Dietary Mannan-oligosaccharides potentiate the beneficial effects of Bifidobacterium bifidum in broiler chicken

This study investigated the effects of dietary Bifidobacterium bifidum (BFD) and mannan-oligosaccharide (MOS), as a synbiotic, on the production performance, gut microbiology, serum biochemistry, antioxidant profile and health indices of broiler chicken. Six dietary treatments were T1 (negative control), T2 (positive control-20 mg antibiotic BMD kg⁻¹ diet; BMD: bacitracin methylene disalicylate), T3 (0·1% MOS + 10⁶ CFU BFD per g feed), T4 (0·1% MOS + 10⁷ CFU BFD per g feed), T5 (0·2% MOS + 10⁶ CFU BFD per g feed) and T6 (0·2% MOS + 10⁷ CFU BFD per g feed). Significantly (P < 0·01) better growth performance and efficiency was observed in birds supplemented with 0·2% MOS along with 10⁶ CFU BFD per g of feed compared to BMD and control birds. Supplementation with 0·2% MOS along with either 10⁶ or 10⁷ CFU BFD per g feed reduced (P < 0·01) the gut coliform, Escherichia coli, total plate count, and Clostridium perfringens count and increased the Lactobacillus and Bifidobacterium count. Significantly (P < 0·01) higher serum and liver antioxidant enzyme pool, serum HDL cholesterol and lower serum glucose, triglyceride, total cholesterol, cardiac risk ratio, atherogenic coefficient and atherogenic index of plasma were observed in birds supplemented with 0·2% MOS along with 10⁶ CFU BFD per g of feed compared to control or BMD supplemented birds. Better production performance, gut microbial composition, serum biochemistry, antioxidant profile and health indices were depicted by broiler chicken supplemented with 0·2% MOS and 10⁶ CFU BFD per g of feed.     

RUNX1T1, a potential prognostic marker in breast cancer,is co-ordinately expressed with ERα, and regulated by estrogen receptor signalling in breast cancer cells

Molecular Biology Reports - RUNX1T1 is extensively studied in the context of AML1-RUNX1T1 fusion protein in acute myeloid leukemia. Little is known about the function of RUNX1T1 itself, although...     

Metals toxicity and its correlation with the gene expression in Alzheimer's disease

Molecular Biology Reports - Alzheimer's disease is a common neurodegenerative disease in the elderly population and a leading cause of dementia. Genetics and environmental risk factors were...     

Palynomorph distribution in a mangrove ecosystem along environmental and salinity gradient: a tool for palaeoecological reconstruction

Pollen assemblages closely reflect the local vegetation that characterizes the salinity status, providing useful analogs for paleoecologxical reconstruction in regional deposits. Palynological evidences of surface sediments from the Coringa mangrove wetland were correlated with the physicochemical and sediment salinity records to observe the relationship between them. The statistical analysis of the data obtained here revealed a marked horizontal salinity gradient from north to south.. In this study, ordination (detrended correspondence analysis) of palynomorph groups has identified a salinity gradient of 1.1 to 3.0 PSU from the north to the south in the wetland. High palynomorph deposition and lower salinity are observed along channel margins due to the mixing of estuarine water during the rainy season. The mudflats along the transects show a lower diversity of plants in the pollen record and high total dissolved solids (TDS) than commonly found in the coastal wetlands. The presence of scrubby halophytic vegetation in the upper saltmarsh and oligohaline-freshwater vegetation in the low tidal saline marshes is a zonation pattern related to the localized influence of freshwater conditions. Palynomarine Index (PMI) reveals the highest freshwater/tidal inundation along Ramannapalem due to the presence of numerous riverine channels while the remaining part of the wetland has restricted tidal inundation leading to the conversion of mangrove forests to salt pans and paddy fields. Thus, the health and productivity of the mangrove ecosystem are also governed by hydrodynamics, catchment land use, water discharge in the channels, and tidal flushing.

     

Endoplasmic reticulum maintains ion homeostasis required for plasma membrane repair

Of the many crucial functions of the ER, homeostasis of physiological calcium increase is critical for signaling. Plasma membrane (PM) injury causes a pathological calcium influx. Here, we show that the ER helps clear this surge in cytoplasmic calcium through an ER-resident calcium pump, SERCA, and a calcium-activated ion channel, Anoctamin 5 (ANO5). SERCA imports calcium into the ER, and ANO5 supports this by maintaining electroneutrality of the ER lumen through anion import. Preventing either of these transporter activities causes cytosolic calcium overload and disrupts PM repair (PMR). ANO5 deficit in limb girdle muscular dystrophy 2L (LGMD2L) patient cells compromises their cytosolic and ER calcium homeostasis. By generating a mouse model of LGMD2L, we find that PM injury causes cytosolic calcium overload and compromises the ability of ANO5-deficient myofibers to repair. Addressing calcium overload in ANO5-deficient myofibers enables them to repair, supporting the requirement of the ER in calcium homeostasis in injured cells and facilitating PMR.     

