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Premature Aging
Published in Nate F. Cardarelli, The Thymus in Health and Senescence, 2019
When the WS karyoplast is fused to a normal young cell, (heterokaryon) DNA synthesis is suppressed.138,139 If the cybrid (normal fused to WS cytoplast) is produced, DNA synthesis also decreases.139 Results would thus indicate that both the nuclear and cytoplasmic environments are involved in retarded DNA synthesis.140 SV40 (Simian virus) infection of WS cells can give a transformed line. Thompson and Holliday report 290 passages form one such line.126 The genes or genes responsible for WS must still be present in this line, but perhaps switched “off”. Ohno and Yamaguchi cultured late phase fibroblasts from WS patients with SV40 injected transformants which activated the fibroblasts resulting in a lifespan increase of 2.3 times to 5.4 times.141 Co-culture with normal cells showed variable effects. DNA replication is retarded, Fujiwara et al. reporting that it seems to “stick” to the nuclear matrix too long.137 Takeuchi et al. note a prolongation of the WS cell cycle in vitro due to an increase in the duration of the S phase from a normal 8.2 to 10.9 h.142
Urinary Incontinence in Older Adults
Published in K. Rao Poduri, Geriatric Rehabilitation, 2017
Nicole Strong, Sara Z. Salim, Jean L. Nickels, K. Rao Poduri
Behavioral and lifestyle modifications are also first-line treatment options. Pharmacologically, both anticholinergic and beta antagonist medication classes have established efficacy in treatment of UUI. Botox is a more invasive third-line treatment option when conservative and pharmacologic measures have not produced significant improvement of symptoms.30 Neuromodulation modalities (neurosacral modulation, pudendal nerves stimulation, and posterior tibial nerve stimulation) are also more invasive techniques that may be used prior or in addition to botulinum toxin as the next step in management of UUI. Insertion of temporary catheter is not recommended as it can aggravate UUI symptoms. Leakage around the catheter may result from bladder spasms. Finally, augmentation cytoplast and urinary diversion are both viable surgical options for severe and refractory cases.
Identification of phenazine analogue as a novel scaffold for thioredoxin reductase I inhibitors against Hep G2 cancer cell lines
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2019
Jianming Liao, Linlin Wang, Zhongxi Wu, Zhixiang Wang, Jun Chen, Yucheng Zhong, Feng Jiang, Yuanyuan Lu
In our previous study, a preliminary mechanism research indicated that a phenazine analogue (Figure 1(A)), namely CPUL1, which demonstrated antitumor activities against both mouse liver carcinoma cell lines (H22–H8D8) implanted xenografted mice in vivo and human liver carcinoma cell line (Hep G2) in vitro, might be acting as dual topoisomerase I and II inhibitors and apoptosis activator11. Intriguingly, with our ongoing study on the detailed antitumor molecular mechanism of compound CPUL1, we found that the compound was prevailingly distributed thoroughly in Hep G2 cell plasma not in cytoplast (Figure 1(B)), which was confirmed by laser scanning confocal microscopy (LSCM). This freakishly phenomenon was distinguishing from typical topoisomerase I/II inhibitors, such as doxorubicin12, etoposide13 and 10-hydroxycamptothecin14, which were reported as locating at nucleus in cancer cell lines by LSCM methods. The discrepant results of CPUL1 between the LSCM and topoisomerase I/II inhibition experiments aroused a suspicion that the CPUL1 might not targeting to the topoisomerase I/II in Hep G2 cell lines. Considering the controversial role of the CPUL1 against Hep G2 cells, the target of CPUL1 against Hep G2 cells becomes the crux of the scene to be unveiled. Thus, we attempted to discover and identify the anticancer target of CPUL1 in this study.
Molecular mechanism analysis of m6A modification-related lncRNA-miRNA-mRNA network in regulating autophagy in acute pancreatitis
Published in Islets, 2022
Xiang Li, Hong Qin, Ali Anwar, Xingwen Zhang, Fang Yu, Zheng Tan, Zhanhong Tang
We further analyzed the functional enrichment of the 21 candidate autophagy genes to identify the main pathways for autophagy to play a role in AP. The results of GO analysis showed that they were mainly enriched in MF such as protein binding (GO: 0005515), ubiquitin-protein ligase binding (GO: 0031625), protein heterodimerization activity (GO: 0046982), in CC such as cytoplast (GO: 0005737), cytosol (GO: 0005829) and autophagosome (GO: 0005776) and in BP including autophagy (GO: 0006914), apoptotic process (GO: 0006915) and autophagy of mitochondrion (GO: 0000422) (Figure 4C). KEGG analysis revealed that in addition to autophagy or apoptosis-related pathways (Figure 4D). These results further verified the representativeness of these 21 genes in autophagy.
Low-dose bisphenol A (BPA)-induced DNA damage and tumorigenic events in MCF-10A cells
Published in Cogent Medicine, 2019
Nasir Jalal, Jing Wei, Yaxin Jiang, Janak L. Pathak, Austin R. Surendranath, Chang Y. Chung
Being a second messenger, imbalance in the cytoplasmic Ca2+ sequestration triggers critical events that lead to tumorigenesis via apoptosis, cell motility or proliferation. Cytoplasmic Ca2+ is partly homeostasized via the secretory pathway of calcium ATPase which has two isoforms SPCA1 and SPCA2. SPCA1 occurs ubiquitously in vertebrates, including Humans, and has orthologs in lower eukaryotes (Missiaen, Dode, Vanoevelen, Raeymaekers, & Wuytack, 2007). SPCA1 (ATP2C1) mutations cause Hailey–Hailey disease that produces stratified epithelium of skin due to loss of intercellular adhesion or Acantholysis (Mascia, Denning, Kopan, & Yuspa, 2012; Missiaen et al., 2004). Both protein isoforms are ATP powered and pump Ca2+ and Mn2+ from cytosol into the lumen of Golgi for protein sorting, processing and glycosylation (Dürr et al., 1998). The siRNA gene silencing of SPCA1 has varying effects on the regulation of calcium-dependent enzymes in MDA MB231 cell line and SPCA1 knockdown in mice causes embryonic lethality (Okunade et al., 2007). SPCA1 inhibition in-vitro alters the cell surface levels of exogenously expressed proteins indicating a functional involvement of SPCA1 in cellular protein trafficking (Lissandron, Podini, Pizzo, & Pozzan, 2010). SPCA1 is a thapsigargin-sensitive intracellular Ca2+ pump found mostly in the Golgi compartment (Sagara, Fernandez-Belda, de Meis, & Inesi, 1992). Contribution of Ca2+ pump to cytosolic Ca2+ signaling in HeLa cells via RNA-mediated interference disrupts the baseline Ca2+ but detectable in the cytoplast (Van Baelen et al., 2003). Moreover, Bis (2-hydroxy-3-tert-butyl-5-methyl-phenyl)-methane is a potent and selective inhibitor of SPCA1 (Lai & Michelangeli, 2012).