Primary mesenteric abscess caused by Klebsiella pneumoniae: A case report.

RATIONALE: Mesenteric abscess, a rare abdominal infection, is regularly mostly secondary to inflammatory bowel disease, diverticula of the small intestine, or tuberculosis. Primary mesenteric abscesses are extremely rare. If not diagnosed and treated in a timely manner, it may lead to serious consequences; computerized tomography is highly beneficial for the diagnosis of this disease; timely surgical intervention, judicious use of antibiotics, and adequate nutritional support are crucial in the management of this disease. PATIENT CONCERNS: A 59-year-old male patient from China was admitted to hospital for intermittent abdominal pain accompanied by poor appetite for 10 days. One week before admission, the patient had been infected with corona virus disease 2019. Past history includes type 2 diabetes and post-operative gastric cancer. DIAGNOSIS: The emergency abdominal computerized tomography examination results of the patient suggested that the mesentery was cloudy with a large amount of effusion and visible bubble. Mesentery abscess was considered, but duodenal perforation could not be excluded. INTERVENTIONS: We adopted exploratory laparotomy to further clarify the diagnosis. Intraoperatically, after fully exposing the duodenum, we found extensive abscess formation in the mesentery, but no duodenal perforation. After operation, the patient developed duodenal leakage and was treated with gastric tube and jejunal nutrition tube. OUTCOMES: Postoperatively, due to poor general condition, the patient was transferred to intensive care unit; after anti-infective treatment, the condition improved on the 5th postoperative day, and duodenal leakage appeared on the 9th postoperative day, and conservative treatment was ineffective, and the patient eventually died. LESSONS: Primary mesenteric abscess is a local tissue infectious disease. Whereas we should consider the physical basic condition of the patient during therapeutic process. We believe adequate postoperative drainage, rational use of antibiotics based on bacterial culture, early ambulation after surgery, and adequate nutritional support might be key points for successful therapy.

Long noncoding RNA MYLK-AS1 promotes growth and invasion of hepatocellular carcinoma through the EGFR/HER2-ERK1/2 signaling pathway.

The epidermal growth factor receptor (EGFR) family members EGFR and HER2 play pivotal roles in oncogenesis and tumor progression. Anticancer drugs targeting EGFR and HER2 have been developed. Long noncoding RNAs (lncRNAs) have been reported to regulate cancer development and progression through signaling pathways. However, lncRNAs that regulate EGFR and HER2 expression remain unknown. Here, we show that lncRNA myosin light chain kinase-antisense RNA 1 (MYLK-AS1) promotes EGFR and HER2 expression and activates their downstream signaling pathway. MYLK-AS1 increases hepatocellular carcinoma (HCC) cell proliferation, migration, and invasion in vitro. Consistently, MYLK-AS1 knockdown hinders tumor growth in vivo. Mechanistically, MYLK-AS1 enhances HCC cell proliferation, migration, and invasion through stimulating the EGFR/HER2-extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway. In addition, MYLK-AS1 is overexpressed in HCC patients and negatively correlated with HCC prognosis. Thus, MYLK-AS1 is an upstream regulator of EGFR/HER2, and acts as an oncogene, suggesting an additional target for cancer therapeutics.

Elevated Transient Receptor Potential Melastatin 8 (TRPM8) Expression Is Correlated with Poor Prognosis in Pancreatic Cancer.

BACKGROUND The transient receptor potential melastatin 8 (TRPM8) was found to be expressed abnormally in a variety of tumors and is associated with unfavorable prognosis in human cancers. However, its clinical significance in pancreatic cancer (PC) is mostly unknown. MATERIAL AND METHODS qRT-PCR was performed to measure the expression of TRPM8 in 110 pairs of PC tissues and the adjacent non-cancerous tissues. The association of TRPM8 expression with the clinical characters of PC patients was analyzed using the chi-square test. Furthermore, the prognostic value of TRPM8 was determined with Kaplan-Meier survival curve and Cox regression analysis. RESULTS We found that the expression level of TRPM8 was significantly elevated in PC tissues compared to the non-cancerous controls (P<0.001). In addition, a close relationship was observed between elevated TRPM8 expression with large tumor size (P=0.001), advanced TNM (P=0.013), and distant metastasis (P=0.034). Survival analysis suggested that patients with high TRPM8 expression has worse OS (P=0.001) and DFS (P<0.001) than those with low TRPM8 expression. Moreover, TRPM8 was confirmed as a valuable prognostic biomarker for OS (HR=1.913; 95% CI: 1.020-3.589; P=0.043) or DFS (HR=2.374; 95% CI: 1.269-4.443; P=0.007) of PC patients. CONCLUSIONS This study shows that TRPM8 expression is significantly up-regulated in PC and it might be a useful prognostic factor for patients with PC.

