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The results suggest that surgical intervention is still the main therapeutic method and the best procedure that should be selected according to causes of disease and patient's condition and history.

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Many studies have evaluated the association between serum levels of mannose-binding lectin (MBL) and sepsis; however, the findings are inconclusive and conflicting. For a better understanding of MBL in sepsis, we conducted a comprehensive meta-analysis. Potential relevant studies were identified covering Science Citation Index, the Cochrane Library, PubMed, Embase, CINAHL, and Current Contents Index databases. Two reviewers extracted data and assessed studies independently. Statistical analyses were conducted with the version 12.0 STATA statistical software. Ten papers were collected for meta-analysis. Results identified that sepsis patients had considerably lower MBL level than those in the controls (standardized mean difference (SMD) = 1.59, 95 % confidence interval (95%CI) = 0.86∼2.31, P < 0.001). Ethnicity-subgroup analysis showed that sepsis patients were associated with decreased serum MBL level in contrast to the healthy controls in Asians (SMD = 3.07, 95%CI = 1.27∼4.88, P = 0.001) and Caucasians (SMD = 1.00, 95%CI = 0.35∼1.65, P = 0.003). In the group-stratified subgroup analysis, subjects with lower serum MBL level did underpin susceptibility to sepsis in the infants subgroup (SMD = 2.57, 95%CI = 1.59∼3.55, P < 0.001); however, this was not the case in the adults subgroup (SMD = 0.13, 95%CI = -1.30∼1.55, P = 0.862). Our study suggests an important involvement of serum MBL level in sepsis patients considering their lower level compared to controls, especially among infants.

Emodin has a direct excitatory effect on circular smooth muscle cells in rat colon mediated via Ca(2+)/CaM dependent pathways. Furthermore, emodin-induced peak [Ca(2+)]i increase may be attributable to the Ca(2+) release from IP(3) sensitive stores, which further promote Ca(2+) release from ryanodine-sensitive stores through CICR mechanism. Additionally, Ca(2+) influx from extracellular medium contributes to the sustained increase in [Ca(2+)]i.

Rationale:Spontaneous isolated dissection of the superior mesenteric artery (SID-SMA) is a rare arterial disease that is difficult to differentiate from other diseases because of lack of specific clinical manifestation and for which there is no available optimal management strategy.Patient concerns:A 58-year-old male patient visited our emergency room with sudden onset of moderate-severe epigastric abdominal pain of uncertain cause.Diagnoses:Computed tomography scanning showed a characteristic “double lumen sign” of the superior mesenteric artery, and further computed tomography angiography findings revealed a dissected segment of the superior mesenteric artery.Interventions:Conservative management was administered for 5 days, but the abdominal pain remained. Subsequently, an endovascular stent was placed in the affected superior mesenteric artery. Postoperative antiplatelet therapy was administered for 6 months.Outcomes:The abdominal pain was relieved. Six months later, a follow-up of computed tomography angiography showed that the stent placed had no interval narrowing.Lessons:Based on our review and the illustration of this case, endovascular stenting may be a preferred rescue treatment in SID-SMA patients for whom initial conservative treatment fails.

Aim: To clarify the contributions of ulinastatin to cellular immune responses in vivo, we examined the functional alterations of splenocytes and quantitatively evaluated the effects of ulinastatin on the splenocyte function during experimental severe acute pancreatitis. Methods: Severe acute pancreatitis was induced in rats by retrograde injection of 3% sodium deoxycholate. Thirty minutes after induction of pancreatitis, the rats were randomly assigned to four groups, receiving either saline or 50,000 U/kg of ulinastatin, respectively. Splenocytes were obtained aseptically and stimulated with concanavalin A for 24 h. Then the proliferative activity of cultured splenocytes was measured by using an MTT cellular proliferation assay, and the cytokine concentrations in the culture supernatants were measured by enzyme-linked immunosorbent assays. Results: Upon stimulation, the release of interleukin-2, interleukin-10, and interferon-γ was significantly decreased in the splenocytes from rats with pancreatitis as compared with those from sham operation and control groups. The splenocyte proliferation was also significantly suppressed in this group. In contrast, the proliferative as well as the cytokine-releasing capacities of the splenocytes from rats treated with ulinastatin were significantly increased as compared with those from rats with pancreatitis. Conclusions: The deficiencies in proliferation and cytokine release in response to antigen stimulation demonstrated an anergic state of splenocytes during severe acute pancreatitis. Treatment with ulinastatin contributed to the recovery of the immune function by improving proliferative responses and cytokine release of splenocytes. These data suggest that a protease-modulating therapy may be an effective strategy for the treatment of immunosuppression induced by severe acute pancreatitis.

AIM:To investigate the effects induced by emodin on single smooth muscle cells from rat colon in vitro, and to determine the signal pathways involved. METHODS: