SOCS

Soil organic carbon stock (SOCS) assessments at a national level are essential in the climate change mitigation role. Our study provides the first assessment of the SOC stored in entire Spanish surface soils obtained from one sampling protocol within a regular sampling framework in a short edaphic time. In this study, we analysed topsoil samples (0–30 cm) from 4401 locations. SOC, soil bulk density and stoniness were measured to estimate SOCS. The results showed that half the Spanish areas obtained a SOC value below 1%. There is inherently wide spatial variability in SOC contents in Spainwith lowSOC concentration levels located in southern areas. The lowest SOC levelswere associatedwith agricultural soils. However, no statistically significant differences were found between forestlands and grasslands. The mean SOCS in the Spanish topsoil layer was 56.57 Mg C ha−1 and the total stored in topsoil was 2.8 Pg C. We were surprised to find that our estimates were 40% lower than those known to date for Spain. The results herein highlight the potential land use change for SOC sequestration in Spanish soils. Certain changes in agricultural practises (conservation tillage) or converting some unproductive croplands into grasslands or forestlands can increase carbon sequestration in soils

15-deoxy-Δ12,14-prostagandin J2 (15d-PGJ2) is produced in the inflamed cells and tissues as a consequence of upregulation of cyclooxygenase-2 (COX-2). 15d-PGJ2 is known to be the endogenous ligand of peroxisome proliferator-activated receptor gamma (PPARγ) with multiple physiological properties. Though one of the terminal products of the COX-2-catalyzed reactions, this cyclopentenone prostaglandin exerts potent anti-inflammatory actions, in part, by antagonizing the activities

The development of hepatic fibrosis is the principal cause of morbidity and mortality in human beings infected with schistosoma. In this study, we investigated the effect of polyinosinic–polycytidylic acid (poly I:C) on Schistosoma japonicum (S. japonicum) egg-induced liver fibrosis. S. japonicum cercariae infected mice were injected with poly I:C at the onset of egg granuloma formation (early phase poly I:C treatment) or after the formation of liver fibrosis (late phase poly I:C treatment). Our results showed that both early and late phase poly I:C treatment significantly reduced collagen deposition and hepatic stellate cell activation in the liver. Poly I:C is one of the most effective adjuvants for Th1 type responses, and its protective effect on liver fibrosis was accompanied by increased IFN-α, IFN-β, IFN-γ, IL-12, TNF-α, and IL-10 mRNA expression, and decreased IL-4 and IL-5 mRNA expression. Moreover, poly I:C injection also enhanced the mRNA expression of natural killer group 2 member D (NKG2D) and tumor necrosis factor related apoptosis-inducing ligand (TRAIL). Therefore, it is indicated that poly I:C can significantly attenuate S. japonicum egg-induced hepatic fibrosis, which may be partly dependent on the increased Th1 response and decreased Th2 response.Poly I:C treatment significantly attenuated Schistosoma japonicum egg-induced hepatic fibrosis via increasing Th1 cytokine mRNA expression and decreasing Th2 cytokine mRNA expression.► We used C57BL/6 mice infected with Schistosoma japonicum to examine the role of poly I:C in liver fibrosis. ► Poly I:C treatment significantly attenuated hepatic fibrosis caused by the eggs. ► Poly I:C treatment increased mRNA expression of Th1 cytokines, IL-10, NKG2D, and TRAIL in the liver of infected mice. ► Poly I:C treatment decreased intrahepatic Th2 cytokine mRNA expression.

Receptor-activated Ca 2+ influx is mediated largely by store-operated channels (SOCs). TRPC channels mediate a significant portion of the receptor-activated Ca 2+ influx. However, whether any of the TRPC channels function as a SOC remains controversial. Our understanding of ...

Despite the essential role of the fibrinogen gamma-chain as a blood clotting factor, the fibrinogen gamma-chain contains a number of interaction sites to recruit other factors such as leukocytes important for prevention of pathogen entry and propagation of the repair process. Interleukin-6 (IL-6) is known as the major inducer of gamma-fibrinogen synthesis in hepatocytes, whereas IL-1beta has been shown to act as a potent inhibitor of gamma-fibrinogen expression. Studies on the rat fibrinogen gamma-chain promoter suggest that nuclear factor (NF)-kappaB replaces the signal transducer and activator of transcription (STAT) 3 from binding to overlapping NF-kappaB/STAT3 binding sites within the 5' regulatory region of the rat gamma-chain gene promoter. However, despite its physiological relevance, the underlying mechanism responsible for the inhibitory effect of IL-1beta in humans is still not understood and apparently more complex. In contrast to the mechanism described for the rat gene our results indicate that IL-1beta suppresses the IL-6-induced activation of the human gamma-fibrinogen gene particularly by blocking the late phase STAT3-tyrosine phosphorylation NF-kappaB-dependently but independent from de novo protein synthesis. Consequently, blocking NF-kappaB activation restores specifically late phase STAT3 activation as well as the induction of the human gamma-fibrinogen gene. In contrast, specifically early STAT3 activation could be restored by a block of the p38 mitogen-activated protein kinase (p38(MAPK)) pathway. In summary, our results indicate that expression of the gamma-fibrinogen gene is mainly controlled by the strength of late phase STAT3 activation, which in turn is negatively regulated by the extent of IL-1beta-mediated NF-kappaB activity.