Zika virus is a mosquito-borne flavivirus that represents a public health emergency at the ongoing epidemic. Previously, this rare virus was limited to sporadic cases in Africa and Asia until its emergence in Brazil, South America in 2015, where it rapidly spread throughout the world. Recently, a high number of cases were reported in Singapore and other Southeast Asia countries. A combination of factors explains the current Zika virus outbreak although it is highly likely that the changes in the climate and high frequency of travelling contribute to the spread of Aedes vector carrying the Zika virus mainly to the tropical climate countries such as the Southeast Asia. The Zika virus is known to cause mild clinical symptoms similar to those of dengue and chikungunya and transmitted by different species of Aedes mosquitoes. However, neurological complications such as Guillain-Barré syndrome in adults, and congenital anomalies, including microcephaly in babies born to infected mothers, raised a serious concern. Currently, there is no specific antiviral treatment or vaccine available for Zika virus infection. Therefore, international public health response is primarily focused on preventing infection, particularly in pregnant women, and on providing up-to-date recommendations to reduce the risk of non-vector transmission of Zika virus.
this study aimed to examine the impact of BpA exposure on pregnancy and foetuses on cardiac tissues and the expression of cardiac microRnAs (miRnAs) related to heart development and diseases. Pregnancy is known to be the "critical windows" in determining the offspring physical and cells development in their life after birth. The increment of the risk of cardiovascular disease (CVD) in a later stage of life has been reported by few studies demonstrated from prenatal exposure of BpA. BpA has been shown to alter miRNAs expression profiles for organ development, regeneration and metabolic functions. These alterations have been associated with the risk of CVDs. However, the associations between pregnancy outcomes and miRnAs expression in cardiac of mother-and foetuses-exposed to BPA are still not entirely explored. In BPA-exposed pregnant rat groups, a significant weight gained was observed in comparison to control (p < 0.05). Interestingly, significant changes in systolic and diastolic blood pressure between the first and third trimester of BPA-exposed pregnant rats were also observed (p < 0.05). In BPA-exposed pregnant rats, miR-499-5p was significantly altered in the heart (p < 0.01). Meanwhile, altered miR-17-5p,-208-3p, and-210-3p expressions were observed in all heart of the foetuses from BpA-exposed pregnant rats (p < 0.05). In H&E staining, BPA-exposed foetal hearts showed a sign of fibrosis while BPA-exposed pregnant rats showed muscle remnant. Masson trichrome staining further confirmed the presence of fibrosis observed in BPA-exposed foetal heart and reduced expression of cardiac troponin I (cTnI) was also observed in BPA-exposed foetal heart. In summary, altered cardiac miRnAs with histological changes were observed in both mother-and foetus-exposed BPA These findings put forward the importance of future work to further understand how prenatal BPA exposure affect foetuses in their later stage of life. Altered foetal development "programming" may predispose certain individuals to the risk of chronic disease development later in their life. This was suggested by Barker and co-worker who presented the first finding on the increased risk of cardiovascular disease (CVD) in children of malnourished mothers 1. Barker then further extended his theory and linked the CVD development and insulin resistance to the environment of the placenta. His findings have attracted another study to report on the insufficiency of uteroplacental of malnutrition mothers increases the risk of the offspring to type 2 diabetes 2. Another study demonstrated that miR-208, a
Cancer recurrence is often associated with the acquisition of radioresistance by cancer tissues due to failure in radiotherapy. The underlying mechanism leading to the development of acquired radioresistance in the EMT6 mouse mammary carcinoma cell line and the potential pathway involved was investigated by comparing differential gene expressions between parental and acquired radioresistance cells. EMT6 cell line was exposed to 2 Gy/per cycle of gamma-ray and the survival fraction between EMT6-treated and parental cells was compared. EMT6RR_MJI (acquired radioresistance) cells was developed after 8 cycles of fractionated irradiation. The development of EMT6RR_MJI cells was confirmed with further irradiation at different doses of gamma-ray, and both the survival fraction and migration rates were measured. Higher survival fraction and migration rates were obtained in EMT6RR_MJI cells after exposure to 4 Gy and 8 Gy gamma-ray irradiations compared to their parental cells. Gene expression between EMT6RR_MJI and parental cells was compared, and 16 genes identified to possess more than tenfold changes were selected and validated using RT-PCR. Out of these genes, 5 were significantly up-regulated i.e., IL-6, PDL-1, AXL, GAS6 and APCDD1. Based on pathway analysis software, the development of acquired radioresistance in EMT6RR_MJI was hypothesized through JAK/STAT/PI3K pathway. Presently, CTLA-4 and PD-1 were determined to be associated with JAK/STAT/PI3K pathway, where both their expressions were significantly increased in EMT6RR_MJI compared to parental cells in the 1st, 4th and 8th cycle of radiation. As a conclusion, the current findings provided a mechanistic platform for the development of acquired radioresistance in EMT6RR_MJI through overexpression of CTLA-4 and PD-1, and novel knowledge on therapeutic targets for recurrent radioresistant cancers.
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