Dibenzothiophene (DBT) was used as a model compound. A bacteria strain, which can degrade dibenzo-thiophene efficiently, was obtained. This strain was identified as Pseudomonas stutzeris UP-1 according to its morphological, physiological and biochemical characters, and 16S rDNA sequence. The strain exhibits strong degradation capacity of DBT, and the end product of degradation is a kind of soluble compound. After the analysis of product of DBT degradation, it was deduced that the degradation of DBT by Pseudomonas stutzeri UP-1 is in accordance with the Kodama mechanism.

AIMTo study whether store-operated Ca2+ channel (SOC) is present in rat colonic smooth muscle cells.

METHODSIntracellular Ca2+ ([Ca2+]i) changes induced by thapsigargin- or caffeine-activated SOC channel were measured in enzymatically dissociated rat colonic smooth muscle cells with the fluorescent indicator Fura-2/AM.

RESULTSIn the absence of external Ca2+ , the sarco-endoplasmic reticulum Ca2+ pump inhibitor thapsigargin (1 micromol/L) and ryanodine receptor (RyR) activator caffeine both transiently elevated [Ca2+]i from (68.32 +/- 3.43) nmol/L to (240.85 +/- 12.65 ) nmol/L, (481.25 +/- 34.77) nmol/L. A subsequent reintroduction of Ca2+ into the extracellular solution resulted in [Ca2+]i further elevated to (457.55 +/- 19.80) nmol/L, (1005.93 +/- 54.62) nmol/L; (643.88 +/- 34.65) nmol/L, (920.16 +/- 43.25) nmol/L, respectively. And the elevated response was blocked by lanthanum (1 mmol/L), but was insensitive to L-type voltage calcium channels blocker verapamil and membrane depolarization.

CONCLUSIONSOC activated by store depletion are present in rat colonic smooth muscle cells. And we further prove the existence of such Ca2+ channels in excitable cells.

Animals ; Caffeine ; pharmacology ; Calcium ; metabolism ; Calcium Channels ; physiology ; Colon ; cytology ; Fura-2 ; metabolism ; Myocytes, Smooth Muscle ; drug effects ; metabolism ; Rats ; Rats, Wistar ; Thapsigargin ; pharmacology

Contraction of smooth muscle cells is triggered by an increase in cytosolic Ca(2+) upon agonist stimulation. Ca(2+) influx across the plasma membrane constitutes a major component of the agonist-induced response in smooth muscle cells. Traditionally, voltage-operated Ca(2+) channel (VOCC) is considered as the channel mediating the Ca(2+) entry. However, this view has been challenged by recent discoveries, which demonstrated that other types of ion channels, such as store-operated and/or receptor-operated Ca(2+) channels (SOCC and/or ROCC), also participate in Ca(2+) response induced by agonists in smooth muscle cells. SOCC is defined as the channel activated in response to the depletion of the internal Ca(2+) stores, an event secondary to G protein coupled receptor or receptor tyrosine kinase stimulation. The Ca(2+) flow mediated by SOCC is termed as capacitative Ca(2+) entry (CCE). Previous study from other group has demonstrated that VOCC played a predominant role in ACh-induced contraction of distal colon smooth muscle in guinea pig. However, whether SOCC participates in the agonist-induced contractile response in this particular tissue is unknown. The present study was performed to investigate the role of CCE in ACh-induced mechanical activity of distal colon smooth muscle in rats. The contractile function of the smooth muscle was assessed by measuring isometric force of isolated rat distal colon rings. We showed that both high extracellular K(+) (40 mmol/L) and ACh (5 mumol/L) evoked striking contraction of the smooth muscle. The contractile responses were almost abolished by removal of extracellular Ca(2+) with ethylene glycol-bis(2-aminoethylether)-N,N,N',N' tetraacetic acid (EGTA), suggesting a critical contribution of extracellular source of Ca(2+) to the contraction. Verapamil (5 mumol/L), an L-type VOCC blocker, significantly attenuated, but didn't completely eliminate the high K(+)- and ACh-induced contraction (74% and 41% for high K(+) and ACh, respectively), indicating that additional channels might be involved in the contractile mechanism. Furthermore, ACh only induced transient contractions in the absence of extracellular Ca(2+). Readmission of Ca(2+) into the extracellular compartment resulted in a significant and sustained increase in the tension of the smooth muscle. This response was not affected by verapamil (5 mumol/L) and Cd(2+) (5 mumol/L), both of which efficiently block VOCC at the doses. However, La(3+), a known inhibitor of SOCC, significantly suppressed the Ca(2+) readdition-induced contraction in a dose-dependent manner. On the basis of these results, we conclude that contraction of smooth muscle in the distal colon is regulated by multiple Ca(2+) channels. In addition to VOCC-mediated Ca(2+) influx, SOCC-mediated CCE participates in agonist-induced contractile response of distal colon smooth muscle in rats.
Acetylcholine ; physiology ; Animals ; Calcium ; metabolism ; Calcium Channels ; physiology ; Colon ; physiology ; Female ; Male ; Muscle Contraction ; physiology ; Muscle, Smooth ; physiology ; Myocytes, Smooth Muscle ; physiology ; Rats ; Rats, Sprague-Dawley ; Verapamil ; pharmacology

