Structural characteristics of camel-bone gelatin by demineralization and extraction

Camel bone was demineralized through HCl acidulation process at different concentrations (0.0%, 1.5%, 3.0%, and 6.0%) over 1–5 days. The level of demineralization was acid concentration and soaking time dependent. Highest demineralization (62.0%) was recorded in bone sample treated with 6.0% dilute acid for 5 days. Energy dispersive X-ray spectroscopy (EDX) elemental analysis revealed reduction in Ca and increase in N and H, while O remains unaffected. Particulate characteristics by scanning electron microscope showed an increased surface roughness of bone after demineralization. Fourier transform infrared (FT-IR) analysis of ossein depicted the presence of functional group similar to that of bone protein (collagen). Statistical optimization by central composite design (CCD) revealed a significant quadratic model for optimum values of extraction temperature, pH, and extraction time. The highest gelatin yield from camel bone was 23.66% at optimum extraction condition (71.87°C, pH 5.26, and 2.58 h) and the bloom was 205.74 g. Camel bone is suitable for production of gelatin with good potentials in food and nonfood applications.     

Synthetic-based blended electrospun scaffolds in tissue engineering applications

Journal of Materials Science - Electrospinning, as one of the most common methodologies in nanofibers production, involves applying high voltages to a polymeric solution that is entrapped in a...     

Optimal Operational Scheduling of Pumps to Improve the Performance of Water Distribution Networks

Widely used software packages might still be deficient when it comes to optimal pump scheduling as they allow concurrent Variable Speed Pumps (VSPs) at low speeds and low efficiency. In this study, a new method is developed to optimize the Number of Active Pumps (NAPs) and their variable setting, not only to address the mentioned issue, but also to improve pressure reliability, leakage, and electrical power consumption in Water Distribution Networks (WDNs). For this purpose, an Active Pumps Index (API) is proposed to find the optimal NAPs at each time step and a single-objective Network Pressure Reliability Index (NPRI) is used to optimize VSP setting. Particle Swarm Optimization (PSO) algorithm is developed in MATLAB and linked with EPANET as the hydraulic simulator. The proposed method is applied to a sample and a real WDN. The results in both cases show a significant reduction in NAPs, as well as energy costs, while tangibly improving leakage and pressure reliability, especially in big pump stations with several pumps.

     

Vanillic Acid,a Bioactive Phenolic Compound,Counteracts LPS-Induced Neurotoxicity by Regulating c-Jun N-Terminal Kinase in Mouse Brain

The receptor for advanced glycation end products (RAGE), a pattern recognition receptor signaling event, has been associated with several human illnesses, including neurodegenerative diseases, particularly in Alzheimer’s disease (AD). Vanillic acid (V.A), a flavoring agent, is a benzoic acid derivative having a broad range of biological activities, including antioxidant, anti-inflammatory, and neuroprotective effects. However, the underlying molecular mechanisms of V.A in exerting neuroprotection are not well investigated. The present study aims to explore the neuroprotective effects of V.A against lipopolysaccharides (LPS)-induced neuroinflammation, amyloidogenesis, synaptic/memory dysfunction, and neurodegeneration in mice brain. Behavioral tests and biochemical and immunofluorescence assays were applied. Our results indicated increased expression of RAGE and its downstream phospho-c-Jun n-terminal kinase (p-JNK) in the LPS-alone treated group, which was significantly reduced in the V.A + LPS co-treated group. We also found that systemic administration of LPS-injection induced glial cells (microglia and astrocytes) activation and significantly increased expression level of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-KB) and secretion of proinflammatory cytokines including tumor necrosis factor alpha (TNF-α), interleukin-1 β (IL1-β), and cyclooxygenase (COX-2). However, V.A + LPS co-treatment significantly inhibited the LPS-induced activation of glial cells and neuroinflammatory mediators. Moreover, we also noted that V.A treatment significantly attenuated LPS-induced increases in the expression of AD markers, such as β-site amyloid precursor protein (APP)–cleaving enzyme 1 (BACE1) and amyloid-β (Aβ). Furthermore, V.A treatment significantly reversed LPS-induced synaptic loss via enhancing the expression level of pre- and post-synaptic markers (PSD-95 and SYP), and improved memory performance in LPS-alone treated group. Taken together; we suggest that neuroprotective effects of V.A against LPS-induced neurotoxicity might be via inhibition of LPS/RAGE mediated JNK signaling pathway; and encourage future studies that V.A would be a potential neuroprotective and neurotherapeutic candidate in various neurological disorders.