Potential of plant extracts in combination with bacterial antagonist treatment as biocontrol agent of red rot of sugarcane

Plant extracts and antifungal microorganisms were tested singly and in combination for biocontrol of sugarcane red rot disease (Colletotrichum falcatum) using two sugarcane (Saccharum officinarum L.) cultivars, CoC671 and CoC92061, in pot and field experiments. Leaf extracts of Abrus precatorius and Bassia latifolia and the rhizome extract of Curcuma longa reduced Colletotrichum falcatum mycelial growth by 80%, 58%, and 57%, respectively. Although sugarcane- planting materials (setts) treated individually with either Pseudomonas fluorescens Md1 or A. precatorius in pot experiments had the lowest incidences of red rot, 20.1% and 24.2%, respectively, none of the plant extracts were effective in the field. In contrast, when the two varieties were tested separately in two field locations, the setts treated with A. precatorius in combination with a spray or soil application of P. fluorescens Md1 had the lowest incidence of red rot in both locations, e.g., 3.1% and 3.4% incidence for CoC92061 in one location, and had a similar response to the chemical control. The results suggest the applicability of plant-based extracts for the suppression of sugarcane red rot disease in the field as an environment-friendly tool in combination with antagonists.     

Effect of T. chebula on mitochondrial alterations in experimental myocardial injury

Mitochondria play a central role in molecular events leading to tissue damage in ischemia. The present study examines the role of the alcoholic extract of T. chebula (TCE) pretreatment (50 mg/100 g body weight) to attenuate the isoproterenol (ISO) (20mg/100g body wt, sc) induced alterations on heart mitochondrial ultrastucture and function in experimental rats. ISO induced cardiotoxicity was evidenced by a significant rise in the level of lactate, decrease in enzyme activities of tricarboxylic acid cycle (TCA), mitochondrial respiration, levels of adenosine triphosphate (ATP) and oxidative phosphorylation. TCE intervention significantly attenuated the above alterations by ISO and retained near normal function of the mitochondria. Electron microscopic studies of the mitochondria further support the isoproterenol induced deleterious changes and accredit the protective effect of TCE on mitochondrial structure and energy metabolism.     

UNC5B receptor deletion exacerbates DSS‐induced colitis in mice by increasing epithelial cell apoptosis

The netrin-1 administration or overexpression is known to protect colon from acute colitis. However, the receptor that mediates netrin-1 protective activities in the colon during colitis remains unknown. We tested the hypothesis that UNC5B receptor is a critical mediator of protective function of netrin-1 in dextran sodium sulfate (DSS)-induced colitis using mice with partial deletion of UNC5B receptor. DSS colitis was performed in mice with partial genetic UNC5B deficiency (UNC5B^+/− mice) or wild-type mice to examine the role of endogenous UNC5B. These studies were supported by in vitro models of DSS-induced apoptosis in human colon epithelial cells. WT mice developed colitis in response to DSS feeding as indicated by reduction in bw, reduction in colon length and increase in colon weight. These changes were exacerbated in heterozygous UNC5B knockout mice treated with DSS. Periodic Acid-Schiff stained section shows damages in colon epithelium and mononuclear cell infiltration in WT mice, which was further increased in UNC5B heterozygous knockout mice. This was associated with large increase in inflammatory mediators such as cytokine and chemokine expression and extensive apoptosis of epithelial cells in heterozygous knockout mice as compared to WT mice. Overexpression of UNC5B human colon epithelial cells suppressed DSS-induced apoptosis and caspase-3 activity. Moreover, DSS induced large amount of netrin-1 and shRNA mediated knockdown of netrin-1 induction exacerbated DSS-induced epithelial cell apoptosis. Our results suggest that UNC5B is a critical mediator of cell survival in response to stress in colon.     

Cyclic nucleotides and mitogen-activated protein kinases: regulation of simvastatin in platelet activation

Background  

3-Hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have been widely used to reduce cardiovascular risk. These statins (i.e., simvastatin) may exert other effects besides from their cholesterol-lowering actions, including inhibition of platelet activation. Platelet activation is relevant to a variety of coronary heart diseases. Although the inhibitory effect of simvastatin in platelet activation has been studied; the detailed signal transductions by which simvastatin inhibit platelet activation has not yet been completely resolved.     