TSG-6 secreted by human umbilical cord-MSCs attenuates severe burn-induced excessive inflammation via inhibiting activations of P38 and JNK signaling.

The hMSCs have become a promising approach for inflammation treatment in acute phase. Our previous study has demonstrated that human umbilical cord-MSCs could alleviate the inflammatory reaction of severely burned wound. In this study, we further investigated the potential role and mechanism of the MSCs on severe burn-induced excessive inflammation. Wistar rats were randomly divided into following groups: Sham, Burn, Burn+MSCs, Burn+MAPKs inhibitors, and Burn, Burn+MSCs, Burn+Vehicle, Burn+siTSG-6, Burn+rhTSG-6 in the both experiments. It was found that MSCs could only down-regulate P38 and JNK signaling, but had no effect on ERK in peritoneal macrophages of severe burn rats. Furthermore, suppression of P38 and JNK activations significantly reduced the excessive inflammation induced by severe burn. TSG-6 was secreted by MSCs using different inflammatory mediators. TSG-6 from MSCs and recombinant human (rh)TSG-6 all significantly reduced activations of P38 and JNK signaling induced by severe burn and then attenuated excessive inflammations. On the contrary, knockdown TSG-6 in the cells significantly increased phosphorylation of P38 and JNK signaling and reduced therapeutic effect of the MSCs on excessive inflammation. Taken together, this study suggested TSG-6 from MSCs attenuated severe burn-induced excessive inflammation via inhibiting activation of P38 and JNK signaling.

MicroRNA­506 participates in pancreatic cancer pathogenesis by targeting PIM3.

MicroRNA (miRNA) is a type of short non-coding RNA that suppresses the expression of protein coding genes by partial complementary binding to the 3'­untranslated regions (UTRs) of mRNAs. miRNA expression alterations are involved in the initiation, progression and metastasis of human cancer and it has been suggested that miRNAs function as tumor suppressors as well as oncogenes in cancer development. PIM-3 is a member of the proto-oncogene PIM family, the aberrant expression of which exists in human pancreatic cancer tissues. There are reports indicating that overexpression of PIM3 is associated with the promotion of pancreatic cancer cell proliferation. The aim of the present study was to identify micro (mi)RNAs that regulate the expression of the oncogene PIM3 in PC. It was confirmed that the expression of PIM3 was regulated by miRNAs through an AGO2 knockout experiment. Subsequently, a dual luciferase assay system was constructed and used to screen 13 selected miRNAs that may target the PIM3 3'UTR directly. The results indicated that miR­15a/b, miR­16, miR­33a/b, miR­124, miR­195 and miR­506 repressed the luciferase activity by targeting the PIM3 3'UTR. However, only the expression of miR­506 was negatively correlated with PIM3 expression in PC tissues (r=­0.38, P=0.017). Furthermore, a biological functional study indicated that miR­506 functioned as a tumor suppressor by repressing PC cell proliferation, which was partially reversed by PIM3 overexpression. To the best of our knowledge, the present study was the first to reveal the tumor suppressor function of miR­506 in PC, which has the potential to be employed in the diagnosis and treatment of PC.

Comparison of systemic inflammation response and vital organ damage induced by severe burns in different area.

