Investigation of the optical properties of a deep-ultraviolet LED with an Al nanograting structure.

The optical properties of deep-ultraviolet (DUV) light-emitting diode (LED) with Al nanograting structure are investigated by three-dimensional (3D) finite-difference time-domain (FDTD) simulation. The peak intensity of TE and TM polarization radiation recombination rate of the grating structure is increased by 33.3% and 22.0% as compared to the control structure with Al plane. The light extraction efficiency (LEE) of the emitted light whose propagation direction is in the plane perpendicular to the Al-grating ridge is much higher than that in the plane parallel to the Al-grating ridge due to the scattering of the grating. Without considering the lateral surface extraction and packaging, the total LEE of the grating structure can be improved by 41.4% as compared to the control structure. The peak intensity of the output spectrum of the DUV LED with the grating structure can be increased by 70.3%.

Colistin sulfate for decontamination of preservation fluid in kidney transplantation to decrease the incidence of donor-derived infections caused by multidrug-resistant Gram-negative bacteria.

BACKGROUND: Preservation fluid (PF) contamination, especially by multidrug-resistant (MDR) Gram-negative bacteria (GNB), poses a high risk of donor-derived infection (DDI) and severe clinical outcomes. We sought to determine whether the use of colistin sulfate to decontaminate PF in kidney transplantation can decrease the incidence of probable DDI (p-DDI) caused by MDR GNB. METHODS: In a retrospective study of 916 recipients who received deceased donation, 864 PF samples were collected and cultured, and microbiological contaminants were recorded with the recipients' clinical data and outcomes. From March 2016 to May 2019, 624 samples were decontaminated with ceftizoxime, and from June 2019 to March 2021, 240 samples were decontaminated with colistin sulfate. Between-group comparisons were performed to assess the ability of the two decontamination regimens to decrease the incidence of p-DDI, especially MDR GNB-related infection. RESULTS: The overall PF contamination rate was 54.51% (471/864), and 80 samples were positive for MDR GNB contamination. All p-DDIs occurred in the ceftizoxime group (p < 0.001), and 67.65% of p-DDIs were MDR GNB-related. In the ceftizoxime group, 23 of 61 cases of MDR GNB contamination led to related p-DDIs, while none occurred in the colistin sulfate group (p = 0.002). Among the 23 patients with p-DDIs, 5 died due to severe infection, and 2 experienced graft loss. CONCLUSIONS: The goal of decontamination should be to decrease the risk of MDR GNB-related p-DDI, and colistin sulfate could be an effective and feasible option.

Circ_0120175 promotes laryngeal squamous cell carcinoma development through up-regulating SLC7A11 by sponging miR-330-3p.

The aim of our study was to illustrate the role of circular RNA 0120175 (circ_0120175) and its associated mechanism in laryngeal squamous cell carcinoma (LSCC) development. The abundance of circ_0120175, microRNA-330-3p (miR-330-3p) and solute carrier family 7, membrane 11 (SLC7A11) messenger RNA and protein was measured by quantitative real time polymerase chain reaction and Western blot assay. Cell proliferation, apoptosis, migration and invasion were assessed by cell counting kit-8 assay, flow cytometry and transwell migration and invasion assays, respectively. The interaction between miR-330-3p and circ_0120175 or SLC7A11 was confirmed by dual-luciferase reporter assay. Murine xenograft model was established to test the function of circ_0120175 in tumor growth in vivo. Circ_0120175 abundance was aberrantly increased in LSCC tissues and cell lines, and LSCC patients with high level of circ_0120175 were associated with advanced tumor staging, lymph node metastasis and short survival time. Circ_0120175 interference suppressed cell proliferation, migration and invasion and induced cell apoptosis of LSCC cells. Circ_0120175 could sponge and negatively regulate miR-330-3p expression in LSCC cells. The addition of anti-miR-330-3p partly reversed circ_0120175 knockdown-induced effects in LSCC cells. SLC7A11 bound to miR-330-3p. Circ_0120175 enhanced the abundance of SLC7A11 through sponging miR-330-3p in LSCC cells. Circ_0120175 silencing-mediated influences in LSCC cells were partly counteracted by the overexpression of SLC7A11. Circ_0120175 interference notably suppressed xenograft tumor growth in vivo. Circ_0120175 promoted proliferation, migration and invasion while impeded cell apoptosis of LSCC cells through miR-330-3p/SLC7A11 axis, which provided novel therapeutic targets for LSCC.

