Construction of a disulfide-stabilized diabody against fibroblast growth factor-2 and the inhibition activity in targeting breast cancer.

Fibroblast growth factor-2 (FGF-2) is one of the most important angiogenic factors to promote tumor growth, progression and metastasis. Neutralizing antibodies against FGF-2 may suppress the growth of tumor cells by blocking the FGF-2 signaling pathway. In this study, a disulfide-stabilized diabody (ds-Diabody) that specifically targets FGF-2 was designed. Compared to its parent antibody, the introduction of disulphide bonds in the diabody could significantly increase the stability of ds-Diabody and maintain its antigen binding activity. The ds-Diabody against FGF-2 could effectively inhibit the tube formation and migration of vascular endothelial cells and block the proliferation and invasion of human breast cancer cells. In the mouse model of breast cancer xenograft tumors, the ds-Diabody against FGF-2 could significantly inhibit the growth of tumor cells. Moreover, the densities of microvessels stained with CD31 and lymphatic vessels stained with LYVE1 in tumors showed a significant decrease following treatment with the ds-Diabody against FGF-2. Our data indicated that the ds-Diabody against FGF-2 could inhibit tumor angiogenesis, lymphangiogenesis and tumor growth.

Novel ionic liquid with both Lewis and Brønsted acid sites for Michael addition.

Ionic liquid with both Lewis and Brønsted acid sites has been synthesized and its catalytic activities for Michael addition were carefully studied. The novel ionic liquid was stable to water and could be used in aqueous solution. The molar ratio of the Lewis and Brønsted acid sites could be adjusted to match different reactions. The results showed that the novel ionic liquid was very efficient for Michael addition with good to excellent yields within several min. Operational simplicity, high stability to water and air, small amount used, low cost of the catalyst used, high yields, chemoselectivity, applicability to large-scale reactions and reusability are the key features of this methodology, which indicated that this novel ionic liquid also holds great potential for environmentally friendly processes.

Upregulation of Stress-Induced Protein Kinase CK1 Delta is associated with a Poor Prognosis for patients with Hepatocellular Carcinoma.

Objective: This study was designed to analyze the expression of CSNK1D in hepatocellular carcinoma (HCC) and investigate the relationship between the expression of CSNK1D and the prognosis of HCC patients. Methods: The CSNK1D and alpha-fetoprotein (AFP) expression levels in patients with HCC and their corresponding clinical data were downloaded from The Cancer Genome Atlas (TCGA) and sorted with a Perl program. CSNK1D and AFP expression differences in liver tissue and liver cancer were compared and analyzed, based on the online database human cancer metastasis database, the relationships between the expression levels of CSNK1D and AFP and the proliferation and metastases of HCC were explored. The immunohistochemical data obtained from the Human Protein Atlas Database further verified the differences in the expression levels of CSNK1D and AFP in liver tissues and liver cancer tissues. Through Kaplan-Meier survival analysis, the effects of CSNK1D and AFP expression levels on the prognosis of patients with HCC were investigated, and the influences of and patients' gender, age and grades of cancer cells, tumor size, the status of lymph node metastasis, distant metastasis, and tumor stage on the expression of CSNK1D were analyzed with R language. The influence of differential expressions of CSNK1D on survival time was compared and the prognostic factors influencing the survival of HCC patients were statistically explored by univariate analysis and multivariate analysis. The potential influencing mechanism of CSNK1D on the prognosis of HCC patients was explored by Gene Set Enrichment Analysis (GSEA) enrichment. Results: The expression level of CSNK1D and AFP in cancer foci was significantly higher than that in normal tissues, However, in the same patient, the expression levels of AFP in paracarcinoma tissues and cancer tissues showed no significant difference. The expression level of CSNK1D in HCC with distant metastases was higher than that in those without metastasis, but the expression level of AFP in metastatic HCC was lower than that in those HCC without metastases. In immunohistochemical tests, CSNK1D was moderately positive in normal liver tissues, slightly positive in normal bile duct tissues, and highly positive in HCC. AFP was slightly positive in normal liver tissues and negative in HCC, but it was not detected in normal intrahepatic bile duct tissue. Survival analysis results suggested that the higher expression level of CSNK1D corresponded to the shorter survival period, whereas the expression level of AFP showed no significant influence on survival time. The expression level of CSNK1D was not correlated with gender, age, the status of lymph node metastasis status, or distant metastasis of patients. The main factors influencing the expression level of CSNK1D included tumor size, cancer cell grade, and tumor stage. The expression levels of CSNK1D in T2 and T3 were higher than that in T1. The expression levels of CSNK1D in G3 and G4 were higher than that in G1. The expression levels of CSNK1D in Stage II and Stage III were higher than that in Stage I. Univariate analysis suggested that tumor size, cell grade, distant metastasis, clinical stage, and CSNK1D expression level were the prognostic factors influencing the survival of patients. Multivariate analysis suggested that CSNK1D expression level was an independent factor influencing the prognosis of HCC patients. GSEA enrichment analysis indicated that CSNK1D mainly affected the prognosis of HCC patients through cell cycle, WNT signaling pathway, amino acid degradation metabolism, and other pathways. Conclusion: CSNK1D is an independent influencing factor for the prognosis of HCC patients and has the potential to be developed as a potential therapeutic target for HCC, and better than AFP in predicting the prognosis of HCC.

