S),an SAP group (group P),and a Bindarit group(group T).The SAP model was induced by retrograde infusion of 4%sodium taurocholate into the bilio-pancreatic duct.Based on the SAP model,Bindarit was injected intraperitoneally in group T,and 0.5% methyl cellulose was injected intraperitoneally in groups S and P.In group S,saline was retrogradely infused into the bili- pancreatic duct.Serum amylase levels and the histological changes in the pancreas were assessed at different time- points in each group.Expression of MCP-1 in serum was measured by enzyme-linked immunoadsorbent assay(ELISA). MCP-1 protein and mRNA expression levels were detected by immunohistochemistry,Western blotting,and semi- quantitative reverse transcriptase-polymerase chain reaction (RT-PCR). RESULTS:Serum amylase levels in groups P and T were higher than those in group S.Serum amylase levels were significantly lower in group T than in group P at 6 and 12 hours after operation.The levels of MCP-1 in serum at 6 and 12 hours after operation in group P were significantly higher than in group S,and significantly lower in group T than in group P at 6 and 12 hours after operation.The pathological damage in the pancreas was milder in group T than in group P.MCP-1 protein and mRNA expression levels in the pancreas were higher in groups P and T than in group S.These expression levels were positively correlated with the pathological damage of pancreatic tissues.The activity of MCP-1 in group T was significantly lower than in group P.CONCLUSION:MCP-1 may play important roles in the pathogenesis of SAP.The data suggest that Bindarit ameliorates SAP by inhibiting the activity of MCP-1 in vivo.
基金supported by grants from the Project of Elitist Peak in Six Fields(No.2006-B-063)the Projectof Medical Sciences(H200727),the Bureau of Health,Jiangsu Province,China
文摘BACKGROUND:Hepatocellular carcinoma(HCC)is one of the most common malignant tumors.We analyzed the expression of nuclear-transcription factor-kappa B(NF-κB) during hepatocarcinogenesis in order to evaluate its dynamic expression and its clinical value in the development and diagnosis of HCC. METHODS:Hepatoma models were induced by oral administration of 2-acetamidoflurene(2-FAA)to male Sprague-Dawley rats.Morphological changes were observed after hematoxylin and eosin staining.The cellular distribution of NF-κB expression during different stages of cancer development was investigated by immunohistochemistry, and the level of NF-κB expression in liver tissues was quantitatively analyzed by ELISA.The gene fragments of hepatic NF-κB were amplified by nested-polymerase chain reaction assay. RESULTS:Hepatocytes showed vacuole-like degeneration during the early stages,then had a hyperplastic nodal appearance during the middle stages,and finally progressed to tubercles of cancerous nests with high differentiation. The NF-κB-positive material was buff-colored,fine particles localized in the nucleus,and the incidence of NF-κB-positive cells was 81.8%in degeneration,83.3%in precancerous lesions,and 100%in cancerous tissues.All of these values were higher than those in controls(P<0.01). Hepatic NF-κB expression and hepatic NF-κB-mRNA were also higher during the course of HCC development(P<0.01).CONCLUSION:The NF-κB signal transduction pathway is activated during the early stages of HCC development, and its abnormal expression may be associated with the occurrence of HCC.
文摘BACKGROUND:Pancreatic cancer is one of the most common malignant tumors.Early diagnosis of pancreatic cancer is difficult because of the latent onset and lack of good biomarkers.This study aimed to look for and identify differentially expressed proteins in tissues of pancreatic cancer and adjacent noncancerous tissues by proteomic approaches so as to provide information about possible pancreatic cancer markers and therapeutic targets.METHODS:Proteins extracted from 3 paired adjacent noncancerous and cancerous pancreatic tissue specimens were separated by two-dimensional gel electrophoresis(2-DE).The protein spots exhibiting statistical alternations between the two groups through computerized image analysis were then identified by matrix-assisted laser desorption ionization time-of-flight mass spectrometry(MALDI-TOF-MS).In addition,Western blotting and immunohistochemistry were performed to verify the expression of certain candidate proteins.RESULTS:Twelve proteins were significantly upregulated and 4 were downregulated between cancerous and paired adjacent noncancerous pancreatic tissues.Several proteins(S100A11,Ig gamma-1 chain C region,GSTO1 and peroxiredoxin 4) were found for the first time to be associated with pancreatic cancer.Differential expression of some identified proteins was further confirmed by Western blotting analysis and/or immunohistochemical analysis.CONCLUSIONS:Comparative proteomic analysis using 2-DE and MALDI-TOF-MS is an effective method for identifying differentially expressed proteins that may be the potential diagnostic biomarkers and therapeutic targets for pancreatic cancer.
基金The study was supported by grants-in-aid from the Key Project of Medical Science of Jiangsu Province, China (RC2003100)the Science and Technology Project for Social Development of Nantong, China (No. S40034).
文摘BACKGROUND: Hepatocellular carcinoma (HCC) is characterized by multicause, obvious multistage and multifocal processes of tumor progression. The development of HCC is related intimately to overexpression and signal transduction of many cellular factors. This study was undertaken to investigate the dynamic expression and alteration of heat shock protein (HSP) gp96 along with its gene during HCC development. METHODS: A rat model of hepatoma induced with 2-fluorenylacetamide (2-FAA, 0.05%) was established in male Sprague-Dawley rats. Total RNA and pathological changes were observed during hepatocarcinogenesis. Total RNAs were transcribed into cDNA by reverse transcription and the gene fragment of gp96 was amplified by nested RT-PCR. The gp96 expression in rat liver tissues was semi-quantitatively analyzed by immunohistochemistry. RESULTS: Histological examination suggested that hepato-cytes in rats fed with 2-FAA showed vacuole-like denaturation at the early stages, then dysplastic nodules appeared at the middle stage, and finally progressed to tubercles of cancerous nests. A tendency of increasing liver gp96 protein level was found from normal liver to precancerous to cancerous tissues during hepatoma development (P<0.01), and was in accordance with the changes in gp96 mRNA (P<0.05).CONCLUSION: HSP gp96 is involved in HCC development and its overexpression may be a useful marker for early diagnosis.
