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Distinguishing light-echoed nerves from surrounding structures is challenging but may be important in nerve block administration. We evaluated the effect of patient characteristics on the echogenicity or visibility of the popliteal sciatic nerve (PSN).This study included adult patients who presented to the operating room as volunteers. The primary outcome was the success rate of nerve identification by ultrasound using different PSN access paths. The secondary outcome included the PSN visibility score (VIS), scan time, and PSN depth. Logistic regression analysis was used to identify factors associated with the PSN identification success rate. The Body Mass Index (BMI) proximal-based cut-off was used to compare the PSN identification success rate through different access paths.The PSN was successfully identified in 89.7% of the volunteers. The access paths (P0.01) and BMI (P=0.01) were identified as independent predictors of successful PSN identification. A higher PSN identification success rate (P=0.01), a higher VIS (P0.01), a more superficial PSN depth (P0.01), and a shorter scan time (P0.01) were observed in the above-knee lateral approach. Among volunteers with BMI≥26.77 kg/mThe ultrasound-guided above-knee lateral approach for PSN block improved the PSN identification success rate, ensured a more superficial nerve location, and provided a clearer image.

Activated pancreatic stellate cells (PSCs) play a crucial role in the progression of pancreatic fibrosis. Transforming growth factor-β (TGF-β) is one of the strongest stimulator inducing fibrosis. The mitogen-activated protein kinase (MAPK) proteins (including ERK, JNK and p38 MAPK) are known to contribute to PSC activation and pancreatic fibrosis. Previous studies have identified PSC activation induced by TGF-β1 is related to MAPK pathway, but the respective role of MAPK family members in PSC activation still unclear, and which family member may be the key mediator in mice PSC activation still controversial. In this study, we investigated the influence of different MAPK family member (JNK, ERK, and p38 MAPK) on mice PSC activation using an in vivo and in vitro model. The results showed p-JNK, p-ERK and p-p38 MAPK were all over-expressed in CP group, and p-JNK, p-ERK, and p-p38 MAPK were co-expressed with activated PSC. In vitro, TGF-β1 induced JNK and ERK over-expression in PSCs. In contrast, p38 MAPK expression in PSC showed only a very weak increase. JNK- and ERK-specific inhibitors inhibited FN and α-SMA mRNA expression in PSCs, and a p38 MAPK inhibitor had no effect on PSC activation. These findings indicate that JNK and ERK were directly involved in the PSCs activation induced by TGF-β1 and the development of pancreatic fibrosis. p38 MAPK participate in the progression of CP, but it does not respond to TGF-β1 directly and may not be regarded as the target of TGF-β1 induced PSC activation.

AIM To explore the role of macrophages in chronic pancreatitis (CP) and the effect of Dachaihu decoction (DCHD) on pancreatic fibrosis in mice. METHODS KunMing mice were randomly divided into a control group, CP group, and DCHD group. In the CP and DCHD groups, mice were intraperitoneally injected with 20% L-arginine (3 g/kg twice 1 d/wk for 6 wk). Mice in the DCHD group were administered DCHD intragastrically at a dose of 14 g/kg/d 1 wk after CP induction. At 2 wk, 4 wk and 6 wk post-modeling, the morphology of the pancreas was observed using hematoxylin and eosin, and Masson staining. Interleukin-6 (IL-6) serum levels were assayed using an enzyme-linked immunosorbent assay. Double immunofluorescence staining was performed to observe the co-expression of F4/80 and IL-6 in the pancreas. Inflammatory factors including monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1α (MIP-1α) and IL-6 were determined using real time-polymerase chain reaction. Western blot analysis was used to detect fibronectin levels in the pancreas. RESULTS Compared with the control group, mice with 20% L-arginine-induced CP had obvious macrophage infiltration and a higher level of fibrosis. IL-6 serum concentrations were significantly increased. Double immunofluorescence staining showed that IL-6 and F4/80 were co-expressed in the pancreas. With the administration of DCHD, the infiltration of macrophages and degree of fibrosis in the pancreas were significantly attenuated; IL-6, MCP-1 and MIP-1α mRNA, and fibronectin levels were reduced. CONCLUSION The dominant role of macrophages in the development of CP was mainly related to IL-6 production. DCHD was effective in ameliorating pancreatic fibrosis by inhibiting macrophage infiltration and inflammatory factor secretion in the pancreas.

It is significant to explore the fatigue contact damage of bi-layer ceramic composites in order to improve the long-time mechanical reliability of bi-layer structured dental restorations. In this study, Hertz contact test was used to compare the fracture modes and the ability of anti-fatigue damage of zirconia and alumina bi-layer composites, to analyze the effect of loading rate and other factors on the damage mechanisms of bi-layer ceramic composites. Cyclic spherical fatigue loading was put on the bi-layer alumina and zirconia composites with different substrates. The samples were observed by high depth of field stereomicroscope and digital optical microscope after test. The results showed that the fatigue contact damage mode of zirconia bi-layer composite was the porcelain fracture from radial cracks without the damage of zirconia core. The fatigue contact damage mode of alumina bi-layer composite was the alumina core failure from radial cracks as the function of contact load. For both of zirconia and alumina bi-layer samples, the number of cycles to the sample failure as the function of same maximum contact load with high loading rate was obviously smaller than low loading rate. The mechanical properties of the substrate materials had limited effects on the number of cycles to the failure of both zirconia and alumina bi-layer samples from contact-induced radial cracks as maximum contact load with low loading rate. The ability of the zirconia bi-layer composites to resist fatigue damage was much higher than that of the alumina bi-layer composites.