Hes1 is associated with long non-coding RNAs in colorectal cancer.

BACKGROUND: Long noncoding RNAs (lncRNAs) play important roles in the development and pathophysiology of colorectal cancer (CRC). Our previous study showed that Hes1 was involved in the self-renewal and tumorigenicity of stem-like cancer cells in CRC. METHODS: ArrayStar Human LncRNA/mRNA Expression Microarray Version 3.0 was used to detect lncRNA expression in CRC tissues compared with their matched non-tumoral tissues. RNA-binding protein immunoprecipitation and sequencing (RIP-seq) assay was used to detect lncRNAs binding to Hes1. Real-time qPCR was used to detect expression of specific lncRNAs in CRC tissues. RESULTS: We found significantly up-regulated as well as down-regulated lncRNAs in CRC tissues compared with their matched non-tumoral tissues. We also screened a number of lncRNAs interacting with Hes1 in CRC cells. Interestingly, we found several lncRNAs binding to Hes1 (such as, GNAS-AS1, RP11-89K10.1, and RP11-465L10.10) were up-regulated in CRC tissues showed by the tissue microarray. Next, we confirmed that Hes1 directly interacted with these lncRNAs using RIP-qPCR and RNA pulldown assay. Finally, we verified the expression of these lncRNAs in 32 CRC samples as well as the adjacent non-tumoral tissues using real-time qPCR. CONCLUSIONS: Based on these, we speculate that Hes1 interacts with one or more lncRNAs which contribute to the development and progression of CRC.

Preservation of non-heart-beating donor livers in extracorporeal liver perfusion and histidine-trytophan-ketoglutarate solution.

AIM: To compare the preservation of non-heart-beating donor (NHBD) livers in cold histidine-trytophan-ketoglutarate (HTK) solution and extracorporeal liver perfusion (ECLP). METHODS: Livers harvested from healthy pigs were stored for 10 h in cold HTK solution (group A, n = 4) or perfused with oxygenated autologous blood at body temperature (group B, n = 4). Both groups were then tested on the circuit for 4 h. Bile production, hemodynamic parameters, hepatocyte markers and reperfusion injury of extracorporeal livers were tested in each group. Liver tissues from each group were examined at the end of reperfusion. RESULTS: At 1, 2, 3 and 4 h after reperfusion, bile production, hemodynamic parameters, hepatocyte markers and reperfusion injury of livers in group A were statistically different from those in group B (P < 0.05 or P < 0.01). CONCLUSION: ECLP is better than HTK solution to preserve NHBD livers. ECLP can assess the graft viability before liver transplantation.