A switch thrombin aptamer sensor was constructed based on the host-guest competition mode ofβ-cyclodextrin (β-CD ) . The aptamer that modified with ferrocene ( Fc ) at its terminal was fixed on the surface of the gold electrode via the host-guest recognization with β-CD. When thrombin was present, the configuration of aptamer transformed from vertical linear to "G-quadruplex" and far away from the electrode surface, which resulted in a decrease in the redox current of the aptamer probe and produce "Signal-off"effect. On the basis of this, a high sensitive detection of thrombin was made. The detection result indicated that the thrombin concentration had a consideration linear response to the signal of aptasensor between 5 . 0 × 10-13-5. 0 × 10-9 mol/L, and as low as 2. 0 × 10-13 mol/L thrombin had been detected. This method for thrombin detection showed a higher specificity compared to other protein molecules. Besides, the sensor was constructed easily and possessed excellent regeneration, which provided a significant platform for highly efficient real-time detection of thrombin in biological serum samples.

OBJECTIVETo analyze the effects of surgical treatment for gastrointestinal stromal tumors (GISTs) and influential factors of survival.

METHODSThe clinical data and the tissue slices including immunohistochemical staining of 153 cases of GISTs from January 1990 to March 2006 were rechecked retrospectively. All patients were followed up carefully. More attention was paid to the surgical effects and the influential factors of survival.

RESULTSThe overall survival rates at 1-, 2-, 3-, 4- and 5-year were 94.9%, 83.3%, 73.3%, 70.5% and 64.3%, respectively. The median survival time for patients with tumor resected completely was 66.0 months, and the 2- and 5-year survival rate were 89.4% and 70.9% respectively. The median survival time was 23.8 months for the patients with tumor resected partly, and only two of these patients survived over 2 years. Gender, tumor sites, preoperative metastasis, tumor size, pathological type, karyokinesis and recurrence and metastasis were related with survival rates for the patients with tumor resected completely on univariate analysis, but tumor size, pathology type, recurrence and metastasis were related with survival rates on Cox regression multivariate analysis (P < 0.05).

CONCLUSIONSSurgery should still be the main therapy for GISTs. Local complete resection is the principal treatment. The survival cannot be improved by extensive resection and lymph nodes clearance.

Adult ; Aged ; Aged, 80 and over ; Antigens, CD34 ; analysis ; Female ; Follow-Up Studies ; Gastrointestinal Stromal Tumors ; metabolism ; mortality ; surgery ; Humans ; Immunohistochemistry ; Kaplan-Meier Estimate ; Male ; Middle Aged ; Proto-Oncogene Proteins c-kit ; analysis ; Retrospective Studies ; Survival Rate ; Treatment Outcome

OBJECTIVETo study the molecular risk factors of lymph node metastasis in stage T1 and T2 colorectal cancers by tissue microarray and immunohistochemistry techniques.

