Change in Phylogenetic Community Structure during Succession of Traditionally Managed Tropical Rainforest in Southwest China

Tropical rainforests in Southeast Asia are facing increasing and ever more intense human disturbance that often negatively affects biodiversity. The aim of this study was to determine how tree species phylogenetic diversity is affected by traditional forest management types and to understand the change in community phylogenetic structure during succession. Four types of forests with different management histories were selected for this purpose: old growth forests, understorey planted old growth forests, old secondary forests (∼200-years after slash and burn), and young secondary forests (15–50-years after slash and burn). We found that tree phylogenetic community structure changed from clustering to over-dispersion from early to late successional forests and finally became random in old-growth forest. We also found that the phylogenetic structure of the tree overstorey and understorey responded differentially to change in environmental conditions during succession. In addition, we show that slash and burn agriculture (swidden cultivation) can increase landscape level plant community evolutionary information content

(E)-Methyl 2-chloro-4-dicyclo­hexyl­amino-4-oxobut-2-enoate

In the title compound, C17H26ClNO3, both cyclo­hexyl rings have chair conformations. In the crystal, mol­ecules are linked by weak inter­molecular C—H⋯O hydrogen bonds

Quantum electrodynamics in a whispering-gallery microcavity coated with a polymer nanolayer

Quasi-transverse-electric and -transverse-magnetic fundamental whispering gallery modes in a polymer-coated silica microtoroid are theoretically investigated and demonstrated to possess very high-quality factors. The existence of a nanometer-thickness layer not only evidently reduces the cavity mode volume but also draws the maximal electric field's position of the mode to the outside of the silica toroid, where single quantum dots or nanocrystals are located. Both effects result in a strongly enhanced coherent interaction between a single dipole (for example, a single defect center in a diamond crystal) and the quantized cavity mode. Since the coated microtoroid is highly feasible and robust in experiments, it may offer an excellent platform to study strong-coupling cavity quantum electrodynamics, quantum information, and quantum computation

1,2-Bis(4-nitro­benzo­yl)hydrazine

The title mol­ecule, C14H10N4O6, crystallizes with one half-mol­ecule in the asymmetric unit; the mid-point of the N—N bond lies on an inversion centre. The nitro and amide groups are twisted with respect to the benzene ring, making dihedral angles of 14.6 (5) and 31.1 (5)°, respectively. In the crystal structure, mol­ecules are linked through N—H⋯O hydrogen bonding between the imino and carbonyl groups

Effect of rosiglitazone on rabbit model of myocardial ischemia-reperfusion injury

AbstractObjectiveTo explore mechanism and protective effect of rosiglitazone on myocardial ischemia reperfusion (I/R) injury.MethodsA total of 48 male Japanese white big-ear rabbits were randomly divided into control group (A), I/R group (B), low dose of rosiglitazone group (C), high dose of rosiglitazone group (D). Plasma concentration of and also reduced the concentration of plasma serum creatine kinase (CK), CK-MB, high-sensitivity C-reactive protein (hsCRP), ultra-superoxide dismutase (SOD), malondialdehyde (MDA), lactic acid glutathione skin peroxidase (GSH-PX), nitric oxide (NO) and endothelin (ET) were measured 1 h later after I/R. Twenty-four hours after I/R the hearts were harvested for pathological and ultrastructural analysis. Area of myocardial infarction were tested.ResultsPlasma concentration of CK, CK-MB, hsCRP, NO, MDA and ET were decreased in C, D group compared with group B. Plasma concentration of T-SOD and GSH-Px were increased significantly in C, D group compared with group B. Compared with group B, pathological and ultrastructural changes in C and D group were slightly. There was significant difference in myocardial infarction area between group C, D and group B (P<0.05). Myocardial infarction area and arrhythmia rate were lower in group C, D compare with group B.ConclusionsRosiglitazone may protect myocardium from I/R injury by enhancing T-SOD and GSH-Px concentration, inhibit inflammatory reaction, and improve endothelial function

Bis{2-[3-(dimethyl­ammonio)­propyl­imino­methyl-κN]-6-meth­oxy­phenolato-κO 1}bis­(thio­cyanato-κN)nickel(II)