Protective effects of L-arginine against ischemia-reperfusion injury in non-heart beating rat liver graft.

BACKGROUND: Although the use of non-heart beating donors (NHBDs) could bridge the widening gap between organ demand and supply, its application to liver transplantation is limited due to the high incidence of primary graft loss. Prevention of liver injury in NHBDs will benefit the results of transplantation. This study was conducted to evaluate the protective effects of L-arginine on liver grafts from NHBDs. METHODS: One hundred and four Wistar rats were randomly divided into 7 groups: normal control (n=8), controls 1, 2 and 3 (C1, C2, C3, n=16), and experimental 1, 2 and 3 (E(1), E(2), E(3), n=16). For groups C(1) and E(1), C(2) and E(2), and C(3) and E(3), the warm ischemia time was 0, 30, and 45 minutes, respectively. Liver grafts were flushed with and preserved in 4 degree centigrade Euro-collins solution containing 1 mmol/L L-arginine for 1 hour in each experimental group. Recipients of each experimental group were injected with L-arginine (10 mg/kg body weight) by tail vein 10 minutes before portal vein reperfusion. Donors and recipients of each experimental control group were treated with normal saline. Then transplantation was performed. At 1, 3, and 24 hours after portal vein reperfusion, blood samples were obtained to determine the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), nitric oxide (NO) and plasma endothelin (ET). At 3 hours after portal vein reperfusion, grafts samples were fixed in 2.5% glutaraldehyde for electron microscopic observation. RESULTS: At 1 hour after portal vein reperfusion, the levels of NO in groups E(1), E(2), E(3) and C(1), C(2), C(3) were lower, while the levels of plasma ET, serum ALT and AST were higher than those in the normal control group (P<0.05). At 1, 3, and 24 hours, the levels of NO in groups E(1), E(2), E(3) were higher, while the levels of plasma ET, serum ALT and AST were lower than those in the corresponding control groups (C(1), C(2), C(3) (P<0.05). The levels of NO in groups C(2) and C(3) were lower than in group C1 (P<0.05), and the level of NO in group C(3) was lower than in group C(2) (P<0.05). At 1, 3 and 24 hours, the levels of plasma ET, serum ALT, and AST in groups E1, E2, E3 were lower than those in the corresponding control groups (C(1), C(2), C(3)) (P<0.05). The levels of plasma ET, serum ALT, and AST were lower in group C(3) than in groups C(1) and C(2) (P<0.05). Pathological changes in groups E(1), E(2), E(3) were milder than those in the corresponding experimental control groups (C(1), C(2), C(3)). CONCLUSIONS: The imbalance between NO and ET plays an important role in the development of ischemia-reperfusion injury of liver grafts from NHBDs. L-arginine can attenuate injury in liver grafts from NHBDs by improving the balance between NO and ET.

[Encapsulating hepatocytes with chitosan in physiological conditions].

Prepared from 15.3% N-acetylated chitosan (FNC), half N-acetylated chitosan (HNC) possesses a good solubility in a weak basic solution, guaranteeing the formation of microcapsules by the coacervating reaction between HNC and methacrylic acid (MAA)-hydroxyethyl methacrylate (HEMA)-methyl methacrylate (MMA) (MAA-HEMA-MMA) terpolymer under physiological conditions. When hepatocytes were encapsulated in such 3-dimensional microenvironment, as compared to monolayer culture, cell functions, including P450 activity, urea production and albumin release, were well supported. The prepared microcapsules have good mechanical stability and permeability.

Differentiation of UC-MSCs into hepatocyte-like cells in partially hepatectomized model rats.

