Objective To investigate Hysterothylacium aduncum (Anisakidae) infection in marine fishes from Bohai Sea and Yellow Sea. Methods Nematodes were collected from the digestive tract of fishes, fixed with hot 4% formalin and preserved in 70% ethanol for study. The specimens were cleared in lactophenol for light microscopical examination, and properly treated for scanning electron microscopy (SEM). Results Among the fishes examined, 14 out of 93 species (15.1%) were found infected by H.aduncum, with a higher prevalence in the fish of Lophius litulon(66.7%), Scomber-omorus niphonius(47.5%), and Gadus macrocephalus(33.3%). H.aduncum infection was first recorded in elasmobranch-Raja smirnovi. Morphological differences of H.aduncum were observed, including the width of lateral alae and the length of intestinal caecum. Conclusion H.aduncum in fishes of Bohai Sea and Yellow Sea in China may be a complex species, and its high prevalence in some fishes reminds the risk of anisakiasis by eating raw fishes.

Background and purpose:Pancreatic cancer is one of the most deadly human malignant neoplasms. Resistance to chemotherapeutic drugs is a major reason responsible for poor prognosis in the treatment of pancreatic cancer patients. MicroRNA (miRNA, miR) is a family of small non-coding RNA molecules, dysregulated miRNA is associated with various tumor biological function. miR-33a has been widely reported as a metabolism-related miRNA, while its relationship with drug resistance has little understand. This study was focused on the effect of miR-33a on gemcitabine chemoresistance in pancreatic cancer to bring the novel theoretical basis to chemotherapy for pancreatic cancer.Methods:In situ hybridization and Real-time PCR were used to analyze the miR-33a expressions in pancreatic cancer tissue sample and cell lines, respectively. Cell counting kit 8 (CCK-8) assay was used to calculate the IC50 value of different pancreatic cancer cells.Results:miR-33a was down-regulated in pancreatic cancer tissue and cell lines compared with para-cancerous tissues and normal HEK293T cells. Moreover, miR-33a over expression not only could enhance the chemosensitivity to gemcitabine in pancreatic cancer cells, but also rescue the gemcitabine resistance in pancreatic cancer cells.Conclusion:Down regulation of miR-33a in pancreatic cancer decreases the chemosensitivity to gemcitabine, resulting in development of acquired gemcitabine chemoresistance. It provides the theoretical basis to develop a new molecular targeted drug to combine with chemotherapy for pancreatic cancer.

aused by the wrong maneuvers by inexperienced operators.

OBJECTIVE:To establish an HPLC method for the determination of triterpenoid in the roots of Actinidia deliciosa from Guangxi. METHODS: With the content of 2?,3?,24-trihydroxyursa-12-en-28-oic acid used as index. The separation was performed on Thermo Hypersil BDS C18 column (250 mm?4.6 mm,5 ?m) with 2?,3?,24-trihydroxyursa-12-en-28-oic acid as standard substance. The mobile phase consisted of methanol-0.2% phosphoric acid (73 ∶ 27) with column temperature set at 20 ℃. The flow rate was set at 1.0 mL?min-1 and detection wavelength was 210 nm. RESULTS: The linear range of 2?,3?,24-trihydroxyursa-12-en-28-oic acid were 0.025～0.200 mg?mL-1(r=0.999 8). The average recovery was 99.79%(RSD=1.54%,n=6). CONCLUSION: The method is accurate, reliable and reproducible for the quality control of the roots of A. deliciosa from Guangxi.

In the present study, a new compound named 17-(6-cinnamamido-hexylamino-)-17-demethoxygeldanamycin (CDG) was obtained by introducing the cinnamic acid (CA) group into the 17-site of geldanamycin (GDM). The anti-cancer effects of CDG in vitro and in vivo were evaluated. MTT assay was used to examine the inhibitory effect of CDG on the proliferation of MCF-7, HepG2, H460 and SW1990 cells. Immunofluorescent staining flow cytometry combined with Annexin V-FITC/PI staining were used to detect apoptotic cells. Transwell assay was used to analyze the effect of CDG on cell invasion and migration ability. Western blotting was used to detect the expression levels of RAF-1, EGFR, AKT, CDK4 and HER-2 of MCF-7, HepG2 and H460 cells. The toxicities of CDG and GDM were evaluated in mice. Using the subcutaneously transplanted MCF-7 xenograft in nude mice, inhibitory effect was evaluated in vivo. The results showed that CDG inhibited the proliferation of cancer cells (IC50: 13.6-67.4 microg.mL-1). After exposure to CDG for 48 h, most cells presented typical morphologic changes of apoptosis such as chromatin condensation or shrunken nucleus. The rates of apoptosis of MCF-7, HepG2, H460 and SW1990 cells incubated with 10 microg.mL-1 CDG were 23.16%, 27.55%, 22.21%, 20.47%, respectively. A dose-dependent reduction of migration of four cell lines was found after exposure to CDG. The decreased levels of RAF-1, EGFR, AKT, CDK4 and HER-2 showed that CDG possessed HSP90 inhibitory effect. The result of animal toxicity test on the mice suggested that CDG had lower toxicity than GDM. Meanwhile, CDG inhibited the growth of MCF-7 xenografts of athymic mice.

