Aluminium-induced enhancement of ageing-related biochemical and electrophysiological parameters in rat brain regions

We investigated alterations in the ageing-related parameters: multiple-unit action potentials, Na(+), K(+)-ATPase activity, glutathione-s-transferase (GST) activity, glutathione peroxidase (GPx) activity, lipid peroxidation and lipofuscin contents in the brain regions cerebral cortex, striatum, hippocampus and thalamus, resulting from the chronic administration of aluminium chloride (AlCl3) in drinking water to rats of 6 and 12 months of age. Aluminium treatment significantly depressed Na(+), K(+)-ATPase, GST and GPx activities, elevated lipid peroxidation and lipofuscin contents, and produced intense epileptiform activity in the electroencephalograms of the studied brain regions together with a concomitant increase in the multiple-unit action potentials (MUA) indicating a vigorous neuronal epileptic hyperactivity. Taken together the aluminium-induced alterations in these parameters are indicative of an accelerated ageing process.     

IL-10 Signaling Remodels Adipose Chromatin Architecture to Limit Thermogenesis and Energy Expenditure

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Caffeic acid phenethyl ester induces adrenoleukodystrophy (Abcd2) gene in human X-ALD fibroblasts and inhibits the proinflammatory response in Abcd1/2 silenced mouse primary astrocytes

X-linked adrenoleukodystrophy (X-ALD) is a peroxisomal disorder caused by mutations in the ABCD1 gene. Accumulation of very long chain fatty acids (VLCFA) that have been attributed to reduced peroxisomal VLCFA β-oxidation activity are the hallmark of the disease. Overexpression of ABCD2 gene, the closest homolog of ABCD1, has been shown to compensate for ABCD1, thus correcting the VLCFA derangement. The accumulation of VLCFA leads to a neuroinflammatory disease process associated with demyelination of the cerebral white matter. The present study underlines the importance of caffeic acid phenethyl ester (CAPE) in inducing the expression of ABCD2 (ALDRP), and normalizing the peroxisomal β-oxidation as well as the levels of saturated and monounsaturated VLCFAs in cultured human skin fibroblasts of X-ALD patients. The expression of ELOVL1, the single elongase catalyzing the synthesis of both saturated VLCFA (C26:0) and mono-unsaturated VLCFA (C26:1), was also reduced by CAPE treatment. Importantly, CAPE upregulated Abcd2 expression and peroxisomal β-oxidation and lowered the VLCFA levels in Abcd1-deficient U87 astrocytes and B12 oligodendrocytes. In addition, using Abcd1/Abcd2-silenced mouse primary astrocytes we examined the effects of CAPE in VLCFA-induced inflammatory response. CAPE treatment decreased the inflammatory response as the expression of inducible nitric oxide synthase, inflammatory cytokine, and activation of NF-κB in Abcd1/Abcd2-silenced mouse primary astrocytes was reduced. The observations indicate that CAPE corrects both the metabolic disease of VLCFA as well as secondary inflammatory disease; therefore, it may be a potential drug candidate to be tested for X-ALD therapy in humans.     

Theaflavins induce G2/M arrest by modulating expression of p21waf1/cip1, cdc25C and cyclin B in human prostate carcinoma PC-3 cells

Cancer of the prostate gland (PCA) is the most common invasive malignancy and is the second leading cause of cancer-related death in males. The polyphenolic constituents of black tea have gained considerable attention as chemopreventive agents. Many studies have shown that black tea reduces the risk of several cancer types. In the present study, we studied the effect of a black tea polyphenol, theaflavin (TF), on cellular proliferation and cell death in the human prostate cancer cell line, PC-3. We showed that TF inhibits cell proliferation in a dose- and time-dependent manner. Studies on cell cycle progression have shown that the anti-proliferative effect of TF is associated with an increase in the G2/M phase of PC-3 cells. Western blot results showed that TF-induced G2/M phase arrest was mediated through the inhibition of cyclin-regulated signaling pathways. TF induces cyclin kinase inhibitor p21(waf1/cip1) expression and inhibits cdc25C and cyclin B expression. Increased exposure time to TF caused apoptosis of PC-3 cells, which was associated with up-regulation of the pro-apoptotic proteins Bax, caspase-3 and caspase-9 and down-regulation of anti-apoptotic protein Bcl-2. The role of caspase-induced apoptosis was further confirmed by a reduction in mitochondria membrane potential and the appearance of a DNA laddering pattern. Thus, it can be concluded that TF acts as an effective anti-proliferative agent by modulating cell growth regulators in prostate cancer cells.     

An efficient and quick protocol for in vitro multiplication of snake plant,Sansevieria trifasciata var. Laurentii [Prain]

Plant Cell, Tissue and Organ Culture (PCTOC) - Plant germ cells, such as pollen grains, can be affected by exposure to metal nanoparticles (NPs) that have diffused into the environment. The...     

Oil field microorganisms cause highly localized corrosion on chemically inhibited carbon steel

Carbon steel pipelines, a means for crude oil transportation, occasionally experience highly localized perforation caused by microorganisms. While microorganisms grown in laboratory culture tend to corrode steel specimens unevenly, they rarely inflict a corrosion morphology consistent with that of pipelines, where centimetre-sized corrosion features are randomly distributed within vast stretches of otherwise pristine metal surface. In this study, we observed that corrosion inhibitors (CIs), widely used for the control of acid gas (H₂S, CO₂) corrosion in oil fields, also affect microbial growth and activity. Inhibited carbon steel resisted biofilm formation and underwent negligible corrosion (< 0.002 mm Fe⁰ year⁻¹), despite 15 months of exposure to oil field waters harbouring a diverse microbiome. In contrast, physical scavenging of CI in these waters led to severe and highly localized corrosion (up to 0.93 mm Fe⁰ year⁻¹) underneath biofilms dominated by methanogenic archaea and sulfate-reducing bacteria. A sharp decline in CI concentration, as well as its active components, quaternary ammonium compounds (QACs), correlated with microbial sulfidogenesis. CIs are ubiquitously present in oil field waters and play an underappreciated role in microbial corrosion mitigation. Physical and biological scavenging of CIs may create local differences in steel inhibition effectiveness and thus result in highly localized corrosion.     

Strengthening data collection for neglected tropical diseases: What data are needed for models to better inform tailored intervention programmes?

Locally tailored interventions for neglected tropical diseases (NTDs) are becoming increasingly important for ensuring that the World Health Organization (WHO) goals for control and elimination are reached. Mathematical models, such as those developed by the NTD Modelling Consortium, are able to offer recommendations on interventions but remain constrained by the data currently available. Data collection for NTDs needs to be strengthened as better data are required to indirectly inform transmission in an area. Addressing specific data needs will improve our modelling recommendations, enabling more accurate tailoring of interventions and assessment of their progress. In this collection, we discuss the data needs for several NTDs, specifically gambiense human African trypanosomiasis, lymphatic filariasis, onchocerciasis, schistosomiasis, soil-transmitted helminths (STH), trachoma, and visceral leishmaniasis. Similarities in the data needs for these NTDs highlight the potential for integration across these diseases and where possible, a wider spectrum of diseases.