Effect of Lawsonia inermis on tumor expression induced by Dalton’s lymphoma ascites in Swiss albino mice

The purpose of this study was investigating experimentally the possible antitumor effect of ethanol extract of root of Lawsonia inermis against Dalton’s lymphoma ascites (DLA) bearing mice.Mice were administered with L. inermis at a dosage of 180 mg/kg of body weight for 15 days after 24 h of DLA inoculation. The ethanolic root extract of L. inermis reverted the increased number of the WBC count, platelets and lymphocytes and decreased the number of the RBC count, hemoglobin content and monocytes. The effect of root extract of L. inermis also increased the pathophysiological marker enzyme, lipid profile and decreased the enzymic and non enzymic antioxidants. A histopathological result shows the loss of liver hepatocytes and kidney architecture in DLA bearing mice. However, mice treatment with L. inermis extract improves the liver and kidney function and rearranges more or less normal architecture. The present work indicates that the ethanol extract of L. inermis exhibited significant antitumor activity.     

The differential stress response of adapted chromite mine isolates Bacillus subtilis and Escherichia coli and its impact on bioremediation potential

In the current study, indigenous bacterial isolates Bacillus subtilis VITSUKMW1 and Escherichia coli VITSUKMW3 from a chromite mine were adapted to 100 mg L^?1 of Cr(VI). The phase contrast and scanning electron microscopic images showed increase in the length of adapted E. coli cells and chain formation in case of adapted B. subtilis. The presence of chromium on the surface of the bacteria was confirmed by energy dispersive X-ray spectroscopy (EDX), which was also supported by the conspicuous Cr–O peaks in FTIR spectra. The transmission electron microscopic (TEM) images of adapted E. coli and B. subtilis showed the presence of intact cells with Cr accumulated inside the bacteria. The TEM–EDX confirmed the internalization of Cr(VI) in the adapted cells. The specific growth rate and Cr(VI) reduction capacity was significantly higher in adapted B. subtilis compared to that of adapted E. coli. To study the possible role of Cr(VI) toxicity affecting the Cr(VI) reduction capacity, the definite assays for the released reactive oxygen species (ROS) and ROS scavenging enzymes (SOD and GSH) were carried out. The decreased ROS production as well as SOD and GSH release observed in adapted B. subtilis compared to the adapted E. coli corroborated well with its higher specific growth rate and increased Cr(VI) reduction capacity.     

DIACAN: Integrated Database for Antidiabetic and Anticancer Medicinal Plants

Medicinal plants and plant derived molecules are widely used in traditional cultures all over the world and they are becoming large popular among biomedical researchers and pharmaceutical companies as a natural alternative to synthetic medicine. Information related to medicinal plants and herbal drugs accumulated over the ages are scattered and unstructured which make it prudent to develop a curated database for medicinal plants. The Antidiabetic and Anticancer Medicinal Plants Database (DIACAN) aims to collect and provide an integrated platform for plants and phytochemiclas having antidiabetic or anticancer activity.

Availability

http://www.kaubic.in/diacan     

E-cadherin supports steady-state Rho signaling at the epithelial zonula adherens

In simple polarized epithelial cells, the Rho GTPase commonly localizes to E-cadherin-based cell–cell junctions, such as the zonula adherens (ZA), where it regulates the actomyosin cytoskeleton to support junctional integrity and tension. An important question is how E-cadherin contributes to Rho signaling, notably whether junctional Rho may depend on cadherin adhesion. We sought to investigate this by assessing Rho localization and activity in epithelial monolayers depleted of E-cadherin by RNAi. We report that E-cadherin depletion reduced both Rho and Rho-GTP at the ZA, an effect that was rescued by expressing a RNAi-resistant full-length E-cadherin transgene. This impact on Rho signaling was accompanied by reduced junctional localization of the Rho GEF ECT2 and the centralspindlin complex that recruits ECT2. Further, the Rho signaling pathway contributes to the selective stabilization of E-cadherin molecules in the apical zone of the cells compared with E-cadherin at the lateral surface, thereby creating a more defined and restricted pool of E-cadherin that forms the ZA. Thus, E-cadherin and Rho signaling cooperate to ensure proper ZA architecture and function.     

Adaptability in protein structures: structural dynamics and implications in ligand design

The basic framework of understanding the mechanisms of protein functions is achieved from the knowledge of their structures which can model the molecular recognition. Recent advancement in the structural biology has revealed that in spite of the availability of the structural data, it is nontrivial to predict the mechanism of the molecular recognition which progresses via situation-dependent structural adaptation. The mutual selectivity of protein–protein and protein–ligand interactions often depends on the modulations of conformations empowered by their inherent flexibility, which in turn regulates the function. The mechanism of a protein’s function, which used to be explained by the ideas of ‘lock and key’ has evolved today as the concept of ‘induced fit’ as well as the ‘population shift’ models. It is felt that the ‘dynamics’ is an essential feature to take into account for understanding the mechanism of protein’s function. The design principles of therapeutic molecules suffer from the problems of plasticity of the receptors whose binding conformations are accurately not predictable from the prior knowledge of a template structure. On the other hand, flexibility of the receptors provides the opportunity to improve the binding affinity of a ligand by suitable substitution that will maximize the binding by modulating the receptors surface. In this paper, we discuss with example how the protein’s flexibility is correlated with its functions in various systems, revealing the importance of its understanding and for making applications. We also highlight the methodological challenges to investigate it computationally and to account for the flexible nature of the molecules in drug design.     

Dynamic environments of fungus‐farming termite mounds exert growth‐modulating effects on fungal crop parasites

This study investigated for the first time the impact of the internal mound environment of fungus‐growing termites on the growth of fungal crop parasites. Mounds of the termite Odontotermes obesus acted as (i) temperature and relative humidity (RH) ‘stabilisers’ showing dampened daily variation and (ii) ‘extreme environments’ exhibiting elevated RH and CO₂ levels, compared to the outside. Yet, internal temperatures exhibited seasonal dynamics as did daily and seasonal CO₂ levels. During in situ experiments under termite‐excluded conditions within the mound, the growth of the crop parasite Pseudoxylaria was greater inside than outside the mound, i.e., Pseudoxylaria is ‘termitariophilic’. Also, ex situ experiments on parasite isolates differing in growth rates and examined under controlled conditions in the absence of termites revealed a variable effect with fungal growth decreasing only under high CO₂ and low temperature conditions, reflecting the in situ parasite growth fluctuations. In essence, the parasite appears to be adapted to survive in the termite mound. Thus the mound microclimate does not inhibit the parasite but the dynamic environmental conditions of the mound affect its growth to varying extents. These results shed light on the impact of animal‐engineered structures on parasite ecology, independent of any direct role of animal engineers.     

PAMPer and tRIGer: ligand-induced activation of RIG-I

Retinoic-acid-inducible gene-I (RIG-I) is an important component of the innate immune response to many RNA viruses that limits viral replication until adaptive immunity becomes available to clear the infection. Upon binding to the nucleic acid genomes and replication intermediates of these viruses, RIG-I undergoes a complex activation process that involves post-translational modifications and structural rearrangements. Once activated, RIG-I upregulates well-studied signal transduction pathways that lead to the production of type-I interferons (IFNs) and a large variety of antiviral IFN-stimulated genes. Thus, an effective antiviral response is dependent on the interaction between pathogen-derived ligands and RIG-I. Recent work has begun to clarify the required characteristics of RIG-I activators and is setting the stage for the identification of authentic ligands used during viral infection.