The aim of the study was to investigate the possibility of human umbilical cord mesenchymal stem cells (UC-MSCs) surviving and differentiating into hepatocyte-like cells in partially hepatectomized model rats. MSCs were isolated from human umbilical cord and cultured with collagenase digestion. Cell surface markers were detected and fifth generation UC-MSCs were labeled with PKH26. The partially hepatectomized model rats were injected with the labeled human umbilical cord MSCs and transplanted through the portal vein. The survival of the labeled cells, in differentiation conditions and the expression of hepatic marker albumin were observed at post-transplantation 1, 2 and 3 weeks under a fluorescence microscope. It was found that the human umbilical cord MSCs could be cultured and amplified in vitro. Following transplantation to the partially hepatectomized liver of the model rat, the cells survived and expresses the hepatic marker albumin in vivo. After being labeled with PKH26, the cells were visualized as red fluorescence under a fluorescence microscope. In the frozen sections of the liver, the marked cells scattered around and most of them expressed albumin with green fluorescence under the fluorescence microscope. In conclusion, the transplanted human umbilical cord MSCs survived and differentiated into hepatocyte-like cells. The human umbilical cord MSCs may therefore be a main source of hepatocytes in transplantation.

Encapsulating live cells with water-soluble chitosan in physiological conditions.

A new class of microcapsules was prepared under physiological conditions by polyelectrolyte complexation between two oppositely-charged, water-soluble polymers. The microcapsules consisted of an inner core of half N-acetylated chitosan and an outer shell of methacrylic acid (MAA) (20.4%)-hydroxyethyl methacrylate (HEMA) (27.4%)-methyl methacrylate (MMA) (52.2%) (MAA-HEMA-MMA) terpolymer. Both 400 and 150 kDa half N-acetylated chitosans maintained good water solubility and supplied enough protonated amino groups to coacervate with terpolymer at pH 7.0-7.4, in contrast to other chitosan-based microcapsules which must be prepared at pH <6.5. The viscosity of half N-acetylated chitosan solutions between 80 and 3000 cPas allowed the formation of microcapsules with spherical shape. Molar mass, pH and concentration of half N-acetylated chitosan, and reaction time, influenced the morphology, thickness and porosity of the microcapsules. Microcapsules formed with high concentration of half N-acetylated chitosan exhibited improved mechanical stability, whereas microcapsules formed with low concentration of half N-acetylated chitosan exhibited good permeability. This 3D microenvironment has been configured to cultivate sensitive anchorage-dependent cells such as hepatocytes to maintain high level of functions.

Characterization of amphoteric multilayered thin films by means of zeta potential measurements.

Multilayer films of amphoteric methylated collagen were assembled on SOURCE 15S or SOURCE 15Q beads by sequential electrostatic deposition with negatively charged methylacrylic acid-hydroxyethyl methacrylate-methyl methacrylate (MAA-HEMA-MMA) terpolymer. Methylated collagen and terpolymer were deposited under conditions where they were oppositely charged to one another, thereby facilitating growth of the films through electrostatic interactions. Measurements revealed alternating positive and negative zeta-potential with the deposition of each methylated collagen and terpolymer layer, respectively. Assembly pH had a remarkable influence on zeta-potential of the assembled multilayers and the deposition of methylated collagen will be frustrated when the assembly pH is up to 9.0. In addition, ionic strength (NaCl concentration) showed an intricate effect on zeta-potential of the films of amphoteric methylated collagen.

[The relationship between leukemia inhibitory factor and neurokinin receptors in a rat model of asthma].

