环纹矮柳(杨柳科)的后选模式指定及形态描述订正

环纹矮柳(Salix annulifera C. MarquandAiry Shaw)的模式标本材料F. K. Ward 5870包括2个完全不同的种。根据深圳法规的相应条款,在此指定F. K. Ward 5870 (K-000335077)为S. annulifera的后选模式;将F. K. Ward 5870 (K-000335083)从S. annulifera中排除,并鉴定为藏南柳(S. austrotibetica N. Chao)。此外,对环纹矮柳的形态描述进行了相应的订正。     

Detection of endo-xylanase activities in electrophoretic gels with congo red staining

Summary A modification of the Congo Red zymographic technique is used to analyse multiple xylanase activities of Bacillus sp. MIR-32 after PAGE and SDS-PAGE. Xylanase activities are associated with at least two major proteins of 18.4 and 19.6 kDa.     

Toll like receptor 2 knock-out attenuates carbon tetrachloride (CCl4)-induced liver fibrosis by downregulating MAPK and NF-κB signaling pathways

Innate immune signaling associated with Toll-like receptors (TLRs) is a key pathway involved in the progression of liver fibrosis. In this study, we reported that TLR2 is required for hepatic fibrogenesis induced by carbon tetrachloride (CCl₄). After CCl₄ treatment, TLR2^−/− mice had reduced liver enzyme levels, diminished collagen deposition, decreased inflammatory infiltration and impaired activation of hepatic stellate cells (HSCs) than wild type (WT) mice. Furthermore, after CCl₄ treatment, TLR2^−/− mice demonstrated downregulated expression of profibrotic and proinflammatory genes and impaired mitogen-activated protein kinases (MAPK) and nuclear factor kappa B (NF-κB) activation than WT mice. Collectively, our data indicate that TLR2 deficiency protects against CCl₄-induced liver fibrosis.     

Algicidal effects of yellow clay and the thiazolidinedione derivative TD49 on the fish-killing dinoflagellate Cochlodinium polykrikoides in microcosm experiments

In order to evaluate the potential to control the fish-killing dinoflagellate Cochlodinium polykrikoides, we compared the algicidal effects of the thiazolidinedione derivative TD49 with those of yellow clay in 10-L microcosms. The responses of higher trophic level marine organisms and microbial loop communities to the algicide were also evaluated. In the yellow clay treatments, the concentration of C. polykrikoides was slightly reduced at day 1 of the experiment but remained higher than that of the control, suggesting that the reduction ratio of C. polykrikoides was <20 %. In the 0.8-μM TD49 treatment, the abundance of C. polykrikoides declined by 98 % 1 day following the addition of the algicide. The algicide did not affect nontarget algae including Chaetoceros spp., Skeletonema spp., Cylindrotheca spp., and other species. In all microcosms, bacterial abundance increased abruptly after day 1, then declined over the next 2 days as a result of predation by heterotrophic nanoflagellates and the small protozoan Uronema sp. Predation by the large protozoan species Euplotes sp. on Uronema sp. gradually increased with increasing incubation time in the TD49 treatment. Zooplankton were particularly affected by the environmental changes that occurred in the microcosms following collapse of the C. polykrikoides populations. Striped beak perch were not affected by the yellow clay treatments and concentrations of TD49?C. polykrikoides, whereas the algicide TD49 is effective in controlling the harmful alga. The results imply that the algicide has positive effects on natural microbial communities and is not toxic to nonharmful algae and higher trophic level marine organisms.     

Hormone‐induced mitochondrial fission is utilized by brown adipocytes as an amplification pathway for energy expenditure

Adrenergic stimulation of brown adipocytes (BA) induces mitochondrial uncoupling, thereby increasing energy expenditure by shifting nutrient oxidation towards thermogenesis. Here we describe that mitochondrial dynamics is a physiological regulator of adrenergically‐induced changes in energy expenditure. The sympathetic neurotransmitter Norepinephrine (NE) induced complete and rapid mitochondrial fragmentation in BA, characterized by Drp1 phosphorylation and Opa1 cleavage. Mechanistically, NE‐mediated Drp1 phosphorylation was dependent on Protein Kinase‐A (PKA) activity, whereas Opa1 cleavage required mitochondrial depolarization mediated by FFAs released as a result of lipolysis. This change in mitochondrial architecture was observed both in primary cultures and brown adipose tissue from cold‐exposed mice. Mitochondrial uncoupling induced by NE in brown adipocytes was reduced by inhibition of mitochondrial fission through transient Drp1 DN overexpression. Furthermore, forced mitochondrial fragmentation in BA through Mfn2 knock down increased the capacity of exogenous FFAs to increase energy expenditure. These results suggest that, in addition to its ability to stimulate lipolysis, NE induces energy expenditure in BA by promoting mitochondrial fragmentation. Together these data reveal that adrenergically‐induced changes to mitochondrial dynamics are required for BA thermogenic activation and for the control of energy expenditure.     

