1] To better constrain the ongoing rates of deformation in northern Tibet, the ages of fluvial and glacial geomorphic markers left-laterally displaced by the Altyn Tagh Fault have been determined by radiocarbon and 10 Be-26 Al cosmic ray exposure dating. Two sites were investigated: Cherchen He and Sulamu Tagh, both near Tura ($37.6°N, 86.6°E). The sites are geomorphologically distinct with Cherchen He dominated by fluvial processes and the Sulamu Tagh by glacial action. Nine offsets ranging from 166 to 3660 m with ages between 6 and 113 ka yield an average slip rate of 26.9 ± 6.9 mm/yr. Landscape evolution appears to have been modulated by climate change and is temporally consistent with the d 18 O record from the Guliya ice cap in the West Kunlun; the features of interest were all formed by glacial and fluvial processes subsequent to marine isotope stage 5e, with the youngest features having formed during the early Holocene Optimum. This ''near-field,'' morphochronological slip rate is averaged over many earthquake cycles and is hence little affected by interseismic strain. It is kinematically consistent with other, somewhat lower, geomorphic slip rate measurements to the east. The average rate, and lower bounds obtained from alternate interpretational models, 18.4 mm/yr, cannot be reconciled with the most rece geodetic measurements ($7 mm/yr), suggesting that interseismic strain and interactions with adjacent faults may lead to disparate geologic and geodetic rate estimates. This late Pleistocene-Holocene, morphochronologic rate would imply that, at this longitude, the Altyn Tagh Fault, on the north edge of Tibet, might absorb almost as much of India's convergence relative to Siberia as the Himalayan Main Frontal Thrust does on the southern edge of the plateau.
In vivo experience induces changes in synaptic NMDA receptor (NMDAR) subunit components, which are correlated with subsequent modifications of synaptic plasticity. However, little is known about how these subunit changes regulate the induction threshold of subsequent plasticity. At hippocampal Schaffer collateral-CA1 synapses, we first examined whether a recent history of neuronal activity could affect subsequent synaptic plasticity through its actions on NMDAR subunit components. We found that prior activity history produced by priming stimulations (PSs) across a wide range of frequencies (1-100 Hz) could induce bidirectional changes in the NR2A/NR2B ratio, which governs the threshold for subsequent long-term potentiation/long-term depression (LTP/LTD). Manipulating the NR2A/NR2B ratio through partial NR2 subunit blockade mimicked the PS regulation of the LTP/LTD threshold. Our results demonstrate that activity-dependent changes in the NR2A/NR2B ratio can be critical factors in metaplastic regulation of the LTP/LTD threshold.
Hepatocellular carcinoma (HCC) is an aggressive malignancy and the second leading cause of cancer-related deaths worldwide. Conventional biomarkers exhibit poor performance in the surveillance, diagnosis, and prognosis of HCC. MicroRNAs (miRNAs) are a class of evolutionarily conserved small non-coding RNAs that are involved in the regulation of gene expression and protein translation, and they play critical roles in cell growth, differentiation, and the development of various types of cancers, including HCC. Recent evidence revealed the role of miRNAs as potential novel and ideal biomarkers for HCC. miRNAs are released to extracellular spaces, and they are extremely stable in bodily fluids, including serum or plasma, where they are packaged into various microparticles or associated with RNA-binding proteins. Numerous studies have demonstrated that circulating miRNAs have potential applications as minimally invasive biomarkers for HCC diagnosis and prognosis. The present review highlights current understanding of miRNA biogenesis and the origins and types of circulating miRNAs. We summarize recent progress in the use of circulating miRNAs as diagnostic and prognostic biomarkers for HCC. We also discuss the challenges and perspectives of the clinical utility of circulating miRNAs in HCC.
The mammalian target of rapamycin (mTOR) plays a critical role for cell growth and survival in many cell types. While substantial progress has been made in understanding the abnormal activation of mTORC1 in the pathogenesis of kidney disease, little is known about mTORC2 in kidney disease such as acute kidney injury (AKI). To study this, we generated a mouse model with tubule-specific deletion of Rictor (Tubule-Rictor-/-). The knockouts were born normal and no obvious kidney dysfunction or kidney morphologic abnormality was found within 2 months of birth. However, ablation of Rictor in the tubular cells exacerbated cisplatin-induced AKI compared to that in the control littermates. As expected, tubular cell apoptosis, Akt phosphorylation (Ser473), and autophagy were induced in the kidneys from the control littermates by cisplatin treatment. Less cell autophagy or Akt phosphorylation and more cell apoptosis in the kidneys of the knockout mice were identified compared with those in the control littermates. In NRK-52E cells in vitro, Rictor siRNA transfection sensitized cell apoptosis to cisplatin but with reduced cisplatin-induced autophagy. Metformin, an inducer of autophagy, abolished cell death induced by Rictor siRNA and cisplatin. Thus, endogenous Rictor/mTORC2 protects against cisplatin-induced AKI, probably mediated by promoting cell survival through Akt signaling activation and induction of autophagy.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.