SIRT3 protects kidneys from ischemia-reperfusion injury by modulating the DRP1 pathway to induce mitochondrial autophagy.

Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury (AKI) and may influence renal graft survival. In this study, we investigate the involvement of SIRT3 and DRP1 in mitochondrial autophagy and AKI in a mouse model of IRI. Autophagy was detected in the absence of SIRT3, and hypoxic reoxygenation (H/R) experiments using renal tubular epithelial cells NRK52E were performed in vitro to validate these results. We found that autophagosomes increased following IRI and that the expression of autophagy-related genes was up-regulated. The inhibition of autophagy with 3-methyladenine exacerbated IRI, whereas the DRP1 inhibitor Mdivi-1 reversed this inhibition. Mdivi-1 did not reverse the inhibition of autophagy in the absence of SIRT3. During IRI, Mdivi-1 reduced autophagy and DRP1 expression, whereas SIRT3 overexpression attenuated this condition. Rescue experiment showed that autophagy was increased when both SIRT3 or DRP1 were over- or under-expressed or just DRP1 was under-expressed but expression was reduced when just SIRT3 was under-expressed. However, the expression of DRP1-related molecules was reduced when SIRT3 was overexpressed and when DRP1 was under-expressed. Taken together, these findings indicate that SIRT3 protects against kidney damage from IRI by modulating the DRP1 pathway to induce mitochondrial autophagy.

Multiorgan Transplant From a Donor With Solid Renal Masses: An Initial Experience and Clinical Considerations.

BACKGROUND: Patients with early-stage renal cell carcinoma (RCC) are considered to be eligible donors. Although preliminary experience in using kidneys of specific pathologic types, mainly those with small renal masses (SRMs), have been established, multiorgan utilization of the same donor with SRMs is limited. METHODS: One deceased donor whose left-side kidney was diagnosed with Fuhrman grade I RCC was included. The tumor mass in the kidney was removed through partial nephrectomy according to the gold standard. Then, 3 transplant surgeries were performed, in which 1 recipient accepted kidney transplant after tumor exeresis, 1 simultaneous heart-kidney (the contralateral one) transplant, and 1 liver transplant. Recipients were followed up according to our standard protocol for renal cancers. (All allografts were allocated in compliance with the Declaration of Helsinki and the Declaration of Istanbul.) RESULTS: After 32 months, no radiographic findings showed any morphologic changes of the lesion, and all patients were in good condition, with neither tumor recurrence nor allograft rejection or infection. No complaints such as pain, oliguria, dyspnea, nausea, or fatigue were recorded. CONCLUSIONS: To the best of knowledge, this initial work takes the lead in elaborating the organ utilization of multiorgan donors with SRMs. We hope the experience will provide support for cross discussion concerned with multiorgan transplant from tumor-affected donors in clinical practices, further expand the donor pool and address the donor shortage problem.

CIRBP promotes ferroptosis by interacting with ELAVL1 and activating ferritinophagy during renal ischaemia-reperfusion injury.

Renal ischaemia-reperfusion (IR) is a major cause of acute kidney injury (AKI). Cold-inducible RNA-binding protein (CIRBP) may contribute to AKI because its deficiency protects against renal IR injury in a mechanism believed to involve ferroptosis. We aimed to investigate whether ferroptosis is associated with CIRBP-mediated renal damage. The differential expression of CIRBP was examined in tubular epithelial (HK2) cells during hypoxia-reoxygenation (HR) or in response to erastin, an inducer of ferroptosis. CIRBP expression was increased in response to HR or erastin in HK2 cells but the silencing of CIRBP inhibited HR and erastin-induced ferroptosis together with ferritinophagy. We discovered an interaction between CIRBP and ELAVL1 using STRING software, which was verified through co-immunoprecipitation and fluorescence colocalization assays. We found that ELAVL1 is a critical regulator in the activation of ferritinophagy and the promotion of ferroptosis. HR or erastin also induced the expression of ELAVL1. An autophagy inhibitor (hydroxychloroquine) or si-ELAVL1 transfection reversed CIRBP-enhanced ferritinophagy activation and ferroptosis in HK2 cells under HR. Injection of anti-CIRBP antibody into a mouse model of IR inhibited ferroptosis and decreased renal IR injury in vivo. In summary, our results provide evidence that ferritinophagy-mediated ferroptosis could be responsible for CIRBP-enhanced renal IR injury.