OBJECTIVE: To study the expression of leukemia inhibitory factor (LIF) and neurokinin receptors (NKR) in the lungs of asthmatic rats, and to evaluate the role of LIF in airway neurogenic inflammation. METHODS: Twenty-four Wistar rats were randomly divided into a control group (group A, n = 8), an asthma group (group B, n = 8) and a dexamethasone treated group (group C, n = 8). The rat asthmatic model was made by intraperitoneal injection and nebulized aspiration of ovalbumin (OVA) at the concentrations of 10% and 1% respectively. Expression levels of lung LIF, NK-1R and NK-2R were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot two weeks after challenge, and the localization of NK-1R was determined by immunohistochemistry. RESULTS: After challenge, the expressions of lung LIF mRNA in group A, B and C were 0.240 +/- 0.020, 0.510 +/- 0.130, 0.180 +/- 0.050, and protein levels were 23 110 +/- 8 018, 40 832 +/- 12 964, 16 160 +/- 2 108 respectively. The expressions of lung NK-1R mRNA in group A, B and C were 0.240 +/- 0.020, 1.040 +/- 0.480, 0.170 +/- 0.040, and protein levels were 16 538 +/- 4 342, 32 292 +/- 4 564, 15 018 +/- 1 488 respectively. The mRNA and protein levels of LIF and NK-1R in group B were significantly elevated as compared with group A and C (all P < 0.01). The expressions of lung NK-2R mRNA in group A, B and C were 0.240 +/- 0.040, 0.200 +/- 0.030 and 0.210 +/- 0.040, and no difference was found among three groups (all P > 0.05). In group B, there was a positive correlation between LIF and NK-1R at mRNA (r = 0.850, P < 0.01) and protein (r = 0.868, P < 0.01) levels respectively. NK-1R immunoreactivity was observed primarily in bronchial epithelial cells. CONCLUSION: LIF and NK-1R were excessively expressed and closely correlated in lungs of the rat asthmatic model, suggesting that LIF may be involved in modulating airway neurogenic inflammation.

Vascular endothelial growth factor receptor tyrosine kinase inhibitors versus bevacizumab in metastatic colorectal cancer: A systematic review and meta-analysis.

Bevacizumab has demonstrated a survival benefit in patients with metastatic colorectal cancer (mCRC) when combined with chemotherapy. Several randomized clinical trials comparing the efficacy and toxicity of vascular endothelial growth factor receptor (VEGFR) tyrosine kinase inhibitors (TKIs) against bevacizumab have been reported. The present meta-analysis was conducted to identify the potentially significant benefit of the combined treatment regimens in patients with mCRC. PubMed, Embase and Cochrane Library databases were searched for the randomized controlled trials published on or before September 2014, which compared the efficacy and toxicity of VEGFR TKIs with bevacizumab in combination with chemotherapy in patients with mCRC. The primary endpoints included progression-free survival (PFS), overall survival (OS) and overall response rate (ORR), and secondary endpoints were the toxicity profiles. Relative risks (RRs) with 95% confidence intervals (CIs) for response rate and adverse events (AEs) were calculated, as well as hazard ratios (HRs) for PFS and OS. The final analysis included 4 studies comprising a total of 1,929 intent-to-treat patients with mCRC, which compared VEGFR TKIs (cediranib and axitinib) plus chemotherapy with bevacizumab plus chemotherapy. Results demonstrated that VEGFR TKIs plus chemotherapy significantly resulted in a modest but significantly shorter PFS [hazard ratio (HR), 1.12; 95% CI, 1.00-1.25; P=0.05] compared with that of bevacizumab plus chemotherapy but not in OS (HR, 1.10; 95% CI, 0.88-1.17; P=0.87) and ORR (RR, 0.95; 95% CI, 0.85-1.05; P=0.30). VEGFR TKIs treatment showed a less favorable AE profile compared with bevacizumab, with higher rates of grade-III/IV diarrhea, fatigue, hypertension, neutropenia and thrombocytopenia, whereas a higher incidence of peripheral neuropathy associated with the bevacizumab group was observed. In conclusion, the addition of VEGFR TKIs to chemotherapy resulted in a modest but significantly shorter PFS but not in OS and ORR compared with bevacizumab. The VEGFR TKIs group showed a less favorable AE profile with higher rates of diarrhea, fatigue, hypertension, neutropenia and thrombocytopenia, whereas a higher incidence of peripheral neuropathy associated with the bevacizumab was observed.

