PacBio single-molecule long-read sequencing provides new insights into the complexity of full-length transcripts in oriental river prawn, macrobrachium nipponense.

BACKGROUND: Oriental river prawn (Macrobrachium nipponense) is one of the most dominant species in shrimp farming in China, which is a rich source of protein and contributes to a significant impact on the quality of human life. Thus, more complete and accurate annotation of gene models are important for the breeding research of oriental river prawn. RESULTS: A full-length transcriptome of oriental river prawn muscle was obtained using the PacBio Sequel platform. Then, 37.99 Gb of subreads were sequenced, including 584,498 circular consensus sequences, among which 512,216 were full length non-chimeric sequences. After Illumina-based correction of long PacBio reads, 6,599 error-corrected isoforms were identified. Transcriptome structural analysis revealed 2,263 and 2,555 alternative splicing (AS) events and alternative polyadenylation (APA) sites, respectively. In total, 620 novel genes (NGs), 197 putative transcription factors (TFs), and 291 novel long non-coding RNAs (lncRNAs) were identified. CONCLUSIONS: In summary, this study offers novel insights into the transcriptome complexity and diversity of this prawn species, and provides valuable information for understanding the genomic structure and improving the draft genome annotation of oriental river prawn.

Impact of a novel prognostic model on allogeneic hematopoietic stem cell transplantation outcomes in patients with CMML.

Chronic myelomonocytic leukemia (CMML) is a clonal hematopoietic stem cell malignancy, and allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the only curable treatment. The outcomes after transplant are influenced by both disease characteristics and patient comorbidities. To develop a novel prognostic model to predict the post-transplant survival of CMML patients, we identified risk factors by applying univariable and multivariable Cox proportional hazards regression to a derivation cohort. In multivariable analysis, advanced age (hazard ratio [HR] 3.583), leukocyte count (HR 3.499), anemia (HR 3.439), bone marrow blast cell count (HR 2.095), and no chronic graft versus host disease (cGVHD; HR 4.799) were independently associated with worse survival. A novel prognostic model termed ABLAG (Age, Blast, Leukocyte, Anemia, cGVHD) was developed and the points were assigned according to the regression equation. The patients were categorized into low risk (0-1), intermediate risk (2, 3), and high risk (4-6) three groups and the 3-year overall survival (OS) were 93.3% (95%CI, 61%-99%), 78.9% (95%CI, 60%-90%), and 51.6% (95%CI, 32%-68%; p < .001), respectively. In internal and external validation cohort, the area under the receiver operating characteristic (ROC) curves of the ABLAG model were 0.829 (95% CI, 0.776-0.902) and 0.749 (95% CI, 0.684-0.854). Compared with existing models designed for the nontransplant setting, calibration plots, and decision curve analysis showed that the ABLAG model revealed a high consistency between predicted and observed outcomes and patients could benefit from this model. In conclusion, combining disease and patient characteristic, the ABLAG model provides better survival stratification for CMML patients receiving allo-HSCT.

The Correlation of Inflammation, Oxidative Stress, and Hippocampal Perfusion in Patients with Atrial Fibrillation.

Atrial fibrillation (AF) is closely related to abnormal cerebral blood flow. Inflammation and oxidative stress have always been important factors in the pathophysiology of AF. It remains unknown whether inflammation and oxidative stress are correlated to hippocampal perfusion in patients with AF.Sixty-three patients with AF with normal hippocampal blood perfusion (NHBP) were compared to 71 patients with AF with abnormal hippocampal blood perfusion (AHBP) using a case-control study design. The serum levels of inflammation and oxidative stress were measured. The hippocampal perfusion was detected. (1) The serum levels of high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and oxidized low-density lipoprotein (ox-LDL) were statistically higher in the AHBP group than in the NHBP group. In the AHBP subgroup analysis, the serum levels of hs-CRP and IL-6 were statistically higher in patients with persistent AF than those with paroxysmal AF. (2) The relative cerebral blood volume (rCBV), mean transit time (MTT), and the time-to-peak (TTP) were statistically higher in the AHBP group than in the NHBP group. Moreover, cerebral blood flow (rCBF) was statistically lower in the AHBP group than in the NHBP group. (3) relative cerebral blood volume (rCBV), rCBF, MTT, and TTP were passively associated with serum hs-CRP and IL-6; rCBV, rCBF, and MTT were positively associated with ox-LDL. The serum levels of hs-CRP, IL-6, and ox-LDL were associated with AHBP in patients with AF after multivariate logistic regression analysis.Oxidative stress and inflammatory biomarkers were increased in patients with AF with AHBP, in which the serum levels of hs-CRP and IL-6 in the persistent AF group were statistically higher than those in the paroxysmal AF group. The serum levels of hs-CRP, IL-6, and ox-LDL were associated with AHBP in patients with AF.