AIM: To search for a new chronic pancreatitis model in mice suitable for investigating the pathophysiological processes leading to pancreatic fibrosis. METHODS: The mice were randomly divided into 2 groups (n = 50), control group and model group. The mice in model group were given ethanol (10%) in drinking water after injection of dibutyltin dichloride (DBTC) (8 mg/kg BW) in tail vein. The mice in control group were injected with only solvent into tail vein (60% ethanol, 20% glycerine and 20% normal saline) and drank common water. At days 1, 7, 14, 28, and 56 after application of DBTC or solvent, 10 mice in one group were killed at each time point respectively. Blood was obtained by inferior vena cava puncture. The activity of amylase, concentration of bilirubin and hyaluronic acid in serum were assayed. The pancreas was taken to observe the pancreatic morphology by HE staining, and to characterize the pancreatic fibrosis by Masson staining. The expression of F4/80, CD3 and fibronectin (FN) were assayed by immuno-histochemistry or Immunofluorescence technique. Collagen type I (COL1A1) in pancreas were detected by Western blot. The expression of matrix metalloproteinase-1 (MMP-1) and tissue inhibitor of metalloproteinases-1 (TIMP-1) mRNA in the pancreas was assessed by real time PCR. RESULTS: DBTC induced an acute edematous pancreatitis within 1 d. The dilated acini, scattered acinar cell necrosis, and inflammatory cells were found at day 7. Extensive infiltration with inflammatory cells following deposition of connective tissue was observed at day 14. At day 28, level of pancreatic fibrosis was aggravated. The pancreatic tissue was replaced by an extended interstitial fibrosis at the end of 2 mo. There was significant difference in the level of amylase, bilirubin and hyaluronic acid in serum between control group and model group (P < 0.05). The level of COL1A1 and FN in pancreas increased. The expression of MMP-1 mRNA in pancreas decreased, but TIMP-1 mRNA increased at model group. CONCLUSION: DBTC joint Ethanol drinking can induce chronic pancreatitis in accordance with the pathophysiological modification of human. DBTC joint Ethanol-induced pancreatitis in mice is an effective and handy experimental method. The model is suitable to study the mechanism of pancreatic fibrosis in chronic pancreatitis.

Bi-layer all-ceramic dental crowns comprise an inner core made of alumina or zirconia and an outer porcelain shell. The veneer safe from damage is mainly depended on the properties of core materials due to the poor strength and toughness of porcelain. The fracture modes and crack transformation of zirconia/porcelain and alumina/porcelain bi-layer composites reveal the potential feasibilities of improving the fatigue life of all-ceramic restorations. The failure modes of bi-layer composites were confirmed under cyclic spherical fatigue loading by dynamic microcosmic observation. Crack modes and evolvement of bi-layered composites were explored inflecting with fatigue load, cycles, frequency and water environment. Microcosmic morphology of the samples was observed by high depth of field stereomicroscope to determine degree and modes of fatigue damage. The appearance of cone cracks of porcelain surface was almost consistent in both of zirconia and alumina bi-layer composites. However, the pattern and process of the damage are different under cycle fatigue load. Furthermore, process of fatigue damage of bi-layer composites were observed to failure rapidly under water environment in both of zirconia and alumina bi-layer composites.

This study aimed to investigate the efficacy and safety of transcatheter arterial chemoembolization (TACE) in combination with three-dimensional conformal radiotherapy (3D-CRT) in the treatment for locally advanced unresectable hepatocellular carcinoma (HCC).From March 2000 to March 2009 a total of 158 patients with unresectable HCC treated and followed at our hospital were divided into TACE group (N=80) and TACE combined with 3D-CRT group (N=78). The TACE group was treated 3-6 times. In the combination group, 2-3 TACE courses were administered and 3D-CRT was performed 2 weeks after the last TACE. Three months after the end of treatment, imaging and serum AFP were carried out to assess the treatment efficacy.The response rates of TACE and the combination groups were 53.7% (43/80) and 71.8% (58/78) (p0.05). The 1, 2, and 3-year survival rates of patients in the TACE and combination groups were 58.75, 36.25, 16.25%, and 78.48, 55.12 and 25.64% (p0.05), respectively. Treatment compliance was good, with at least 2 TACE administrations for each case and at least 52 Gy for radiotherapy. In the TACE and the combination group, there were 2 and 3 cases with grade III/IV toxicity, respectively, without treatment-related death.3D-CRT in combination with TACE significantly improve the therapeutic outcome in patients with locally advanced unresectable HCC, without creating severe toxicity.

To investigate the effectiveness and adverse effects of gemcitabine by fixed-dose rate infusion plus oxaliplatin (GEMOX regimen) as second-line therapy for advanced ovarian cancer.64 patients with advanced ovarian cancer were divided into an experimental group (44 cases) and a control group (20 cases). The experimental group was treated with continuous intravenous infusion of gemcitabine at 1000 mg/m(2) with a fixed-dose rate of 10 mg/m(2)/min, on days 1 and 8 and oxaliplatin at 100 mg/m(2) on day 1, IVGTT, repeated every 3 weeks. The control group was treated with intravenous infusion of gemcitabine at 1000 mg/m(2) within 30 min on days 1 and and oxaliplatin at 100 mg/m(2) on day 1, IVGTT, again repeated every 3 weeks. CT scans or MRI were used for review every 1-2 cycles.The effective rate in the experimental group was significantly high than control group (43.2% vs 35.0%; P0.05), with no obvious difference of hematologic or non-hematologic toxicity between the two groups (P0.05).GEMOX regimen is very effective to treat advanced ovarian cancer, with low toxicity, good tolerance and improved life quality in patients.