BACKGROUND: In this study, we will establish a stable and optimized rat model that can meet strictly diagnosed criteria and serve as a tool to investigate the potential of novel therapeutics in this preclinical model through comparative analysis of systemic alterations, levels of pro-inflammatory cytokines in serum and infiltrated numbers of inflammatory cells in distant organ between 30% and 50% TBSA with a full-thickness burn. MATERIALS AND METHODS: The adult male Wistar rats were randomly divided into the following groups: control group, 30% TBSA with a full-thickness burn group, and 50% TBSA with a full-thickness burn group. The blood and serum samples in the 3 groups were collected and detected by blood routine examination and biochemical detection at 6 h, 12 h, 24 h and 48 h post burn. The levels of TNF-α, IL-1ß and IL-6 in serum were detected by ELISA. The sections of lung, renal, liver and heart were analyzed by H&E and immunohistochemical staining detection. RESULTS: Our results showed that temperature in 50% TBSA with a full-thickness burn group was always hypothermia, and lower than 36°C at defined timepoints post burn, that was in 30% TBSA with a full-thickness burn group was lower than 36°C only at 48 h post burn. The levels of TNF-α, IL-1ß and IL-6 were significantly increased in 30% and 50% groups at 6 h, 12 h, 24 h and 48 h post burn. The apoptosis in distant organs and the biochemical parameters such as ALT, AST, troponin, CK, CK-MB, LDH, urea and creatinine in 30% and 50% groups were also increased at different degrees at defined timepoints after burn, but changes in 50% group were more obvious than that in 30% group. CONCLUSION: We choose 50% TBSA with a full-thickness burn to establish a stable and optimized rat model that can meet strictly diagnosed criteria and serve as a tool to investigate the potential of novel therapeutics in this preclinical model.

Effects of intensive insulin therapy combined with low molecular weight heparin anticoagulant therapy on severe pancreatitis.

The current study explored the effects of intensive insulin therapy (IIT) combined with low molecular weight heparin (LMWH) anticoagulant therapy on severe acute pancreatitis (SAP). A total of 134 patients with SAP that received treatment between June 2008 and June 2012 were divided randomly into groups A (control; n=33), B (IIT; n=33), C (LMWH; n=34) and D (IIT + LMWH; n=34). Group A were treated routinely. Group B received continuous pumped insulin, as well as the routine treatment, to maintain the blood sugar level between 4.4 and 6.1 mmol/l. Group C received a subcutaneous injection of LMWH every 12 h in addition to the routine treatment. Group D received IIT + LMWH and the routine treatment. The white blood cell count, hemodiastase, serum albumin, arterial partial pressure of oxygen and prothrombin time were recorded prior to treatment and 1, 3, 5, 7 and 14 days after the initiation of treatment. The intestinal function recovery time, incidence rate of multiple organ failure (MOF), length of hospitalization and fatality rates were observed. IIT + LMWH noticeably increased the white blood cell count, hemodiastase level, serum albumin level and the arterial partial pressure of oxygen in the patients with SAP (P<0.05). It markedly shortened the intestinal recovery time and the length of stay and reduced the incidence rate of MOF, the surgery rate and the fatality rate (P<0.05). It did not aggravate the hemorrhagic tendency of SAP (P>0.05). IIT + LMWH had a noticeably improved clinical curative effect on SAP compared with that of the other treatments.

Human umbilical cord mesenchymal stem cells transplantation promotes cutaneous wound healing of severe burned rats.

BACKGROUND: Severe burns are a common and highly lethal trauma. The key step for severe burn therapy is to promote the wound healing as early as possible, and reports indicate that mesenchymal stem cell (MSC) therapy contributes to facilitate wound healing. In this study, we investigated effect of human umbilical cord MSCs (hUC-MSCs) could on wound healing in a rat model of severe burn and its potential mechanism. METHODS: Adult male Wistar rats were randomly divided into sham, burn, and burn transplanted hUC-MSCs. GFP labeled hUC-MSCs or PBS was intravenous injected into respective groups. The rate of wound closure was evaluated by Image Pro Plus. GFP-labeled hUC-MSCs were tracked by in vivo bioluminescence imaging (BLI), and human-specific DNA expression in wounds was detected by PCR. Inflammatory cells, neutrophils, macrophages, capillaries and collagen types I/III in wounds were evaluated by histochemical staining. Wound blood flow was evaluated by laser Doppler blood flow meter. The levels of proinflammatory and anti-inflammatory factors, VEGF, collagen types I/III in wounds were analyzed using an ELISA. RESULTS: We found that wound healing was significantly accelerated in the hUC-MSC therapy group. The hUC-MSCs migrated into wound and remarkably decreased the quantity of infiltrated inflammatory cells and levels of IL-1, IL-6, TNF-α and increased levels of IL-10 and TSG-6 in wounds. Additionally, the neovascularization and levels of VEGF in wounds in the hUC-MSC therapy group were markedly higher than those in other control groups. The ratio of collagen types I and III in the hUC-MSC therapy group were markedly higher than that in the burn group at indicated time after transplantation. CONCLUSION: The study suggests that hUC-MSCs transplantation can effectively improve wound healing in severe burned rat model. Moreover, these data might provide the theoretical foundation for the further clinical application of hUC-MSC in burn areas.

