GENO PROTECTIVE AND ANTI-APOPTOTIC EFFECT OF GREEN TEA AGAINST PERINATAL LIPOPOLYSACCHARIDE-EXPOSURE INDUCED LIVER TOXICITY IN RAT NEWBORNS

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Correlation between vitamin D levels and apoptosis in geriatric patients infected with hepatitis C virus genotype 4

Sami A Gabr,1,2 Ahmad H Alghadir,1 Ahmed A Allam,3,4 Jamaan Ajarem,3 Ghada Al-Basher,3 Mostafa A Abdel-Maksoud,3 Ayman A Ghfar,5 Alaa Aboud6 1Rehabilitation Research Chair, College of Applied Medical Sciences, King Saud University, Riyadh, Kingdom of Saudi Arabia; 2Department of Anatomy, Faculty of Medicine, Mansoura University, Mansoura, Egypt; 3Zoology Department, College of Science, King Saud University, Riyadh, Saudi Arabia; 4Zoology Department, Faculty of Science, Beni-Suef University, Beni Suef, Egypt; 5Department of Chemistry, College of Science, King Saud University, Riyadh, Saudi Arabia; 6Internal Endemic Medicine Department, College of Medicine, Beni-Suef University, Beni Suef, Egypt Background: Vitamin D levels play a pivotal role in most biological processes and differ according to age. A deficiency of vitamin D in chronic hepatitis C (CHC) patients has been shown to be linked with the severity of liver fibrosis, but little is known about the mechanism of this association. Objective: In this study, we evaluate the potential interrelation between vitamin D levels, oxidative stress, and apoptosis, based on liver fibrosis in geriatric patients infected with hepatitis C virus (HCV) genotype 4. Subjects and methods: A total of 120 adult individuals aged 30–68 years were recruited in this study. Of these, 20 healthy subjects (15 men and five women) with a mean age of 48.3±6.1 years were selected as controls, and 100 patients with a mean age of 47.8±4.9 years with chronic HCV (CHC) who had undergone liver biopsy (80 men and 20 women) were included in this study. Based on liver radiographic (computed tomography, magnetic resonance imaging) and histological Metavir system analyses, the CHC patients were classified into three groups: asymptomatic CHC carriers (n=30), fibrosis (n=25), and cirrhosis (n=45). HCV RNA, HCV genotypes, inflammatory cytokines AFP and TNFα, 25-hydroxyvitamin D (25[OH]D) levels, apoptotic markers single-stranded DNA (ssDNA) and soluble Fas (sFas), and oxidative stress markers nitric oxide (NO) and total antioxidant capacity (TAC) were estimated by using molecular, immunoassay, and colorimetric techniques. Results: Approximately 30% of the study population (n=30) were diagnosed as asymptomatic CHC carriers, and 70% of the study population (n=70) had severe fibrosis; these were classified into fibrosis and cirrhosis. There was a significant reduction in 25(OH)D levels and TAC activity, along with an increase in levels of NO, AFP, TNFα, ssDNA, and sFas in fibrosis and cirrhosis subjects compared with those of asymptomatic CHC carriers and health controls. The deficiency in 25(OH)D levels correlated positively with sFas, ssDNA, AFP, TNFα, NO, and TAC, and negatively with age, sex, liver function, body mass index, homeostatic model assessment – insulin resistance, HCV RNA, and viral load. Significant intercorrelation was reported between serum 25(OH)D concentrations and apoptotic and oxidative markers, which suggested progression of liver pathogenesis and fibrogenesis via oxidative and apoptotic mechanisms. Conclusion: The data showed that vitamin D status was significantly correlated with pathogenesis and fibrogenesis of the liver in geriatric patients infected with HCV genotype 4. The deficiency in 25(OH)D levels was shown to have a pivotal role in the pathogenesis of liver via apoptotic, oxidative stress, and inflammatory mechanistic pathways. The data point to adequate vitamin D levels being recommended for a good response to treatment strategies, especially in older CHC patients. Keywords: 25(OH)D, HCV, apoptosis, Fas antigen, liver fibrosis, oxidative stress, geriatric

