Explore chapters and articles related to this topic
Machine Learning Applications to Recognize Autism and Alzheimer's Disease
Published in Rashmi Priyadarshini, R M Mehra, Amit Sehgal, Prabhu Jyot Singh, Artificial Intelligence, 2023
Touko Tcheutou Stephane Borel, Rashmi Priyadarshini
The genetic origins of this disorder in neuron development have been shown to be difficult via whole exome sequencing (WES) and cytogenetics. Likewise, studies of twins and families suggest that ASD’s heritability is more than 80%. The principal ASD- associated syndromes are fragile X syndrome (FXS) and tuberous sclerosis (TS), both of which have similar pathophysiological processes to those of ASD, including deviant mRNA translation and elevated synthesis of protein. FXS is a genetic disease caused by aninconsistent increase of the FMR1 gene’s multiple CGG repeat and is characterized by abnormal facial features as well as variously severe cognitive deficiencies. TS presents asepilepsy, learning challenges, and social interactive issues. More than 40% of patients with TS also suffer from ASD, hence the elevated incidence of epileptic seizures in both ASD and TS sufferers.
Effect of intra-session exercise sequence of an 8-week concurrent training program on the components of physical fitness in recreationally trained young adults
Published in Journal of Sports Sciences, 2022
Santiago A. Ruiz-Alias, Felipe García-Pinillos, Diego Jaén-Carrillo, Alejandro Pérez-Castilla
This additive effect that RT and ET combination has on health requires the consideration of how the musculoskeletal system adapts to each stimulus. The combination of both exercise modes within the same training session or day, defined as concurrent training (CT; Hickson, 1980), has been associated with the interference phenomenon. Each exercise mode activates and/or represses specific genes and cellular signalling pathways (Hawley, 2009). While RT induces myofibrillar protein synthesis (actin and myosin) by the mechanistic target of rapamycin (mTOR), ET increases mitochondrial protein synthesis by the increased adenosine monophosphate (AMP) concentration in muscle during exercise (Hawley, 2009). The resulted activation of AMP protein kinase (AMPK) may inhibit mTOR signalling via tuberous sclerosis complex and suppress myofibrillar protein synthesis (Hawley, 2009).
Transcriptome alterations in zebrafish gill after exposure to different sizes of microplastics
Published in Journal of Environmental Science and Health, Part A, 2022
Ying-Hao Xue, Tao Jia, Ning Yang, Zhan-Xiang Sun, Zhi-Yu Xu, Xin-Li Wen, Liang-Shan Feng
As one of the most frequently mutated tumor suppressor gene, PTEN antagonizes the activity of PI3K (phosphoinositide-3-kinase). The balance between them finally affect proliferation, cell migration, apoptosis, cell survival, angiogenesis, and metabolism.[52] In zebrafish, lack of PTEN function arrested proliferation of embryo cells and enhanced the apoptosis.[53] In the present study, both pten and pi3k were upregulated in response to MPs exposure. However, their downstream gene TSC1/2 (tuberous sclerosis complex 1/2) was upregulated, which has been reported to protect stress-induced apoptosis in HeLa cells.[54] Therefore, the upregulation of pten and TSC1/2 might inhibit cell apoptosis in response to the physical damage caused by MPs.