Comparison analysis in synchronous and metachronous metastatic colorectal cancer based on microarray expression profile.

BACKGROUND/AIMS: Colorectal cancer (CRC) is one of the most common malignancies, and liver metastasis is one of the major causes of death of CRC. This study aimed to compare the genetic difference between metachronous lesions (MC) and synchronous lesions (SC) and explore the molecular pathology of CRC metastasis. METHODOLOGY: Microarray expression profile data (GSE10961) including 8 MC and 10 SC was downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs) between the two groups were identified based on T test. Furthermore, GO enrichment analysis was performed for the down-regulated DEGs using DAVID. Finally, Classify validation of known CRC genes based on previous studies between MC and SC samples was conducted. RESULTS: Total of 36 DEGs including 35 down-regulated DEGs and 1 up-regulated DEGs were identified. The expressional differences of the 5 informative oncogenes: EGFr, PIK3R1, PTGS2 (COX-2), PTGS1 (COX1), and ALOX5AP between SC and MC were really tiny. CONCLUSIONS: Some DEGs, such as NFAT5, OLR1, ERAP2, HOXC6 and TWIST1 might play crucial roles in the regulation of CRC metastasis (both SC and MC) and by disrupting some pathways. However, our results indeed demand further research and experiment.

Prognostic significance of microRNA-141 expression and its tumor suppressor function in human pancreatic ductal adenocarcinoma.

Increasing evidence shows that dysregulation of microRNAs is correlated with tumor development. This study was performed to determine the expression of miR-141 and investigate its clinical significance in pancreatic ductal adenocarcinoma (PDAC). Taqman quantitative RT-PCR was used to detect miR-141 expressions in 94 PDAC tissues and 16 nontumorous pancreatic tissues. Correlations between miR-141 expression and clinicopathologic features and prognosis of patients were statistically analyzed. The effects of miR-141 expression on growth and apoptosis of PDAC cell line (PANC-1) were determined by MTT, colony formation, and flow cytometry assays. Potential target genes were identified by luciferase reporter and Western blot assays. The expression level of miR-141 in PDAC tissues was significantly lower than that in corresponding nontumorous tissues. Downregulation of miR-141 correlated with poorer pT and pN status, advanced clinical stage, and lymphatic invasion. Also, low miR-141 expression in PDAC tissues was significantly correlated with shorter overall survival, and multivariate analysis showed that miR-141 was an independent prognostic factor for PDAC patients. Further, functional researches suggested that miR-141 inhibits growth and colony formation, and enhances caspase-3-dependent apoptosis in PANC-1 cells by targeting Yes-associated protein-1 (YAP1). Therefore, miR-141 is an independent prognostic factor for PDAC patients, and functions as a tumor suppressor gene by targeting YAP1.

Expression of microRNA-218 in human pancreatic ductal adenocarcinoma and its correlation with tumor progression and patient survival.

BACKGROUND: Our aim was to analyze clinicopathologic and prognostic values of microRNA (miR)-218 in pancreatic ductal adenocarcinima (PDAC). METHODS: TaqMan quantitative RT-PCR was used to determine the expression of miR-218 in human PDAC cells and tissue samples. The association of miR-218 expression with clinicopathologic variables was analyzed. Kaplan-Meier survival analysis was performed to analyze the association of miR-218 expression with recurrence-free survival or overall survival of patients. Univariate and multivariate Cox regression analyses were performed. RESULTS: The relative level of miR-218 in PDAC cells was significantly lower than that in normal human pancreatic duct epithelial cell line. Also, the mean level of miR-218 in PDAC tissues was significantly lower than that in normal pancreatic tissues. Statistical analyses indicated that low miR-218 expression was closely associated with poor tumor differentiation, advanced tumor stage, higher incidence of lymph node metastasis, and tumor recurrence. Kaplan-Meier survival analyses showed that patients with low miR-218 expression had lower recurrence-free and overall survival than those with high miR-218 expression. Univariate and multivariate Cox regression analyses showed that miR-218 might be an independent prognostic factor. CONCLUSION: Reduced miR-218 in PDAC tissues was correlated with tumor progression, and might be an independent poor prognostic factor for patients.

