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Kouki Abe Kentarou Baba Liguo Huang Koay Teng Wei Kazunori Okano Yoichiroh Hosokawa Naoyuki Inagaki 《Biophysical journal》2021,120(17):3566-3576
Mechanical properties of the extracellular environment modulate axon outgrowth. Growth cones at the tip of extending axons generate traction force for axon outgrowth by transmitting the force of actin filament retrograde flow, produced by actomyosin contraction and F-actin polymerization, to adhesive substrates through clutch and cell adhesion molecules. A molecular clutch between the actin filament flow and substrate is proposed to contribute to cellular mechanosensing. However, the molecular identity of the clutch interface responsible for mechanosensitive growth cone advance is unknown. We previously reported that mechanical coupling between actin filament retrograde flow and adhesive substrates through the clutch molecule shootin1a and the cell adhesion molecule L1 generates traction force for axon outgrowth and guidance. Here, we show that cultured mouse hippocampal neurons extend longer axons on stiffer substrates under elastic conditions that correspond to the soft brain environments. We demonstrate that this stiffness-dependent axon outgrowth requires actin-adhesion coupling mediated by shootin1a, L1, and laminin on the substrate. Speckle imaging analyses showed that L1 at the growth cone membrane switches between two adhesive states: L1 that is immobilized and that undergoes retrograde movement on the substrate. The duration of the immobilized phase was longer on stiffer substrates; this was accompanied by increases in actin-adhesion coupling and in the traction force exerted on the substrate. These data suggest that the interaction between L1 and laminin is enhanced on stiffer substrates, thereby promoting force generation for axon outgrowth. 相似文献
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Genotoxicity of diacetoxyscirpenol (DAS) was studied on laboratory mice after intraperitoneal injection with single and repeated
doses. DAS was administrated at three different dose levels (0.5, 0.75, and 1.0 mg/kg body weight). The study was conducted
on both somatic and germ cells additional to the sperm morphology analysis. DAS treatment resulted in a significant reduction
(P<0.01) in mitotic activity at all levels of doses tested, confirming that DAS is a potent protein and DNA synthesis inhibitor.
At somatic cells (bone marrow) both structural and numerical chromosome abnormalities were observed. Single dose treatment
showed significant abnormalities only with high dose treatment. In contrast, at repeated dose similar abnormalities were also
observed with some significance but no systematic relation between the administrated dose and abnormalities ratio could be
settled. In germ cells (testicles), structural and numerical abnormalities were also observed. In general, the frequencies
of scored abnormalities at germ cells were lower than that the somatic cells. Sperm count test revealed a decrease in the
number of released sperm after toxin treatment. Abnormalities of sperm shape (head and tail) were observed, confirming the
positive correlation between cytogenetic damage and sperm abnormality.
The results also proved that DAS is a very toxic mycotoxin, in addition to inducing chromosomal abnormalities, it causes a
severe inhibition of DNA synthesis which subsequently affects the cell cycle and cell division. A good system for good harvesting
practice and good food technology can lower the risk for the consumers. 相似文献
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Deborah Amanda Goh Yanhong Dong Wah Yean Lee Way Inn Koay Stephen Ziyang Tay Danny Soon Christopher Chen Claire Frances Brittain Stephen Loucian Lowe Boon-Seng Wong 《PloS one》2014,9(5)
Background
Diabetes is reported to be linked to poorer cognitive function. The purpose of this study is to examine (a) clinical correlation between cognitive function and the biochemical perturbations in T2DM, and (b) the impact of statin treatment on cognitive function in diabetic subjects.Methods
Forty Singaporean Chinese males with diabetes and twenty Singaporean Chinese males without diabetes were recruited for this study. Twenty-two of the diabetic subjects were on statin therapy and all subjects were non-demented. This was a 2-period non-interventional case-control study in which subjects were assessed for cognitive function in period 1 and blood samples taken over 2 periods, approximately 1 week apart. Blood was collected to determine the level of total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), triglycerides, glucose and insulin. Cognitive performance was measured by a neuropsychological battery covering domains of attention, language, verbal and visual memory, visuomotor speed and executive function. Z-scores were derived for each cognitive domain using the mean and standard deviations (SDs), and they were used to compare between (a) diabetic and non-diabetic groups, and (b) diabetic subjects with and without statin treatment. ANCOVAs with age, education, BMI, and the duration of diabetes as covariates were employed to examine differences in mean score of cognitive domains and subtests between the two groups.Results
Overall cognitive function was similar among diabetics and age matched non-diabetic controls. Among diabetic statin users, HDL, LDL and total cholesterol were negatively correlated with executive function, whereas peripheral insulin levels and insulin resistance were negatively associated with attention.Conclusion
Diabetic statin users were likely to have poorer performance in attention and executive function. Increasing levels of the peripheral biomarkers are likely to contribute to poorer cognitive performance. 相似文献107.
Yeonju Lee Eugene J. Koay Weijia Zhang Lidong Qin Dickson K. Kirui Fazle Hussain Haifa Shen Mauro Ferrari 《PloS one》2014,9(10)
We report cell mechanical changes in response to alteration of expression of the human equilibrative nucleoside transporter-1 (hENT1), a most abundant and widely distributed plasma membrane nucleoside transporter in human cells and/or tissues. Modulation of hENT1 expression level altered the stiffness of pancreatic cancer Capan-1 and Panc 03.27 cells, which was analyzed by atomic force microscopy (AFM) and correlated to microfluidic platform. The hENT1 knockdown induced reduction of cellular stiffness in both of cells up to 70%. In addition, cellular phenotypic changes such as cell morphology, migration, and expression level of epithelial-mesenchymal transition (EMT) markers were observed after hENT1 knockdown. Cells with suppressed hENT1 became elongated, migrated faster, and had reduced E-cadherin and elevated N-cadherin compared to parental cells which are consistent with epithelial-mesenchymal transition (EMT). Those cellular phenotypic changes closely correlated with changes in cellular stiffness. This study suggests that hENT1 expression level affects cellular phenotype and cell elastic behavior can be a physical biomarker for quantify hENT1 expression and detect phenotypic shift. Furthermore, cell mechanics can be a critical tool in detecting disease progression and response to therapy. 相似文献
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Ingunn MS Engebretsen Karen M Moland Jolly Nankunda Charles A Karamagi Thorkild Tylleskär James K Tumwine 《International breastfeeding journal》2010,5(1):1-11