202 research outputs found

    Polarization-based cyclic weak value metrology for angular velocity measurement

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    Weak value has been proved to amplify the detecting changes of the meters at the cost of power due to post-selection. Previous power-recycling schemes enable the failed post-selection photons to be reselected repeatedly, thus surpassing the upper noise limit and improving the precision of interferometric systems. Here we introduce three cyclic methods to improve the sensitivity of polarization-based weak-value-based angular velocity measurement: power-, signal- and dual-recycling schemes. By inserting one or two partially transmitting mirrors inside the system, both the power and precision of detected signals are greatly enhanced, and the dual-recycling scheme has wider optimal region than that of power- or signal-recycling schemes. Compared to non-polarization schemes, polarization-based schemes enjoy lower optical loss and unique cyclic directions. These reduce the crosstalk among different paths of light and, theoretically, eliminate the walk-off effect, thus towering in both theoretical performance and application.Comment: 7 pages, 3 figure

    Multiple functions and regulatory network of miR-150 in B lymphocyte-related diseases

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    MicroRNAs (miRNAs) play vital roles in the post-transcriptional regulation of gene expression. Previous studies have shown that miR-150 is a crucial regulator of B cell proliferation, differentiation, metabolism, and apoptosis. miR-150 regulates the immune homeostasis during the development of obesity and is aberrantly expressed in multiple B-cell-related malignant tumors. Additionally, the altered expression of MIR-150 is a diagnostic biomarker of various autoimmune diseases. Furthermore, exosome-derived miR-150 is considered as prognostic tool in B cell lymphoma, autoimmune diseases and immune-mediated disorders, suggesting miR-150 plays a vital role in disease onset and progression. In this review, we summarized the miR-150-dependent regulation of B cell function in B cell-related immune diseases

    Silencing of lncRNA PKIA-AS1 Attenuates Spinal Nerve Ligation-Induced Neuropathic Pain Through Epigenetic Downregulation of CDK6 Expression

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    Neuropathic pain (NP) is among the most intractable comorbidities of spinal cord injury. Dysregulation of non-coding RNAs has also been implicated in the development of neuropathic pain. Here, we identified a novel lncRNA, PKIA-AS1, by using lncRNA array analysis in spinal cord tissue of spinal nerve ligation (SNL) model rats, and investigated the role of PKIA-AS1 in SNL-mediated neuropathic pain. We observed that PKIA-AS1 was significantly upregulated in SNL model rats and that PKIA-AS1 knockdown attenuated neuropathic pain progression. Alternatively, overexpression of PKIA-AS1 was sufficient to induce neuropathic pain-like symptoms in uninjured rats. We also found that PKIA-AS1 mediated SNL-induced neuropathic pain by directly regulating the expression and function of CDK6, which is essential for the initiation and maintenance of neuroinflammation and neuropathic pain. Therefore, our study identifies PKIA-AS1 as a novel therapeutic target for neuroinflammation related neuropathic pain

    Dynamic diffusion tensor imaging reveals structural changes in the bilateral pyramidal tracts after brain stem hemorrhage in rats

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    Background and Purpose: Few studies have concentrated on pyramidal tract (PY) changes after brain stem hemorrhage (BSH). In this study, we used a diffusion tensor imaging (DTI) technique and histologic identification to investigate longitudinal PY changes on both the contralateral and ipsilateral sides after experimental BSH. Methods: BSH was induced in 61 Sprague-Dawley rats by infusing 30 μl of autogenous tail blood into each rat’s right pons. DTI and motor function examinations were performed repeatedly on days 1, 3, 7, 14, and 28 after surgery. Fractional anisotropy, mean diffusivity, axial diffusivity, and radial diffusivity were measured in the bilateral PYs. The axon and myelin injury in the PY were evaluated by histologic study. Results: As compared with normal controls, the bilateral PYs in rats with induced BSH showed an early decrease and a late increase in fractional anisotropy and an early increase and a late decrease in mean diffusivity. A progressive decrease in axial diffusivity with dramatic axon loss from day 1 to day 28 after BSH was found bilaterally. The bilateral PYs showed an early increase and a late decrease in radial diffusivity. Early myelin injury and late repair were also detected pathologically in the bilateral PYs of rats with BSH. Thus, the early motor function deficits of rats with BSH began to improve on day 14 and had almost completely disappeared by day 28. Conclusions: DTI revealed dynamic changes in the bilateral PYs after BSH, which was confirmed by histologic findings and which correlated with motor function alteration. These findings support the idea that quantitative DTI can track structural changes in the bilateral PYs and that DTI may serve as a noninvasive tool to predict the prognoses of patients with BSH

    Myofilament Ca2+ desensitization mediates positive lusitropic effect of neuronal nitric oxide synthase in left ventricular myocytes from murine hypertensive heart

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    AbstractNeuronal nitric oxide synthase (NOS1 or nNOS) exerts negative inotropic and positive lusitropic effects through Ca2+ handling processes in cardiac myocytes from healthy hearts. However, underlying mechanisms of NOS1 in diseased hearts remain unclear. The present study aims to investigate this question in angiotensin II (Ang II)-induced hypertensive rat hearts (HP). Our results showed that the systolic function of left ventricle (LV) was reduced and diastolic function was unaltered (echocardiographic assessment) in HP compared to those in shams. In isolated LV myocytes, contraction was unchanged but peak [Ca2+]i transient was increased in HP. Concomitantly, relaxation and time constant of [Ca2+]i decay (tau) were faster and the phosphorylated fraction of phospholamban (PLN-Ser16/PLN) was greater. NOS1 protein expression and activity were increased in LV myocyte homogenates from HP. Surprisingly, inhibition of NOS1 did not affect contraction but reduced peak [Ca2+]i transient; prevented faster relaxation without affecting the tau of [Ca2+]i transient or PLN-Ser16/PLN in HP, suggesting myofilament Ca2+ desensitization by NOS1. Indeed, relaxation phase of the sarcomere length–[Ca2+]i relationship of LV myocytes shifted to the right and increased [Ca2+]i for 50% of sarcomere shortening (EC50) in HP. Phosphorylations of cardiac myosin binding protein-C (cMyBP-C282 and cMyBP-C273) were increased and cardiac troponin I (cTnI23/24) was reduced in HP. Importantly, NOS1 or PKG inhibition reduced cMyBP-C273 and cTnI23/24 and reversed myofilament Ca2+ sensitivity. These results reveal that NOS1 is up-regulated in LV myocytes from HP and exerts positive lusitropic effect by modulating myofilament Ca2+ sensitivity through phosphorylation of key regulators in sarcomere
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