L-Cysteine attenuates osteopontin-mediated neuroinflammation following hypoxia-ischemia insult in neonatal mice by inducing S-sulfhydration of Stat3.

We previously show that L-Cysteine administration significantly suppresses hypoxia-ischemia (HI)-induced neuroinflammation in neonatal mice through releasing H2S. In this study we conducted proteomics analysis to explore the potential biomarkers or molecular therapeutic targets associated with anti-inflammatory effect of L-Cysteine in neonatal mice following HI insult. HI brain injury was induced in postnatal day 7 (P7) neonatal mice. The pups were administered L-Cysteine (5 mg/kg) at 24, 48, and 72 h post-HI. By conducting TMT-based proteomics analysis, we confirmed that osteopontin (OPN) was the most upregulated protein in ipsilateral cortex 72 h following HI insult. Moreover, OPN was expressed in CD11b+/CD45low cells and infiltrating CD11b+/CD45high cells after HI exposure. Intracerebroventricular injection of OPN antibody blocked OPN expression, significantly attenuated brain damage, reduced pro-inflammatory cytokine levels and suppressed cerebral recruitment of CD11b+/CD45high immune cells following HI insult. L-Cysteine administration reduced OPN expression in CD11b+/CD45high immune cells, concomitant with improving the behavior in Y-maze test and suppressing cerebral recruitment of CD11b+/CD45high immune cells post-HI insult. Moreover, L-Cysteine administration suppressed the Stat3 activation by inducing S-sulfhydration of Stat3. Intracerebroventricular injection of Stat3 siRNA not only decreased OPN expression, but also reversed HI brain damage. Our data demonstrate that L-Cysteine administration effectively attenuates the OPN-mediated neuroinflammation by inducing S-sulfhydration of Stat3, which contributes to its anti-inflammatory effect following HI insult in neonatal mice. Blocking OPN expression may serve as a new target for therapeutic intervention for perinatal HI brain injury.

Screening for Immune-Related RNA Biomarkers of Aneurysmal Subarachnoid Hemorrhage.

PURPOSE: Through comprehensive bioinformatics analysis based on the immune microenvironment, this study aimed to identify immune-related RNA biomarkers that indicate aneurysmal subarachnoid hemorrhage (aSAH). METHODS: The GSE73378 dataset was downloaded from the National Center for Biotechnology Information GEO database, providing blood from 107 normal controls and 103 patients with aSAH. The immune infiltration types in the aSAH blood samples were assessed and RNAs that were differentially expressed (DE) between 1) the aSAH and control groups and 2) the immune infiltration groups (high and low) were identified. The intersecting genes were subjected to weighted gene co-expression network analysis followed by co-expression network construction. The aSAH-related genes and pathways were identified from the Comparative Toxicogenomics Database: update 2019. RESULTS: A total of three DE long non-coding RNAs (lncRNAs) and 301 DE mRNAs were identified. Of the 301 mRNAs, 91 were significantly enriched in three modules. Based on the 91 mRNAs and three lncRNAs, a co-expression network related to the disease pathway was constructed. This pathway consisted of 16 factors, including the 13 mRNAs (e.g., TNFSF13B, TNFSF10, MYD88, GNA12 and NSMAF) and three lncRNAs (FAM66A, LINC00954 and CELF2-AS2), as well as six pathways, including the NF-κB, toll-like receptor, and sphingolipid signalling pathways. CONCLUSION: TNFSF13B, MYD88, GNA12, NSMAF, FAM66A, LINC00954 and CELF2-AS2 may serve as biomarkers for aSAH. The NF-κB, toll-like receptor and sphingolipid signalling pathways may play critical roles in the progression of aSAH.

