Behavioral response of Panonychus citri (McGregor) (Acari: Tetranychidae) to synthetic chemicals and oils.

BACKGROUND: Panonychus citri (McGregor) (Acari: Tetranychidae) population outbreaks after the citrus plantation's chemical application is a common observation. Dispersal behavior is an essential tool to understand the secondary outbreak of P. citri population. Therefore, in the current study, the dispersal activity of P. citri was observed on the leaf surfaces of Citrus reticulata (Rutaceae) treated with SYP-9625, abamectin, vegetable oil, and EnSpray 99. METHOD: Mites were released on the first (apex) leaf of the plant (adaxial surface) and data were recorded after 24 h. The treated, untreated, and half-treated data were analyzed by combining the leaf surfaces (adaxial right, adaxial left, abaxial right, and abaxial left). All experiments were performed in open-air environmental conditions. RESULTS: The maximum number of mites was captured on the un-treated or half-treated surfaces due to chemicals repellency. Chemical bioassays of the free-choice test showed that all treatments significantly increased the mortality of P. citri depending on application method and concentration. A significant number of mites repelled away from treated surfaces and within treated surfaces except adaxial left and abaxial right surfaces at LC30. In the no-choice test, SYP-9625 gave maximum mortality and dispersal by oils than others. No significant differences were observed within the adaxial and abaxial except abaxial surface at LC30. Therefore, the presence of tested acaricides interferes with P. citri dispersal within leaf surfaces of plantations depending on the mites released point and a preferred site for feeding.

Mineral Composition and Its Control on Nanopores of Marine-Continental Transitional Shale from the Ningwu Basin, North China.

There is a large difference between the sedimentary environment and maturity of organic matter between marine shale and marine-continental transitional shale. It is of great significance to discuss the effect of inorganicminerals on the pores for marine-continental transitional shale gas exploration. In this study, scanning electron microscopy (SEM), low temperature liquid nitrogen adsorption and Xray diffraction (XRD) were conducted on eight marine-continental transitional shale samples from the Ningwu Basin, Shanxi Province, China. The pore structure differences in the different minerals were discussed, and the relationship between the mineral content and pore parameters was analysed. The results show that the mineral composition of shale is dominated by clay minerals, quartz, carbonate minerals and a small amount of pyrite. The clay minerals content is between 39.5% and 77.0%, with an average of 59.9%. The quartz content ranges from 21.8% to 47.8%, with an average of 31.9%. The carbonate minerals content in shale is between 0.6% and 23.9%, and the average is 6.3%. The clay minerals are composed of mixed illite-montmorillonite layer, kaolinite and chlorite. The content of mixed illite-montmorillonite layer is between 13.8% and 27.4%, with an average of 20.4%. The kaolinite content ranges from 57.0% to 86.2%, with an average of 76.0%. The content of chlorite is between 0 and 15.6%, with an average of 5.7%. The types of pores are mainly intergranular pores and interlaminar pores, which are mostly presented as slit and parallel plates. The mixed illite-montmorillonite layer contributes more to the specific surface area, which is favourable for shale gas adsorption. The pores in kaolinite are more developed than those of the mixed illite-montmorillonite layer, but the pore diameter is relatively large. The quartz granule has a complete crystal type, and intergranular pores with a large pore size are often developed at the mineral contacts. Compared with clay minerals and quartz, the pore development in the carbonate minerals is relatively poor and develops more micro-fractures. The pyrite contributes a certain number of intergranular pores and mold pores.

Combined administration on You-Gui Yin and low-dose Raloxifene partially attenuates the bone loss in ovariectomized mice through the proliferation and osteogenic differentiation of bone marrow stromal cells.

