Separation of Halloysite Nano Tubes (HNTs) by Homogenization of Quartz Contaminated Kaolins.

Natural halloysite kaolin contains a lot of impurities such as quartz phases and varies in morphology and size during their formation in the earth. So to utilize as a new type of natural nano material, removing quartz impurities from kaolin clays without scathe the tube morphologies are necessary. So to remove quartz impurities from kaolin by forming a well deflocculated aqueous slip without fracturing the morphology of tubes, the slip of homogenized halloysite clay was recovered by adding polyvalent metallic cations and anionic polyelectrolyte flocculants simultaneously to selectively flocculate the mixture of quartz and halloysite, whereby the halloysite particles form floes and the tubular halloysite remains in suspensions. Then, the uniform size and tubular shape of halloysite was obtained which could be suitably used as a container or a carrier to encapsulate nanomaterials.

The effects of Curcumin on HCT-116 cells proliferation and apoptosis via the miR-491/PEG10 pathway.

Paternally expressed gene-10 (PEG10) could participate in several carcinomas and might be regulated by miR-491. To now, miR-491 was found to play an important role in the sensitivity and mechanism of drug usage in the treatment of colorectal cancer, and drug resistance is a key factor to affect the disease healing. In this study, miR-491, PEG10, Wnt1, and ß-catenin expression levels and their correlation with colorectal cancer were assessed in cancer tissues and adjacent parts. And the target relationship between PEG10 and miR-491 was verified. Meanwhile, the impaction of Curcumin on miR-491, PEG10, and Wnt/ß-catenin signaling pathway were analyzed in HCT-116 cells. The effects of PEG10 and Curcumin on human HCT-116 cells proliferation and apoptosis were investigated by MTT and flow cytometry assay. Results showed that the expression of miR-491 in colon cancer tissues was decreased, but PEG10, Wnt1, and ß-catenin were higher than that in adjacent tissues. The PEG10 gene 3' UTR could combine with miR-491 seed sequence and miR-491 overexpression could cause a decrease in PEG10, Wnt1, and ß-catenin levels in human HCT-116 cells. Furthermore, PEG10 overexpression increased the expression levels of Wnt1 and ß-catenin, thereby promoting cell proliferation and inhibiting apoptosis. In addition, Curcumin could up-regulate miR-491, inhibit PEG10, and Wnt/ß-catenin signaling pathway. Consequently, Curcumin reduced HCT-116 cells proliferation and promoted cells apoptosis via the miR-491/PEG10 pathway. In conclusion, PEG10 was a target gene of miR-491, miR-491/PEG10 strengthen the sensitivity of Curcumin in HCT-116 cells proliferation and apoptosis, which might act as an ideal diagnostic biomarker treatment methods.

Microscale tribological behavior and in vitro biocompatibility of graphene nanoplatelet reinforced alumina.

Graphene nanoplatelets were added as reinforcement to alumina ceramics in order to enhance microscale tribological behavior, which would be beneficial for ceramic-on-ceramic hip implant applications. The reduction in microscale wear is critical to hip implant applications where small amounts of wear debris can be detrimental to patients and to implant performance. The addition of the GNPs lead to improvements in fracture toughness and wear (scratch) resistance of 21% and 39%, respectively. The improved wear resistance was attributed to GNP-induced toughening, which generates fine (~100nm) microcracks on the scratch surface. In addition, active participation of GNPs was observed in the scratch subsurface of GNP-reinforced samples through focused ion beam sectioning. Friction coefficients are not significantly influenced by the addition of GNPs, and hence GNPs do not act as solid state lubricants. In vitro biocompatibility with human osteoblasts was assessed to evaluate any possible cytotoxic effects induced by GNPs. Osteoblast cells were observed to survive and proliferate robustly in the GNP-reinforced samples, particularly those with high (10-15vol%) GNP content.

Stercoral colonic diverticulum perforation with jejunal diverticulitis mimicking upper gastrointestinal perforation.

Stercoral perforation of the colon is an unusual pathological condition with fewer than 150 cases reported in the literature to date. We present a case of stercoral colonic perforation mimicking upper gastrointestinal perforation, which was diagnosed by computed tomography preoperatively. However, at laparotomy, stercoral colonic diverticulum perforation with jejunal diverticulitis became the most appropriate diagnosis.

Sulfated polymannuroguluronate inhibits Tat-induced SLK cell adhesion via a novel binding site, a KKR spatial triad.

AIM: Sulfated polymannuroguluronate (SPMG), a candidate anti-AIDS drug, inhibited HIV replication and interfered with HIV entry into host T lymphocytes. SPMG has high binding affinity for the transactivating factor of the HIV-1 virus (Tat) via its basic domain. However, deletion or substitution of the basic domain affected, but did not completely eliminated Tat-SPMG interactions. Here, we sought to identify other SPMG binding sites in addition to the basic domain. METHODS: The potential SPMG binding sites were determined using molecular simulation and a surface plasmon resonance (SPR) based competitive inhibition assay. The effect of SPMG on Tat induced adhesion was evaluated using a cell adhesion assay. RESULTS: The KKR domain, a novel high-affinity heparin binding site, was identified, which consisted of a triad of Lys12, Lys41, and Arg78. The KKR domain, spatially enclosed SPMG binding site on Tat, functions as another binding domain for SPMG. Further functional evaluation demonstrated that SPMG inhibits Tat-mediated SLK cell adhesion by directly binding to the KKR region. CONCLUSION: The KKR domain is a novel high-affinity binding domain for SPMG. Our findings provide important new insights into the molecular mechanisms of SPMG and a potential therapeutic intervention for Tat-induced cell adhesion.

