Biomedical subjects

C W Wu

Publications and source records attributed to C W Wu.

At least 55 records · Page 3Linked to original sources

PubMed2000

Human gastric cancer kinase profile and prognostic significance of MKK4 kinase.

Alterations of protein tyrosine kinase are often associated with uncontrolled cell growth and tumor progression. Knowledge of the overall expression pattern of tyrosine kinases should prove beneficial in understanding the signaling pathways involved in gastric cancer oncogenesis and in providing possible biomarkers for gastric cancer progression. To establish a general tyrosine-kinase expression profile, degenerated polymerase chain reaction primers designed from the consensus catalytic kinase motifs were used to amplify protein tyrosine kinase molecules from gastric cancer tissues. We observed more than 50 tyrosine and serine/threonine kinases from matching pairs of gastric cancer tissue and normal mucosa. Based on this new kinase profile information, we selected the MKK4 gene for further immunohistochemical studies. Statistical analysis of MKK4 protein expression and clinicopathological features indicated that MKK4 kinase expression could serve as a significant prognostic factor for relapse-free survival and for overall survival. We demonstrated a simple and sensitive method for establishing protein tyrosine-kinase expression profiles of human gastric cancer tissues as well as for discovering novel and useful clinical biomarkers from such kinase expression profiles.

Aged↗

PubMed2000

Spinal cord atrophy and reorganization of motoneuron connections following long-standing limb loss in primates.

Primates with long-standing therapeutic amputations of a limb at a young age were used to investigate the possibility that deefferented motor nerves sprout to new muscle targets. Injections of anatomical tracers into the muscles proximal to the amputated stump labeled a larger extent of motoneurons than matched injections on the intact side or in normal animals, including motoneurons that would normally supply only the missing limb muscles. Although the total numbers of distal limb motoneurons remained normal, some distal limb motoneurons on the amputated side were smaller in size and simpler in form. These results suggest that deprived motoneurons survive and retain function by reinnervating new muscle targets. The sprouted motor efferents may account for some of the reorganization of primary motor cortex that follows long-standing amputation.

Amputation, Surgical↗

PubMed2000

Perioperative safety and prognosis in hepatocellular carcinoma patients with impaired liver function.

BACKGROUND: The benefits of liver resection for hepatocellular carcinoma (HCC) patients with concomitant impaired liver function were often considered questionable because of poor postoperative prognosis. This study will clarify whether an acceptable operative risk exists and whether limited resection will compromise the outcomes of these patients. STUDY DESIGN: Between July 1991 and December 1996, a total of 168 patients with HCC who underwent hepatectomies were enrolled and divided into normal (group A) and impaired (group B) liver function groups according to the value of indocyanine green retention rate at 15 minutes. Clinical features, surgical related features, pathologic features, and disease-free and overall survivals were compared between the groups. RESULTS: Operative morbidity and mortality in group A were 27.3% and 1.6%, and in group B were 40.0% and 2.5%, respectively (p = 0.129 and 0.506). Disease-free survival and overall survival at 5 years in group A were 43.2% and 59.6%, respectively, and in group B they were 30.6% and 56.8%, respectively (p = 0.607 and 0.378). CONCLUSIONS: Limited liver resection is safe and provides favorable prognosis in HCC patients with concomitant impaired liver function.

Adult↗

PubMed2000

Clinical significance of microscopic tumor venous invasion in patients with resectable hepatocellular carcinoma.

BACKGROUND: Tumor venous invasion in patients with resectable hepatocellular carcinoma (HCC) is frequent and can be macroscopic and microscopic or microscopic alone. Although macroscopic invasion is a well-established prognostic indicator, the clinical significance of microscopic invasion remains unclear. METHODS: There were 322 patients enrolled who had undergone curative resection for HCC. The clinicopathologic factors and prognostic significance associated with macroscopic and microscopic venous invasion were analyzed. RESULTS: Macroscopic invasion was observed in 50 patients (15.5%) and microscopic invasion in 190 (59.0%). The larger the tumor, the more the incidence of venous invasion. There were 140 patients with microscopic invasion only (Group 1). Patients with macroscopic invasion (Group 2, n = 50) also had microscopic invasion. Compared with patients without venous invasion (Group 3, n = 132), Group 1 had a higher alpha-fetoprotein level, a larger tumor size, and more tumors without encapsulation. For group 1, the 1-, 3-, and 5-year disease-free survival rates were 65.6%, 41.6%, and 30.8%, respectively. The 1-, 3-, and 5-year overall survival rates were 87. 8%, 60.0%, and 52.7%, respectively. The survival rates of group 1 were lower than those of group 3 and higher than those of group 2 (P <.05). Multivariate analysis indicated that microscopic and macroscopic venous invasion, surgical margin, indocyanine-green retention, and tumor size and number were significant predictors of postresectional survival. CONCLUSIONS: In HCC patients, microscopic venous invasion is frequent and related independently to postresectional outcome.