[Comparison of different methods for the isolation of human umbilical cord mesenchymal stem cells].

OBJECTIVE: To explore the most appropriate method for the isolation of human umbilical cord mesenchymal stem cells (MSCs) through a comparison of different methods. METHODS: Fifteen umbilical cord specimens from full-term healthy fetus with caesarean birth were completely rinsed with phosphate buffer saline (PBS) and sliced into 1 mm(3) tissue blocks after removal of umbilical vessels and external membrane. These tissue blocks were averagely divided into 4 groups after washing and centrifuge. Then four methods for the isolation of human umbilical cord MSCs were compared: an explant culture and three enzymatic methods of collagenaseII, collagenaseII/trypsin and collagenaseII/hyaluronidase. The count of living cells was evaluated by trypan blue dye exclusion test. Cell morphology was observed under inverted microscope. The expressions of cell surface markers CD105, CD90, CD73, CD31, CD44, CD45, human leukocyte antigen-I (HLA-I) and human leukocyte antigen class IImolecules (HLA-DR) were detected by immunofluorescent staining. Cell proliferation was assayed by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT). RESULTS: The human umbilical cord MSCs were successfully isolated by four isolated methods. However the isolation method used profoundly altered the cell number and proliferation capacity of isolated cells. Isolated cells using four methods were counted at (5.44 ± 0.21)×10(5), (4.03 ± 0.24)×10(5), (4.91 ± 0.33)×10(5) and (5.94 ± 0.40)×10(5) respectively. More cells were obtained with collagenaseII/hyaluronidase than other three methods (all P < 0.05). Cells out of tissue blocks were observed at Day 9-11 and cells were observed at Day 2 with three types of enzyme digestion. The fusion time of cells were (18.5 ± 3.5), (8.0 ± 1.0), (7.5 ± 1.5) and (3.5 ± 0.5) days respectively. The fusion time of cells obtained with collagenaseII/hyaluronidase was lower than other methods (all P < 0.05). Cell morphology: polygonal, irregular and of large volume for explant culture; relatively short and small for collagenaseII and collagenaseII/trypsin methods; thin spindle for collagenaseII/hyaluronidase method. Immunofluorescent staining revealed that CD105, CD73, CD90 and CD44 were expressed in all groups while there was no expression of CD31, CD45 or HLA-DR. And the cells obtained with collagenaseII/hyaluronidase method were in a higher cell proliferation rate and activity compared to other methods. CONCLUSION: The collagenaseII/hyaluronidase method is optimal for the isolation of human umbilical cord MSCs than other methods.

Basic fibroblast growth factor/vascular endothelial growth factor in the serum from severe burn patients stimulates the proliferation of cultured human umbilical cord mesenchymal stem cells via activation of Notch signaling pathways.

BACKGROUND: Mesenchymal stem cells (MSCs) are the leading cellular constituents used in regenerative medicine. MSCs repair and reconstruct wounds of acute traumata and radiation-induced burns through proliferation, differentiation, and trophic activity. However, repair effect of MSCs on severe burn wounds remain to be clarified because severe burns are much more complex traumata than radiation-induced burns. Survival and proliferation of MSCs in microenvironments affected by severe burns are very important for improving wound repair/regeneration. This study aimed to elucidate the survival and proliferation effects and the potential proliferation mechanism of serum from severe burn patients (BPS) on human umbilical cord MSCs (hUCMSCs) in vitro. METHODS: The hUCMSCs were isolated, cultured, and identified. Next, we evaluated the effects of BPS on cell numbers, cell cycle progression, cyclin D expression, and key proteins and genes of the Notch signaling pathway. Putative mechanisms underlying the proliferation of hUCMSCs were investigated. RESULTS: BPS markedly increased the number of hUCMSCs, and the results of the cell cycle studies indicated that BPS induced cell cycle progression into the M phase. Cyclin D expression was higher with BPS than in the control group. Moreover, Notch-1, a key determinant of hUCMSC activation and proliferation, and its target gene Hes-1 were overexpressed after BPS treatment. Proliferation numbers of hUCMSC, rate of proliferation period (G2/M+S), and the expression of cyclin D, Notch-1, and Hes-1 were markedly decreased by Notch signaling inhibitors (DAPT/GSI). In the case of BPS, basic fibroblast growth factor and vascular endothelial growth factor were the key factors that promoted hUCMSC proliferation. CONCLUSION: This study provides novel evidence for the role of BPS in the survival and rapid proliferation of hUCMSCs and suggests that these cells could be used for cell therapy-based clinical applications for treating severe burns. Furthermore, hUCMSC proliferation was induced by basic fibroblast growth factor/vascular endothelial growth factor in BPS through activation of Notch signal.