Pediatric kidney transplantation in China: an analysis from the IPNA Global Kidney Replacement Therapy Registry.

BACKGROUND: The International Pediatric Nephrology Association (IPNA) Global Kidney Replacement Therapy (KRT) Registry was established to evaluate the incidence and outcomes of kidney replacement therapy (dialysis and transplantation) provided to children worldwide. Analysis of registry data for separate regions is feasible. METHODS: Three centers located in Shanghai, Guangzhou, and Zhengzhou, which have the greatest number of pediatric kidney transplantation cases in China, participated in this analysis of transplant data. Data were registered by each center for patients under the age of 19 years who received a single-organ kidney transplant for the first time between 2011 and 2018. RESULTS: In total, 415 patients (59.8% male) aged 1.4-18.7 (median 12.1) years were followed for 0.3-97.1 (median 27.7) months. The number of kidney transplants increased from a total of 129 during 2011-2014 to 286 cases during 2015-2018. 85.8% of patients received the transplanted kidney from a pediatric (age < 19 years) donor, and deceased donors accounted for 94% of all donors. 8.0% of grafts were lost. One and 5-year patient survival rates were 97.6% and 95.5%, respectively. The major cause of death was infection (7/14). Similar graft and patient survival rates were observed for organs from pediatric and adult donors in 6-11 and 12-18 year recipient age groups, whereas recipients < 6 years showed inferior patient and graft survival. CONCLUSIONS: Pediatric kidney transplantation shows favorable short-term and medium-term outcomes in China. Our experience supports use of pediatric donors in pediatric kidney transplantation, but attention directed to the outcome of recipients aged under 6 is necessary. Graphical abstract.

ZnO UV Photodetectors Modified by Ag Nanoparticles Using All-Inkjet-Printing.

To further improve the performance of all-inkjet-printing ZnO UV photodetector and maintain the advantages of inkjet printing technology, the inkjet printing Ag nanoparticles (NPs) were deposited on the inkjet printing ZnO UV photodetector for the first time. The inkjet printing Ag NPs can passivate the surface defects of ZnO and work as surface plasmons from the characterization of photoluminescence (PL), X-ray photoelectron spectroscopy (XPS), and finite difference time domain method (FDTD) simulation. The normalized detectivity (D*) of the Ag NP-modified detector reaches to 1.45 × 1010 Jones at 0.715 mW incident light power, which is higher than that of 5.72 × 109 Jones of the bare ZnO photodetector. The power-law relationship between the photocurrent and the incident light power of the Ag NP-modified ZnO detector is Ipc ∝ P2.34, which means the photocurrent is highly sensitive to the change of incident light power.

On the origin of enhanced hole injection for AlGaN-based deep ultraviolet light-emitting diodes with AlN insertion layer in p-electron blocking layer.

For the [0001] oriented AlGaN-based deep ultraviolet light-emitting diodes (DUV LEDs), the holes in the p-type electron blocking layer (p-EBL) are depleted due to the polarization induced positive sheet charges at the last quantum barrier (LQB)/p-EBL interface. The hole depletion effect significantly reduces the hole injection capability across the p-EBL. In this work, we propose inserting a thin AlN layer between the LQB and the p-EBL, which can generate the hole accumulation at the AlN/p-EBL interface. Meanwhile, the holes can obtain the energy when traveling from the p-EBL into the multiple quantum wells (MQWs) by intraband tunneling through the thin AlN layer. As a result, the hole injection and the external quantum efficiency (EQE) have been remarkably enhanced. Moreover, we point out that the thick AlN insertion layer can further generate the hole accumulation in the p-EBL and increase the hole energy which helps to increase the hole injection. We also prove that the intraband tunneling for holes across the thick AlN insertion layer is facilitated by using the optimized structure.

SHP-1 inhibits renal ischemia reperfusion injury via dephosphorylating ASK1 and suppressing apoptosis.

