Use of Two Industrial Wastes as Soil Amendments: Effect on Dissolved Reactive Phosphorus in Runoff

To control the dissolved reactive phosphorus (DRP) concentration in a soil solution, a number of soil amendments were tested. In the current study, Blast Furnace Slag (BFS) and Water Treatment Residues (WTR) were tested on bare soil under two rainfall intensities and two soil roughness levels. The soil was fertilized with P (KH₂PO₄) at a rate of 400 kg ha^?1 while BFS and WTR were applied at a rate of 5 g per 100 g of soil. Two soil roughness levels were exposed to artificial rainfall intensities of 30 and 65 mm h^?1. Three rainfall events were performed on each treatment. The runoff water generated over an area of 0.5 m² with a slope of 8% was collected at different time intervals and analyzed for DRP, Al, Fe, and K concentrations. The results showed that, regardless of rainfall intensity and soil roughness, the concentration of DRP in the runoff water increased with increasing runoff time from the unamended plots. However, in the BFS- and WTR-amended soils, the DRP concentration decreased with runoff time. Dissolved reactive P and DRP loads were the lowest from the WTR-amended plots, followed by the control and the BFS treatment plots. Water treatment residues reduced the mean DRP concentration by 27.3% and the DRP load by 32% compared to unamended plots. The two rainfall intensities significantly affected the DRP concentration and load. Under the low rainfall intensity, the DRP concentration and load were higher compared to the high rainfall intensity. The overall DRP concentration was not affected by changes in soil roughness. However, the DRP loads were higher from the plots with low soil roughness levels, especially during the first and second runs. Both the BFS and WTR were also effective in reducing the DRP concentrations in the drain water collected during the runoff events. The concentrations of Al, Fe, and K in the runoff water were not affected by the soil amendments. However, the electrical conductivity and pH readings were higher from the BFS-amended plots.     

A stable biologically motivated learning mechanism for visual feature extraction to handle facial categorization

The brain mechanism of extracting visual features for recognizing various objects has consistently been a controversial issue in computational models of object recognition. To extract visual features, we introduce a new, biologically motivated model for facial categorization, which is an extension of the Hubel and Wiesel simple-to-complex cell hierarchy. To address the synaptic stability versus plasticity dilemma, we apply the Adaptive Resonance Theory (ART) for extracting informative intermediate level visual features during the learning process, which also makes this model stable against the destruction of previously learned information while learning new information. Such a mechanism has been suggested to be embedded within known laminar microcircuits of the cerebral cortex. To reveal the strength of the proposed visual feature learning mechanism, we show that when we use this mechanism in the training process of a well-known biologically motivated object recognition model (the HMAX model), it performs better than the HMAX model in face/non-face classification tasks. Furthermore, we demonstrate that our proposed mechanism is capable of following similar trends in performance as humans in a psychophysical experiment using a face versus non-face rapid categorization task.     

Targeting bone remodeling by isoflavone and 3,3'-diindolylmethane in the context of prostate cancer bone metastasis

Prostate cancer (PCa) bone metastases have long been believed to be osteoblastic because of bone remodeling leading to the formation of new bone. However, recent studies have shown increased osteolytic activity in the beginning stages of PCa bone metastases, suggesting that targeting both osteolytic and osteoblastic mediators would likely inhibit bone remodeling and PCa bone metastasis. In this study, we found that PCa cells could stimulate differentiation of osteoclasts and osteoblasts through the up-regulation of RANKL, RUNX2 and osteopontin, promoting bone remodeling. Interestingly, we found that formulated isoflavone and 3,3'-diindolylmethane (BR-DIM) were able to inhibit the differentiation of osteoclasts and osteoblasts through the inhibition of cell signal transduction in RANKL, osteoblastic, and PCa cell signaling. Moreover, we found that isoflavone and BR-DIM down-regulated the expression of miR-92a, which is known to be associated with RANKL signaling, EMT and cancer progression. By pathway and network analysis, we also observed the regulatory effects of isoflavone and BR-DIM on multiple signaling pathways such as AR/PSA, NKX3-1/Akt/p27, MITF, etc. Therefore, isoflavone and BR-DIM with their multi-targeted effects could be useful for the prevention of PCa progression, especially by attenuating bone metastasis mechanisms.     