The asymmetric unit of the title complex, [Ni(NCS)2(C13H20N2O2)2], consists of two half-mol­ecules, both of which are completed by crystallographic inversion symmetry (Ni2+ site symmetry = in both cases). Both metal ions are six-coordinated in distorted trans-NiO2N4 geometries arising from two N,O-bidentate Schiff base ligands and two N-bonded thio­cyanate ions. The mol­ecular conformations are reinforced by two intra­molecular N—H⋯O hydrogen bonds

{N,N-Dimethyl-N′-[1-(2-pyrid­yl)ethyl­idene]propane-1,3-diamine}bis(thio­cyanato-κN)­copper(II)

In the title complex, [Cu(NCS)2(C12H19N3)], the CuII atom is five-coordinated in a square-pyramidal geometry defined by one pyridine N, one imine N, and one amine N atom of the tridentate Schiff base ligand and two N-bonded thio­cyanate ions (one of the latter occupying the apical site). The three bridging C atoms and the two terminal C atoms of the Schiff base are disordered over two sets of sites, with occupancies of 0.465 (2) and 0.535 (2)

{3-Methyl-2-[(1-oxido-2-naphth­yl)methyl­idene­amino-κ2 O,N]butano­ato-κO}(1H-pyrazole-κN 2)nickel(II)

In either of the two independent mol­ecules within the asymmetric unit of the title compound, [Ni(C16H15NO3)(C3H4N2)], the NiII atom is coordinated by the two N atoms and two O atoms in a distorted square-planar geometry. The crystal packing is stabilized by strong and weak inter­molecular C—H⋯O hydrogen bonds, as well as weak centroid–centroid π-stacking inter­actions [centroid–centroid separation = 3.526 (3) Å]

Anti-HER-2 engineering antibody ChA21 inhibits growth and induces apoptosis of SK-OV-3 cells

<p>Abstract</p> <p>Background and Aims</p> <p>Anti-HER-2 antibodies targeting distinct epitopes have different biological functions on cancer cells. In a previous study, we demonstrated that anti-HER-2 engineering antibody ChA21 was able to bind to subdomain I of HER-2 extracellular domain. In this study, The effects of ChA21 on growth and apoptosis against ovarian carcinoma cell SK-OV-3 over-expressing HER-2 <it>in vitro </it>and <it>in vivo </it>were investigated.</p> <p>Methods</p> <p>Cell growth inhibition was evaluated by MTT assay. Apoptosis was detected by TUNEL stain, transmission electron microscopy and flow cytometry on cultured cells and tissue sections from nude mice xenografts. The apoptosis-related proteins Bax and Bcl-2 were assessed by immunohistochemistry.</p> <p>Results</p> <p>We found that treatment of ChA21 caused a dose-dependent decrease of cell proliferation <it>in vitro </it>and a significant inhibition of tumor growth <it>in vivo</it>. ChA21 therapy led to a significant increase in the induction of apoptosis, and up-regulated the expression of Bax, while the expression of Bcl-2 was down-regulated.</p> <p>Conclusion</p> <p>These data suggest that ChA21 inhibits the growth and induces apoptosis of SK-OV-3 via regulating the balance between Bax and Bcl-2.</p

Deficiency of Mkrn2 causes abnormal spermiogenesis and spermiation, and impairs male fertility.

Although recent studies have shed insights on some of the potential causes of male infertility, new underlining molecular mechanisms still remain to be elucidated. Makorin-2 (Mkrn2) is an evolutionarily conserved gene whose biological functions are not fully known. We developed an Mrkn2 knockout mouse model to study the role of this gene, and found that deletion of Mkrn2 in mice led to male infertility. Mkrn2 knockout mice produced abnormal sperms characterized by low number, poor motility, and aberrant morphology. Disruption of Mkrn2 also caused failure of sperm release (spermiation failure) and misarrangement of ectoplasmic specialization (ES) in testes, thus impairing spermiogenesis and spermiation. To understand the molecular mechanism, we found that expression of Odf2, a vital protein in spermatogenesis, was significantly decreased. In addition, we found that expression levels of Odf2 were decreased in Mkrn2 knockout mice. We also found that MKRN2 was prominently expressed in the sperm of normal men, but was significantly reduced in infertile men. This result indicates that our finding is clinically relevant. The results of our study provided insights into a new mechanism of male infertility caused by the MKRN2 downregulation