Optimized Design of a Pump Laser System for a Spin Exchange Relaxation Free Inertial Measurement Device.

In order to improve the precision and beam quality of a pump laser for a spin exchange relaxation free inertial measurement device, we applied one scheme to achieve the square wave modulation and power stability control of the pump laser and another one to obtain the uniform intensity distribution of the laser beam, in which the acousto-optic modulator (AOM) and proportion integration differentiation (PID) controller were used to achieve the former, and the freeform surface lens was designed and optimized to achieve the latter based on the TracePro software. In experiments, the first-order diffraction light beam coming through the AOM had a spot size of about 1.1×0.7 mm2, and a spherical vapor cell with a radius of 7 mm was placed behind the freeform surface lens. Results show that the uniformity of the reshaped intensity distribution is higher than 90% within the target area with a radius of 7 mm both in the simulation and the experiment, which ensure that the uniform laser beam covers the area of cell. On the other hand, the power stability of the pump laser is controlled to be less than 0.05%. Compared with traditional methods, the complicated calculation process in optical design is better solved, and a higher uniformity with slight energy loss is achieved.

Effects of Levosimendan on Systemic Perfusion in Patients with Low Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) Score: Experience from a Single Center in Taiwan.

BACKGROUND: Patients with cardiogenic shock have a high risk of mortality. Intravenous levosimendan can provide pharmacologic inotrope support. OBJECTIVES: We aimed to investigate the effect of levosimendan in patients with extremely severe cardiogenic shock and low Interagency Registry for Mechanically Assisted Circulatory Support (INTERMACS) score with or without mechanical circulatory support. METHODS: From January 2017 to May 2019, 24 patients with INTERMACS 1-4 were enrolled in this retrospective study. All patients had systemic malperfusion and were treated with levosimendan. Biochemistry data related to systemic perfusion were recorded and compared before and at 24 and 72 hours after levosimendan administration. Echocardiography and Kansas City Cardiomyopathy Questionnaire (KCCQ) were completed 2 months later to assess left ventricular ejection fraction (LVEF) and quality of life (QoL), respectively. RESULTS: Arterial pressure and heart rate did not significantly differ before and after levosimendan administration. Atrial fibrillation and ventricular premature complex increased without significance. The dose of inotropes could be significantly tapered down. There were no significant differences in blood urea nitrogen, creatinine, and lactate levels. Urine output significantly increased (p = 0.018), and liver-related enzymes improved but without significance. B-type natriuretic peptide significantly decreased (p = 0.007) at 24 hours after levosimendan administration. Echocardiography showed significantly improved LVEF 2 months later (22.43 ± 8.13% to 35.87 ± 13.4%, p = 0.001). KCCQ showed significantly improved physical activity and greater relief of symptoms (p = 0.003). The survival-to-discharge rate was 75%. CONCLUSIONS: We observed a decrease in B-type natriuretic peptide, better urine output, and alleviated hepatic injury in the levosimendan group. Most patients who survived without transplantation had significantly improved LVEF and better QoL after levosimendan administration.

Decoy receptor 2 mediation of the senescent phenotype of tubular cells by interacting with peroxiredoxin 1 presents a novel mechanism of renal fibrosis in diabetic nephropathy.