Aged↗

PubMed2000

Serum interleukin-10 but not interleukin-6 is related to clinical outcome in patients with resectable hepatocellular carcinoma.

OBJECTIVE: To evaluate the clinical significance of preoperative serum levels of interleukin-10 (IL-10) and interleukin-6 (IL-6) in patients with resectable hepatocellular carcinoma (HCC). SUMMARY BACKGROUND DATA: IL-10 is an immunosuppressive factor and IL-6 is a multifunctional cytokine that plays a role in host defense mechanisms. Both have been reported to be related to the disease prognosis in some human solid tumors. Their role in human HCC has not been investigated. METHODS: Preoperative serum samples of 67 patients with HCC who underwent potentially curative resection and 27 normal healthy donors were assayed. Levels of IL-10 and IL-6 were determined by enzyme-linked immunosorbent assay. The clinical significance of serum IL-10 and IL-6 was evaluated and compared with conventional clinicopathologic factors. RESULTS: Levels of IL-10 and IL-6 were significantly higher in patients with HCC than in healthy subjects. There was no correlation between IL-10 and IL-6 levels. Tumor resection resulted in a decrease in IL-10 and IL-6 levels. On univariate analysis, patients with high IL-10 levels had a worse disease-free survival, but IL-6 levels had no correlation with the disease-free survival. Multivariate analysis identified IL-10 levels as a predictor of postresectional outcome, in addition to the well-established clinical risk factors. CONCLUSIONS: In patients with HCC, the preoperative serum IL-10 level is related to the clinical outcome. IL-10 may play an important role in the progression of HCC.

Carcinoma, Hepatocellular↗

PubMed2000

Tumor necrosis factor gene polymorphism and septic shock in surgical infection.

OBJECTIVES: To evaluate the relationship of the genotype distribution of the tumor necrosis factor (TNF)-alpha polymorphism with regard to the plasma TNF-alpha concentration and the development of septic shock as well as mortality of infected patients in a surgical intensive care unit (SICU). DESIGN: A total of 112 postoperative critically ill infected patients were prospectively enrolled. SETTING: SICU of a tertiary university-affiliated medical center. PATIENTS: Patients who were consecutively admitted to the SICU because of surgical infection with sepsis. INTERVENTION: Blood sampling. MEASUREMENTS AND MAIN RESULTS: Blood sample was obtained 24 hrs after intensive care unit (ICU) admission or within 2 hrs after the onset of septic shock to determine the plasma TNF-alpha level and to analyze the genotype of the biallelic polymorphism of the TNF-alpha. RESULTS: The allele frequency of the TNF2 in our infected ICU patients was 12%. Forty-two (37.5%) patients admitted fulfilled the criteria of septic shock during their ICU stay. Patients carrying the TNF2 allele were not more likely to develop septic shock, nor did they have a higher mortality rate. In the patients with septic shock, those carrying the TNF2 allele had a significantly higher mortality rate than those with the homozygous TNF1 genotype (92% vs. 62%, p < .05). In those who developed septic shock, the TNF2 allele was significantly associated with higher TNF levels. CONCLUSION: In patients admitted to SICU with surgical infection, the frequency of TNF2 allele was higher than in the general population. SICU patients with TNF2 allele did not show a higher incidence of developing septic shock, nor was there a higher baseline TNF-alpha level after infection. However, once septic shock had developed, the mortality rate was higher in those patients carrying the TNF2 allele.

APACHE↗

PubMed2000

Variations of the cystic artery in Chinese adults.

