Arabidopsis SYT1 maintains stability of cortical endoplasmic reticulum networks and VAP27-1-enriched endoplasmic reticulum–plasma membrane contact sites

Arabidopsis synaptotagmin 1 (SYT1) is localized on the endoplasmic reticulum–plasma membrane (ER–PM) contact sites in leaf and root cells. The ER–PM localization of Arabidopsis SYT1 resembles that of the extended synaptotagmins (E-SYTs) in animal cells. In mammals, E-SYTs have been shown to regulate calcium signaling, lipid transfer, and endocytosis. Arabidopsis SYT1 was reported to be essential for maintaining cell integrity and virus movement. This study provides detailed insight into the subcellular localization of SYT1 and VAP27-1, another ER–PM-tethering protein. SYT1 and VAP27-1 were shown to be localized on distinct ER–PM contact sites. The VAP27-1-enriched ER–PM contact sites (V-EPCSs) were always in contact with the SYT1-enriched ER–PM contact sites (S-EPCSs). The V-EPCSs still existed in the leaf epidermal cells of the SYT1 null mutant; however, they were less stable than those in the wild type. The polygonal networks of cortical ER disassembled and the mobility of VAP27-1 protein on the ER–PM contact sites increased in leaf cells of the SYT1 null mutant. These results suggest that SYT1 is responsible for stabilizing the ER network and V-EPCSs

Actin3 promoter reveals undulating F-actin bundles at shanks and dynamic F-actin meshworks at tips of tip-growing pollen tubes

The dynamic actin cytoskeleton of pollen tubes is both the driver of the tip growth and the organizer of cell polarity. In order to understand this fast re-arranging cytoskeletal system, we need reliable constructs expressed under relevant promoters. Here we are reporting that the Lifeact reporter, expressed under the pollen-specific Actin3 promoter, visualizes very dynamic F-actin elements both in germinating pollen grains and tip-growing pollen tubes. Importantly, we have documented very active actin polymerization at the cell periphery, especially in the bulging area during pollen germination and in the apical clear zone. Expression of the Lifeact reporter under control of the pollen-specific Actin3 promoter revealed 2 new aspects: (i) long F-actin bundles in pollen tube shanks are dynamic, showing undulating movements, (ii) subapical ‘actin collars’ or ‘fringes’ are absent

Application of Plasticity Theory to Reinforced Concrete Deep Beams

yesThis paper reviews the application of the plasticity theory to reinforced concrete deep beams. Both the truss analogy and mechanism approach were employed to predict the capacity of reinforced concrete deep beams. In addition, most current codes of practice, for example Eurocode 1992 and ACI 318-05, recommend the strut-and-tie model for designing reinforced concrete deep beams. Compared with methods based on empirical or semi-empirical equations, the strut-and-tie model and mechanism analyses are more rational, adequately accurate and sufficiently simple for estimating the load capacity of reinforced concrete deep beams. However, there is a problem of selecting the effectiveness factor of concrete as reflected in the wide range of values reported in the literature for deep beams

Neural network modelling of RC deep beam shear strength

YesA 9 x 18 x 1 feed-forward neural network (NN) model trained using a resilient back-propagation algorithm and early stopping technique is constructed to predict the shear strength of deep reinforced concrete beams. The input layer covering geometrical and material properties of deep beams has nine neurons, and the corresponding output is the shear strength. Training, validation and testing of the developed neural network have been achieved using a comprehensive database compiled from 362 simple and 71 continuous deep beam specimens. The shear strength predictions of deep beams obtained from the developed NN are in better agreement with test results than those determined from strut-and-tie models. The mean and standard deviation of the ratio between predicted capacities using the NN and measured shear capacities are 1.028 and 0.154, respectively, for simple deep beams, and 1.0 and 0.122, respectively, for continuous deep beams. In addition, the trends ascertained from parametric study using the developed NN have a consistent agreement with those observed in other experimental and analytical investigations

Tuftsin Promotes an Anti-Inflammatory Switch and Attenuates Symptoms in Experimental Autoimmune Encephalomyelitis

Multiple sclerosis (MS) is a demyelinating autoimmune disease mediated by infiltration of T cells into the central nervous system after compromise of the blood-brain barrier. We have previously shown that administration of tuftsin, a macrophage/microglial activator, dramatically improves the clinical course of experimental autoimmune encephalomyelitis (EAE), a well-established animal model for MS. Tuftsin administration correlates with upregulation of the immunosuppressive Helper-2 Tcell (Th2) cytokine transcription factor GATA-3. We now show that tuftsin-mediated microglial activation results in shifting microglia to an anti-inflammatory phenotype. Moreover, the T cell phenotype is shifted towards immunoprotection after exposure to tuftsin-treated activated microglia; specifically, downregulation of pro-inflammatory Th1 responses is triggered in conjunction with upregulation of Th2-specific responses and expansion of immunosuppressive regulatory T cells (Tregs). Finally, tuftsin-shifted T cells, delivered into animals via adoptive transfer, reverse the pathology observed in mice with established EAE. Taken together, our findings demonstrate that tuftsin decreases the proinflammatory environment of EAE and may represent a therapeutic opportunity for treatment of MS