Premature senescence of renal tubular epithelial cell (RTEC), which is involved in kidney fibrosis, is a key event in the progression of diabetic nephropathy. However, the underlying mechanism remains unclear. Here we investigated the role and mechanism of decoy receptor 2 (DcR2) in kidney fibrosis and the senescent phenotype of RTEC. DcR2 was specifically expressed in senescent RTEC and associated with kidney fibrosis in patients with diabetic nephropathy and mice with streptozotocin-induced with diabetic nephropathy. Knockdown of DcR2 decreased the expression of α-smooth muscle actin, collagen I, fibronectin and serum creatinine levels in streptozotocin-induced mice. DcR2 knockdown also inhibited the expression of senescent markers p16, p21, senescence-associated beta-galactosidase and senescence-associated heterochromatic foci and promoted the secretion of a senescence-associated secretory phenotype including IL-6, TGF-ß1, and matrix metalloproteinase 2 in vitro and in vivo. However, DcR2 overexpression showed the opposite effects. Quantitative proteomics and validation studies revealed that DcR2 interacted with peroxiredoxin 1 (PRDX1), which regulated the cell cycle and senescence. Knockdown of PRDX1 upregulated p16 and cyclin D1 while downregulating cyclin-dependent kinase 6 expression in vitro, resulting in RTEC senescence. Furthermore, PRDX1 knockdown promoted DcR2-induced p16, cyclin D1, IL-6, and TGF-ß1 expression, whereas PRDX1 overexpression led to the opposite results. Subsequently, DcR2 regulated PRDX1 phosphorylation, which could be inhibited by the specific tyrosine kinase inhibitor genistein. Thus, DcR2 mediated the senescent phenotype of RTEC and kidney fibrosis by interacting with PRDX1. Hence, DcR2 may act as a potential therapeutic target for the amelioration of diabetic nephropathy progression.

Retraction Note to: Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC­1 cell apoptosis via activating the mROS­HtrA2/Omi pathways.

[This retracts the article DOI: 10.1186/s12935-018-0665-1.].

Efficacy and safety of rivaroxaban on the resolution of left atrial/left atrial appendage thrombus in nonvalvular atrial fibrillation patients.

Data on LA/LAA thrombus resolution after rivaroxaban treatment has not been established. The aim of the present study was to compare the efficacy and safety on the resolution of LA/LAA thrombus between rivaroxaban and warfarin in nonvalvular atrial fibrillation (AF) patients. 80 AF patients with LA/LAA thrombus between January 2013 and June 2016 were randomized divided into warfarin group (n = 40) and rivaroxaban group (n = 40). Compared to warfarin group, thrombin time (TT; p < 0.0001), plasma prothrombin time (PT; p < 0.0001), and activated partial thromboplastin time (APTT; p = 0.0019) were significantly lower, and fibrinogen (FIB; p < 0.0001) was significantly higher in rivaroxaban group. TEE shown the average length (p < 0.0001), average width (p = 0.0008) and average area (p < 0.0001) of thrombus were significantly lower in rivaroxaban group compared to warfarin group after 6-week treatments. No major or fatal bleeding and ischemic stroke occurred in both two groups. The 20 mg dose Rivaroxaban is more effective than warfarin on the resolution of LA/LAA thrombus in nonvalvular AF patients especially after 6-week treatments. The results suggest that rivaroxaban is a potential option for the treatment of LA/LAA thrombus in patients with nonvalvular AF.

Prediction of lifetime by lumen degradation and color shift for LED lamps, in a non-accelerated reliability test over 20,000 h.

Although the predicted lifetime of the classical 6000 h test given by Energy Star is taken as the normal lifetime of LED products in most research and applications, the aim of this study is to explore the error in lifetime prediction of LED lamps based on the 6000 h test. A non-accelerated aging test with 10 LED lamps is conducted for 20,000 h (from March 2016 to now) under room temperature, which is long enough for this kind of lamp reaching the real lifetime with the normalized luminous flux dropping to 70% naturally. At different aging periods, the correspondent lifetime of each sample is predicted by the lumen degradation, and the median lifetime τ0.5 of 10 samples is obtained by applying the Weibull distribution. Result shows that the τ0.5 of the real lifetime is 16,867 h in this work, and the aging time should be at least 9000 h to make the error in predicting the lifetime less than 3%. On the other hand, the Du'v' values of 0.006, 0.007, and 0.008 are taken as the three thresholds for predicting the lifetime by color shift. For the case of 0.008, the calculated shape parameter of 8.4 in Weibull distribution is similar with that of the real lifetime, which means the Du'v' of 0.008 for this kind of lamp gives the same failure mechanism as that of lumen degradation of 70%.