METHODSTwo hundred and three patients with stage T1 and T2 colorectal carcinoma who underwent radical surgery from 1999 to 2010 in our department were included in this study. Their clinicopathological data were retrospectively analyzed. Expression of the following 14 molecular markers were selected and assayed by tissue microarray and immunohistochemistry: VEGFR-3, HER2, CD44v6, CXCR4, TIMP-1, EGFR, IGF-1R, IGF-2, IGFBP-1, ECAD, MMP-9, RKIP, CD133, MSI. Chi-squared test and logistic regression were used to evaluate the variables as potential risk factors for lymph node metastasis.

RESULTSThe positive expression rates of biomarkers were as following: VEGFR-3 (44.3%), EGFR (30.5%), HER-2 (28.1%), IGF-1R (63.5%), IGF-2 (44.8%), IGFBP-1 (70.9%), ECAD (45.8%), CD44v6 (51.2%), MMP-9 (44.3%), TIMP-1 (41.4%), RKIP (45.3%), CXCR4 (40.9%), and CD133 (49.8%). The positive rate of MSI expression was 22.2%. Both univariate and multivariate analyses showed that VEGFR-3, HER-2, and TIMP-1 were significant predictors of lymph node metastasis. Univariate analysis showed that CD44v6 and CXCR4 were significant significant predictors of lymph node metastasis.

CONCLUSIONSVEGFR-3, HER2 and TIMP-1 are independent factors for lymph node metastasis in stage T1 and T2 colorectal cancers.

Aged ; Biomarkers, Tumor ; metabolism ; Colonic Neoplasms ; metabolism ; pathology ; Female ; Humans ; Hyaluronan Receptors ; metabolism ; Immunohistochemistry ; Lymphatic Metastasis ; Male ; Microsatellite Instability ; Middle Aged ; Neoplasm Staging ; Oligonucleotide Array Sequence Analysis ; Receptor, ErbB-2 ; metabolism ; Receptors, CXCR4 ; metabolism ; Rectal Neoplasms ; metabolism ; pathology ; Retrospective Studies ; Tissue Inhibitor of Metalloproteinase-1 ; metabolism ; Vascular Endothelial Growth Factor Receptor-3 ; metabolism

OBJECTIVETo analyze the outcome of the patients with gastric gastrointestinal stromal tumor(GIST) after surgical treatment and identify the associated risk factors.

METHODSClinical data and the tissue slices including immunohistochemistry staining of 140 patients with gastric GIST from January 1990 to December 2008 were retrospectively reviewed. SPSS 16.0 for Windows software package was used for statistical analysis.

RESULTSThe overall survival rates of 1-, 3-, 5-year were 96.8%, 86.7% and 79.3%, respectively. The survival rates of 1-, 3-, 5-year were 98.1%, 90.0% and 85.4% in patients who underwent complete tumor resection. But the survival rates of 1-, 3-, 5-year were 38.1%, 0 and 0 in patients with incomplete tumor resection. The differences were statistically significant (P<0.05). Gender, preoperative metastasis, tumor size,pathology type,karyokinesis, recurrence and metastasis were associated with survival rates in patients with complete tumor resection by univariate analysis. However, only tumor size, karyokinesis, recurrence and metastasis were associated with survival rates by Cox regression multivariable analysis(P<0.05).

CONCLUSIONSurgery remains the main treatment for gastric GIST. Local complete resection is the principal treatment.

Adult ; Aged ; Aged, 80 and over ; Female ; Gastrointestinal Stromal Tumors ; surgery ; Humans ; Male ; Middle Aged ; Prognosis ; Retrospective Studies ; Stomach Neoplasms ; surgery ; Survival Rate ; Treatment Outcome ; Young Adult