Apoptosis of tubular epithelium cells (TECs) plays critical roles in renal ischemia reperfusion (I/R) injury, but the molecular regulatory mechanisms of apoptosis still require further investigation. Recently, phosphatase family members have been suggested to regulate multiple aspects of the injury and regeneration response. However, the roles of SHP-1, an important protein-tyrosine phosphatase, in the regulation of renal I/R injury remain unknown. Here, we found that SHP-1 knockdown in vivo significantly increased renal I/R injury and aggravated the apoptosis of TECs. Consistently, after SHP-1 knockdown in TECs in vitro, a sharp increase of apoptosis induced by cobalt dichloride was found. The protective role of SHP-1 was also validated in a TEC cell line stably overexpressing SHP-1. Mechanistically, the ASK1/MKK4/JNK pro-apoptosis signal was over activated after SHP-1 knockdown, and SHP-1 could bind to and dephosphorylate ASK1 to inhibit its activation, thus repressing apoptosis.

Growth of pediatric recipients after renal transplantation from small pediatric deceased donors weighing less than 15 kg.

RTx is currently the best treatment for children with ESRD. This study retrospectively analyzed the outcomes of growth after RTx using the pediatric-to-pediatric allocation strategy and some factors that may affect it. From March 2012 to August 2016, 8 en bloc and 38 single pediatric RTxs were performed at our center using organs from small pediatric deceased donors (weight < 15 kg). Growth before and after RTx was analyzed according to the height-for-age z-score at RTx, the 3-year follow-up, and adulthood and compared between the procedures. The chi-square test and multiple linear regression analysis were used for statistical analyses. Overall, 79.2% of children were diagnosed with chronic nephritis before RTx; 14.6% of cases were due to congenital urinary tract malformation, and 6.3% of cases were due to unknown causes. All grafts and patients survived postoperatively. The mean estimated GFRs were 92.7 ± 28.6 mL/min/1.73 m2 , 100.9 ± 32.3 mL/min/1.73 m2 , and 110.1 ± 34.8 mL/min/1.73 m2 at 1, 2, and 3 years' postoperatively, respectively. The children's postoperative growth and development, particularly during the first year postoperatively, improved but were negatively correlated with age and the height-for-age z-score before RTx. The growth of children after RTx was moderate and accelerated during prepubescence. The rate of post-RTx growth during the first year postoperatively was unrelated to the recipient's sex or duration of dialysis (P > 0.05) but was negatively correlated with age at RTx (r = -0.349, P = 0.043). Future studies on the long-term outcomes are still needed.

SIRT3 Protects Against Acute Kidney Injury via AMPK/mTOR-Regulated Autophagy.

Acute kidney injury (AKI), which involves the loss of kidney function caused by damage to renal tubular cells, is an important public health concern. We previously showed that sirtuin (SIRT)3 protects the kidneys against mitochondrial damage by inhibiting the nucleotide-binding domain (NOD)-like receptor protein 3 (NLRP3) inflammasome, attenuating oxidative stress, and downregulating proinflammatory cytokines. In this article, we investigated the role of autophagy, mediated by a mammalian target of rapamycin (mTOR) and AMP-activated protein kinase (AMPK), in the protective effect of SIRT3, against sepsis-induced AKI, in a mouse model of cecal ligation and puncture (CLP). The AKI in CLP mice was associated with the upregulation of autophagy markers; this effect was abolished in SIRT3- mice in parallel with the downregulation of phospho (p)-AMPK and the upregulation of p-mTOR. Pretreatment with the autophagy inhibitor 3-methyladenine (3-MA) or AMPK inhibitor compound isotonic saline (C), exacerbated AKI. SIRT3 overexpression promoted autophagy, upregulated p-AMPK and downregulated p-mTOR in CLP mice, attenuating sepsis-induced AKI, tubular cell apoptosis, and inflammatory cytokine accumulation in the kidneys. The blockage of autophagy induction largely abolished the protective effect of SIRT3 in sepsis-induced AKI. These findings indicate that SIRT3 protects against CLP-induced AKI by inducing autophagy through regulation of the AMPK/mTOR pathway.

Influence of Quantum-Well Width on the Electroluminescence Properties of AlGaN Deep Ultraviolet Light-Emitting Diodes at Different Temperatures.