BACKGROUND: Osteoporosis is a systemic skeletal disease of fragility fractures due to the loss of mass and deterioration of the microarchitecture of bone. PURPOSE: The aim of the study was to assess the osteogenic effects and the underlying mechanisms of the combined administration of You-Gui Yin (YGY) and Raloxifene hydrochloride (RLX) in ovariectomized (OVX) mice. METHODS: First, a classic animal model was used to mimic postmenopausal osteoporosis through the removal of the ovary of mice. Second, the OVX mice were administered YGY, RLX, and YGY + RLX for 12 weeks. Next, the bone microtomographic histomorphometry and bone mineral density (BMD) were assessed by micro-CT, and the biochemical markers of procollagen type I N-terminal propeptide (P1NP) and beta-isomerized C-telopeptide (ß-CTX) in serum were assessed. Finally, primary bone marrow stromal cells (BMSCs) were isolated from the tibia and cultured to evaluate cell proliferation and osteogenic differentiation. RESULTS: The results showed that BMD on the YGY + RLX group was higher than that on the RLX group (p < 0.05) and did not have a significant difference when compared with the sham group. Notably, the YGY + RLX group had a dramatically increased trabecular number (Tb.N) compared with that of the YGY group (p < 0.05). Moreover, the BV/TV (bone volume/total volume) and Tb.N in the YGY + RLX group were higher than that in the RLX group (p < 0.05), and the Tb.Sp (trabecular separation) was lower than that in the RLX group (p < 0.05). Moreover, the serum level of P1NP from the YGY + RLX group dramatically increased when compared with that from the YGY and RLX groups (YGY group: p < 0.05; RLX groups: p < 0.01). Notably, there was no significant difference between the YGY and YGY + RLX groups. In addition, cell proliferation from the co-administration of YGY and RLX was clearly higher than a single use of YGY and RLX (p < 0.01, respectively). The ALP/BCA (alkaline phosphatase/bicinchoninic acid) in the YGY + RLX group was higher than that in the RLX group (p < 0.01). CONCLUSION: Overall, co-administered YGY and RLX could partially attenuate bone loss and were more effective than individually using either one; this outcome might be associated with the proliferation and osteogenic differentiation of BMSCs.

An iminocoumarin sulfonamide based turn-on fluorescent probe for the detection of biothiols in aqueous solution.

A new chemodosimeter for the highly selective sensing and imaging of biothiols was designed and realized in phosphate-buffered saline solution at pH 7.4 through a fluorescence "off-on" response. A unique mechanism featuring a two-step cascade (biothiols→H2 O) sequence for this remarkable recognition is disclosed for the first time.

Comparison of the efficacy of Lamivudine plus adefovir versus entecavir in the treatment of Lamivudine-resistant chronic hepatitis B: a systematic review and meta-analysis.

BACKGROUND: Hepatitis B virus infection remains 1 of the major health threats worldwide. Currently, lamivudine plus adefovir combination therapy or entecavir monotherapy is usually used for the treatment of patients with lamivudine-resistant chronic hepatitis B (CHB). However, there are few systematic comparisons between the efficacy of lamivudine plus adefovir and the efficacy of entecavir in the treatment of these patients. OBJECTIVE: The goal of this systematic study and meta-analysis was to assess the efficacy of lamivudine plus adefovir compared with entecavir for the treatment of patients with lamivudine-resistant CHB. METHODS: A comprehensive literature search of PUBMED, Web of Science, WANFANG database, the Cochrane Central Register of Controlled Trials, and the Cochrane Database of Systematic Review, were screened to obtain citations from January 1990 to January 2012 in this study. Data analysis was done by using the Review Manager Software 5.1. RESULTS: Eight studies were suitable for analysis. A total of 696 patients with lamivudine-resistant CHB were studied and grouped according to treatment: 341 patients in the entecavir group and 355 patients in the lamivudine plus adefovir group. The results found that the rates of undetectable hepatitis B virus DNA levels, alanine aminotransferase normalization, hepatitis B e antigen loss, and hepatitis B e antigen seroconversion were not significantly different between the lamivudine plus adefovir group and the entecavir group. Moreover, the rate of adverse reactions was also not significantly different between the 2 groups. However, virologic breakthrough for the patients with lamivudine resistance was higher in the entecavir group than in the lamivudine plus adefovir group. CONCLUSIONS: For these CHB patients with lamivudine resistance, lamivudine plus adefovir was a better treatment option than entecavir alone.

HMGB1 release by human liver L02 and HepG2 cells induced by lipopolysaccharide.