[Effect of serum from severe burn patients on biology characteristics of human umbilical cord mesenchymal stem cells].

OBJECTIVE: To investigate the effect of the serum from severe burn patients on the biology characteristics of human umbilical cord mesenchymal stem cells (hUCMSCs) in vitro, so as to explore the feasibility of hUCMSCs transplantation for treating severe burn. METHODS: The 3rd passage of hUCMSCs were randomly divided into 3 groups: 10% fetal bovine serum group (group A), 10% normal serum group (group B), and 10% burn serum group (group C). At 24 hours, 72 hours, and 6 days after culture, the cell morphology and density were observed by inverted microscope; the cell proliferation was assessed by MTT; after 6 days of culture, the cell cycle by propidium iodide staining and flow cytometry, the apoptosis by acridine orange/ ethidium bromide staining, and the cell senescence by beta-galactosidase staining; the levels of tumor necrosis factor alpha (TNF-alpha), interleukin 1 (IL-1), platelet-derived growth factor (PDGF), and insulin-like growth factor 1 (IGF-1) in serum were detected by a double-antibody sandwich ELISA kit. RESULTS: hUCMSCs were long spindle/polygon in 3 groups. The cell fusion of group C was obviously faster than that in group A and group B. The cell proliferation curves showed that the velocity and number of cell proliferation in group C were significantly higher than those in group A and group B at 2-6 days after culture (P < 0.05). The rates of proliferation period (S) of hUCMSCs were 9.21% +/- 1.02%, 11.79% +/- 1.87%, and 20.54% +/- 2.03%, respectively in groups A, B, and C at 6 days, and group C was significantly higher than that of group A and group B (P < 0.05). The hUCMSCs showed normal morphology and structure in 3 groups, and no apoptosis cells was observed. The positive cells percentage of group C (2.6% +/- 0.1%) was significantly lower than that of group A (4.8% +/- 0.2%) and group B (3.8% +/- 0.4%) (P < 0.05). The levels of TNF-alpha, IL-1, PDGF, and IGF-1 in group C were significantly higher than those in group B (P < 0.05). CONCLUSION: The higher levels of cytokines in serum from the severe burn patients can significantly stimulate hUCMSCs proliferation, prevent cells apoptosis, and reduce cells senescence. Therefore, it is feasible to use hUCMSCs transplantation for treating severe burn patients.

Retroperitoneal laparoscopic debridement and drainage of infected retroperitoneal necrosis in severe acute pancreatitis.

OBJECTIVE: To explore the effect of retroperitoneal laparoscopic debridement and drainage on infected necrosis in severe acute pancreatitis. MATERIALS AND METHODS: This retrospective study included 18 patients with severe acute pancreatitis (SAP) undergoing retroperitoneal laparoscopic debridement and drainage from May 2006 to April 2012 in our hospital. All patients had infected retroperitoneal necrosis and single or multiple peritoneal abscesses. Eleven patients transferred to our hospital were treated with the retroperitoneal laparoscopic debridement and drainage within 24-72 hours after admission. Conservative treatments were given to eight patients. Retroperitoneal laparoscopic debridement and drainage were applied 3-11 days after admission. RESULTS: All patients had infection of necrotic pancreas or peripancreatic tissues. Twelve patients had organ failure. Three patients underwent secondary surgery. Laparotomy with debridement and drainage were applied to one patient who had a huge lesser sac abscess 7 days after first surgery. The other two patients were given secondary retroperitoneal laparoscopic debridement and drainage. One case was complicated by retroperitoneal hemorrhage, four cases had pancreatic leakage, and no intestinal fistula was found. The patients' heart rate, respiration, temperature, and white blood cell count were significantly improved 48 hours after surgery compared with those prior to surgery (p<0.05). The average length of stay in hospitals was 40.8 days (range, 6-121 days), and the drainage tube indwelling time was 44.4 days (range, 2-182 days). CONCLUSION: Retroperitoneal laparoscopic debridement and drainage is an SAP surgical treatment with a minimally invasive procedure and a good effect, and can be applied for infected retroperitoneal necrosis in early SAP.

