(E)- and (Z)-1,2,4-triazolylchromanone oxime ethers as conformationally constrained antifungals

A series of 1,2,4-triazolylchromanone oxime ethers were synthesized and tested for in vitro antifungal activity. Many of these derivatives exhibit high activity against Candida albicans, Saccharomyces cerevisiae, Aspergillus niger and Microsporum gypseum.     

Effect of Hydro and KNO3 Priming on Seed Germination of Cotton (Gossypium hirsutum L.) Under Gnotobiotic Conditions

Journal of Plant Growth Regulation - Cotton (Gossypium hirsutum L.) is an important cash crop; its germination is very susceptible to salinity. Saline conditions result in a severe decline in yield...     

Different aspects of bacterial communication signals

The communication or quorum-sensing signal molecules (QSSM) are specialized molecules used by numerous gram-negative bacterial pathogens of animals and plants to regulate or modulate bacterial virulence factor production. In plant-associated bacteria, genes encoding the production of these signal molecules, QSSMs, were discovered to be linked with the phenotype of bacterium, because mutation of these genes typically disrupts some behaviors of bacteria. There are other regulator genes which respond to the presence of signal molecule and regulate the production of signal molecule as well as some virulence factors. The synthesis and regulator genes (collectively called quorum-sensing genes hereafter) are repressed in low bacterial population but induced when bacteria reach to high cell density. Multiple regulatory components have been identified in the bacteria that are under control of quorum sensing. This review describes different communication signal molecules, and the various chemical, physical and genomic factors known to synthesize signals. Likewise, the role of some signal-degrading enzymes or compounds and the interaction of QSSMs with eukaryotic metabolism will be discussed here.     

The Role of Peptide-Based Tumor Vaccines on Cytokines of Adaptive Immunity: A Review

International Journal of Peptide Research and Therapeutics - Recently, peptide-based materials have been applied to solving many therapeutic problems and have shown particular efficacy as cancer...     

Role of mechanosignaling on pathology of varicose vein

Varicose veins are the most common vascular disease in humans. Veins have valves that help the blood return gradually to the heart without leaking blood. When these valves become weak, blood and fluid collect and pool by pressing against the walls of the veins, causing varicose veins. In the cardiovascular system, mechanical forces are important determinants of vascular homeostasis and pathological processes. Blood vessels are constantly exposed to a variety of hemodynamic forces, including shear stress and environmental strains caused by the blood flow. In varicose veins within the leg, venous blood pressure rises in the vein of the lower extremities due to prolonged standing, creating a peripheral tension in the vessel wall thereby causing mechanical stimulation of endothelial cells and vascular smooth muscle. Studies have shown that long-term increased exposure to vascular wall tension is associated with the overexpression of HIF-1α and HIF-2α and increased levels of MMP-2 and MMP-9, thereby reducing venous contraction and progressive venous dilatation, which is involved in the development of varicose veins. Following the expression of metalloproteinase, the expression of type 1 collagen increases, and the amount of type 3 collagen decreases. Therefore, collagen imbalance will cause the varicose veins to not stretch. Loss of structural proteins (type 3 collagen and elastin) in the vessel wall causes the loss of the biophysical properties of the varicose vein wall. This review article tries to elaborate on the effect of mechanical forces and sensors of these forces on the vascular wall in creating the mechanism of mechanosignaling, as well as the role of the onset of molecular signaling cascades in the pathology of varicose veins.     

Epigenetics in osteoarthritis: Novel spotlight

Osteoarthritis (OA) is the most common type of arthritis and no longer is considered as an absolute consequence of joint mechanical use (wear and tear); rather recent data demonstrate the pivotal role of inflammatory mediators in the development and progression of this disease. This multifactorial disease results from several environmental and inherited factors. Genetic cannot solely explain all the contribution share of inheritance and, this way, it is speculated that epigenetics can play a role, too. Moreover, environmental factors can induce local epigenetic changes. The epigenetic contribution to OA pathogenesis occurs at all of its levels, DNA methylation, histone modification, microRNA, and long noncoding RNA. In fact, during early phases of OA pathogenesis, environmental factors employ epigenetic mechanisms to provide a positive feedback for the OA-related pathogenic mechanisms and pathways with an ultimate outcome of a well-established clinical OA. These epigenetic changes stay during clinical disease and prevent the body natural healing and regenerative processes to work properly, resulting in an incurable disease condition. In this review article, we aimed to have an overview on the studies performed with regard to understanding the role of epigenetics in the etiopathogenesis of OA and highlighted the importance of such kind of regulatory mechanisms within this context.     

Synthesis and antibacterial activity of N-(5-benzylthio-1,3,4-thiadiazol-2-yl) and N-(5-benzylsulfonyl-1,3,4-thiadiazol-2-yl)piperazinyl quinolone derivatives

A series of N-(5-benzylthio-1,3,4-thiadiazol-2-yl) and N-(5-benzylsulfonyl-1,3,4-thiadiazol-2-yl) derivatives of piperazinyl quinolones was synthesized and evaluated for antibacterial activity against Gram-positive and Gram-negative microorganisms. Some of these derivatives exhibit high activity against Gram-positive bacteria; Staphylococcus aureus and Staphylococcus epidermidis, comparable or more potent than their parent N-piperazinyl quinolones norfloxacin and ciprofloxacin as reference drugs. The SAR of this series indicates that both the structure of the benzyl unit and the S or SO(2) linker dramatically impact antibacterial activity.