Solvent-Free Synthesis,Characterization, and In Vitro Biological Activity Study of Xanthenediones and Acridinediones

Russian Journal of Bioorganic Chemistry - The present work highlights the broad range of oxygen and nitrogen heterocycles and their applications in medicinal field. A facial approach has been...     

The Enantioselectivity of the Cellular Deoxynucleoside Kinases

Abstract

Cytosolic thymidine kinase (TK1) and deoxycytidine kinase (dCK) and the mitochondrial thymidine kinase (TK2) and deoxyguanosine kinase (dGK), phosphorylate deoxynucleosides and their analogs. Recombinant human TK1 only phosphorylated β-D Thd, but recombinant TK2, dCK and dGK all phosphorylated equally well β-D and β-L as well as to some extent α-D and α-L deoxynucleosides.     

Purification and characterization of an extracellular antifungal chitinase from Penicillium ochrochloron MTCC 517 and its application in protoplast formation

A highly chitinolytic strain Penicillium ochrochloron MTCC 517 was procured from MTCC, Chandigarh, India. Culture medium supplemented with 1% chitin was found to be suitable for maximum production of chitinase. Purification of extracellular chitinase was done from the culture medium by organic solvent precipitation and DEAE-cellulose column chromatography. The chitinase was purified 6.92-fold with 29.9% yield. Molecular mass of purified chitinase was found to be 64 kDa by SDS-PAGE. The chitinase showed optimum temperature 40 °C and pH 7.0. The enzyme activity was completely inhibited by Hg²⁺, Zn²⁺, K⁺ and NH₄⁺. The enzyme kinetic study of purified chitinase revealed the following characteristics, such as apparent K_m 1.3 mg ml^?1, V_max 5.523 × 10^?5 moles l^?1 min^?1 and K_cat 2.37 s^?1 and catalytic efficiency 1.82 s^?1 M^?1. The enzyme hydrolyzed colloidal chitin, glycol chitin, chitosan, glycol chitosan, N,N′-diacetylchitobiose, p-nitrophenyl N-acetyl-β-d-glucosaminide and 4-methylumbelliferyl N-acetyl-β-d-glucosaminide. The chitinase of P. ochrochloron MTCC 517 is an exoenzyme, which gives N-acetylglucosamine as the main hydrolyzate after hydrolysis of colloidal chitin. Protoplasts with high regeneration capacity were obtained from Aspergillus niger using chitinase from P. ochrochloron MTCC 517. Since it also showed antifungal activity, P. ochrochloron MTCC 517 seems to be a promising biocontrol agent.     

Delphinidin Reduces Cell Proliferation and Induces Apoptosis of Non-Small-Cell Lung Cancer Cells by Targeting EGFR/VEGFR2 Signaling Pathways

Epidermal growth factor receptor (EGFR) and vascular endothelial growth factor receptor 2 (VEGFR2) have emerged as two effective clinical targets for non-small-cell lung cancer (NSCLC). In the present study, we found that delphinidin, an anthocyanidin, present in pigmented fruits and vegetables, is a potent inhibitor of both EGFR and VEGFR2 in NSCLC cells that overexpress EGFR/VEGFR2. Using these cells, we next determined the effects of delphinidin on cell growth and apoptosis in vitro and on tumor growth and angiogenesis in vivo. Delphinidin (5-60 µM) treatment of NSCLC cells inhibited the activation of PI3K, and phosphorylation of AKT and MAPKs. Additionally, treatment of NSCLC cells with delphinidin resulted in inhibition of cell growth without having significant toxic effects on normal human bronchial epithelial cells. Specifically, treatment of NCI-H441 and SK-MES-1 cells with delphindin (5-60 µM) resulted in (i) cleavage of PARP protein, (ii) activation of caspase-3 and -9, (iii) downregulation of anti-apoptotic proteins (Bcl2, Bcl-xL and Mcl-1), (iv) upregulation of pro-apoptotic proteins (Bax and Bak), and (v) decreased expression of PCNA and cyclin D1. Furthermore, in athymic nude mice subcutaneously implanted with human NSCLC cells, delphinidin treatment caused a (i) significant inhibition of tumor growth, (ii) decrease in the expression of markers for cell proliferation (Ki67 and PCNA) and angiogenesis (CD31 and VEGF), and (iii) induction of apoptosis, when compared with control mice. Based on these observations, we suggest that delphinidin, alone or as an adjuvant to current therapies, could be used for the management of NSCLC, especially those that overexpress EGFR and VEGFR2.