Can Micro RNA-24 Affect the Cardiovascular Morbidity in Systemic Lupus Erythematosus by Targeting YKL-40?

Background:Systemic lupus erythematosus (SLE) is an autoimmune disease with inflammatory nature. One of the leading causes of death in SLE patients is cardiovascular (CVS) morbidity. MiRNA-24 is highly expressed in vascular endothelial cells (VECs). This dysregulated expression pattern is associated with dysfunction or even damage of VECs and leads to the occurrence of cardiovascular diseases. YKL- 40 is an inflammatory glycoprotein involved in the pathogenesis of endothelial dysfunction and thereby atherosclerosis. In this work, we aimed at illustrating the possible role of miR-24 and its target YKL-40 in the pathogenesis of the CVS morbidity associated with SLE.Methods:This work was conducted on 40 SLE patients and 40 healthy controls. Quantitative real-time PCR (qPCR) was done to estimate the expression level of miRNA-24 in serum. In addition, we measured the serum level of YKL-40 using ELISA.Results:miR-24-fold change was found to be down-regulated, whereas serum YKL- 40 was up-regulated among SLE patients with observed significant and negative correlation between the two parameters.Conclusion:Our study provided an insight about the role of miR-24 and its target serum YKL-40 protein in the development of SLE-related inflammation and atherosclerosis.Key Words: miRNA-24, SDC-1, SLE, VCAM, YKL-40     

A Ca(v)3.2/syntaxin-1A signaling complex controls T-type channel activity and low-threshold exocytosis

T-type calcium channels represent a key pathway for Ca(2+) entry near the resting membrane potential. Increasing evidence supports a unique role of these channels in fast and low-threshold exocytosis in an action potential-independent manner, but the underlying molecular mechanisms have remained unknown. Here, we report the existence of a syntaxin-1A/Ca(v)3.2 T-type calcium channel signaling complex that relies on molecular determinants that are distinct from the synaptic protein interaction site (synprint) found in synaptic high voltage-activated calcium channels. This interaction potently modulated Ca(v)3.2 channel activity, by reducing channel availability. Other members of the T-type calcium channel family were also regulated by syntaxin-1A, but to a smaller extent. Overexpression of Ca(v)3.2 channels in MPC 9/3L-AH chromaffin cells induced low-threshold secretion that could be prevented by uncoupling the channels from syntaxin-1A. Altogether, our findings provide compelling evidence for the existence of a syntaxin-1A/T-type Ca(2+) channel signaling complex and provide new insights into the molecular mechanism by which these channels control low-threshold exocytosis.     

Antioxidant defense responses: physiological plasticity in higher plants under abiotic constraints

Environmental stresses (salinity, drought, heat/cold, light and other hostile conditions) may trigger in plants oxidative stress, generating the formation of reactive oxygen species (ROS). These species are partially reduced or activated derivatives of oxygen, comprising both free radical and non-radical (H₂O₂) forms, leading to cellular damage, metabolic disorders and senescence processes. In order to overcome oxidative stress, plants have developed two main antioxidants defense mechanisms that can be classified as non-enzymatic and enzymatic systems. The first class (non-enzymatic) consists of small molecules such as vitamin (A, C and E), glutathione, carotenoids and phenolics that can react directly with the ROS by scavenging them. Second class is represented by enzymes among them superoxide dismutase, peroxidase and catalase which have the capacity to eliminate superoxide and hydrogen peroxide. In this review, we have tried to explore the related works, which have revealed the changes in the basic antioxidant metabolism of plants under various abiotic constraints.     

Synthesis of AZT analogues: 7-(3-azido-2-hydroxypropyl)-, 7-(3-amino-2-hydroxypropyl)-,7-(3-triazolyl-2-hydroxypropyl)theophylline

Nucleophilic displacement of the tosyloxy group in 7-(2-hydroxy-3-p-toluenesulfonyloxypropyl)theophylline (1) with azide anion afforded 7-(3-azido-2-hydroxypropyl)theophylline (2). Reduction of the 3-azido group in 2 with Ph3P/Py/NH4OH afforded the 3-amino derivative 4, alternatively obtained by regioselective amination of 7-(2,3-epoxypropyl)theophylline (3). Selective acetylation of 4 gave the N-acetyl derivative 5. 1,3-Dipolar cycloaddition of the azide group in 2 with N1-propargyl thymine (6) afforded the regioisomeric triazole 7.     

Dual-mode security authentication of SrAl2O4:Eu,Dy phosphor encapsulated in electrospun cellulose acetate nanofibrous films

Photochromic inks have been an attractive authentication strategy to improve the anti-counterfeiting efficiency of commercial products. However, recent reports have shown significant disadvantages with photochromic inks, including poor durability and high cost. In this context, we developed novel photochromic nanofibres for advanced anti-counterfeiting applications. Lanthanide-doped strontium aluminate (LdSA) nanoparticles (NPs) were prepared and immobilized into electrospun cellulose acetate nanofibres (CANF). Authentication materials immobilized with inorganic photochromic agents can warranty durability and photostability. Therefore, the ultraviolet-stimulated photochromism of LdSA-encapsulated cellulose acetate nanofibres (LdSA@CANF) demonstrated high reversibility and photostability. A broad range of cellulose acetate nanofibres with unique emission characteristics was developed when applying different ratios of LdSA NPs. LdSA@CANF appeared colourless under visible daylight, whereas a green emission was monitored under ultraviolet-light illumination. The shape and chemical content of the photochromic fibrous films were examined using various analytical techniques. The mechanical characteristics of LdSA@CANF-coated paper were investigated. The emission wavelength was detected at 514 nm to designate green colour, whereas the excitation wavelength was detected at 369 nm to indicate transparency. The prepared cellulose acetate nanofibrous film can be described as an efficient strategy for the anti-counterfeiting of commercialized items.     

An immunohistochemical method for identifying fibroblasts in formalin-fixed, paraffin-embedded tissue.

Fibroblasts are critical for tissue homeostasis, and their inappropriate proliferation and activation can result in common and debilitating conditions including fibrosis and cancer. We currently have a poor understanding of the mechanisms that control the growth and activation of fibroblasts in vivo, in part because of a lack of suitable fibroblast markers. We have taken advantage of an antibody previously shown to stain stromal cells in frozen tissues (TE-7) and identified conditions in which it can be used to stain fibroblasts and myofibroblasts in the paraffin-embedded tissue samples routinely collected for pathological analysis. We show that this antibody recognizes growing and quiescent fibroblasts and myofibroblasts by immunohistochemistry, immunofluorescence, and ELISA assays. We also present its staining patterns in normal tissue samples and in breast tumors.