Bioinformatic analysis to explore key genes associated with brain ischemia-reperfusion injury in rats.

Objectives: Ischemia-reperfusion (I/R) injury can aggravate the dysfunction and structural damage of tissues and organs. This study aimed at investigating the pathogenesis of I/R injury. Methods: GSE82146 was extracted from Gene Expression Omnibus database, which included 12 nonischemic control (NIC) hippocampal tissues and 15 complete global brain ischemia (CGBI)-reperfusion hippocampal tissues. After processing the original data using the affy package, the differentially expressed genes (DEGs) between CGBI and NIC samples were analysed by the limma package. An enrichment analysis for the DEGs was implemented based on the MATHT online tool. Using Cytoscape software, a protein-protein interaction (PPI) network was built and significant network modules were obtained. Finally, miRNA-gene pairs were predicted using the miRWalk2.0 tool, and the miRNA-gene regulatory network was built using the Cytoscape software. Results: Overall, 322 DEGs (279 upregulated and 43 downregulated) were present in the CGBI samples. In PPI network, JUN, STAT3, ATF3, VEGFA and ATF4 had higher degrees. Four significant modules (modules a, b, c and d) were obtained from PPI network. Enrichment analysis suggested that FGF2 in module d was involved in MAPK signalling pathway. In the miRNA-gene regulatory network, rno-miR-125a-5p and rno-miR-125b-5p were among the top 10 miRNAs. Conclusion: JUN, STAT3, ATF3, VEGFA, ATF4, FGF2, rno-miR-125a-5p and rno-miR-125b-5p might affect the development and progression of I/R injury.

The implication of seniority of supervising attending surgeon on the reexploration rate following elective coronary artery bypass grafting.

BACKGROUND AND AIMS: During coronary artery bypass graft (CABG) surgery, the residual hemostasis procedures, from weaning cardiopulmonary bypass to closing sternotomy, are always completed by residents and supervised by attending surgeons. We want to evaluate the teaching effectiveness for residents under the supervision of attending surgeons with different levels of seniority. MATERIALS AND METHODS: Between January 1st 2001 and December 31st 2010, 2279 consecutive CABG surgeries were performed in our medical center. In total, 83 patients underwent a reexploration for postoperative bleeding. All causes of bleeding were identified and recorded. Competent attending surgeons were defined as having >3 years' experience and young attending surgeons with ≦3 years' experience. We compared the reexploration rate and aimed to identify the common sources of bleeding by the two groups. We also assessed the impact of attending experience on the outcomes and major complications after reexploration. RESULTS: There were 36 surgical bleeding and 17 non-surgical bleeding in the young group and 16 surgical bleeding and 14 non-surgical bleeding in the competent group. The young group experienced more mediastinal drainage before a reexploration and a longer time interval to a reexploration. However, both are without statistical significance. Furthermore, the young group has a significant longer hospital stay. The most common intra-pericardium surgical bleeding included two-stage cannulation, side branch of the left internal mammary artery (LIMA), and side branch of vein grafts. The most common extra-pericardium surgical bleeding included a puncture hole by sternal wires, LIMA bed, and fragile sternum. CONCLUSION: Young attending surgeons indeed had both higher incidence of reexploration and surgical bleeding after a CABG. However, the supervisor experience only impacted hospital stay, not major complications or mortality after a reexploration. This might imply the competent attending surgeons provide higher teaching effectiveness for the hemostasis procedure after CABG.

Excessive mitochondrial fragmentation triggered by erlotinib promotes pancreatic cancer PANC-1 cell apoptosis via activating the mROS-HtrA2/Omi pathways.

