Killing two enemies with one stone? Genomics of resistance to two sympatric pathogens in Norway spruce.

Trees must cope with the attack of multiple pathogens, often simultaneously during their long lifespan. Ironically, the genetic and molecular mechanisms controlling this process are poorly understood. The objective of this study was to compare the genetic component of resistance in Norway spruce to Heterobasidion annosum s.

Association genetics identifies a specifically regulated Norway spruce laccase gene, PaLAC5, linked to Heterobasidion parviporum resistance.

It is important to improve the understanding of the interactions between the trees and pathogens and integrate this knowledge about disease resistance into tree breeding programs. The conifer Norway spruce (Picea abies) is an important species for the forest industry in Europe. Its major pathogen is Heterobasidion parviporum, causing stem and root rot.

300 mm Wafer-level, ultra-dense arrays of Au-capped nanopillars with sub-10 nm gaps as reliable SERS substrates.

The 193 nm deep UV immersion lithography is leveraged to fabricate highly dense and uniform arrays of Au-capped Si nanopillars on a 300 mm wafer level, and the substrates are applied in surface enhanced Raman spectroscopy for reliable molecule detection. Due to the sub-10 nm gap sizes and ultra-high array density with the lattice constant less than 100 nm, our nanopillar based substrates outperform the current commercial products in terms of the signal intensity, reproducibility and fabrication scale.

Effect of vascular endothelial growth factor and its receptor KDR on the transendothelial migration and local trafficking of human T cells in vitro and in vivo.

In these studies, we find that the vascular endothelial growth factor (VEGF) receptor KDR is expressed on subsets of mitogen-activated CD4(+) and CD8(+) T cells in vitro. We also found that KDR colocalizes with CD3 on mitogen-activated T cells in vitro and on infiltrates within rejecting human allografts in vivo. To evaluate whether VEGF and KDR mediate lymphocyte migration across endothelial cells (ECs), we used an in vitro live-time transmigration model and observed that both anti-VEGF and anti-KDR antibodies inhibit the transmigration of both CD4(+) and CD8(+) T cells across tumor necrosis factor α (TNFα)-activated, but not unactivated ECs.

Thyroid hormone-induced cardiac mechano growth factor expression depends on beating activity.

The mechano growth factor (MGF), a splice variant of the IGF-I gene, was first discovered in mechanically overloaded skeletal muscle and was shown to play an important role in proliferation of muscle stem cells. Since then, the presence and effects of MGF have been demonstrated in other tissues. MGF has been shown to act neuroprotectively during brain ischemia, and pretreatment with MGF before myocardial infarction improves cardiac function.

The role of nitric oxide in renal transplantation.

This review discusses the concept that nitric oxide synthase (NOS) may orchestrate both the inflammatory response to the renal allograft and anti-inflammatory defense in the graft itself. NO is produced by endothelial, epithelial, as well as inflammatory cells. In the setting of transplantation, the endothelium is the first lining to be subjected to the early response to injury.

Anti-inflammatory effects of tetrahydrobiopterin on early rejection in renal allografts: modulation of inducible nitric oxide synthase.

Oxidative stress contributes to the development of early transplant failure. As nitric oxide synthases (NOS) can act as sources of superoxide, we investigated the effect of the NOS cofactor tetrahydrobiopterin (BH4) on oxyradical production and early rejection in a rat kidney transplantation model. Allograft transplantation (Brown Norway to Lewis) showed more renal superoxide production and monocyte infiltration when compared with isografts (Lewis to Lewis).

Inducible nitric oxide synthase in renal transplantation.

The importance of the endothelial isoform of nitric oxide synthase (eNOS) has been well established. Endothelium-derived nitric oxide has been shown to be essential for vascular homeostasis and modulation of eNOS has thus become a target in prevention of cardiovascular disease. The role of the inducible form of nitric oxide synthase (iNOS) in vascular biology, however, is less clear.

L-arginine supplementation improves function and reduces inflammation in renal allografts.

Recovery from ischemia/reperfusion and immune-mediated injury in the renal transplant is associated with reduced renal hemodynamics and increased leukocyte infiltration. In diverse models of renal failure, L-arginine supplementation improved hemodynamics and reduced inflammation. However in a proinflammatory environment, L-arginine can worsen renal injury.

Dysfunctional renal nitric oxide synthase as a determinant of salt-sensitive hypertension: mechanisms of renal artery endothelial dysfunction and role of endothelin for vascular hypertrophy and Glomerulosclerosis.

This study investigated the role of renal nitric oxide synthase (NOS), endothelin, and possible mechanisms of renovascular dysfunction in salt-sensitive hypertension. Salt-sensitive (DS) and salt-resistant (DR) Dahl rats were treated for 8 wk with high salt diet (4% NaCl) alone or in combination with the ET(A) receptor antagonist LU135252 (60 mg/kg per d). Salt loading markedly increased NOS activity (pmol citrulline/mg protein per min) in renal cortex and medulla in DR but not in DS rats by 270 and 246%, respectively.