Numerical investigation of GHz repetition rate fundamentally mode-locked all-fiber lasers

GHz repetition rate fundamentally mode-locked lasers have attracted great interest for a variety of scientific and practical applications. A passively mode-locked laser in all-fiber format has the advantages of high stability, maintenance-free operation, super compactness, and reliability. In this paper, we present numerical investigation on passive mode-locking of all-fiber lasers operating at repetition rates of 1-20 GHz. Our calculations show that the reflectivity of the output coupler, the small signal gain of the doped fiber, the total net cavity dispersion, and the modulation depth of the saturable absorber are the key parameters for producing stable fundamentally mode-locked pulses at GHz repetition rates in very short all-fiber linear cavities. The instabilities of GHz repetition rate fundamentally mode-locked all-fiber lasers with different parameters were calculated and analyzed. Compared to a regular MHz repetition rate mode-locked all-fiber laser, the pump power range for the mode-locking of a GHz repetition rate all-fiber laser is much larger due to the several orders of magnitude lower accumulated nonlinearity in the fiber cavity The presented numerical study provides valuable guidance for the design and development of highly stable mode-locked all-fiber lasers operating at GHz repetition rates.National Science Foundation Engineering Research Center for Integrated Access Networks [EEC-0812072]; Technology Research Initiative Fund (TRIF) Photonics Initiative of the University of Arizona; National Natural Science Foundation of China (NSFC) [61575075]Open access journalThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

<i>Myo</i>-Inositol Supplementation Alleviates Cisplatin-Induced Acute Kidney Injury via Inhibition of Ferroptosis

Myo-inositol, a carbocyclic sugar, is believed to be relevant to renal pathobiology since the kidney is the major site for its catabolism. Its role in acute kidney injury (AKI) has not been fully investigated. Ferroptosis, a unique form of regulated cell death, is involved in various types of renal injuries. The relevance of myo-inositol with respect to the process of ferroptosis has not been explored either. Herein, our current exploratory studies revealed that supplementation of myo-inositol attenuates cisplatin-induced injury in cultured Boston University mouse proximal tubular (BUMPT) cells and renal tubules in vivo. Moreover, our studies unraveled that metabolic parameters pertaining to ferroptosis were disrupted in cisplatin-treated proximal tubular cells, which were seemingly remedied by the administration of myo-inositol. Mechanistically, we noted that cisplatin treatment led to the up-regulation of NOX4, a key enzyme relevant to ferroptosis, which was normalized by the administration of myo-inositol. Furthermore, we observed that changes in the NOX4 expression induced by cisplatin or myo-inositol were modulated by carboxy-terminus of Hsc70-interacting protein (CHIP), an E3 ubiquitin ligase. Taken together, our investigation suggests that myo-inositol promotes CHIP-mediated ubiquitination of NOX4 to decelerate the process of ferroptosis, leading to the amelioration of cisplatin-induced AKI

The Adenosine A1 Receptor Antagonist DPCPX Inhibits Tumor Progression via the ERK/JNK Pathway in Renal Cell Carcinoma

Background/Aims: The adenosine A1 receptor (A1R) has been reported to be involved in the pathogenesis of various cancers, and the effects of A1R on different cancers are pleiotropic. However, the role of A1R in renal cell carcinoma (RCC) remains not well-known. Methods: The expression of A1R in RCC cells was detected by quantitative real-time PCR and Western blotting analysis. Cell proliferation was detected using an MTT assay and a colony formation assay. Tumor growth was also evaluated in nude mice. Cell invasion and migration were evaluated using a wound healing assay and a transwell assay. Cell cycle distribution and apoptosis rates were analyzed by flow cytometry. Results: A1R was the main subtype of ARs and was up-regulated in 786-O and ACHN cells. Functionally, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX), an A1R antagonist, inhibited RCC cell proliferation in vitro and tumor growth in vivo. Furthermore, DPCPX inhibited RCC cell migration, while N6-Cyclopentyladenosine (CPA), a selective A1 agonist, was able to rescue RCC cell migration. In addition, DPCPX promoted 786-O and ACHN cell apoptosis and induced an S phase cell cycle arrest. Finally, we demonstrated that DPCPX inhibited tumor progression in part via the ERK/JNK pathway. Conclusion: These findings suggest the potentially important role of DPCPX in the control of RCC cell proliferation and migration by regulating the ERK/JNK signaling pathway

