In recent years, studies related to the expression profiles of miRNAs in the dairy goat mammary gland were performed, but regulatory mechanisms in the physiological environment and the dynamic homeostasis of mammary gland development and lactation are not clear. In the present study, sequencing data analysis of early and late lactation uncovered a total of 1,487 unique miRNAs, including 45 novel miRNA candidates and 1,442 known and conserved miRNAs, of which 758 miRNAs were co-expressed and 378 differentially expressed with P < 0.05. Moreover, 76 non-redundant target genes were annotated in 347 GO consortiums, with 3,143 candidate target genes grouped into 33 pathways. Additionally, 18 predicted target genes of 214 miRNAs were directly annotated in mammary gland development and used to construct regulatory networks based on GO annotation and the KEGG pathway. The expression levels of seven known miRNAs and three novel miRNAs were examined using quantitative real-time PCR. The results showed that miRNAs might play important roles in early and late lactation during dairy goat mammary gland development, which will be helpful to obtain a better understanding of the genetic control of mammary gland lactation and development.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5607250 | PMC |
http://dx.doi.org/10.1038/s41598-017-12297-4 | DOI Listing |
JAMA Netw Open
January 2025
Department of Health Policy and Management, Yale School of Public Health, New Haven, Connecticut.
Importance: Disparities in cognition, including dementia occurrence, persist between non-Hispanic Black (hereinafter, Black) and non-Hispanic White (hereinafter, White) older adults, and are possibly influenced by early educational differences stemming from structural racism. However, the association between school racial segregation and later-life cognition remains underexplored.
Objective: To investigate the association between childhood contextual exposure to school racial segregation and cognitive outcomes in later life.
Calcif Tissue Int
January 2025
Department of Medicine, Surgery and Neurosciences, University of Siena, Policlinico Santa Maria Alle Scotte, Siena, Italy.
Aromatase deficiency (ORPHA:91; OMIM: 613,546) is a rare, autosomal recessive disorder due to loss of function mutations in the CYP19A1 gene, described in both genders with an estimated incidence below 1/1000000. While in female the clinical manifestations generally occur at birth or in early infancy, and mainly involve sexual characteristics, in men clinical signs of aromatase deficiency mostly occur in puberty and especially in late puberty, so that diagnosis is generally established after the second decade due to tall stature, unfused epiphyses and reduced bone mass. Here we review the available information concerning the skeletal and extraskeletal phenotype and the clinical management of bone health in patients with aromatase CYP19A1 gene mutations.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Laboratory for Neuropathology, KU Leuven, Leuven, Belgium.
Background: In 43-63% of symptomatic Alzheimer's disease (AD) patients, there is an observed accumulation of misfolded alpha-synuclein (αSyn). Two primary αSyn subtypes have been identified based on the underlying spreading pattern of this pathology: caudo-rostral and amygdala-predominant. Interactions between pathological TDP-43, Tau, and αSyn can aggravate their spread and aggregation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Michigan, Ann Arbor, MI, USA.
Background: Inhibitory interneurons normally regulate neural networks underlying memory and cognition, but are disrupted in Alzheimer's disease. Proper interneuron activity reduces amyloid-beta, whereas hyperexcitability elevates amyloid levels. Still, the underlying pathologic processes mediating interneuron dysfunction remain unknown.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
NYU Grossman School of Medicine, New York, NY, USA.
Background: How tauopathy disrupts direct entorhinal cortex (EC) inputs to CA1 and their plasticity is understudied, despite its critical role in memory. Moreover, dysfunction of lateral EC (LEC) input is less clear, despite its relevance to early Alzheimer's disease pathogenesis. Here we examined how tau impacts long-term potentiation (LTP) of LEC→CA1 input in a transgenic model of tauopathy.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!