23 research outputs found

    Meiosis initiation: a story of two sexes in all creatures great and small

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    Meiosis facilitates diversity across individuals and serves as a major driver of evolution. However, understanding how meiosis begins is complicated by fundamental differences that exist between sexes and species. Fundamental meiotic research is further hampered by a current lack of human meiotic cells lines. Consequently, much of what we know relies on data from model organisms. However, contextualising findings from yeast, worms, flies and mice can be challenging, due to marked differences in both nomenclature and the relative timing of meiosis. In this review, we set out to combine current knowledge of signalling and transcriptional pathways that control meiosis initiation across the sexes in a variety of organisms. Furthermore, we highlight the emerging links between meiosis initiation and oncogenesis, which might explain the frequent re-expression of normally silent meiotic genes in a variety of human cancers

    A Novel Respiratory Rate Estimation Algorithm from Photoplethysmogram Using Deep Learning Model

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    Respiratory rate (RR) is a critical vital sign that can provide valuable insights into various medical conditions, including pneumonia. Unfortunately, manual RR counting is often unreliable and discontinuous. Current RR estimation algorithms either lack the necessary accuracy or demand extensive window sizes. In response to these challenges, this study introduces a novel method for continuously estimating RR from photoplethysmogram (PPG) with a reduced window size and lower processing requirements. To evaluate and compare classical and deep learning algorithms, this study leverages the BIDMC and CapnoBase datasets, employing the Respiratory Rate Estimation (RRest) toolbox. The optimal classical techniques combination on the BIDMC datasets achieves a mean absolute error (MAE) of 1.9 breaths/min. Additionally, the developed neural network model utilises convolutional and long short-term memory layers to estimate RR effectively. The best-performing model, with a 50% train–test split and a window size of 7 s, achieves an MAE of 2 breaths/min. Furthermore, compared to other deep learning algorithms with window sizes of 16, 32, and 64 s, this study’s model demonstrates superior performance with a smaller window size. The study suggests that further research into more precise signal processing techniques may enhance RR estimation from PPG signals

    Dependency of NELF-E-SLUG-KAT2B epigenetic axis in breast cancer carcinogenesis.

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    Cancer cells undergo transcriptional reprogramming to drive tumor progression and metastasis. Using cancer cell lines and patient-derived tumor organoids, we demonstrate that loss of the negative elongation factor (NELF) complex inhibits breast cancer development through downregulating epithelial-mesenchymal transition (EMT) and stemness-associated genes. Quantitative multiplexed Rapid Immunoprecipitation Mass spectrometry of Endogenous proteins (qPLEX-RIME) further reveals a significant rewiring of NELF-E-associated chromatin partners as a function of EMT and a co-option of NELF-E with the key EMT transcription factor SLUG. Accordingly, loss of NELF-E leads to impaired SLUG binding on chromatin. Through integrative transcriptomic and genomic analyses, we identify the histone acetyltransferase, KAT2B, as a key functional target of NELF-E-SLUG. Genetic and pharmacological inactivation of KAT2B ameliorate the expression of EMT markers, phenocopying NELF ablation. Elevated expression of NELF-E and KAT2B is associated with poorer prognosis in breast cancer patients, highlighting the clinical relevance of our findings. Taken together, we uncover a crucial role of the NELF-E-SLUG-KAT2B epigenetic axis in breast cancer carcinogenesis

    Erk1/2 Activity Promotes Chromatin Features and RNAPII Phosphorylation at Developmental Promoters in Mouse ESCs