Characterization of hepatitis B virus genotypes/subgenotypes in 1,301 patients with chronic hepatitis B in North China.

BACKGROUND: There is still a paucity of data on hepatitis B virus (HBV) subgenotype prevalence in North China based on sequencing of large-size samples. In addition, whether HBV genotypes impact drug-resistance-associated and HBV e antigen (HBeAg)-loss-associated mutations in patients with chronic hepatitis B (CHB) is still under investigation. This study aimed to disclose clinical prevalence of HBV genotypes/subgenotypes in North China and the clinical implications of HBV genotype classification in respect to HBeAg loss and drug-resistant occurrence. METHODS: Sera were collected from 1301 nucleos(t)ide analog-experienced CHB patients. Viral DNA was extracted and used as template for HBV genome amplification by nested PCR. DNA sequencing was performed for the analysis of HBV genotypes/subgenotypes, drug-resistance-associated mutations in polymerase gene and HBeAg-loss-associated mutations in precore/basal core promoter (BCP) regions. RESULTS: HBV/B, HBV/C, and HBV/D were detected in 190 (14.6%), 1096 (84.2%), and 15 (1.2%) patients, respectively. HBV/B2 (182/190), HBV/C2 (1069/1096), and HBV/D1 (12/15) were predominant subgenotypes within individual genotypes. By contrast, C2 prevalence is relatively lower in Beijing area (77.2%) than in other north areas (84.9% - 87.4%). HBV/C-infected patients had an older age and a lower serum albumin level but similar HBV DNA and alanine aminotransferase (ALT) levels compared to HBV/B-infected patients. HBV/C infection had a higher incidence of lamivudine-resistant mutations rtM204I/V (44.9% vs. 30.2%, P < 0.01) and BCP mutations A1762T+G1764A (65.8% vs. 40.0%, P < 0.01) compared with HBV/B infection. CONCLUSIONS: C2 is the most prevalent HBV subgenotype followed by B2 in CHB patients in North China; and HBV genotype prevalence is influenced by immigrant population. HBV/C infection is likely to have longer disease duration and severer liver functional impairment and might be more susceptible to develop lamivudine resistance compared to HBV/B infection.

[Experimental study of protective effects of hepatotrophic factors on hepatic functions in rats with portal hypertension after portacaval shunt].

OBJECTIVE: To investigate the protective effects of hepatotrophic factors (hepatocyte growth-promoting factor and insulin) on hepatic functions and pathology in rats with portal hypertension after portacaval shunt. METHODS: The rats of hepatic cirrhosis with portal hypertension were randomly assigned into 1 control group, 1 model group and 4 treatment groups (NS, HGF, INS, HGF + INS). An end-side portacaval shunt was performed in the treatment group. The hepatotrophic factors were respectively injected into portal vein. After treatment, the serum levels of ALT (alanine aminotransferase), AST (aspartate aminotransferase), HA (hyaluronic acid) and LN (laminin) were determined by radioimmunoassay. And then according to the hematoxylin and eosin (H&E) staining results, the tissue slides were prepared. RESULTS: The serum levels of ALT (30.13 ± 4.12 U/L), AST (133.75 ± 21.18 U/L), HA (322.49 ± 52.33 µg/L) and LN (23.89 ± 5.03 µg/L) were lower in the HGF + INS group than those in the NS group (all P < 0.01); the scores of hepatic fibrosis stages (1.63 ± 0.74) and collagen semiquantitative of Masson stain (10.17 ± 1.14 × 10(-2)) were significantly reduced in the HGF + INS group than those in the NS group (all P < 0.01). CONCLUSION: The injection of hepatotrophic factors through portal vein after portacaval shunt can improve hepatic functions, reduce the damages of hepatocyte and improve the degree of hepatic fibrosis.

Peroxisome proliferator-activated receptor gamma ligands suppress liver carcinogenesis induced by diethylnitrosamine in rats.

AIM: Peroxisome proliferator-activated receptor gamma (PPARgamma) is known to regulate growth arrest and terminal differentiation of adipocytes and is used clinically as a new class of antidiabetic drugs. Recently, several studies have reported that treatment of cancer cells with PPARgamma ligands could induce cell differentiation and apoptosis, suggesting a potential application as chemopreventive agents against carcinogenesis. In the present study, 3 different kinds of PPARgamma ligands were subjected to the experiments to confirm their suppressive effects on liver carcinogenesis. METHODS: Three PPARgamma ligands, pioglitazone (Pio) (200 ppm), rosiglitazone (Rosi) (200 ppm), and troglitazone (Tro) (1,000 ppm) were investigated on the induction of the placental form of rat glutathione S-transferase (rGST P) positive foci, a precancerous lesion of the liver, and liver cancer formation using a diethylnitrosamine-induced liver cancer model in Wistar rats, and dose dependency of a PPARgamma ligand was also examined. RESULTS: PPARgamma ligands reduced the formation of rGST P-positive foci by diethylnitrosamine and induction of liver cancers was also markedly suppressed by a continuous feeding of Pio at 200 ppm. CONCLUSION: PPARgamma ligands are potential chemopreventive agents for liver carcinogenesis.