The influence of quantum-well (QW) width on electroluminescence properties of AlGaN deep ultraviolet light-emitting diodes (DUV LEDs) was studied at different temperatures. The maximum external quantum efficiency (EQE) ratios of LED with 3.5 nm QW to that with 2 nm increased from 6.8 at room temperature (RT) to 8.2 at 5 K. However, the ratios for LED with 3.5 nm QW to that with 5 nm QW decreased from 4.8 at RT to 1.6 at 5 K. The different changes of EQE ratios were attributed to the decrease of non-radiative recombination and the increase of volume of the active region. From theoretical analysis, the LED with 2-nm wells had a shallowest barrier for electron overflow due to the quantum-confined effect, whereas the LED with 5-nm wells showed the least overlap of electron and hole due to the large internal field. Therefore, the LED with 3.5 nm QW had the highest maximum EQE at the same temperature. As temperature decreased, the current for maximum EQE decreased for all the LEDs, which was believed to be due to the increase of electron which overflowed out of QWs and the decrease of hole concentration. The results were helpful for understanding the combination of polarization effect and electron overflow in DUV LEDs.

Astronomical tuning and magnetostratigraphy of Neogene biogenic reefs in Xisha Islands, South China Sea.

Biogenic reefs are one of two major depositional types in the South China Sea, and are constructed by coral, algae and bryozoa. The West Pacific is a major area of biogenic reef development and plays a critical role in the global carbon cycle. However, the lack of geochronological studies in previous works inhibits our understanding of their contributions. Herein, we conduct a cyclostratigraphic and magnetostratigraphic study on Neogene biogenic reefs using the XK-1 core that was drilled at the Shidao Island, Xisha (Paracel) Islands. The main findings of this study are: (1) the establishment of reliable magentostratigraphy for Ledong, Huangliu, Meishan and Sanya Formations; (2) the magnetic susceptibility variation can be inferred as growth index and tuned to the 405-ka long eccentricity cycle; (3) the astronomical geochronology suggests that the bottom ages for Ledong, Yinggehai, Huangliu, Meishan, and Sanya Formations are 2.2 Ma, 5.7 Ma, 10.4 Ma, 16.6 Ma, and 24.3 Ma, respectively; and (4) Earth's eccentricity and obliquity played predominant roles in biogenic reef establishment on orbital to tectonic timescales. Thus, the reported geochronology offers an opportunity to test the contributions of various factors and hypothesize their roles in the global carbon cycle in future.

Characterization of new bone morphogenetic protein (Bmp)-2 regulatory alleles.

Bone morphogenetic protein 2 (BMP2, HGNC:1069, GeneID: 650) is a classical morphogen; a molecule that acts at a distance and whose concentration influences cell proliferation, differentiation, and apoptosis. Key events requiring precise Bmp2 regulation include heart specification and morphogenesis and neural development. In mesenchymal cells, the concentration of BMP2 influences myogenesis, adipogenesis, chondrogenesis, and osteogenesis. Because the amount, timing, and location of BMP2 synthesis influence pattern formation and organogenesis, the mechanisms that regulate Bmp2 are crucial. A sequence within the 3'UTR of the Bmp2 mRNA termed the "ultra-conserved sequence" (UCS) has been largely unchanged since fishes and mammals diverged. Cre-lox mediated deletion of the UCS in a reporter transgene revealed that the UCS may repress Bmp2 in proepicardium, epicardium, and epicardium-derived cells (EPDC) and in tissues with known epicardial contributions (coronary vessels and valves). The UCS also repressed the transgene in the aorta, outlet septum, posterior cardiac plexus, cardiac and extra-cardiac nerves, and neural ganglia. We used homologous recombination and conditional deletion to generate three new alleles in which the Bmp2 3'UTR was altered as follows: a UCS flanked by loxP sites with or without a neomycin resistance targeting vector, or a deleted UCS. Deletion of the UCS was associated with elevated Bmp2 mRNA and BMP signaling levels, reduced fitness, and embryonic malformations.

Protective effects of sirtuin 3 in a murine model of sepsis-induced acute kidney injury.