The origin and course of the cystic artery related to the Calot triangle were studied in 72 autopsies. The cystic artery arises from many possible origins; the right hepatic artery is the most common origin (76.6%). The Calot triangle (hepatocystic triangle), which is an important imaginary referent area for biliary surgery, is bounded by the common hepatic duct (CHD), the cystic duct, and the cystic artery. Of all the cystic arteries, 86.1% coursed through the Calot triangle, and 100% of the cystic arteries originating from the right hepatic artery coursed through the Calot triangle. However, only 54% of the cystic arteries that originated from the left, bifurcation, proper, and common hepatic arteries ran through the triangle. None of the cystic arteries that originated from the gastroduodenal, celiac, superior mesentery, or superior pancreaticoduodenal arteries passed through the triangle. Furthermore, 72.7% of the cystic arteries that originated from the right hepatic artery ran beneath the CHD as they entered the Calot triangle; the others ran anterior to the CHD. Of the cystic arteries that arose from locations other than the right hepatic artery, 29.4% ran posterior to the CHD, and 11.8% ran anterior to the CHD. The current study provides detailed information about anatomic variance in Chinese adults that may help avoid injury during open or laparoscopic cholecystectomies.

Adult↗

PubMed2000

Stability and peptide binding specificity of Btk SH2 domain: molecular basis for X-linked agammaglobulinemia.

X-linked agammaglobulinemia (XLA) is caused by mutations in the Bruton's tyrosine kinase (Btk). The absence of functional Btk leads to failure of B-cell development that incapacitates antibody production in XLA patients leading to recurrent bacterial infections. Btk SH2 domain is essential for phospholipase C-gamma phosphorylation, and mutations in this domain were shown to cause XLA. Recently, the B-cell linker protein (BLNK) was found to interact with the SH2 domain of Btk, and this association is required for the activation of phospholipase C-gamma. However, the molecular basis for the interaction between the Btk SH2 domain and BLNK and the cause of XLA remain unclear. To understand the role of Btk in B-cell development, we have determined the stability and peptide binding affinity of the Btk SH2 domain. Our results indicate that both the structure and stability of Btk SH2 domain closely resemble with other SH2 domains, and it binds with phosphopeptides in the order pYEEI > pYDEP > pYMEM > pYLDL > pYIIP. We expressed the R288Q, R288W, L295P, R307G, R307T, Y334S, Y361C, L369F, and 1370M mutants of the Btk SH2 domain identified from XLA patients and measured their binding affinity with the phosphopeptides. Our studies revealed that mutation of R288 and R307 located in the phosphotyrosine binding site resulted in a more than 200-fold decrease in the peptide binding compared to L295, Y334, Y361, L369, and 1370 mutations in the pY + 3 hydrophobic binding pocket (approximately 3- to 17-folds). Furthermore, mutation of the Tyr residue at the betaD5 position reverses the binding order of Btk SH2 domain to pYIIP > pYLDL > pYDEP > pYMEM > pYEEI. This altered binding behavior of mutant Btk SH2 domain likely leads to XLA.

Agammaglobulinaemia Tyrosine Kinase↗

PubMed2000

Adeno-associated virus major Rep78 protein disrupts binding of TATA-binding protein to the p97 promoter of human papillomavirus type 16.

Adeno-associated virus type 2 (AAV) is known to inhibit the promoter activities of several oncogenes and viral genes, including the human papillomavirus type 16 (HPV-16) E6 and E7 transforming genes. However, the target elements of AAV on the long control region (LCR) upstream of E6 and E7 oncogenes are elusive. A chloramphenicol acetyltransferase assay was performed to study the effect of AAV on the transcription activity of the HPV-16 LCR in SiHa (HPV-positive) and C-33A (HPV-negative) cells. The results reveal that (i) AAV inhibited HPV-16 LCR activity in a dose-dependent manner, (ii) AAV-mediated inhibition did not require the HPV gene products, and (iii) the AAV replication gene product Rep78 was involved in the inhibition. Deletion mutation analyses of the HPV-16 LCR showed that regulatory elements outside the core promoter region of the LCR may not be direct targets of AAV-mediated inhibition. Further study with the electrophoretic mobility shift assay demonstrated that Rep78 interfered with the binding of TATA-binding protein (TBP) to the TATA box of the p97 core promoter more significantly than it disrupted the preformed TBP-TATA complex. These data thus suggest that Rep78 may inhibit transcription initiation of the HPV-16 LCR by disrupting the interaction between TBP and the TATA box of the p97 core promoter.

Cell Line↗

PubMed2000

Profiling the downstream genes of tumor suppressor PTEN in lung cancer cells by complementary DNA microarray.