Liver cells release the high mobility group box-1 (HMGB1) protein when exposed to lipopolysaccharides (LPSs). However, the timing and levels of protein released remain unclear. The present study aimed to characterize the secretion of the late pro-inflammatory cytokine HMGB1 by liver L02 and HepG2 cells. The human mononuclear macrophage cell line U937 was used as a control. Various concentrations of LPS were added to human U937, L02 and HepG2 cells for different durations, and the cells were analyzed at different time-points following this addition. Reverse transcription polymerase chain reaction (RT-PCR) was used to measure cellular HMGB1 mRNA levels, western blotting was performed to detect HMGB1 in cellular supernatants and the translocation of HMGB1 from the nucleus to the cytosol was examined using immunofluorescence staining. L02 and HepG2 cells exhibited higher HMGB1 mRNA levels compared with the control U937 cells 20 and 24 h following continuous exposure to LPS. U937 cells exhibited higher HMGB1 mRNA levels compared with the corresponding L02 and HepG2 cells 16 h following LPS exposure. The phase of HMGB1 protein detected in the cellular supernatants of L02 and HepG2 cells (16 h) was later than that of U937 cells (8 h). For the three cell lines, HMGB1 levels demonstrated a time dependency; however, the protein level was the highest in U937 cells. In the three cell lines, translocation of HMGB1 from the nucleus to the cytosol occurred; however, the phases of HMGB1 translocation in L02 and HepG2 cells occurred later than in U937 cells. LPS-induced secretion of the late pro­inflammatory cytokine HMGB1 by liver cells is characterized by a late phase of release and smaller quantity, and the process of HMGB1 secretion appears to be associated with HMGB1 translocation.

Evaluation of predation abilities of Blattisocius dolichus (Acari: Blattisociidae) on a plant-parasitic nematode, Radopholus similis (Tylenchida: Pratylenchidae).

Predation and predatory behavior of Blattisocius dolichus on Radopholus similis were tested both in experimental arenas and on potted plants. Predation occurred in all active stages of B. dolichus. Blattisocius dolichus preferred live R. similis when offered together with Caneorhabditis elegans and dead R. similis in a choice test. Consumption rate was affected by temperature, prey density and duration of starvation. Maximum consumption rates were observed at 25 °C, for both adult males and females after being starved for 96 and 72 h, respectively. Consumption rate increased with increasing prey density until satiation was reached, when the predator-prey ratio was 1:250 for both male and female predators. Anthurium andraeanum seedlings, artificially infested with R. similis (1,000 per pot), were used to evaluate the biological control efficiency of B. dolichus. The nematode density decreased by 66 % 10 days after a release of 500 mites per pot.

Protective role of α2HS-glycoprotein in HBV-associated liver failure.

In this study, levels of plasma α2-Heremans-Schmid glycoprotein, serum tumor necrosis factor-α, serum liver function parameters and short-term mortality were measured in 100 hepatitis B patients. Release of interleukin-6 and tumor necrosis factor-α from the lipopolysaccharide-stimulated peripheral blood mononuclear cells in the presence/absence of spermine and α2-Heremans-Schmid glycoprotein were analyzed by enzyme-linked immunosorbent assay to determine the significance and potential mechanism of α2-Heremans-Schmid glycoprotein in hepatitis B virus-associated liver damage. Results showed that serum α2-Heremans-Schmid glycoprotein levels in acute-on-chronic liver failure patients were significantly lower than that in chronic hepatitis B patients or healthy controls (p < 0.05). A negative dependence between serum human α2-Heremans-Schmid glycoprotein and tumor necrosis factor-α levels was observed. Interleukin-6 and tumor necrosis factor-α levels in the lipopolysaccharide-induced peripheral blood mononuclear cell supernates were significantly reduced by spermine and/or α2-Heremans-Schmid glycoprotein. The latter two proteins jointly inhibited cytokine release. These observations suggest that plasma α2-Heremans-Schmid glycoprotein is an independent marker of liver damage and a prognostic indicator of hepatitis B virus chronicity. It may reduce liver inflammation by partially inhibiting release of inflammatory factors from activated peripheral blood mononuclear cells.

Protective effect of Acanthopanax gracilistylus-extracted Acankoreanogenin A on mice with fulminant hepatitis.