Objective: To explore the influence and mechanism of overexpression of SOCS2 on diabetic nephropathy (DN) rats and cells. Methods: STZ was used to induce male SD rats and SOCS2 was injected into left renal vein. Rats were divided into DN group, DN-Ad-null group and DN-Ad-SOCS2 group. Glucose with high and normal concentration was used to culture HBZY-1 cells and then transfect Ad-SOCS2. HG group, HG-Ad-null group, HG-Ad-SOCS2 group, CG group, CG-Ad-null group, and CG-Ad-SOCS2 group were created. The expression of inflammatory cytokines (MCP-1, TNF-α and IL-6) in kidney tissue of rats, fibrosis related protein (FN, Collagen IV and TGF-β) in kidney tissue and cells of rats, and JAK/STAT signaling pathway related proteins (p-JAK2 and p-STAT3) were tested by western blot. ELISA was used to test the expression of inflammatory cytokines (TNF-α and IL-6) in cells. Results: The expression of inflammatory cytokines in DN rats (MCP-1, TNF-α and IL-6) and cell (TNF-α and IL-6) were increased (P < 0.01) significantly. However, SOCS2 could decrease the overexpression of mediated inflammatory cytokines in DN animal models and cell models (P < 0.01). The expression of fibrosis related protein in DN rats and cells increased while SOCS2 decreased the overexpression of mediated fibrosis related protein in DN model rats and cells (P < 0.01). The expression of JAK/STAT pathway related protein in both DN rats and cells increased and the JAK/STAT signaling pathway was activated. Yet, SOCS2 obviously suppressed the expression of the JAK/STAT signaling pathway as well as the related proteins (p-JAK2 and p-STAT3) in both DN rats and cells. Conclusions: The overexpression of SOCS2 can decrease the expression of inflammatory cytokines and fibrosis related proteins in DN rats and cells, and meanwhile suppress the activation of JAK/STAT signaling pathway mediated by DN.

Glucolipid metabolic disease (GLMD), a complex of interrelated disorders in glucose and lipid metabolism, has become one of the leading chronic diseases causing public and clinical problem worldwide. As the metabolism of lipid and glucose is a highly coordinated process under both physiological and diseased conditions, the impairment in the signals corresponding to the metabolism of either lipid or glucose represents the common mechanism underlying the pathogenesis of GLMD. The liver and adipose tissue are the major metabolic organs responsible for energy utilization and storage, respectively. This review article aims to summarize the current advances in the investigation of the functional roles and the underling mechanisms of the interplay between the liver and adipose tissue in the modulation of GLMD development. Fibroblast growth factor 21 (FGF21) and adiponectin represent the two major hormones secreted from the liver and adipose tissues, respectively. FGF21 exerts pleiotropic effects on regulating glucose and lipid homeostasis majorly through inducing the expression and secretion of adiponectin. Therefore, FGF21-adiponectin axis functions as the key mediator for the crosstalk between the liver and adipose tissue to exert the beneficial effects on the maintenance of the homeostasis of energy consumption. The liver- and adipose tissue-derived factors with pleiotropic effects on regulating of lipid and glucose metabolism function as the key mediator for the crosstalk between these two highly active metabolic organs, thereby coordinating the initiation and development of GLMD.

Objective To investigate the relationship between serum angiotensin converting enzyme (ACE) and angiotensinogen (AGT) and gestational hypertension syndrome (HDCP) and the risk factors of HDCP. Methods A total of 135 pregnant hypertensive patients (HDCP group) and 100 normal pregnant women as control check (CK) group were selected. Serum ACE and AGT levels were measured by ELISA, and correlation analysis was performed. The age and gestational age of the two groups, pre-pregnancy body mass index (BMI), parity, number of births, family history of hypertension, family history, education, and other general information, single factor analysis of risk factors for maternal HDCP, single factor regression analysis Statistically significant factors were all used for multivariate logistic regression analysis. Results The serum ACE level in the HDCP group (90.49±47.65) μg/L was significantly higher than that in the CK group (58.72±27.58) μg/L, P<0.05, the difference was statistically significant. The serum AGT level in the HDCP group was (64.57±19.71) μg/L was higher than CK group (58.22±18.64) μg/L, P>0.05, the difference was not statistically significant; single factor analysis showed; age, BMI, hypertension, family history of diabetes, ACE level was maternal (P<0.05), while gestational age, parity, number of births, and education were no significant differences in risk factors for HDCP (P>0.05). Multivariate analysis showed: age, BMI, history of hypertension and ACE. It was a risk factor for pregnancy-induced hypertension. Conclusion ACE levels are associated with HDCP. AGT levels are not associated with HDCP. Patients with a high age, high BMI, and hypertension history have an increased risk of gestational hypertension syndrome.