Soluble production and function of vascular endothelial growth factor/basic fibroblast growth factor complex peptide.

Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) are important proangiogenic factors in tumor procession. The autocrine and paracrine bFGF and the VEGF in tumor tissue can promote tumor angiogenesis, tumor growth, and metastasis. A VEGF/bFGF Complex Peptide (VBP3) was designed on the basis of epitope peptides from both VEGF and bFGF to elicit in vivo production of anti-bFGF and anti-VEGF antibodies. In this study, we reported on the production of recombinant VBP3 using high cell density fermentation. Fed-batch fermentation for recombinant VBP3 production was conducted, and the production procedure was optimized in a 10-L fermentor. The fraction of soluble VBP3 protein obtained reached 78% of total recombinant protein output under fed-batch fermentation. Purified recombinant VBP3 could inhibit tumor cell proliferation in vitro and stimulate C57BL/6 mice to produce high titer anti-VEGF and anti-bFGF antibodies in vivo. A melanoma-grafted mouse model and an immunohistochemistry assay showed that tumor growth and tumor angiogenesis were significantly inhibited in VBP3-vaccinated mice. These results demonstrated that soluble recombinant VBP3 could be produced by large-scale fermentation, and the product, with good immunogenicity, elicited production of high-titer anti-bFGF and anti-VEGF antibodies, which could be used as a therapeutic tumor vaccine to inhibit tumor angiogenesis and tumor growth.

Use of ultrathin shell microcapsules of hepatocytes in bioartificial liver-assist device.

We previously encapsulated hepatocytes in ultrathin shell microcapsules and showed them to have enhanced differentiated functions over cells cultured in monolayer. Here we have used these microencapsulated hepatocytes in a bioartificial liver-assisted device (BLAD) with a rat hepatectomy model. Primary rat hepatocytes were encapsulated in 150- to 200-microm microcapsules, using an electrostatic droplet generator. The microencapsulated hepatocytes exhibited good in vitro urea synthesis activity in plasma from rats with fulminant hepatic failure (FHF). The ex vivo hemoperfusion was conducted in FHF rats by perfusing plasma at a rate of 1-2 mL/min through 1.5-2 x 10(8) encapsulated hepatocytes packed into a packed-bed bioreactor. Hemoperfusion with the bioreactor was initiated 5 h after operative induction of liver failure and continued for 7 h. The BLAD-treated rats showed improvements over the control groups in survival time and metabolic indicators, including ammonia and total bilirubin levels. Furthermore, expanded bed adsorption (EBA) detoxification technology using Streamline-SP resin was explored to complement the bioreactor with microencapsulated hepatocytes. In vitro experiments indicated that serum ammonia could be specifically removed in dose-dependent manner, whereas the total serum proteins were unaffected by the resin. In ex vivo experiments, hemoperfusion with the resin was initiated 3 h after operative induction of liver failure and continued for 7 h. The resin-treated rats showed obvious serum ammonia removal with no observable total blood protein and blood cell adsorption. Therefore, Streamline-SP resin can potentially be integrated into a BLAD for improved efficacy.

Leukemia inhibitory factor in the neuroimmune communication pathways in allergic asthma.

