Bone and Bones ; pathology ; Humans ; Immunologic Deficiency Syndromes ; diagnosis ; Osteochondrodysplasias ; diagnosis

Objective To summarize the pathological features of nonalcoholic fatty liver disease(NAFLD)in China based on a histological scoring system for NAFLD designed by the Pathology Committee of NASH Clinical Research Network(NASH-CRN).Methods The specimens of liver needle biopsy from 130 patients with NAFLD were examined with light microscopy after haematoxylin eosin,reticular fiber,and Masson trichrome staining.Immunohistochemistry staining of the sections,combined with clinical data,was used to exclude non-NAFLD cases.Results Hepatic steatosis,lobular inflammation,hepatocyte ballooning and fibrosis existed extensively in 130 cases NAFLD liver tissues.Furthermore,macrovesicular steatosis predominantly located in acinar zone 3 was the main pathological feature of NAFLD,and lobular inflammation was usually mild.Hepatocyte ballooning was observed in 94.6 percent of 130 cases.Mild perisinusoidal fibrosis and periportal fibrosis were often observed in stage 1.According to the statistic analysis,hepatic steatosis was positively correlated with lobular inflammation,hepatocyte ballooning and fibrosis(r=0.587,0.488,0.374,respectively;all P value

Objective To explore the expression of leptin and its receptors in liver tissue of nonalcoholic steatohepatitis(NASH)patient and its significance in pathogenesis.Methods Samples of 59 liver biopsies of NASH patients were divided into three groups G,S and F according to their degree of inflammation and steatosis and stage of fibrosis.The expression of leptin and its receptors including Ob-R,the short form of Ob-R(Ob-Ra)and the long form of Ob-R(Ob-Rb)were semi-quantitatively determined at the protein and/or mRNA expression levels by using immunohistochemistry,in situ hybridization and image analysis.Results The expressions of leptin in NASH liver tissues were found in KC,HSC and MNC,which were mainly situated in zone 3 near steatotic hepatocytes and perisinusoidal or portal fibrosis areas.Leptin mRNA(Ob)positive cells were distributed in hepatocytes in zone 3.The expression of leptin at protein and mRNA levels in the NASH liver tissues was significantly increased in NASH compared with normal liver tissues(P

Objective To investigate the expressions of pivotal cytokines such as TNF-? and TGF-?_1, and leptin in human nonalcoholic lipoid hepatitis (NALH), and to explore their potential roles in the pathogenesis of NALH. Methods Liver tissue obtained from 59 patients pathologically diagnosed as nonalcoholic lipoid hepatitis and 10 healthy adult liver tissues were examined in the present study. The respective expression of TNF-?, TGF-?_1 and Leptin was qualitatively and semi-quantitatively determined at the protein expression levels by using immunohistochemical method and image analysis. Results In NALH liver tissue the expression of TNF-? appeared mainly in inflammatory cells and lining cells of liver sinusoids in zone 3, lipogranulomas and portal tract, where obvious inflammation was found. The expression was parallel to different degrees of inflammation in NALH, significant correlation was found between degree of inflammation and fibrosis and extent of expression (P

Objective To investigate the risk factors and prognosis of acute kidney injury (AKI) in elderly patients with sepsis in intensive care unit (ICU).Methods Clinical data of 108 elderly patients diagnosed as sepsis admitted in ICU in our hospital,from May 2010 to May 2014 were analyzed retrospectively.Patients were divided into two groups:the AKI group and the non-AKI group.Clinical characteristics,laboratory and physiologic data were compared between groups.Multivariate Logistic regression analysis was used to analyze the independent risk factors for AKI in these patients,and clinical outcome was retrospectively analyzed.Results Among the 108 elderly patients,60 patients developed AKI and the incidence was 55.6％.Baseline glomerular filtration rate (GFR) and mean arterial pressure (MAP) were lower in the AKI group than in non-AKI group (t=4.536 and 3.28).Prothrombin time (PT) (t=3.053),multiple organ dysfunction score (MODS) (t =2.201),acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score (t=3.423),the incidence of septic shock (x2 =5.400) and patients undergoing surgical operation within two weeks (x2 =5.625) were higher or longer in AKI group than in non-AKI group (all P＜0.05).Multivariate Logistic regression analysis showed that MAP (OR =0.833),baseline GFR (OR=0.776),MODS (OR=2.039) were independent risk factors for AKI occurrence.Hospital mortality,length of stay in ICU and hospitalization time were higher or longer in AKI group than in non-AKI group (P=0.001,0.026 and 0.042).Conclusions MAP,baseline GFR and MODS are the independent risk factors for AKI occurrence in elderly adults with sepsis in ICU.Hospital mortality,length of stay in ICU and hospitalization time are increased in sepsis patients combined with AKI.