One Step Synthesis of Oxygen Defective Bi@Ba2TiO4/BaBi4Ti4O15 Microsheet with Efficient Photocatalytic Activity for NO Removal

Photocatalysis is an effective technology for NO removal even at low concentrations in the ambient atmosphere. However, the low efficiency of this advanced process and the tendency of producing toxic byproducts hinder the practical application of photocatalysis. To overcome these problems, the Bi@Ba2TiO4/BaBi4Ti4O15 photocatalytic composites were successfully prepared by a one-step hydrothermal method. The as-synthesized photocatalysts exhibited an efficient photocatalytic performance and generated low amounts of toxic byproducts. X-ray diffraction studies show that Bi3+ is successfully reduced on the surface of Ba2TiO4/BaBi4Ti4O15 (BT/BBT). After L-Ascorbic acid (AA) modification, the photocatalytic NO removal efficiency of Bi@Ba2TiO4/BaBi4Ti4O15 is increased from 25.55% to 67.88%, while the production of the toxic byproduct NO2 is reduced by 92.02%, where the initial concentration of NO is diluted to ca. 800 ppb by the gas stream and the flow rate is controlled at 301.98 mL·min−1 in a 150 mL cylindrical reactor. Furthermore, ambient humidity has little effect on the photocatalytic performance of theBi@Ba2TiO4/BaBi4Ti4O15, and the photocatalyst exhibits excellent reusability after repeated cleaning with deionized water. The improved photocatalytic effect is attributed to the addition of AA in BT/BBT being able to reduce Bi3+ ions to form Bi nanoparticles giving surface plasmon effect (SPR) and generate oxygen vacancies (OVs) at the same time, thereby improving the separation efficiency of photogenerated carriers, enhancing the light absorption, and increasing the specific surface areas. The present work could provide new insights into the design of high-performance photocatalysts and their potential applications in air purification, especially for NO removal

Impaired auditory discrimination learning following perinatal nicotine exposure or β2 nicotinic acetylcholine receptor subunit deletion

Maternal smoking during pregnancy can impair performance of the exposed offspring in tasks that require auditory stimulus processing and perception; however, the tobacco component(s) responsible for these effects and the underlying neurobiological mechanisms remain uncertain. In this study, we show that administration of nicotine during mouse perinatal development can impair performance in an auditory discrimination paradigm when the exposed animals are mature. This suggests that nicotine disrupts auditory pathways via nicotinic acetylcholine receptors (nAChRs) that are expressed at an early stage of development. We have also determined that mice which lack nAChRs containing the β2 subunit (β2* nAChRs) exhibit similarly compromised performance in this task, suggesting that β2* nAChRs are necessary for normal auditory discrimination or that β2* nAChRs play a critical role in development of the circuitry required for task performance. In contrast, no effect of perinatal nicotine exposure or β2 subunit knockout was found on the acquisition and performance of a differential reinforcement of low rate task. This suggests that the auditory discrimination impairments are not a consequence of a general deficit in learning and memory, but may be the result of compromised auditory stimulus processing in the nicotine-exposed and knockout animals

Nicotine-induced plasticity during development: modulation of the cholinergic system and long-term consequences for circuits involved in attention and sensory processing.

Despite a great deal of progress, more than 10% of pregnant women in the USA smoke. Epidemiological studies have demonstrated correlations between developmental tobacco smoke exposure and sensory processing deficits, as well as a number of neuropsychiatric conditions, including attention deficit hyperactivity disorder. Significantly, data from animal models of developmental nicotine exposure have suggested that the nicotine in tobacco contributes significantly to the effects of developmental smoke exposure. Consequently, we hypothesize that nicotinic acetylcholine receptors (nAChRs) are important for setting and refining the strength of corticothalamic-thalamocortical loops during critical periods of development and that disruption of this process by developmental nicotine exposure can result in long-lasting dysregulation of sensory processing. The ability of nAChR activation to modulate synaptic plasticity is likely to underlie the effects of both endogenous cholinergic signaling and pharmacologically administered nicotine to alter cellular, physiological and behavioral processes during critical periods of development