In the pathogenesis of asthma, central sensitization is suggested to be an important neural mechanism, and neurotrophins and cytokines are likely to be the major mediators in the neuroimmune communication pathways of asthma. However, their impact on the central nervous system in allergic asthma remains unclear. We hypothesize that central neurogenic inflammation develops in the pathogenesis of allergic asthma, and nerve growth factor (NGF) and leukemia inhibitory factor (LIF) are important mediators in its development. An asthma model of rats was established by sensitization and challenged with ovalbumin (OVA). For further confirmation of the role of LIF in neurogenic inflammation, a subgroup was pretreated with intraperitoneally (i.p.) LIF antibody before OVA challenge. The levels of LIF and NGF were measured with reverse transcription and polymerase chain reaction (RT-PCR), in situ hybridization (ISH) and immunohistochemistry stain in lung tissue, airway-specific dorsal root ganglia (DRG, C7-T5) and brain stem of asthmatic rats, anti-LIF pretreated rats and controls. A significantly increased number of LIF- and NGF-immunoreactive cells were detected in lung tissue, DRG and the brain stem of asthmatic rats. In the asthma group a significantly increase level of mRNA encoding LIF and NGF in lung tissue was detected, but not in DRG and the brain stem. Pretreatment with LIF antibody decreased the level of LIF and NGF in all tissues. LIF is an important mediator in the crosstalk between nerve and immune systems. Our study demonstrate that the increased level of LIF and NGF in DRG and brain stem may be not based on result from de novo synthesis, but rather on result from retrograde nerve transport or passage across the blood-brain-barrier.

[Diagnostic values of pressure aggravation test and breath aggravation test in the early acute appendicitis].

OBJECTIVE: To compare the applied value of the pressure aggravation test and breath aggravation test in the diagnosis of early acute appendicitis. METHODS: A total of 101 cases with epigastralgia, middle or upper abdomen pain, disease duration within 6 hours undergoing pressure aggravation test and breath aggravation test respectively in our hospital between October 2010 and December 2012 were prospectively enrolled. By comparing with the postoperative pathological diagnosis (early acute appendicitis and other abdominal pain), the sensitivity and specificity of these two tests were calculated. Through analyzing the receiver operating characteristic (ROC) curve, the diagnostic value of early acute appendicitis was evaluated. RESULTS: Fifty-two cases of early acute appendicitis and 49 cases of other abdominal pain were diagnosed by postoperative pathologic results. The sensitivity and specificity of the pressure aggravation test were 87.5% and 72.1% and of the breath aggravation test were 53.8% and 83.7% respectively. The area under the ROC curve of the pressure aggravation test was 0.786 (95% CI: 0.693-0.878), similar to that of the breath aggravation test (0.688, 95% CI: 0.583-0.792). CONCLUSION: The pressure aggravation test has higher value to diagnose early acute appendicitis, while the breath aggravation test has better specificity.

[Indications for non-surgical management of traumatic splenic rupture: report of 36 cases].

OBJECTIVE: To investigate the indications for non-surgical management of traumatic splenic rupture. METHODS: From Jan. 2002 to Jan. 2008, 36 patients with traumatic splenic rupture underwent non-surgical management in the First Affiliated Hospital of Jinan University. RESULTS: Of the 36 cases, 32 were successfully managed without surgical interventions, and 4 converted to open surgery. No death occurred in these patients, nor was delayed splenic rupture identified 1 to 5 years after the treatment. CONCLUSION: Hemodynamically index is an important reference to select the patients, and the degree of splenic rupture, the patient's age and conditions of the hospital should be considered.

[Surgical management of serious hepatic injuries].

OBJECTIVE: To explore an effective method of treating serious hepatic injuries. METHODS: A retrospective analysis was conducted on 92 consecutive cases of serious hepatic injuries during recent 21 years. RESULTS: Eighty-four cases were treated with operation, and 8 cases with nonoperation management (NOM). Of these patients, 77 (83.5%) were healed, and 15 (16.5%) died. There were complications in 30 patients (31.5%). Hospital stay was 22.3 days. CONCLUSION: Ultrasonography is a valuable diagnostic measure for hepatic injuries. When hemodynamic was stable, CT scanning was especially necessary for patients with complex injuries. Hemostasis is a key measure during operation. Debridement of nonviable hepatic parenchyma is effective management for the decrease of operative complications. If hypotension cannot be corrected actively, clamping of the upper abdominal aorta is an effective measure for patients with hepatic injuries. Serious hepatic injuries can be treated with NOM selectively.