The Adenosine A1 Receptor Antagonist DPCPX Inhibits Tumor Progression via the ERK/JNK Pathway in Renal Cell Carcinoma

Background/Aims: The adenosine A1 receptor (A1R) has been reported to be involved in the pathogenesis of various cancers, and the effects of A1R on different cancers are pleiotropic. However, the role of A1R in renal cell carcinoma (RCC) remains not well-known. Methods: The expression of A1R in RCC cells was detected by quantitative real-time PCR and Western blotting analysis. Cell proliferation was detected using an MTT assay and a colony formation assay. Tumor growth was also evaluated in nude mice. Cell invasion and migration were evaluated using a wound healing assay and a transwell assay. Cell cycle distribution and apoptosis rates were analyzed by flow cytometry. Results: A1R was the main subtype of ARs and was up-regulated in 786-O and ACHN cells. Functionally, 1,3-dipropyl-8-cyclopentylxanthine (DPCPX), an A1R antagonist, inhibited RCC cell proliferation in vitro and tumor growth in vivo. Furthermore, DPCPX inhibited RCC cell migration, while N6-Cyclopentyladenosine (CPA), a selective A1 agonist, was able to rescue RCC cell migration. In addition, DPCPX promoted 786-O and ACHN cell apoptosis and induced an S phase cell cycle arrest. Finally, we demonstrated that DPCPX inhibited tumor progression in part via the ERK/JNK pathway. Conclusion: These findings suggest the potentially important role of DPCPX in the control of RCC cell proliferation and migration by regulating the ERK/JNK signaling pathway

An ionic liquid-based synergistic extraction strategy for rare earths

In this work, a novel IL-based synergistic extraction system utilizing the ionic liquid tricaprylmethyl-ammonium nitrate ([A336][NO3]) and the commercial extractant di(2-ethylhexyl) 2-ethylhexyl phosphonate (DEHEHP) was developed for the extraction of rare earth (RE) nitrates. Pr(III) was used as a model RE and the effects of key factors, i.e. the ratio of [A336][NO3] to DEHEHP, the acidity of feed solutions, and the concentration of a salting-out reagent, were systematically studied. Our results demonstrate that the mixture of [A336][NO3] and DEHEHP had an obviously synergistic extraction effect for the extraction of Pr(III). The maximum synergistic enhancement coefficient of 3.44 was attained at X-A = 0.4 (v%). Alternatively, a mixture of [A336][Cl] and DEHEHP hardly extracted Pr(III) from chloride media. Moreover, we investigated the Pr(III) extraction mechanism and demonstrated that Pr(III) can be extracted as the neutral complexation species Pr(NO3)(3)center dot chi DEHEHP and the ion-type species [A336](y)center dot Pr(NO3)(3+y). These extraction processes can effectively hamper the release of organic cation-ligands into the aqueous phase. The synergistic extraction effect is mainly derived from the enhanced solubility of the extracted species in the ionic liquid phase. The extraction behaviors of Pr(III) could be properly described by Langmuir and pseudo-second-order rate equations. An increase in temperature was unfavorable for the extraction reaction but greatly improved the extraction rate. Interestingly, the mixed IL extraction system has an obviously synergistic extraction effect for light REs (LREs, La-Eu), but an anti-synergistic effect for heavy REs (HREs, Gd-Lu, Y), thus indicating that our synergistic extraction system is helpful for the separation of LREs from HREs. In addition, the high selectivity between REs and non-REs suggested that the recovery of REs from a complicated high-salt leachate could be highly possible. It demonstrates that the IL-based synergistic extraction strategy developed in this work is promising and sustainable, and as a result the development of an IL-based synergistic extraction process for the recovery of REs is straightforwardly envisaged

Acute rejection after kidney transplantation promotes graft fibrosis with elevated adenosine level in rat.