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    Erk1/2 activation contributes to mouse ES cell pluripotency. We found a direct role of Erk1/2 in modulating chromatin features required for regulated developmental gene expression. Erk2 binds to specific DNA sequence motifs typically accessed by Jarid2 and PRC2. Negating Erk1/2 activation leads to increased nucleosome occupancy and decreased occupancy of PRC2 and poised RNAPII at Erk2-PRC2-targeted developmental genes. Surprisingly, Erk2-PRC2-targeted genes are specifically devoid of TFIIH, known to phosphorylate RNA polymerase II (RNAPII) at serine-5, giving rise to its initiated form. Erk2 interacts with and phosphorylates RNAPII at its serine 5 residue, which is consistent with the presence of poised RNAPII as a function of Erk1/2 activation. These findings underscore a key role for Erk1/2 activation in promoting the primed status of developmental genes in mouse ES cells and suggest that the transcription complex at developmental genes is different than the complexes formed at other genes, offering alternative pathways of regulation

    Cancer and meiotic gene expression: Two sides of the same coin?

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    Meiosis increases genetic diversity in offspring by generating genetically unique haploid gametes with reshuffled chromosomes. This process requires a specialized set of meiotic proteins, which facilitate chromosome recombination and segregation. However, re-expression of meiotic proteins in mitosis can have catastrophic oncogenic consequences and aberrant expression of meiotic proteins is a common occurrence in human tumors. Mechanistically, re-activation of meiotic genes in cancer promotes oncogenesis likely because cancers—conversely to healthy mitosis—are fueled by genetic instability which promotes tumor evolution, and evasion of immune response and treatment pressure. In this review, we explore similarities between meiotic and cancer cells with a particular focus on the oncogenic activation of meiotic genes in cancer. We emphasize the role of histones and their modifications, DNA methylation, genome organization, R-loops and the availability of distal enhancers

    Data on cell spread area and directional contraction in human umbilical vein endothelial cells on fibronectin and on collagen type I-coated micro-posts

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    AbstractFibronectin and collagen type I are abundant extracellular matrix proteins that modulate cell mechanics and they regulate angiogenic sprouting. In this data article, fibronectin- or collagen type I-coated micro-posts were used to examine the traction force, cell spread area and directional contraction of human umbilical vein endothelial cells (HUVECs)

    A method for producing high lipophilic antioxidants noodle products

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    The present invention provides method on preparing noodle product regardless in any form which contain stable delivery of lipophilic antioxidants from the source of red palm olein. A solid state delivery system which is invented was introducedinto the noodle preparation steps. Noodles are prepared by mixing flour, water, red palm olein solid state delivery system and others ingredients into a dough. The dough can be shaped into noodles and precooked with steam. The fresh noodles are dried with a flow of high velocity air at temperature of between 30-110°C to moisture content less than about 15%. Once dried, the product can be packaged as a brick and the product can be stored at ambient temperature for long periods of time

    Prmt5 is essential for early mouse development and acts in the cytoplasm to maintain ES cell pluripotency

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    Prmt5, an arginine methyltransferase, has multiple roles in germ cells, and possibly in pluripotency. Here we show that loss of Prmt5 function is early embryonic-lethal due to the abrogation of pluripotent cells in blastocysts. Prmt5 is also up-regulated in the cytoplasm during the derivation of embryonic stem (ES) cells together with Stat3, where they persist to maintain pluripotency. Prmt5 in association with Mep50 methylates cytosolic histone H2A (H2AR3me2s) to repress differentiation genes in ES cells. Loss of Prmt5 or Mep50 results in derepression of differentiation genes, indicating the significance of the Prmt5/Mep50 complex for pluripotency, which may occur in conjunction with the leukemia inhibitory factor (LIF)/Stat3 pathway

    A method for delivering lipophilic nutrients from red palm olein

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    A method for producing an organoleptic acceptable and quality stable product to act as delivery system of lipophilic nutriens from red palm olein is provided as a preferred embodiment of the present invention. Microcapsules comprised of red palm olein are prepared by preparing oil in water emulsion and subsequently dried with a flow of heat. The microcapsules are in the form of a solid state delivery system. The Moisture content of the product is less than 10%. Once dried, the product can be packaged and stored at room temperature for long periods of time
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