The phosphatase and tensin homology deleted on chromosome 10 (PTEN) is a tumor suppressor gene with sequence homology to tyrosine phosphatases and the cytoskeletal proteins tensin and auxilin. PTEN has recently been shown to inhibit cell migration and the spreading and formation of focal adhesions. This study investigated the role of PTEN in carcinoma invasion in a lung-cancer cell line and examined the downstream genes regulated by PTEN. We have previously established a cell-line model in human lung adenocarcinoma with different invasive abilities and metastatic potentials. Examining PTEN gene expression in these cell lines, we found that a homozygous deletion in exon 5 is associated with high invasive ability. We then constructed stable constitutive and inducible wild-type PTEN-overexpressed transfectants in the highly invasive cell line CL(1-5). We found that an overexpression of PTEN can inhibit invasion in lung cancer cells. To further explore the downstream genes regulated by PTEN, a high-density complementary DNA (cDNA) microarray technique was used to profile gene changes after PTEN overexpression. Our results indicate a panel of genes that can be modulated by PTEN. PTEN overexpression downregulated genes, including integrin alpha(6), laminin beta(3), heparin-binding epidermal growth factor-like growth factor, urokinase-type plasminogen activator, myb protein B, Akt2, and some expressed sequence tag (EST) clones. In contrast, PTEN overexpression upregulated protein phosphatase 2A1B, ubiquitin protease (unph), secreted phosphoprotein 1, leukocyte elastase inhibitor, nuclear factor-kappaB, cyclic adenosine monophosphate response element binding protein, DNA ligase 1, heat shock protein 90, and some EST genes. Northern hybridization and flow cytometry analysis also confirmed that PTEN overexpression results in the reduced expression of the integrin alpha(6) subunit. The results of this study indicate that PTEN overexpression may inhibit lung cancer invasion by downregulation of a panel of genes including integrin alpha(6). The cDNA microarray technique may be an effective tool to study the downstream function of a tumor suppressor gene.

Adenocarcinoma↗

PubMed2000

Binary/ternary combined effects of vitamin K3 with other antitumor agents in nasopharyngeal carcinoma CG1 cells.

Nasopharyngeal carcinoma (NPC) is a prevalent cancer in Taiwan. To improve the treatment of NPC, we have extensively searched for effective combination chemotherapies. Our previous studies indicated that vitamin K3 (VK3) inhibits the growth of NPC CG1 cells in vitro. In this study, we further studied the binary/ternary combined effects of VK3 with other anticancer drugs against NPC cells. The antitumor effects of different VK3 combinations against CG1 cells were determined by using MTT assay, and the combined effects were evaluated by a taibologram, a modified isobolographic method being developed in our laboratory for the analyses of binary/ternary combinations of anticancer agents. Binary combinations of VK3 with doxorubicin (DOX), vinblastine (VBL), or 5-fluorouracil (5-FU) result in synergistic effects. For three-drug combinations, a remarkable synergy was found in the combination of VK3, VBL, and 5-FU. These in vitro results will provide useful information not only for further mechanistic studies and but also for future clinical trials of VK3-based cancer chemotherapy of NPC.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2000

Tissue-specific cancer-related serpin gene cluster at human chromosome band 3q26.

Approximately one quarter of the identified human serpin genes are cancer-related and clustered mainly at two distinct loci: 6p25 and 18q21. We have studied a novel serpin gene cluster at 3q26 containing at least two recently identified members: the pancreas-specific protease inhibitor, pancpin (PI14), and the brain-associated protease inhibitor, neuroserpin (PI12). In this, unlike a previous study, both PI14 and PI12 at 3q26 were found to consist of 9 exons and 8 introns and to share a perfectly conserved gene organization whose pattern is very different from that of the ov-serpin family. This distinct pattern appears identical in the genomic structures of human plasminogen activator inhibitor-1 (PAI1) at 7q21 and protease nexin 1 (PI7) at 2q33-35, confirming that these four genes in three different chromosomes form a discrete subset within the serpin superfamily. As in the other three members whose gene expression is altered during tumorigenesis, PI12 expression was found to be down-regulated in tumor brain tissues and in two brain cancer cell lines: U-87 MG and H4. By screening genomic libraries, we isolated two overlapping clones showing that the marker SGC32223 (centromere) is located within intron F of PI12 and the marker WI-10077 (telomere) is located downstream of the 3'-flanking region of PI14. This finding indicates that the distance between human PI14 and PI12 is approximately 100 kb, and hence we speculate that other tissue-specific cancer-related serpin genes are likely to reside within this 3q26.1 cluster region.

Amino Acid Sequence↗

PubMed2000

Splenic abscess--a changing trend in treatment.

