Identification and characterization of a novel synthetic cannabinoid CP 55,940 binder in rat brain cytosol

We have detected the presence of a specific [³H] CP 55,940 binder in the cytosol of rat cerebral cortex. Competition studies showed that only cold CP 55,940 and to a lesser extent D⁹THC was able to compete with [³H] CP 55,940; little competition was observed with either D⁸;THC or anandamide. Scatchard analysis of the data indicate the presence of two distinct binding components having affinity constants (Kd) of 0.97 ± 0.03 nM, 5.83 ± 0.08 nM, and B_max of 3.31 ± 0.06 pmol/mg protein, 22.2 ± 1.2 pmol/mg protein respectively. The cytosolic CP 55,940 binder was heat stable up to 30øC. Besides the brain cytosol, lesser amounts of binding were also detected in the spleen, and testis. Liver, kidney and muscle cytosol preparations were found to be devoid of this binder. Unlike the previously characterized brain membrane cannabinoid receptor, this binder was found to be salt, sulfhydryl blocking reagents and nucleotide resistant. Interestingly, dithiothreitol (DTT), a protein-disulfide group reducing agent, inhibited the binding of [³H] CP-55,940 to the receptor and approximately 80% binding inhibition was obtained at a 5 mM concentration. Western blot analysis using anti-receptor antibody reveal the presence of a 95-110, 50 and 38 kDa band in the brain, spleen and testis cytosolic preparations. In conclusion, we have identified the presence of a novel CP 55,940 binder in rat cerebral cortex cytosol possessing biochemical properties distinct from those previously observed using rat cerebral cortex membrane cannabinoid receptor.     

Bioextraction Dynamics of Potassium from Feldspar by Heterotrophic Microorganisms Isolated from Ceramic and Rhizospheric Soil

Bioleaching of potassium from feldspar was optimized for five fungal and two bacterial isolates for carbon, nitrogen, agitation, pH and incubation time. Fungal isolates SDS_R and SDS₃ and bacterial isolate SDS₁ released 34, 42 and 28 ppm K in sucrose-amended medium, respectively. Isolate SDS₃ took 10 days for the highest K solubilization, whereas SDS_R required 15 days under 150 rpm shaking condition. The pH of medium was found to decrease from 7.0 to 2.05 after the growth of the organisms. High-performance liquid chromatography analysis of the filtrate showed the presence of citric, tartaric and maleic acid, which could be responsible for the solubilization of potassium.     

Designing of Nucleocapsid Protein Based Novel Multi-epitope Vaccine Against SARS-COV-2 Using Immunoinformatics Approach

International Journal of Peptide Research and Therapeutics - The COVID-19 disease is caused by SARS-CoV-2 and spreading rapidly worldwide with extremely high infection rate. Since effective and...     

Differential Inhibition by Hyperammonemia of the Electron Transport Chain Enzymes in Synaptosomes and Non-Synaptic Mitochondria in Ornithine Transcarbamylase-Deficient spf-Mice: Restoration by Acetyl-L-Carnitine

Sparse-fur (spf) mouse is the ideal animal model to study the neuropathology of congenital ornithine transcarbamylase (OTC) deficiency. Our current hypothesis implies that an ammonia-induced depletion of energy metabolism in the spf mouse, could be due to a reduction in the activities of the enzymes of the electron transport chain and a treatment with acetyl-L-carnitine could normalize this abnormality. We also hypothesized that there might be a differential degree of inhibition in synaptosomal and non-synaptic mitochondria, for the enzymes of the electron transport chain, caused by congenital hyperammonemia. We have therefore measured the activities of NADH-cytochrome C oxidoreductase, succinate cytochrome C oxidoreductase and cytochrome C oxidase in synaptosomes and non-synaptic mitochondria, isolated from spf mice and CD-1 controls with and without acetyl-L-carnitine treatment. Our results indicate a significant reduction (19–34%) in the activities of these complexes in synaptosomes in untreated spf mice, whereas in non-synaptic mitochondria, there was a tendency for the activities to decrease. Acetyl-L-carnitine treatment enhanced these activities (15–64%) for all the three enzyme complexes and its effect was more prominent on succinate cytochrome C oxidoreductase activity (64%). These studies point out that: (a) ammonia-induced disturbances in the energy metabolism could be more pronounced in neuronal mitochondria, and (b) the effect of acetyl-L-carnitine on the restoration of cerebral ATP in hyperammonemia could be through an enhancement of the activities of various electron transport chain enzymes.     

Prostate cancer is known by the companionship with ATM and miRNA it keeps: craftsmen of translation have dual behaviour with tailors of life thread

Research on prostate cancer progression has focused extensively on the concept of miRNA, which can operate either as promoters or as suppressors of carcinogenesis. Moreover, recent genetic studies and emerging functional work show that strikingly similar and overlapping pathways are involved in prostate carcinogenesis. Unswervingly, these elements constitute a recently explored ‘network of networks’ that dynamically reorganizes during DNA damage and is responsible for positively or negatively regulating genome organization and integrity. We consider these facets of convergence and discuss how insights from diametrically opposed interactions of ataxia–telangiectasia mutated and mitrons can inform us about, and possibly help us to get a step closer to personalized medicine. Copyright © 2012 John Wiley & Sons, Ltd.     

Liver aspartate aminotransferase activity as a power function of body weight

Total liver enzyme activity (E) for aspartate aminotransferase (ASAT; EC 2.6.1.1) per gram body weight (W) decreases in six species as body weight increases from mice to cattle according to the equation E/W 0.85 = c, where c is a constant. The 0.85 power of body weight thereby provides a reference standard for the direct arithmetic comparison of liver ASAT activities in six species with different body weights. The use of W 0.85 should provide a tool in clinical studies in which data from experimental animals must be related to humans, e.g., in establishing the relationship between drug dosage (or toxicity) and body weight.