[The clinical study of percutaneous transhepatic radiofrequency ablation combined with tumor edge of percutaneous absolute ethanol injection on liver cancer adjacent to major blood vessels].

OBJECTIVE: To explore the effects of percutaneous transhepatic radiofrequency ablation (PRFA) combined with tumor edge of percutaneous absolute ethanol injection (PEI) on liver cancer adjacent to major blood vessels. METHODS: Seventy five patients with liver cancer adjacent to major blood vessels were randomly divided into two groups: PRFA+PEI therapy group (38 cases) and PRFA control group (37 cases). Tumor necrosis rate, AFP levels, local recurrence rate, median for survival time and cum survival were used as the evaluation index to evaluate the efficacies of the two methods. RESULTS: Tumor necrosis rates of the therapy group and the control group were 84.2% and 54.1% (P < 0.01), respectively; AFP levels of therapy group and control group at 1, 3, 6 and 12 months after treatment were (105.0 ± 35.5) µg/L, (28.4 ± 4.3) µg/L, (58.6 ± 6.7) µg/L, (89.5 ± 12.5) µg/L and (137.2 ± 34.6) µg/L, (84.2 ± 18.4) µg/L, (106.6 ± 20.3) µg/L, (173.7 ± 32.0) µg/L, respectively. The rates of therapy group was significantly lower than of control group. Local recurrence rates of the therapy group and control group were 2.6%, 7.9%, 13.2% and 31.6% vs 10.8%, 21.6% , 40.5% and 62.1% (P < 0.05) at 3, 6, 12 and 24 months after treatment, respectively. Median for survival time of the therapy group and control group were 28.0 ± 2.8 months and 19.0 ± 3.6 months, respectively. Cum survival of the therapy group and control group were 84.2%, 78.9%, 60.5% and 31.6% vs 78.4%, 67.6%, 37.8% and 8.1% (P < 0.05) at 6, 12, 24 and 36 months after treatment, respectively. CONCLUSION: PEI as a supplementary treatment of PRFA can effectively improve the treatment of liver cancer adjacent to major blood vessels and significantly reduce the local recurrence rate and improve long-term survival rates.

Clinical effects of intensive insulin therapy treating traumatic shock combined with multiple organ dysfunction syndrome.

The therapeutic effects of intensive insulin therapy in treatment of traumatic shock combined with multiple organ dysfunction syndrome (MODS) were investigated. A total of 114 patients with traumatic shock combined with MODS were randomly divided into two groups: control group (n=56) treated with conventional therapy, and intensive insulin therapy group (n=58) treated with conventional therapy plus continuous insulin pumping to control the blood glucose level at range of 4.4-6.1 mmol/L. White blood cells (WBC) counts, prothrombin time (PT), serum creatinine (SCr), alanine aminotransferase (ALT), serum albumin and PaO(2) were measured before and at the day 1, 3, 5, 7 and 14 after treatment. The incidence of gastrointestinal dysfunction, the incidence of MODS, hospital stay and the mortality were also observed and compared. After intensive insulin therapy, the WBC counts, SCr, ALT and PT were significantly reduced (P<0.05), but the level of serum albumin was significantly increased (P<0.05) at the day 3, 5, 7 and 14. In the meantime, the PaO2 was significantly elevated at the day 3, 5 and 7 (P<0.01) after intensive insulin therapy. The incidence of gastrointestinal dysfunction, the incidence of MODS, the length of hospital stay and the mortality were markedly decreased (P<0.01). The results suggest early treatment with intensive insulin therapy is effective for traumatic shock combined with MODS and can decrease the length of hospital stay and the mortality.