Chronic allograft nephropathy is a worldwide issue with the major feature of progressive allograft fibrosis, eventually ending with graft loss. Adenosine has been demonstrated to play an important role in process of fibrosis. Our study aimed to investigate the relationship between adenosine and fibrosis in renal allograft acute rejection in rat.Wistar rats and SD rats were selected as experimental animals. Our study designed two groups. In the allograft transplantation group, kidneys of Wistar rats were orthotopically transplanted into SD rat recipients, the same species but not genetically identical, to induce acute rejection. Kidney transplantations of SD rats to SD rats which were genetically identical were served as the control. We established rat models and detected a series of indicators. All data were analyzed statistically. P<0.05 was considered statistically significant.Compared with the control group, levels of adenosine increased significantly in the allograft transplantation group, in which acute rejection was induced (P<0.05). Progressive allograft fibrosis as well as collagen deposition were observed.These findings suggested that level of adenosine was upregulated in acute rejection after kidney allograft transplantation in rat. Acute rejection may promote renal allograft fibrosis via the adenosine signaling pathways

CHIP protects against septic acute kidney injury by inhibiting NLRP3-mediated pyroptosis

Summary: Septic acute kidney injury (S-AKI), the most common type of acute kidney injury (AKI), is intimately related to pyroptosis and oxidative stress in its pathogenesis. Carboxy-terminus of Hsc70-interacting protein (CHIP), a U-box E3 ligase, modulates oxidative stress by degrading its targeted proteins. The role of CHIP in S-AKI and its relevance with pyroptosis have not been investigated. In this study, we showed that CHIP was downregulated in renal proximal tubular cells in lipopolysaccharide (LPS)-induced S-AKI. Besides, the extent of redox injuries in S-AKI was attenuated by CHIP overexpression or activation but accentuated by CHIP gene disruption. Mechanistically, our work demonstrated that CHIP interacted with and ubiquitinated NLRP3 to promote its proteasomal degradation, leading to the inhibition of NLRP3/ACS inflammasome-mediated pyroptosis. In summary, this study revealed that CHIP ubiquitinated NLRP3 to alleviate pyroptosis in septic renal injuries, suggesting that CHIP might be a potential therapeutic target for S-AKI

Image_1_Development and validation of a nomogram for risk prediction of nephrolithiasis recurrence in patients with primary hyperparathyroidism.tif

BackgroundNephrolithiasis is a common complication of primary hyperparathyroidism (PHPT), and the recurrence of nephrolithiasis in patients with PHPT is also an urgent concern. What is worse, there is a scarcity of recommended evaluation to predict the risk of nephrolithiasis recurrence in patients with PHPT. This study was aimed to develop and validate a nomogram to facilitate risk assessment in patients with PHPT.MethodsA total of 197 patients with PHPT were retrospectively included in this study from September 2016 to August 2021. Patients’ demographic data, blood test parameters, urinalysis, stone parameters, and surgical intervention were collected. Extracted variables were submitted to a least absolute shrinkage and selection operator (LASSO) regression model. A nomogram was built and validated according to the area under the curve (AUC) value, calibration curve, and decision curve analysis.ResultsAccording to the LASSO regression and logistic regression analyses, five predictors were derived from 22 variables: creatinine, uric acid, bilateral stone, multiplicity, and surgery. The AUC and concordance index of the training cohort and validation cohort were 0.829 and 0.856, and 0.827 and 0.877, respectively. The calibration curve analysis and the decision curve analysis showed that the nomogram had an adequate prediction accuracy.ConclusionWe built a useful nomogram model to predict the risk of nephrolithiasis recurrence in patients with PHPT. This would assist clinicians to provide appropriate advices and managements for these patients.</p