Objective To explore the effect of suledexide on renal injury and podocalyxin expression of podocytes in STZ diabetic desoxycorticosterone acetate (DOCA)-hypertensive rats. Methods Wistar rats were subjected to subcutaneous injection of streptozotocin(STZ), followed by uninephrectomy and subcutaneous administration of DOCA. Diabetic and hypertensive rats were randomly allocated to treatment with sulodexide or a combination of sulodexide and telmisartan for 8 weeks. Blood pressure (BP), 24-hour urinary albumin were measured every 2 weeks. Blood and urinary samples were collected to detect biochemical indexes of plasma and urinary β-acetyl-β-D-glucosaminidase (NAG) at the end of the study. Immunohistochemistry (IHC), RT-PCR and Western blot were performed to examine the expression and distribution of podocalyxin. Results STZ +DOCA-treated rats progressively developed hypertension, albuminuria and hyperglycemia. Hyperlipidemia and hypoinsulinemia were found in diabetic and hypertensive rats compared with controls. Albuminuia was significantly reduced in sulodexide group at week 8 and sulodexide plus telmisartan group at week 6 and week 8. Blood pressure decreased in sulodexide plus telmisartan group. No significant effects on lipid and glucose metabolism were observed in all treated groups. Histopathological index increased in STZ+DOCA-treated rats, but was significantly lower in sulodexide group as well as sulodexide plus telmisartan group. The number of podocytes on glomerular cross-section of the four groups were comparable. Segmental loss and down-regulation of podocalyxin were detected in STZ+DOCA-treated rats, which were greatly attenuated by sulodexinde, meanwhile, combination treatment preserved more podocalyxin expression in glomeruli than sulodexide monotherapy. Conclusion Sulodexide effectively reduces albuminuria, prevents loss of podocyte podocalyxin and alleviates renal damage in STZ diabetic DOCA-hypertensive rats.

Objective To evaluate effects of glycemic control on refraction in diabetic patients.Methods Twenty newly diagnosed diabetic patients were included in this study. The random blood glucose,glycosylated hemoglobin A1c( HbA1c) levels, fasting C-peptide and postprandial 2 h C-peptide levels were measured before treatment. The patients with random blood glucose ≥ 12. 0 mmol/L and HbA1c ≥ 10. 0%were selected. Refraction, intraocular pressure, radius of the anterior corneal curvature, depth of the anterior chamber, lens thickness, vitreous length, and axial length were measured on admission and at the end of week 1,2, 3 and 4 during glycaemic control. Results A transient hyperopic change occurred in all the patients receiving glycemic control with a mean maximum hyperopic changes of 1.6 D ( 0. 50 D ～ 3.20 D). There was a positive correlation between the magnitude of the maximum hyperopic changes and the HbA1 c levels on admission ( r = 0.84, P ＜ 0.05 ). There was a positive correlation between the magnitude of the maximum hyperopic changes and the daily rate of blood glucose reduction over the first 7 days of the treatment ( r = 0.53, P ＜ 0.05 ). There was no significant correlation between the magnitude of the maximum hyperopic changes and the levels of random blood glucose on admission. No significant correlation was observed between the maximum hyperopic changes and fasting C-peptide or postprandial 2 h C-peptide.There were no significant correlations between the magnitude of the maximum hyperopic changes and age,blood press, body mass index, triglyceride, total cholesterol, low-density lipoprotein or high-density lipoprotein. No significant changes were observed in the intraocular pressure, radius of the anterior corneal curvature, depth of the anterior chamber, lens thickness, vitreous length and axial length during glycemic control. Conclusions Transient hyperopic changes occur after glycemic control in diabetic patients with severe hyperglycaemia. The degrees of transient hyperopia are highly dependent on HbA1c levels before treatment and the rate of reduction of glucose level over the first 7 days of treatment. This is probably due to the decrease of refractive power by lens hydration, not morphological change of lens.

Adenoidectomy ; Female ; Humans ; Infant ; Male ; Retrospective Studies ; Sleep Apnea, Obstructive ; surgery

Aged ; Aged, 80 and over ; Alanine Transaminase ; blood ; Bilirubin ; blood ; Choledochostomy ; methods ; Common Bile Duct ; surgery ; Common Bile Duct Neoplasms ; complications ; Drainage ; Female ; Follow-Up Studies ; Humans ; Jaundice, Obstructive ; blood ; etiology ; surgery ; Jejunum ; surgery ; Male ; Middle Aged ; Pancreatic Neoplasms ; complications ; Survival Rate ; gamma-Glutamyltransferase ; blood

AIM: To evaluate the effects of glycemic control on refraction in diabetic patients. METHODS: Twenty newly diagnosed diabetic patients were included in this study. The random blood glucose, HbA1c levels, fasting C-peptide and postprandial 2h C-peptide were measured before treatment. The patients with random blood glucose higher than 12.0mmol/L and HbA1c level higher than 10.0% were selected. Refraction, intraocular pressure, radius of the anterior corneal curvature, depth of the anterior chamber, lens thickness, vitreous length, and axial length were measured on admission and at the end of week 1, 2, 3 and 4 during glycemic control.RESULTS: A transient hyperopic change occurred in all the patients receiving glycemic control. The maximum hyperopic change was 1.60D (range 0.50±3.20D). Recovery of the previous refraction occurred between two and four weeks after insulin treatment. There was a positive correlation between the maximum hyperopic changes and the HbA1c levels on admission (r=0.84, P<0.05). There was a positive correlation between the maximum hyperopic changes and the daily rate of blood glucose reduction over the first 7 days of the treatment (r=0.53, P<0.05). During transient hyperopia, no significant changes were observed in the intraocular pressure, radius of the anterior corneal curvature, depth of the anterior chamber, lens thickness, vitreous length and axial length.CONCLUSION: Transient hyperopic changes occur after glycemic control in diabetic patients with severe hyperglycemia. The degrees of transient hyperopia are highly dependent on HbA1c levels before treatment and the rate of reduction of the blood glucose level.