文摘BACKGROUND:Telomerase activity is reported to be specific and frequent in human pancreatic cancer.We conducted this study to assess the usefulness of monitoring telomerase activity in exfoliated cells obtained by pancreatic duct brushing during endoscopic retrograde cholangiopancreatography(ERCP)for the diagnosis of pancreatic cancer. METHODS:Exfoliated cells obtained by pancreatic duct brushing during ERCP from 21 patients(18 with pancreatic cancer,3 with chronic pancreatitis) were examined.Telomerase activity was detected by polymerase chain reaction and telomeric repeat amplification protocol assay(PCR-TRAP-ELISA). RESULTS:D450 values of telomerase activity were 0.446± 0.2700 in pancreatic cancer and 0.041±0.0111 in chronic pancreatitis.77.8%(14/18)of patients with pancreatic cancer had cells with telomerase activity.None of the samples from patients with chronic pancreatitis showed telomerase activity,when the cutoff value of telomerase activity was set at 2.0.Cytological examination showed cancer cells in 66.7%(12/18)of the patients. CONCLUSIONS:Telomerase activity may be an early malignant event in pancreatic cancer development Cytology and telomerase activity in cells obtained bypancreatic duct brushing may complement each other for the diagnosis of pancreatic cancer.
基金the National "863" High Technology Research Program of China (2005AA123320)Universities Natural Science Research Project of Jiangsu Province (05KJB510101).
文摘To suppress the interference in the ultra-wideband (AI-UWB) system is a challenging problem. An anti-interference multiband orthogonal frequency-division multiplexing ultra-wideband (AI-UWB) system, based on spreading and interleaving is addressed. It will exploit the frequency diversity across the subcarriers and provide the robustness to narrow-band interference, by spreading the coded bit streams within each sub-band and interleaving across all sub-bands. Simulating results show that the spreading and interleaving provide about 5 dB to 10 dB advantages over the conventional multiband orthogonal frequency-division multiplexing ultra-wideband system in signal-to-interference ratio. Spreading and interleaving is an effective cure for enhancing the robustness to narrow-band interference,
基金Clinical Scientific Research Foundation Project of Nantong University,No. 200626
文摘Skeletal muscle atrophy inevitably occurs in denervated skeletal muscle,and cell apoptosis plays an important role in skeletal muscle atrophy and degeneration.The present study established rat models of simple nerve injury by transecting the ventral or dorsal spinal nerve root and observed rat skeletal muscle cell apoptosis following simple motor nerve injury versus simple sensory nerve injury.Following skeletal muscle denervation for 10 weeks,cell apoptosis was detected in skeletal muscle,which was accompanied by obvious changes in rat behavior and electrophysiological responses.In addition,changes in cross-sectional area and average gray-scale of motor endplates of the gastrocnemius muscle were analyzed following sciatic nerve injury and motor nerve injury.Cell nuclei in denervated skeletal muscle tissue were more densely arranged than in normal skeletal muscle tissue.Cell nuclei were most dense in the sciatic nerve injury group,followed by the motor nerve injury group and the sensory nerve injury group.Fas/FasL expression and the number of apoptotic cells increased in denervated skeletal muscle,and apoptosis-related changes were observed.These findings suggested that motor and sensory nerves provided trophic actions following skeletal muscle and motor nerve injury,resulting in a greater influence on skeletal muscle atrophy than sensory nerve injury.Therefore,reconstruction of motor nerves should be preferentially considered for treating denervation-induced skeletal muscle atrophy.
基金Supported by The National Natural Science Foundation of China (30972530)
文摘AIM: To find evidences about whether NOD1/CARD4 insertion/deletion polymorphism is associated with inflammatory bowel disease by meta-analysis. METHODS: We surveyed the studies on the association of NOD1/CARD4 insertion/deletion polymorphism with inflammatory bowel disease in PubMed. Meta-analysis was performed for genotypes GG/T vs T/T, GG/GG vs T/T, GG/T + GG/GG vs T/T, GG/GG vs T/T + GG/T, and GG allele vs T allele in a fixed/random effect model. RESULTS: We identified 8 studies (6439 cases and 4798 controls) in Caucasian populations using PubMed search. We found no association between NOD1/CARD4 insertion/deletion polymorphism and inflammatory bowel disease, Crohn's disease, and ulcerative colitis. Stratification of cases by age showed that NOD1/CARD4 insertion/deletion polymorphism was associated with inflammatory bowel disease in younger age group at onset (< 40 years) (GG vs T: OR = 0.68, 95% CI: 0.50-0.93, P = 0.02; GG/T + GG/GG vs T/T: OR = 0.71, 95% CI: 0.59-0.85, P = 0.0003). CONCLUSION: This meta-analysis demonstrates an association between NOD1/CARD4 insertion/deletion polymorphism and inflammatory bowel disease in the younger age group at onset (< 40 years) in Caucasian populations.