Purification and characterization of a new glucoamylopullulanase from thermotolerant alkaliphilic Bacillus subtilis DR8806 of a hot mineral spring

We have introduced a novel glucoamylopullulanase from thermostable alkaliphilic Bacillus subtilis DR8806 from a hot mineral spring in Iran. The enzyme was purified by ion-exchange chromatography following to ammonium sulphate precipitation. The molecular weight of the purified enzyme was estimated to be 65.5 kDa using denaturing acrylamide gel electrophoresis. The enzyme showed high activity over a wide pH range, from pH 5.0 to pH 11.0 with the optimum pH 9.5. Our results also indicated an optimum temperature of the enzyme activity at 70 °C. These features justify the characteristics of the alkaliphilic and thermostable bacterial proteins and enzymes. The enzyme did not require calcium and showed extreme stability with regard to surfactants, including SDS and Triton X-100, and oxidizing agents such as H₂O_2. These features of the enzyme suggest a promising potential for application in laundry industry. Furthermore, the enzyme was active on pulullan by 68% relative to normal activity on starch. Such characteristics have not already been reported for this type of enzyme, hence we propose that this is a new alkalophilic and thermostable enzyme.     

Extended access to cocaine self-administration results in reduced glutamate function within the medial prefrontal cortex

Previous studies have shown that brief access to cocaine yields an increase in D2 receptor binding in the medial prefrontal cortex (mPFC), but that extended access to cocaine results in normalized binding of D2 receptors (i.e. the D2 binding returned to control levels). Extended-access conditions have also been shown to produce increased expression of the NR2 subunit of the N-Methyl-D-aspartate receptor in the mPFC. These results implicate disrupted glutamate and dopamine function within this area. Therefore, in the present study, we monitored glutamate and dopamine content within the mPFC during, or 24 hours after, cocaine self-administration in animals that experienced various amounts of exposure to the drug. Na?ve subjects showed decreased glutamate and increased dopamine levels within the mPFC during cocaine self-administration. Exposure to seven 1-hour daily cocaine self-administration sessions did not alter the response to self-administered cocaine, but resulted in decreased basal dopamine levels. While exposure to 17 1-hour sessions also resulted in reduced basal dopamine levels, these animals showed increased dopaminergic, but completely diminished glutamatergic, response to self-administered cocaine. Finally, exposure to 17 cocaine self-administration sessions, the last 10 of which being 6-hour sessions, resulted in diminished glutamatergic response to self-administered cocaine and reduced basal glutamate levels within the mPFC while normalizing (i.e. causing a return to control levels) both the dopaminergic response to self-administered cocaine as well as basal dopamine levels within this area. These data demonstrate directly that the transition to escalated cocaine use involves progressive changes in dopamine and glutamate function within the mPFC.     

Evaluation of persistence and relative toxicity of some pest control products to adults of two native trichogrammatid species in Kenya