Fifteen patients with splenic abscesses were evaluated between 1985 and 1995. The most common predisposing factors were remote infection, diabetes mellitus and heart disease. Common clinical presentations included leucocytosis, fever, left upper quadrant abdominal pain and left pleural effusion. Four patients with splenic abscesses smaller than 4 cm in diameter were treated with antibiotics alone, and 1 in this treatment group died. Among the 10 patients with splenic abscesses larger than 4 cm in diameter receiving percutaneous drainage, 9 (90%) were successfully cured, including 8 with unilocular abscesses and 1 with multilocular abscesses. Two patients underwent splenectomy. In conclusion, percutaneous drainage using ultrasound or computed tomography guidance may be recommended as the treatment of choice for splenic abscess larger than 4 cm in diameter. Antibiotics alone may sometimes be considered for splenic abscesses smaller than 4 cm in diameter. Splenectomy is reserved for those cases where medical treatment has failed.

Abscess↗

PubMed1999

Reorganization in primary motor cortex of primates with long-standing therapeutic amputations.

Intracortical microstimulation was used to investigate the organization of primate primary motor cortex (M1) in three squirrel monkeys and two galagos years after the therapeutic amputation of an injured forelimb or hindlimb. In two squirrel monkeys with forelimb amputation, physiological results were correlated with the distribution of corticospinal neurons after injections of tracers into the lower cervical segments of the spinal cord. Distributions of labeled corticospinal neurons helped identify the locations of the former forelimb cortex in M1. Evoked movements from M1 ipsilateral to the missing limb were not obviously different from M1 of normal controls. Stimulation in the deefferented part of M1 contralateral to the missing limb elicited movements of the remaining proximal muscles as well as movements from adjacent body representations in all cases. Stimulation in the deefferented forelimb cortex evoked shoulder stump, trunk, and orofacial movements, whereas stimulation in the deefferented hindlimb cortex evoked hip stump, trunk, and tail movements. Movements were evoked from all sites in the deprived cortex, so that there were no unresponsive zones. Minimal levels of current necessary to evoke these movements varied from those in the normal range to those of much higher levels, with the average threshold higher than normal. Finally, multiunit recording from the two galagos revealed that the deprived portions of S1 were responsive to touch or taps on the stump and neighboring body parts.

Amputation, Surgical↗

PubMed1999

Inhibition of hTAFII32-binding implicated in the transcriptional repression by central regions of mutant p53 proteins.

We previously identified a movable and regulable inactivation function within the central region (CRts247) of a temperature-sensitive p53 (p53(ts)) mutant, p53(N247I). Here we showed that central regions from several p53(ts) mutants behaved similarly, i.e. they repressed a neighboring activation domain only when existing in the mutant status. Using chimeric protein GAL4VP16-CRts247 as an example, we demonstrated that de novo protein synthesis was not required for the reactivation of the chimeric protein, indicating that a post-translational mechanism was involved in the control of CRts247 activity. The CRts247-conferred thermo-regulability did not work via a mechanism demanding either an alteration of the subcellular compartmentalization of or the inactivation of DNA-binding activity of the GAL4 chimera. Further, CRts247 did not function in trans, eliminating the possibility that the observed repression was because of the competition for a putative factor(s) by the mutant p53 domain. Rather, CRts247 bestowed temperature-dependent interaction with hTAFII32 to the VP16 activation domain. In a parallel experiment, CRts247 also caused a large reduction in the affinity of hTAFII32 to the p53 activation domain at the nonpermissive temperature. These results strongly suggested that inhibition of hTAFII32 binding could be one of the mechanisms responsible for the transcriptional repression by mutant p53 central regions.

Mutation↗

PubMed1999

Effect of magnolol on in vitro mitochondrial lipid peroxidation and isolated cold-preserved warm-reperfused rat livers.

BACKGROUND/AIM: A mechanism suggested to cause injury to preserved organs is the generation of oxygen free radicals. Lipid peroxidation is one of the biological damages caused by oxygen free radicals. It is our aim to investigate whether magnolol, a strong antioxidant, suppresses the generation of oxygen free radicals and improves the viability of cold-preserved warm-reperfused rat livers. MATERIALS AND METHODS: In vitro lipid peroxidation was induced in rat hepatic mitochondria with ADP and FeSO4. The inhibitory effect of magnolol on lipid peroxidation was measured with oxygen consumption and malondialdehyde (MDA) formation. Subsequently, we preserved and reperfused rat livers in preservation solutions that contained magnolol. The hepatic enzymes and liver MDA were measured to assess the protective effect of magnolol on isolated rat livers. RESULTS: In rat hepatic mitochondria, magnolol was 470 times more potent than alpha-tocopherol in inhibiting oxygen consumption and 340 times more potent than alpha-tocopherol in inhibiting MDA formation. Addition of magnolol to Ringer's lactate solution had a protective effect, in terms of MDA formation and leakage of hepatic enzymes, on warm-reperfused but not cold-stored liver tissue. Addition of magnolol to University of Wisconsin (UW) solution, a widely used preservation solution, did not modify the effect of this solution on isolated liver tissues. CONCLUSIONS: We conclude that magnolol is an effective antioxidant and suppresses lipid peroxidation in rat liver mitochondria and can be used as a rinsing solution in protecting transplanted organs from lipid peroxidation during reperfusion, especially for those organs not preserved with UW solution.