Clinical Effects of Intensive Insulin Therapy Treating Traumatic Shock Combined with Multiple Organ Dysfunction Syndrome / 华中科技大学学报（医学）（英德文版）

The therapeutic effects of intensive insulin therapy in treatment of traumatic shock combined with multiple organ dysfunction syndrome (MODS) were investigated.A total of 114 patients with traumatic shock combined with MODS were randomly divided into two groups:control group (n=56) treated with conventional therapy,and intensive insulin therapy group (n=58) treated with conventional therapy plus continuous insulin pumping to control the blood glucose level at range of 4.4-6.1 mmol/L.White blood cells (WBC) counts,prothrombin time (PT),serum creatinine (SCr),alanine aminotransferase (ALT),serum albumin and PaO2 were measured before and at the day 1,3,5,7 and 14 after treatment.The incidence of gastrointestinal dysfunction,the incidence of MODS,hospital stay and the mortality were also observed and compared.After intensive insulin therapy,the WBC counts,SCr,ALT and PT were significantly reduced (P＜0.05),but the level of serum albumin was significantly increased (P＜0.05) at the day 3,5,7 and 14.In the meantime,the PaO2 was significantly elevated at the day 3,5 and 7 (P＜0.01) after intensive insulin therapy.The incidence of gastrointestinal dysfunction,the incidence of MODS,the length of hospital stay and the mortality were markedly decreased (P＜0.01).The results suggest early treatment with intensive insulin therapy is effective for traumatic shock combined with MODS and can decrease the length of hospital stay and the mortality.

[Effects of intensive insulin therapy on serum immunoglobulin, complement levels and phagocytosis of monocytes in patients with severe trauma].

OBJECTIVE: To investigate the influence of intensive insulin therapy on serum immunoglobulin (Ig), complement levels and phagocytosis of monocytes in patients with severe trauma. METHODS: Severe injured patients with injury severity score (ISS)>20 in surgical intensive care unit (ICU) were randomly divided into two groups, intensive insulin therapy and conventional therapy. Blood glucose levels in intensive insulin therapy and conventional therapy groups were maintained at 4-6 mmol/L and <11.1 mmol/L, respectively. Blood samples were obtained on 0, 2, 4, 6 and 8 days after admission. Dynamic changes of immunological parameters including serum IgA, IgG, IgM, complements (C3, C4) levels were determined in each group at various intervals following trauma. Phagocytosis of monocytes was also measured by use of phagotest kits after blood cells were incubated with fluorescein isothiocyanate (FITC)-labeled E. coli in a heated water bath at 37 centigrade. RESULTS: Serum IgA, IgG, IgM, C3 and C4 levels were low in two groups at admission, and elevated after treatment with recovery to normal range on 6-8 days. Serum C3 and C4 levels in intensive insulin therapy group were much lower than those in conventional therapy group (both P<0.05) with delayed recovery to normal range. There were no significant differences in serum IgA, IgG and IgM levels between two groups (all P>0.05). For the patients with intensive insulin therapy, phagocytosis of monocytes was markedly enhanced on 4 and 6 days compared with those at admission (both P<0.05), and E. coli-FITC positive rates were significantly higher than those with conventional therapy on 2, 4 and 6 days after admission (all P<0.05). CONCLUSION: Intensive insulin therapy can markedly improve immune function and enhance phagocytosis of monocytes, which might be used as one of effective methods to increase the host defense ability in traumatic patients.

[Effects of anticoagulation therapy with low molecular weight heparin in acute pancreatitis].

OBJECTIVE: To evaluate the effects of anticoagulation therapy with low molecular weight heparin in acute pancreatitis. METHODS: Low molecular weight heparin, in a dose of 40 mg or 0.01 ml/kg, by subcutaneous injection, every 12 hours, was administered to 17 acute pancreatitis patients combined with conventional therapy. The changes of serum enzymology and prognosis in patients treated with low molecular weight heparin or conventional therapy were observed. RESULTS: Anticoagulation by low molecular weight heparin could significantly decrease the blood white cell count of patients with acute pancreatitis and increase their arterial blood oxygen partial pressure. It could cut down the duration of hospitalization and reduce the aggravation rate, secondary operation rate, and mortality of these patients without increasing hemorrhagic tendency or its related complications. CONCLUSION: Anticoagulation therapy with low molecular weight heparin is safe and effective in the treatment of acute pancreatitis, and it may improve its prognosis.