The incidence and risk factors of gastrointestinal complications after hepatectomy: a retrospective observational study of 1329 consecutive patients in a single center.

BACKGROUND: Despite of the importance of gastrointestinal (GI) complications in morbidity and mortality after major and moderate surgeries, it is not yet specifically studied in patients undergoing hepatectomy. This study was aimed to investigate the in-hospital incidence and potential risk factors of GI complications after open hepatectomy in our hospital. SUBJECTS AND METHODS: Prospectively recorded perioperative data from 1329 patients undergoing elective hepatectomy were retrospectively reviewed. The in-hospital incidence of GI complications was investigated, and independent risk factors were analyzed by multiple logistic regression. RESULTS: GI complications occurrence was 46.4%. Univariate analysis showed that preoperative Child-Pugh score, total bilirubin, aspartate transaminase, anesthesia duration, operation duration, intraoperative blood loss, crystalloid and colloid infusion, blood transfusion, urine output, use of Pringle maneuver were statistically different between patients with and without GI complications (P < 0.05). Moreover, patients with GI complications had a more prolonged postoperative parenteral nutrient supporting time, hospital stay and ICU stay, and higher incidence of other complications than those without GI complications (P < 0.05). Multivariate regression indicated that long duration of anesthesia (odds ratio 2.51, P < 0.001) and use of Pringle maneuver (odds ratio 1.37, P = 0.007) were independent risk factors of GI complications after hepatectomy. CONCLUSIONS: The incidence of GI complications after hepatectomy is high, which is related to an increase of other complications and a prolonged hospital stay. Avoidance of routinely use of Pringle maneuver and shortening the duration of anesthesia are important measures to reduce the postoperative GI complications.

Kallikrein gene-modified EPCs induce angiogenesis in rats with ischemic hindlimb and correlate with integrin αvß3 expression.

BACKGROUND: Human tissue kallikrein (hTK) plays an essential role in the physiological and pathological mechanisms of blood vessels. This study aimed to determine whether angiogenesis induced by endothelial progenitor cells (EPCs) transduced with the adenovirus-mediated hTK gene could improve blood flow in rat hindlimb ischemia in vivo and to establish a promising mechanism in vitro. METHODS: EPCs transduced with adenovirus encoding hTK-162 (i.e., Ad/hTK-transduced EPCs or Ad/GFP-transduced EPCs) were administered to Wister rats with hindlimb ischemia through therapeutic neovascularization. Muscular capillary density (MCD), blood flow (BF), and the number of myofibers were measured at days 7, 14, and 21 after treatment. Expressions of integrin αvß3 and endothelial nitric oxide synthase (eNOS) were detected on the surface of EPCs. RESULTS: MCD, BF, and the number of myofibers in rats with Ad/hTK-transduced EPCs remarkably increased at day 21 after treatment compared with rats with Ad/GFP-transduced EPCs or the control group (P<0.01). Expressions of integrin αvß3 and eNOS protein on the surface of EPCs also increased in rats with Ad/hTK-transduced EPCs. The levels of integrin αvß3 expression were reduced by PI3K and eNOS blockade, and the inhibitor of integrin αvß3 abrogated the migration and adhesion of hTK-transduced EPCs (P<0.05). CONCLUSION: hTK gene delivery in vivo improves the natural angiogenic response to ischemia. The ability of hTK gene-transduced EPCs can be enhanced in vitro, in which integrin αvß3 plays a role in the process.

Molecular cloning and characterization of a cathepsin B from Angiostrongylus cantonensis.

Cysteine proteases, a superfamily of hydrolytic enzymes, have numerous functions in parasites. Here, we reported the cloning and characterization of a cDNA encoding a cathepsin B (AcCPB) from Angiostrongylus cantonensis fourth-stage larvae cDNA library. The deduced amino acid sequence analysis indicated AcCPB is related to other cathepsin B family members with an overall conserved architecture. AcCPB is evolutionarily more close to other parasitic nematode cathepsin B than the ones from hosts, sharing 43-53% similarities to the homologues from other organisms. Real-time quantitative PCR analysis revealed that AcCPB was expressed significantly higher in the fourth-stage larvae (L4) and the fifth-stage larvae (L5) than that in the third-stage larvae (L3) and adult worms (Aw). Unexpectedly, AcCPB was expressed at a higher level in L4 and L5 derived from mice than the larvae at the same stages derived from rats. The protease activity of recombinant AcCPB (rAcCPB) expressed in Escherichia coli showed high thermostability and acidic pH optima. The role in ovalbumin digestion and enzyme activity of rAcCPB could be evidently inhibited by cystatin from A.cantonensis. Furthermore, we found rAcCPB increased the expression levels of CD40, MHC II, and CD80 on LPS-stimulated dendritic cells (DCs). In this study, we provided the first experimental evidence for the expression of cathepsin B in A.cantonensis. Besides its highly specific expression in the stages of L4 and L5 when the worms cause dysfunction of the blood-brain barrier of hosts, AcCPB displayed different expression profiles in non-permissive host- and permissive host-derived larval stages and was involved in the maturation of DCs, suggesting a potential role in the central nervous system invasion and the immunoregulation during parasite-host interactions.