Acute kidney injury (AKI) is a rapid loss of kidney function characterized by damage to renal tubular cells driven by mitochondrial dysregulation and oxidative stress. Here, we used a murine caecal ligation and puncture (CLP) model of sepsis-induced AKI to study the role of sirtuin 3 (SIRT3), a NAD(+) dependent deacetylase critical for the maintenance of mitochondrial viability, in AKI-related renal tubular cell damage and explored the underlying mechanisms. CLP induced alterations in kidney function and morphology were associated with SIRT3 downregulation, and SIRT3 deletion exacerbated CLP-induced kidney dysfunction, renal tubular cell injury and apoptosis, mitochondrial alterations, and ROS production in a knockout mouse model. SIRT3 deletion increased the CLP-induced upregulation of the NLRP3 inflammasome and apoptosis-associated speck-like protein, resulting in the activation of oxidative stress, increased production of the proinflammatory cytokines interleukin (IL)-1ß and IL-18, and the enhancement of apoptosis, and these effects were reversed by antioxidant NAC. Our results suggest that SIRT3 plays a protective role against mitochondrial damage in the kidney by attenuating ROS production, inhibiting the NRLP3 inflammasome, attenuating oxidative stress, and downregulating IL-1ß and IL-18.

Interleukin-22 promotes papillary thyroid cancer cell migration and invasion through microRNA-595/Sox17 axis.

Interleukin-22 (IL-22) is an inflammatory cytokine mainly produced by activated Th17 and Th22 cells. The data presented here demonstrate that IL-22 induced the migration and invasion of papillary thyroid cancer (PTC) cells. MicroRNA expression analysis and functional studies indicated that IL-22-mediated migration and invasion is positively regulated by miR-595. Further mechanistic studies revealed that sex-determining region Y-box 17 (Sox17) is directly targeted by miR-595. We then demonstrated that IL-22 regulated migration and invasion of PTC cells via inhibiting Sox17 expression. Interestingly, in PTC cell lines and PTC tissues, expression of IL-22 and miR-595 was upregulated and Sox17 downregulated compared with normal thyroid, and their expression levels were closely correlated. Taken together, this present study suggests that IL-22 stimulation enhances the migration and invasion of PTC cells by regulating miR-595 and its target Sox17.

Optimizing the utilization of kidneys from small pediatric deceased donors under 15 kg by choosing pediatric recipients.

Currently, most kidneys from small pediatric deceased donors are transplanted into adult recipients (i.e., PTA). However, due to the weight mismatch, there is a high discard rate and a high ratio of EBKTs if adopting PTA. Here, we sought both to optimize utilization of these challenging but scarce donor grafts by selecting pediatric recipients and to characterize the feasibility and efficacy of this PTP allocation strategy. From February 2012 to October 2014, kidneys from 27 infant donors ≤ 15 kg were procured and distributed to 38 pediatric candidates in our center. The grafts were utilized for EBKT if the donor weighed 2.5-5 kg and for SKT if the donor weighed 5-15 kg, leading to 10 EBKTs and 28 SKTs. The overall utilization rate from small pediatric deceased donors was 94.12%. After a follow-up of 3-26 months, the graft survival rate was 89.47%, with four graft losses due to vascular thrombosis. Kidneys from low-body-weight donors should be applied to pediatric recipients, and the kidneys from infant donors ≥ 5 kg can be used in single-kidney-transplant procedures at experienced centers to optimize utilization.

Transformation of organ donation in China.

The organ donation system in China has far lagged behind international levels. Transformation of this situation began in July 2005. A complete organ donation system that ensures fairness, impartiality, transparency, and respect for life has now been developed. This system is composed of regulations and policies, an organizational structure, operational guidelines, organ procurement organizations, registration of donors and recipients, and an organ allocation system. Since March 2010, pilot trials on donation after circulatory death (DCD) have been carried out. In 4 years, organ donation has started in 25 of 32 provinces in the country. From 2010 to 2013, the ratio of DCD liver transplantation to total case numbers in China rose from 1.38% to 26.1%, whereas for kidney, the ratio were 0.59% and 24.6%, respectively. The total number of DCD in China has accumulated to 1564 cases, and 4243 organs were transplanted. To alleviate the further difficulties of donation, establishment of professional organ procurement organizations in transplant hospitals, legislation of brain death, and promulgation of legal guidelines on DCD will be the main targets of organ donation development in China.