Objective To investigate the correlation between immune cell function and the infection after renal transplantation through monitoring of immune function intracellular ATP by Cylex ImmuKnow assay,and explore its significance in individual immunosuppressive therapy of renal transplantion recipients.Method We collected 44 renal transplant patients suffered from pulmonary infection from January 2014 to March 2015.The patients were divided into two groups according to the clinical status,namely,ImmuKnow monitoring group (n =22) and empirical treatment group (n =22).Thirty-two non-infection recipients were collected as controls.All the kidney transplantation recipients received immunosuppressive therapy based on calcineurin inhibitors,mycophenolate mofetil and prednisone,and ATG for induction therapy after transplantatior.The immune cell function levels were measured by Cylex ImmuKnow assay.The whole blood samples were collected before infection onset,at the time of infection,and 1 week after infection resolution.Result When infection occurred,ATP concentrations in CD4+ T cells of the kidney transplant recipients were significantly lower than those in non-infection group [(151.30--71.35 ng/mL vs.(308.34 ± 141.29 ng/mL,P＜0.05).When the infection got controlled,the ATP concentrations in CD4+ T cells increased to those before infection occurred.The average hospitalization time in ImmuKnow monitoring group was 12.27 ± 0.74 days,which was significantly shorter than in empirical treatment group (16.64 ± 1.98 days,P＜ 0.05).The incidence of acute rejection was 4.5％ in ImmuKnow monitoring group,and 13.6％ in empirical treatment group (P＞0.05).Conclusion The examination of ATP in CD4+ T cells by Cylex Immuknow assay could reflect the status of cellular immunity,provide reliable and objective basis for the diagnosis and treatment of infection after renal transplantation,and guide the clinical individualized immunosuppressive therapy.

Objective To investigate the expressions of vascular endothelial growth factor (VEGF)-C,-D and VEGF receptor-3 (VEGFR-3/Flt-4) in pN0 early gastric cancer (ECG) and their relationship with lymph node micrometastasis.Methods From January 2005 to January 2010,the paraffin-embedded specimens of 61 pN0 ECG were collected.The expressions of VEGF-C,VEGF-D and VEGFR-3 in 61 pN0 early gastric cancer tissue,25 adjacent tissue and CAM5.2 expression in 868 hematoxylin-eosin staining negative lymph nodes were detected by immunohistochemical assay.The rate of lymph node micrometastasis of 61 pN0 ECG was evaluated.According to the data type,t test,x2 test or Fisher exact probability were performed for the relationship analysis between the expressions of VEGF-C,VEGF-D and VEGFR-3 in pN0 stage ECG and lymph node micrometastasis.Results The high expressions of VEGF-C,VEGF-D and VEGFR-3 in the 61 pN0 ECG were 34.4％ (21/61),34.4％ (21/61) and 44.3％ (27/61) respectively,which were higher than those of adjacent tissues [12.0％ (3/25),8.0％ (2/25) and 16.0％ (4/25) respectively] (x2=4.433,6.321 and 6.144 respectively,all P＜0.05).There were 10 cases (16.4％) of pN0 ECG with lymph node micrometastasis.In pN0 ECG,the low expressions of VEGF-C and VEGFR-3 in negative Flt-4 vascular invasion (FVI) were common than positive FVI (x2 =15.828,6.879 and 9.244,all P＜0.05).The high expressions of VEGF-C and VEGFR-3 were related to the depth of tumor invasion (x2 =5.561 and 5.678,both P＜0.05),the density of VEGFR 3 positive vascular (FVD) (t=2.987and 5.652,both P＜0.01) and lymph node micrometastasis (x2 =6.705 and 6.192,both P＜0.05),but not related to the degree of differentiation (P＞0.05).However,the high expression of VEGF-D was not related to depth of tumor invasion,FVD and lymph node micrometastasis (all P＞0.05),but related to the degree of differentiation (x2 =8.472,P =0.004).The high expressions of VEGF-C,VEGF-D and VEGFR-3 were not related to gender,age,tumor location,macroscopic type and tumor size (all P＞0.05).Conclusions The high expressions of VEGF-C,VEGFR-3 were related to lymph node micrometastasis in pN0 ECG.Although the high expression of VEGF-D was not related to lymph node micrometastasis,it could indirectly affect lymph node micrometastasis through VEGF-C-VEGFR-3 axis in pN0 ECG.