Bioactive and metal uptake studies of carboxymethyl chitosan-graft-d-glucuronic acid membranes for tissue engineering and environmental applications

Carboxymethyl chitosan-graft-d-glucuronic acid (CMCS-g-d-GA) was prepared by grafting d-GA onto CMCS in the presence of 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDC) and then the membranes were made from it. In this work, the bioactivity studies of CMCS-g-d-GA membranes were carried out and then characterized by SEM, CLSM, XRD and FT-IR. The CMCS-g-d-GA membranes were found to be bioactive. The adsorption of Ni²⁺, Zn²⁺and Cu²⁺ ions onto CMCS-g-d-GA membranes has also been investigated. The maximum adsorption capacity of CMCS-g-d-GA for Ni²⁺, Zn²⁺and Cu²⁺ was found to be 57, 56.4 and 70.2 mg/g, respectively. Hence, these membranes were useful for tissue engineering, environmental and water purification applications.     

Bioactive and osteoblast cell attachment studies of novel α- and β-chitin membranes for tissue-engineering applications

Chitin is a novel biopolymer and has excellent biological properties such as biodegradation in the human body and biocompatible, bioabsorable, antibacterial and wound healing activities. In this work, α- and β-chitin membranes were prepared using α- and β-chitin hydrogel. The bioactivity studies were carried out using these chitin membranes with the simulated body fluid solution (SBF) for 7, 14 and 21 days. After 7, 14 and 21 days the membranes were characterized using SEM, EDS and FT-IR. The SEM, EDS and FT-IR studies confirmed the formation of calcium phosphate layer on the surface of the both chitin membranes. These results indicate that the prepared chitin membranes were bioactive. Cell adhesion studies were also carried out using MG-63 osteoblast-like cells. The cells were adhered and spread over the membrane after 24 h of incubation. These results indicated that the chitin membranes could be used for tissue-engineering applications.     

Prevention of nicotine and streptozotocin treatment induced circulatory oxidative stress by bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione in diabetic rats

Diabetes and smoking have been considered as major health problems individually and their seriousness related to health hazard has been well reported. The role of nicotine in causing or worsening effect on diabetes is not well understood. The aim of our study was to investigate the effect of nicotine on experimental diabetes and to analyze the effect of bis-1,7-(2-hydroxyphenyl)-hepta-1,6-diene-3,5-dione a bisdemethoxy curcumin analog (BDMCA) in streptozotocin and nicotine induced toxicity. Group I: control rats; Group II: nicotine (2.5 mg/kg b.wt); Group III: streptozotocin (STZ) (40 mg/kg b.wt); Group IV: STZ (40 mg/kg b.wt) + nicotine (2.5 mg/kg b.wt); Group V: STZ + nicotine + BDMCA (40 mg/kg b.wt); Group VI: STZ + nicotine + BDMCA (80 mg/kg b.wt). Efficacy of BDMCA was determined by evaluating blood glucose, thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP), activities of marker enzymes alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) and activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). From our study, we have observed that nicotine not only aggravates diabetic complications but also increased the risk for diabetes. BDMCA, at a dose 80 mg/kg body weight was found to be more effective in decreasing toxic effects induced by nicotine and STZ.     

C9 conformation of N-(N alpha-[(tert.-butyloxy)-carbonyl]-L-alanyl)-N,N'-dicyclohexylu rea in solid and solution.

An X-ray diffraction study was carried out on a single crystal of N-(N alpha-[(tert.-butyloxy)-carbonyl]-L-alanyl)-N,N'-dicyclohexylur ea belonging to the tetragonal space group P4(1)2(1)2, having cell dimensions a = b = 10.102(3) A, c = 46.067(7) A, V = 4701.2 A3, Z = 8. The crystal structure was solved by direct methods and refined to an R value of 0.056 for 1602 unique reflections with I greater than 2.5 sigma(I). Crystal structure analysis shows the presence of an intramolecular N-H ... O=C H-bond stabilizing the molecule in a folded form similar to that of a beta turn, forming a nine-membered ring. IR and 1H-NMR studies in CDCl3 solution confirm the stable folded conformation found in the crystalline state, as well as the existence of N-H ... O=C H-bonds in the title compound, as in peptides.