Animals↗

PubMed1999

Diagnostic and prognostic values of CA 19-9 and CEA in periampullary cancers.

BACKGROUND: The roles of carcinoembryonic antigen (CEA) and carbohydrate antigen 19-9 (CA 19-9) in periampullary cancers have not been clearly established. Diagnostic and prognostic values of these two tumor markers were clarified in this study. STUDY DESIGN: Preoperative serum levels of CEA and CA 19-9, and clinicopathologic features were retrospectively reviewed in 143 surgical patients with periampullary cancer from 1989 to 1997. RESULTS: There were 86 resectable and 57 unresectable periampullary cancers. CA 19-9 demonstrated significantly higher sensitivity in detecting these cancers than CEA. The cancer with unresectable lesion, total bilirubin >7.3 mg/dL, or tumor size >2 cm tended to associate with higher CA 19-9 level. CEA level was significantly higher in the tumor >2 cm, not in the tumor < or =2 cm. CA 19-9 was a significant prognostic factor in both resectable and unresectable periampullary cancers, but CEA was significant only in the resectable group. Multivariate analysis revealed that independent prognostic factors included CA 19-9, resectability, primary tumor, and stage, and CA 19-9 was the most important one. CONCLUSION: CA 19-9 provided more important diagnostic and prognostic values than CEA in periampullary cancers and was the most important independent prognostic factor for periampullary cancers. This study recommends serum CA 19-9 as an adjunct in detecting periampullary cancers, in evaluating resectability, and in predicting prognosis.

Ampulla of Vater↗

PubMed1999

Somatic electrical nerve stimulation regulates the motility of sphincter of Oddi in rabbits and cats: evidence for a somatovisceral reflex mediated by cholecystokinin.

Cholecystokinin (CCK) plays an important role in regulating the biliary motility in herbivorous and carnivorous animals. Little is known about how the motility of the sphincter of Oddi (SO) is regulated through a somatic stimulation. It was our aim to test the hypothesis that somatic electrical nerve stimulation (SENS) affects SO motility in animals with different types of SO through CCK-related mechanisms. The activity of SO in anesthetized rabbits and cats was measured by using a continuously perfused open-tip manometric method. SENS was brought about by applying an electric current (2/15 Hz alternatively, 20 min) to two needles positioned near spinal nerves in the 6th and 7th intercostal space in the right midclavicular line. The SO motility before and X min after the start of SENS, designated as pre-SENS and SENS-X respectively, were recorded and saved in a computer equipped with off-line analysis software. The SO activity in rabbits, in terms of phasic contraction pressure and duration of summation peak during SENS were significantly higher than that before SENS. The phasic contraction pressure of pre-SENS, SENS-10, and SENS-16 were 6.83 +/- 0.39 mm Hg, 9.23 +/- 0.83 mm Hg and 10.46 +/- 0.81 mm Hg, respectively (P < 0.03, N = 13). The duration of summation peak in pre-SENS, SENS-10, and SENS-16 were 7.26 +/- 0.41 sec, 10.22 +/- 0.46 sec, and 13.49 +/- 2.31 sec, respectively (P < 0.05, N = 13). The SENS-induced SO hyperactivity was not inhibited by pretreatment with atropine, propranolol, phentolamine, or naloxone, but was blocked by pretreatment with the CCK receptor antagonist, proglumide, and by injection of anti-CCK-8 antibody during SENS in a dose-dependent manner. In contrast, SENS induced an inhibitory SO response in cats. However, in both circumstances, an obvious elevation of plasma CCK level determined by radioimmunoassay was noted after SENS. We conclude that SENS causes secretion of CCK, which in turn affects biliary tract motility in animals with different types of SO. This provides an easily applicable method for those patients who have hyperactive SO function.

Animals↗