Impact of Maternal Air Pollution exposure on children's lung health: An Indian perspective

© 2018 by the authors. Air pollution has become an emerging invisible killer in recent years and is a major cause of morbidity and mortality globally. More than 90% of the world's children breathe toxic air every day. India is among the top ten most highly polluted countries with an average PM 10 level of 134 μg/m 3 per year. It is reported that 99% of India's population encounters air pollution levels that exceed the World Health Organization Air Quality Guideline, advising a PM 2.5 permissible level of 10 μg/m 3 . Maternal exposure to air pollution has serious health outcomes in offspring because it can affect embryonic phases of development during the gestation period. A fetus is more prone to effects from air pollution during embryonic developmental phases due to resulting oxidative stress as antioxidant mechanisms are lacking at that stage. Any injury during this vulnerable period (embryonic phase) will have a long-term impact on offspring health, both early and later in life. Epidemiological studies have revealed that maternal exposure to air pollution increases the risk of development of airway disease in the offspring due to impaired lung development in utero. In this review, we discuss cellular mechanisms involved in maternal exposure to air pollution and how it can impact airway disease development in offspring. A better understanding of these mechanisms in the context of maternal exposure to air pollution can offer a new avenue to prevent the development of airway disease in offspring

Innate Immune Suppression Enables Frequent Transfection with RNA Encoding Reprogramming Proteins

BACKGROUND: Generating autologous pluripotent stem cells for therapeutic applications will require the development of efficient DNA-free reprogramming techniques. Transfecting cells with in vitro-transcribed, protein-encoding RNA is a straightforward method of directly expressing high levels of reprogramming proteins without genetic modification. However, long-RNA transfection triggers a potent innate immune response characterized by growth inhibition and the production of inflammatory cytokines. As a result, repeated transfection with protein-encoding RNA causes cell death. METHODOLOGY/PRINCIPAL FINDINGS: RNA viruses have evolved methods of disrupting innate immune signaling by destroying or inhibiting specific proteins to enable persistent infection. Starting from a list of known viral targets, we performed a combinatorial screen to identify siRNA cocktails that could desensitize cells to exogenous RNA. We show that combined knockdown of interferon-beta (Ifnb1), Eif2ak2, and Stat2 rescues cells from the innate immune response triggered by frequent long-RNA transfection. Using this technique, we were able to transfect primary human fibroblasts every 24 hours with RNA encoding the reprogramming proteins Oct4, Sox2, Klf4, and Utf1. We provide evidence that the encoded protein is active, and we show that expression can be maintained for many days, through multiple rounds of cell division. CONCLUSIONS/SIGNIFICANCE: Our results demonstrate that suppressing innate immunity enables frequent transfection with protein-encoding RNA. This technique represents a versatile tool for investigating expression dynamics and protein interactions by enabling precise control over levels and timing of protein expression. Our finding also opens the door for the development of reprogramming and directed-differentiation methods based on long-RNA transfection

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Not AvailableLuteinizing hormone, insulin like growth factor-1, and epidermal growth factor stimulate vascular endothelial growth factor production in cultured bubaline granulosa cells.Not Availabl

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Not AvailableSuccess in the outcomes of applied assisted reproductive techniques mainly relies on the quality of the semen. Oxidative stress created by Reactive Oxygen Species (ROS) and Lipid Peroxidation (LPO) generated during different steps of semen preservation reduces semen quality. Melatonin and canthaxanthin are potent antioxidants involved in many biological processes. They have excellent capacity to scavenge free radicals, combat against oxidative stress and improve endogenous antioxidant defenses. Melatonin is well established antioxidant in semen preservation to protect against oxidative stress-induced damage; however, little literature is available on use of canthaxanthin as semen extender additive. Melatonin and its metabolites act as direct or indirect scavenger of free radicals arrest LPO and reduce generation of ROS, hence oxidative stress, thereby shielding seminal quality to prolong sperm morphological and functional attributes. Similar to melatonin, canthaxanthin by virtue of its antioxidant potential has shown promising results in preserving the seminal quality as well as their efficiency to reduce and/or prevent sperm damages during storage. This brief review encapsulated new uncovering related to the beneficial antioxidant effects of melatonin and canthaxanthin on semen preservation along with future perspective in respect of different combination and/or concentration along with fertility trails.Not Availabl