Molecular weight dependence of the poly(L-lactide)/poly(D-lactide) Stereocomplex at the air-water interface

The molecular weight dependence of poly(L-lactide)/poly(D-lactide) (PLLA/PDLA) stereocomplex behavior at the air-water interface was studied by surface pressure-area (pi-A) isotherms and atomic force microscopy (AFM). It was found that the compression-induced sterecomplexation of a PDLA/PLLA equimolar blend with high molecular weight (M(w) = 1 x 10(6) and 9.8 x 10(5), respectively) could occur at the air-water interface. This result is in marked contrast with the stereocomplexation of PDLA/PLLA blends in the bulk from the melt or in solutions, where the homocrystallites of either PLLA or PDLA rather than stereocomplex crystallites will be formed preferentially when the molecular weights of both polymers are higher than 1 x 10(5). Unexpectedly, the Langmuir-Blodgett behavior of the PDLA/PLLA blend with lower molecular weight (M(w) = 4 x 10(3) and 3.2 x 10(3), respectively), which should be favored in the stereocomplex, was distinct from that of other higher molecular weight blends. AFM images clearly disclosed for the first time the morphological changes of the equimolar blends of PLLA and PDLA at the air-water interface induced by increasing the surface pressure of the monolayer. Of particular note, the bilayer mechanism for the plateau in the isotherm was directly verified by the AFM height images.     

Proteasome Inhibitor PS-341 Effectively Blocks Infection by the Severe Fever with Thrombocytopenia Syndrome Virus

Severe fever with thrombocytopenia syndrome(SFTS) is an emerging hemorrhagic fever disease caused by SFTSV, a newly discovered phlebovirus that is named after the disease. Currently, no effective vaccines or drugs are available for use against SFTSV infection, as our understanding of the viral pathogenesis is limited. Bortezomib(PS-341), a dipeptideboronic acid analog, is the first clinically approved proteasome inhibitor for use in humans. In this study, the antiviral efficacy of PS-341 against SFTSV infection was tested in human embryonic kidney HEK293 T(293 T) cells. We employed four different assays to analyze the antiviral ability of PS-341 and determined that PS-341 inhibited the proliferation of SFTSV in 293 T cells under various treatment conditions. Although PS-341 did not affect the virus absorption, PS-341 treatment within a non-toxic concentration range resulted in a significant reduction of progeny viral titers in infected cells.Dual-luciferase reporter assays and Western blot analysis revealed that PS-341 could reverse the SFTSV-encoded nonstructural protein(NS) mediated degradation of retinoic acid-inducible gene-1(RIG-I), thereby antagonizing the inhibitory effect of NSs on interferons and blocking virus replication. In addition, we observed that inhibition of apoptosis promotes virus replication. These results indicate that targeting of cellular interferon pathways and apoptosis during acute infection might serve as the bases of future therapeutics for the treatment of SFTSV infections.     

Impaired long-term potentiation and long-term memory deficits in xCT-deficient sut mice

xCT is the functional subunit of the cystine/glutamate antiporter system xc-, which exchanges intracellular glutamate with extracellular cystine. xCT has been reported to play roles in the maintenance of intracellular redox and ambient extracellular glutamate, which may affect neuronal function. To assess a potential role of xCT in the mouse hippocampus, we performed fear conditioning and passive avoidance for long-term memories and examined hippocampal synaptic plasticity in wild-type mice and xCT-null mutants, sut mice. Long-term memory was impaired in sut mice. Normal basal synaptic transmission and short-term presynaptic plasticity at hippocampal Schaffer collateral-CA1 synapses were observed in sut mice. However, LTP (long-term potentiation) was significantly reduced in sut mice compared with their wild-type counterparts. Supplementation of extracellular glutamate did not reverse the reduction in LTP. Taken together, our results suggest that xCT plays a role in the modulation of hippocampal long-term plasticity.     

Review of the South American leafhopper genus Parandanus (Hemiptera,Cicadellidae, Deltocephalinae)

The South American leafhopper genus Parandanus Linnavuori & DeLong (Deltocephalinae: Deltocephalini) is reviewed and four of its six species are illustrated and male genital characters are provided. Three new species from Peru, Parandanus longistylus Duan, sp. n., Parandanus nigricephalus Duan, sp. n. and Parandanus paracruciatus Duan, sp. n. are described. A key to species is also provided.     

Potent inhibition of human immunodeficiency virus type 1 in primary T cells and alveolar macrophages by a combination anti-Rev strategy delivered in an adeno-associated virus vector.

The rate of viral replication appears to play a pivotal role in human immunodeficiency virus type 1 (HIV-1) pathogenesis and disease progression as it outstrips the capacity of the immune system to respond. Important cellular sites for HIV-1 production include T lymphocytes and tissue macrophages. Antiviral strategies, including newer treatment modalities such as gene therapy of HIV-1-susceptible cell populations, must be capable of engendering durable inhibitory effects to HIV-1 replication in both of these primary cell types in order to be effective. Among the potential genetic targets for intervention in the HIV-1 life cycle, the Rev regulatory system, consisting of Rev and its binding site, the Rev-responsive element (RRE), stands out as particularly attractive. Rev is essential for maintaining the stability of the viral genomic RNA as well as viral mRNAs encoding key structural and regulatory proteins. Moreover, it exhibits favorable threshold kinetics, in that Rev concentrations must rise above a critical level to exert their effect. To disable Rev function, primary T cells or macrophages were transduced with anti-Rev single-chain immunoglobulin (SFv) or RRE decoy genes either singly or in combination by employing adeno-associated virus vectors and then challenged with HIV-1. By directing both a protein and a nucleic acid against the normal interaction between Rev and the RRE, this genetic antiviral strategy effectively inhibited infection by either clinical or laboratory virus isolates. These results provide a framework for novel interventions to reduce virus production in the infected host.     