The release of pro-inflammatory cytokines in both acute (IL-1ß and TNF-α) and chronic [high mobility group box 1 protein (HMGB1)] phases, is thought to play important roles in the development of fulminant hepatitis (FH). Triterpenoid Acankoreanogenin A (AA) which is extracted from the leaves of the Acanthopanax gracilistylus W.W. Smith (AGS) has shown its inhibiting effect on TNF-α, IL-1ß and HMGB1 release in vitro in our preliminary experiments. In present study, we investigated the effect of AA on mice with fulminant hepatitis in vivo. Fulminant hepatitis mice model was established by intraperitoneally injecting galactosamine (GalN) and lipopolysaccharide (LPS). The levels of serum of TNF-α, IL-1ß, ALT, AST and HMGB1 from AA-treated mice were measured at different time points. Our results demonstrated that pre-treatment of mice with AA markedly reduced the serum levels of TNF-α, IL-1ß, HMGB1, ALT and AST with the improvement in histological features. And the survival rate from AA-treated fulminant hepatitis mice was increased. Furthermore, delayed administration of AA after peak occurrence of the early pro-inflammatory cytokines still endowed significant protection against GalN/LPS-induced lethality. The post-treatment of AA could significantly attenuate the release of HMGB1, but not the TNF-α and IL-1ß. These results indicate that AA inhibits the systemic release of pro-inflammatory cytokine HMGB1, and dose-dependently rescue the mice from lethal GalN/LPS-induced fulminant hepatitis, which suggests this component as a candidate therapy for fulminant hepatitis.

Hepatitis B virus is inhibited by RNA interference in cell culture and in mice.

BACKGROUND AND AIMS: For chronic hepatitis B virus (HBV) infection the effects of current therapies are limited. Recently, RNA interference (RNAi) of virus-specific genes has emerged as a potential antiviral mechanism. Here we studied the effects of HBV-specific 21-bp short hairpin RNAs (shRNAs) targeted to the surface antigen (HBsAg) region and the core antigen (HBcAg) region both in a cell culture system and in a mouse model for HBV replication. METHODS: HBsAg and hepatitis B e antigen (HBeAg) in the media of the cells and in the sera of the mice were analyzed by time-resolved immunofluorometric assay, intracellular HBcAg by immunofluorescence assay, HBsAg and HBcAg in the livers of the mice by immunohistochemical assay, HBV DNA by fluorogenic quantitative polymerase chain reaction (FQ-PCR) and HBV mRNA by semi-quantitative reverse transcriptase PCR (RT-PCR). RESULTS: Transfection with the shRNAs induced an RNAi response. Secreted HBsAg was reduced by >80% in cell culture and >90% in mouse serum, and HBeAg was also significantly inhibited. Immunofluorescence detection of intracellular HBcAg revealed 76% reduction. In the liver tissues by immunohistochemical detection, there were no HBsAg-positive cells and >70% reduction of HBcAg-positive cells for shRNA-1. And for shRNA-2 the detection of HBsAg and HBcAg also revealed substantial reduction. The shRNAs caused a significant inhibition in the levels of viral mRNA relative to the controls. HBV DNA was reduced by >40% for shRNA-1 and >60% for shRNA-2. CONCLUSIONS: RNAi is capable of inhibiting HBV replication and expression in vitro and in vivo and thus may constitute a new therapeutic strategy for HBV infection.

[Inhibition of hepatitis B virus replication and expression by RNA interference in vivo].

OBJECTIVE: To evaluate the inhibitory effect of small interfering RNA (siRNA) targeting HBV C gene region on hepatitis B virus (HBV) in vivo. METHODS: An animal model of HBV infection was developed hydrodynamically, and pcDNA3.1-HBV and siRNA were together injected into the tail vein of the BALB/c mice. HBsAg was analyzed by time-resolved immunofluorometric assay, HBV DNA was analyzed by fluorogenic quantitative PCR (FQ-PCR), HBV C-mRNA was detected by semi-quantitative RT-PCR, and viral specific proteins (HBsAg and HBcAg) in the mice livers were assayed using immunohistochemical staining. RESULTS: In the mice, the siRNA effectively inhibited HBV replication and expression compared with the controls. The inhibitive effect of siRNA on HBV lasted at least 3 days. CONCLUSION: These results demonstrate that RNAi can substantially inhibit HBV replication and expression in vivo.