The utilization of native trichogrammatids for biocontrol of Helicoverpa armigera (Hbn.) and their potential integration with pesticide use are currently receiving attention. In this study the interaction of adults of Trichogramma sp. nr. mwanzai and Trichogrammatoidea sp. nr. lutea with commonly used pesticide products was investigated. The toxicity of eight pest control products commonly used in vegetable crops in Kenya, were evaluated by exposing the adults of the two species to detached potted tomato leaves at different intervals after spraying. Two biologically derived products, Achook^? (neem-based) and Dipel^? (Bt ssp. kurstaki)—were found to be harmless and had no persistent toxicity on both the trichogrammatid species. Two organophosphate products tested, dimethoate (Rogor^?) and malathion (Malathion^?) were found to be ‘slightly harmful’ and ‘moderately persistent’ respectively. Three other synthetic insecticides, lambdacyhalothrin (Karate^?), bifenthrin (Brigade^?) and alpha-cypermentrin (Fastac^?) were found to be ‘moderately harmful’ and ‘persistent’ respectively. Polytrin^? (mixture of cypermethrin and profenofos) was also found to be persistent but only ‘slightly harmful’. On the basis of five concentrations tested (0.032, 0.016, 0.008, 0.004 and 0.002 of the recommended field rates) the LC₅₀ values for adult T. sp. nr. mwanzai were estimated as 285, 411, 435 and 1,916 (μg active ingredient (a.i) ml^?1) for dimethoate; malathion; lambdacyhalothrin as well as cypermethrin?+?profenofos respectively. The corresponding values for T. sp. nr. lutea were 247, 251, 278 and 697 respectively. Further, Karate^? appeared to be the least toxic among the four products, across all the respective concentrations. The study was an attempt to adopt the methodologies of the IOBC (International Organization for Biological Control) on non-target risk assessment for pest control products to cater for the local needs of integrating the use of the trichogrammatids along with other pest control products.     

TNF-alpha induced NFκB signaling and p65 (RelA) overexpression repress Cldn5 promoter in mouse brain endothelial cells

Inflammatory cytokine TNFα enhances permeability of brain capillaries constituting blood brain barrier (BBB). In the monoculture endothelial models of BBB TNFα alters tight junction (TJ) structure and protein content. Claudin-5 (Cldn5) is a key TJ protein whose expression in the brain endothelial cells is critical to the function of BBB. TNFα reduces Cldn5 promoter activity and mRNA expression in mouse brain derived endothelial cells but the regulatory elements and signaling mechanism involved are not defined. Here we report that TNFα acts through NFκB signaling and requires a conserved promoter region for the down-regulation of Cldn5 expression. Overexpression of the NFκB subunit p65 (RelA) alone repressed Cldn5 promoter activity in mouse brain endothelial cells. We observed partial loss of Cldn5 protein expression after prolonged TNFα treatment in primary endothelial culture isolated from C56BL/6 mice brain. Taken together, our results confirm and extend previous observations of TNFα induced down-regulation of Cldn5 expression in mouse brain endothelial cells.     

High Mobility Group Box 1 Contributes to the Pathogenesis of Experimental Pulmonary Hypertension via Activation of Toll-like Receptor 4

Survival rates for patients with pulmonary hypertension (PH) remain low, and our understanding of the mechanisms involved are incomplete. Here we show in a mouse model of chronic hypoxia (CH)-induced PH that the nuclear protein and damage-associate molecular pattern molecule (DAMP) high mobility group box 1 (HMGB1) contributes to PH via a Toll-like receptor 4 (TLR4)-dependent mechanism. We demonstrate extranuclear HMGB1 in pulmonary vascular lesions and increased serum HMGB1 in patients with idiopathic pulmonary arterial hypertension. The increase in circulating HMGB1 correlated with mean pulmonary artery pressure. In mice, we similarly detected the translocation and release of HMGB1 after exposure to CH. HMGB1-neutralizing antibody attenuated the development of CH-induced PH, as assessed by measurement of right ventricular systolic pressure, right ventricular hypertrophy, pulmonary vascular remodeling and endothelial activation and inflammation. Genetic deletion of the pattern recognition receptor TLR4, but not the receptor for advanced glycation end products, likewise attenuated CH-induced PH. Finally, daily treatment of mice with recombinant human HMGB1 exacerbated CH-induced PH in wild-type (WT) but not Tlr4^−/− mice. These data demonstrate that HMGB1-mediated activation of TLR4 promotes experimental PH and identify HMGB1 and/or TLR4 as potential therapeutic targets for the treatment of PH.