Objective To investigate the incidence and extent of biopsy tract contamination in malignant bone tumors by either core needle biopsy or open biopsy and detect the safe extent in resection of biopsy tract. Methods Forty-eight cases were performed core needle biopsy, including 37 osteosarcomas, 5 malignant fibrous histiocytomas, 1 juxtacortical osteosarcoma, 1 low grade central osteosarcoma, 1 periosteal osteosarcoma, 1 primary malignant melanoma of bone and 2 chondrosarcomas. There were 37 males and 11 females with a mean age of 23.3 years (range, 10-64 years). The mean time between core needle biopsy and definitive surgery was 1.3 months (range, 0-2 months). All the patients were performed limb salvage surgery.Twenty-six cases were performed open biopsy, including 20 osteosareomas, 1 Ewing's sarcoma, 2 chondrosarcomas, 1 mesenchymal chondrosarcoma, 1 malignant fibrous histiocytoma, 1 lymphoma. There were 21males and 5 females with a mean age of 21.9 years (range, 8-59 years). The mean time between open biopsy and definitive surgery was 2.3 months (range, 1-4 months). The tumor and tissue around the biopsy tract at least 2 cm were resected. The pathological examination was performed in specimens via the biopsy tract, including the normal soft tissue outside the tumor, deep fascia, subcutaneous tissue and skin. The incidence and extent of biopsy tract contamination were evaluated with pathological examination. Results Forty-four cases were followed up. The mean follow-up time was 17.6 months (range, 4-39 months). In core needle biopsy group, four of forty-eight cases were found malignant tumor cells seeding in biopsy tract, the positive rate was 8.3%. In open biopsy group, all the cases were followed up with the mean time of 12.9 months (range, 2-29 months), and two of twenty-six cases were found malignant tumor cells seeding in biopsy tract,the positive rate was 7.7%. Conclusion Biopsy of malignant bone tumors has the risk of biopsy tract contamination. The tumor cell seeding exists in both core needle biopsy and open biopsy. The biopsy tract should be performed en bloc resection with the tumor.

AIM: To study the signal pathway involved in up-regulation of LPS-induced HO-1 expression by CCK-8. METHODS: Forty-two SD rats were divided into 7 groups (six rats each) randomly as follows: control group, LPS group, LPS+SP600125 (JNK-specific inhibitor) group, CCK-8+LPS group, CCK-8+LPS+SP600125 group, CCK-8 group and CCK-8 +SP600125 group. Lungs from the rats in these 7 groups were excised 6 h after the agents were administered. HO-1 mRNA expression was examined by RT-PCR. The protein expression of HO-1 was detected by Western blotting and immunofluorescence flow cytometry (FCM). RESULTS: There were significant positive expression of HO-1 mRNA in LPS group compared to control group. CCK-8 enhanced LPS-induced HO-1 mRNA expression and CCK-8 alone induced HO-1 mRNA expression as well. The mRNA expressions of HO-1 in LPS group, CCK-8+LPS group and CCK-8 group were 3.01 (P<0.01), 5.88 (P<0.01) and 3.45 (P<0.01) times as many as that in control group, respectively. SP600125 inhibited the mRNA expression of HO-1 induced by CCK-8 and (or) LPS. The change of HO-1 protein expression was in accordance with that of HO-1 mRNA expression by Western blotting and immunofluorescence FCM. CONCLUSION: These results suggest that JNK/c-Jun signal pathway plays an important role in the up-regulation of LPS-induced HO-1 expression by CCK-8.

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.