GDF11 prevents the formation of thoracic aortic dissection in mice: Promotion of contractile transition of aortic SMCs

Thoracic aortic dissection (TAD) is an aortic disease associated with dysregulated extracellular matrix composition and de-differentiation of vascular smooth muscle cells (SMCs). Growth Differentiation Factor 11 (GDF11) is a member of transforming growth factor β (TGF-β) superfamily associated with cardiovascular diseases. The present study attempted to investigate the expression of GDF11 in TAD and its effects on aortic SMC phenotype transition. GDF11 level was found lower in the ascending thoracic aortas of TAD patients than healthy aortas. The mouse model of TAD was established by β-aminopropionitrile monofumarate (BAPN) combined with angiotensin II (Ang II). The expression of GDF11 was also decreased in thoracic aortic tissues accompanied with increased inflammation, arteriectasis and elastin degradation in TAD mice. Administration of GDF11 mitigated these aortic lesions and improved the survival rate of mice. Exogenous GDF11 and adeno-associated virus type 2 (AAV-2)-mediated GDF11 overexpression increased the expression of contractile proteins including ACTA2, SM22α and myosin heavy chain 11 (MYH11) and decreased synthetic markers including osteopontin and fibronectin 1 (FN1), indicating that GDF11 might inhibit SMC phenotype transition and maintain its contractile state. Moreover, GDF11 inhibited the production of matrix metalloproteinase (MMP)-2, 3, 9 in aortic SMCs. The canonical TGF-β (Smad2/3) signalling was enhanced by GDF11, while its inhibition suppressed the inhibitory effects of GDF11 on SMC de-differentiation and MMP production in vitro. Therefore, we demonstrate that GDF11 may contribute to TAD alleviation via inhibiting inflammation and MMP activity, and promoting the transition of aortic SMCs towards a contractile phenotype, which provides a therapeutic target for TAD.     

Discovering Candidate Chromosomal Regions Linked to Kernel Size-Related Traits via QTL Mapping and Bulked Sample Analysis in Maize

Kernel size-related traits, including kernel length, kernel width, and kernel thickness, are critical components in determining yield and kernel quality in maize (Zea mays L.). Dissecting the phenotypic characteristics of these traits, and discovering the candidate chromosomal regions for these traits, are of potential importance for maize yield and quality improvement. In this study, a total of 139 F2:3 family lines derived from EHel and B73, a distinct line with extremely low ear height (EHel), was used for phenotyping and QTL mapping of three kernel size-related traits, including 10-kernel length (KL), 10-kernel width (KWid), and 10-kernel thickness (KT). The results showed that only one QTL for KWid, i.e., qKWid9 on Chr9, with a phenotypic variation explained (PVE) of 13.4% was detected between SNPs of AX-86298371 and AX-86298372, while no QTLs were detected for KL and KT across all 10 chromosomes. Four bulked groups of family lines, i.e., Groups I to IV, were constructed with F2:3 family lines according to the phenotypic comparisons of KWid between EHel and B73. Among these four groups, Group I possessed a significantly lower KWid than EHel (P = 0.0455), Group II was similar to EHel (P = 0.34), while both Group III and Group IV were statistically higher than EHel (P < 0.05). Besides, except Group IV exhibited a similar KWid to B73 (P = 0.11), KWid of Groups I to III were statistically lower than B73 (P < 0.00). By comparing the bulked genotypes of the four groups to EHel and B73, a stable chromosomal region on Chr9 between SNPs of AX-86298372 to AX-86263154, entirely covered by qKWid9, was identified to link KWid with the positive allele of increasing phenotypic effect to KWid from B73, similar to that of qKWid9. A large amount of enzyme activity and macromolecule binding-related genes were annotated within this chromosomal region, suggesting qKWid9 as a potential QTL for KWid in maize.     

Roseomonas alkaliterrae sp. nov., isolated from an alkali geothermal soil sample in Tengchong,Yunnan, south-west China

An alkalitolerant, thermotolerant and Gram-stain negative bacterium, designated strain YIM 78007^T, was isolated from an alkaline geothermal soil sample from Hehua hot spring, Tengchong, Yunnan province, south-west China. Cells of strain YIM 78007^T were observed to be aerobic and short rod-shaped. The colonies were observed to be orange-red, convex and circular. 16S rRNA gene sequence-based phylogenetic analysis showed that strain YIM 78007^T clustered with members of the genus Roseomonas (with similarities from 97.2 to 92.2 %). Optimal growth of strain YIM 78007 occurs at 40–50 °C and pH 8.0–10.0. The predominant ubiquinone was identified as Q-10 and the major fatty acids were identified as C_18:1 ω7c and C_16:0. The polar lipids were identified as diphosphatidylglycerol, phosphatidylethanolamine, phosphatidylcholine, two unidentified aminolipids and one unknown phospholipid. The G + C content of the genomic DNA was determined to be 63 mol %. The levels of DNA–DNA hybridization relatedness between strain YIM 78007^T and its closet neighbours (Roseomonas lacus JCM 13283^T and Roseomonas terrae JCM 14592^T) were well below the threshold required for the proposal of a novel species. The results of physiological and biochemical characteristics, the phylogenetic analysis, as well as low DNA–DNA hybridization values, allowed the phenotypic and genotypic differentiation of strain YIM 78007^T from its closest phylogenetic neighbours. Therefore, strain YIM 78007^T is considered to represent a novel species of the genus Roseomonas, for which the name Roseomonas alkaliterrae sp. nov. is proposed. The type strain is YIM 78007^T (=BCRC 80644^T = JCM 19656^T).