Light limitation and litter of an invasive clonal plant,Wedelia trilobata,inhibit its seedling recruitment

Background and Aims

Invasive clonal plants have two reproduction patterns, namely sexual and vegetative propagation. However, seedling recruitment of invasive clonal plants can decline as the invasion process proceeds. For example, although the invasive clonal Wedelia trilobata (Asteraceae) produces numerous seeds, few seedlings emerge under its dense population canopy in the field. In this study it is hypothesized that light limitation and the presence of a thick layer of its own litter may be the primary factors causing the failure of seedling recruitment for this invasive weed in the field.

Methods

A field survey was conducted to determine the allocation of resources to sexual reproduction and seedling recruitment in W. trilobata. Seed germination was also determined in the field. Effects of light and W. trilobata leaf extracts on seed germination and seedling growth were tested in the laboratory.

Key Results

Wedelia trilobata blooms profusely and produces copious viable seeds in the field. However, seedlings of W. trilobata were not detected under mother ramets and few emerged seedlings were found in the bare ground near to populations. In laboratory experiments, low light significantly inhibited seed germination. Leaf extracts also decreased seed germination and inhibited seedling growth, and significant interactions were found between low light and leaf extracts on seed germination. However, seeds were found to germinate in an invaded field after removal of the W. trilobata plant canopy.

Conclusions

The results indicate that lack of light and the presence of its own litter might be two major factors responsible for the low numbers of W. trilobata seedlings found in the field. New populations will establish from seeds once the limiting factors are eliminated, and seeds can be the agents of long-distance dispersal; therefore, prevention of seed production remains an important component in controlling the spread of this invasive clonal plant.     

Phase II clinical trial of ex vivo-expanded cytokine-induced killer cells therapy in advanced pancreatic cancer

Second-line chemotherapy in patients with gemcitabine-refractory advanced pancreatic cancer has shown disappointing survival outcomes due to rapid disease progression and performance deterioration. The aim of this phase II trial was to evaluate the efficacy and safety of adoptive immunotherapy using ex vivo-expanded, cytokine-induced killer (CIK) cells in gemcitabine-refractory advanced pancreatic cancer. Patients with advanced pancreatic cancer who showed disease progression during gemcitabine-based chemotherapy were enrolled in this study. For generation of CIK cells, peripheral blood samples were collected from each patient and cultured with anti-CD3 monoclonal antibody and IL-2. Patients received CIK cells intravenously 10 times, every week for 5 weeks and then every other week for 10 weeks. Twenty patients were enrolled between November 2009 and September 2010. The disease control rate was 25 % (4/16 patients). The median progression-free survival (PFS) was 11.0 weeks (95 % CI 8.8–13.2), and the median overall survival (OS) was 26.6 weeks (95 % CI 8.6–44.6). Grade 3 toxicities included general weakness in two patients and thrombocytopenia in one patient. Grade 4 hematologic or non-hematologic toxicity was not observed. Patients showed improvement in pancreatic pain, gastrointestinal distress, jaundice, body image alterations, altered bowel habits, health satisfaction, and sexuality when assessing quality of life (QoL). Adoptive immunotherapy using CIK cells showed comparable PFS and OS to survival data of previous trials that assessed conventional chemotherapies while maintaining tolerability and showing encouraging results in terms of patient QoL in gemcitabine-refractory advanced pancreatic cancer (clinicalTrials.gov number NCT00965718).     

Simultaneous silencing of VEGF and KSP by siRNA cocktail inhibits proliferation and induces apoptosis of hepatocellular carcinoma Hep3B cells

Background

Vascular endothelial growth factor (VEGF) is involved in the growth of new blood vessels that feed tumors and kinesin spindle protein (KSP) plays a critical role in mitosis involving in cell proliferation. Simultaneous silencing of VEGF and KSP, an attractive and viable approach in cancer, leads on restricting cancer progression. The purpose of this study is to examine the therapeutic potential of dual gene targeted siRNA cocktail on human hepatocellular carcinoma Hep3B cells.

Results

The predesigned siRNAs could inhibit VEGF and KSP at mRNA level. siRNA cocktail showed a further downregulation on KSP mRNA and protein levels compared to KSP-siRNA or VEGF-siRNA, but not on VEGF expression. It also exhibited greater suppression on cell proliferation as well as cell migration or invasion capabilities and induction of apoptosis in Hep3B cells than single siRNA simultaneously. This could be explained by the significant downregulation of Cyclin D1, Bcl-2 and Survivin. However, no sigificant difference in the mRNA and protein levels of ANG2, involving inhibition of angiogenesis was found in HUVECs cultured with supernatant of Hep3B cells treated with siRNA cocktail, compared to that of VEGF-siRNA.

Conclusion

Silencing of VEGF and KSP plays a key role in inhibiting cell proliferation, migration, invasion and inducing apoptosis of Hep3B cells. Simultaneous silencing of VEGF and KSP using siRNA cocktail yields promising results for eradicating hepatocellular carcinoma cells, a new direction for liver cancer treatment.