BACKGROUND: Mitochondrial fragmentation drastically regulates the viability of pancreatic cancer through a poorly understood mechanism. The present study used erlotinib to activate mitochondrial fragmentation and then investigated the downstream events that occurred in response to mitochondrial fragmentation. METHODS: Cell viability and apoptosis were determined via MTT assay, TUNEL staining and ELISA. Mitochondrial fragmentation was measured via an immunofluorescence assay and qPCR. siRNA transfection and pathway blockers were used to perform the loss-of-function assays. RESULTS: The results of our study demonstrated that erlotinib treatment mediated cell apoptosis in the PANC-1 pancreatic cancer cell line via evoking mitochondrial fragmentation. Mechanistically, erlotinib application increased mitochondrial fission and reduced mitochondrial fusion, triggering mitochondrial fragmentation. Subsequently, mitochondrial fragmentation caused the overproduction of mitochondrial ROS (mROS). Interestingly, excessive mROS induced cardiolipin oxidation and mPTP opening, finally facilitating HtrA2/Omi liberation from the mitochondria into the cytoplasm, where HtrA2/Omi activated caspase-9-dependent cell apoptosis. Notably, neutralization of mROS or knockdown of HtrA2/Omi attenuated erlotinib-mediated mitochondrial fragmentation and favored cancer cell survival. CONCLUSIONS: Together, our results identified the mROS-HtrA2/Omi axis as a novel signaling pathway that is activated by mitochondrial fragmentation and that promotes PANC-1 pancreatic cancer cell mitochondrial apoptosis in the presence of erlotinib.

Lumen degradation analysis of LED lamps based on the subsystem isolation method.

The lumen degradation of LED lamps undergoing an accelerated aging test is investigated. The entire LED lamp is divided into three subsystems, namely, driver, lampshade, and LED light source. The parameters of output power [Watts (W)], transmittance (%), and lumen flux (lm) are adopted in the analysis of the degradation of the driver, lampshade, and LED light source, respectively. Two groups of LED lamps are aged under the ambient temperatures of 25°C and 85°C, respectively, with the aging time of 2000 h. The lumen degradation of the lamps is from 3.8% to 4.9% for the group under a temperature of 25°C and from 10.6% to 12.7% for the group under a temperature of 85°C. The LED light source is the most aggressive part of the three subsystems, which accounts for 70.5% of the lumen degradation of the LED lamp on average. The lampshade is the second degradation source, which causes 21.5% of the total amount on average. The driver is the third degradation source, which causes 6.5% under 25°C and 2.8% under 85°C of the total amount on average.

Transcription Factor Trps1 Promotes Tubular Cell Proliferation after Ischemia-Reperfusion Injury through cAMP-Specific 3',5'-Cyclic Phosphodiesterase 4D and AKT.

Trichorhinophalangeal 1 (Trps1) is a transcription factor essential for epithelial cell morphogenesis during kidney development, but the role of Trps1 in AKI induced by ischemia-reperfusion (I/R) remains unclear. Our study investigated Trps1 expression during kidney repair after acute I/R in rats and explored the molecular mechanisms by which Trps1 promotes renal tubular epithelial cell proliferation. Trps1 expression positively associated with the extent of renal repair after I/R injury. Compared with wild-type rats, rats with knockdown of Trps1 exhibited significantly delayed renal repair in the moderate I/R model, with lower GFR levels and more severe morphologic injury, whereas rats overexpressing Trps1 exhibited significantly accelerated renal repair after severe I/R injury. Additionally, knockdown of Trps1 inhibited and overexpression of Trps1 enhanced the proliferation of renal tubular epithelial cells in rats. Chromatin immunoprecipitation sequencing assays and RT-PCR revealed that Trps1 regulated cAMP-specific 3',5'-cyclic phosphodiesterase 4D (Pde4d) expression. Knockdown of Trps1 decreased the renal protein expression of Pde4d and phosphorylated Akt in rats, and dual luciferase analysis showed that Trps1 directly activated Pde4d transcription. Furthermore, knockdown of Pde4d or treatment with the phosphatidylinositol 3 kinase inhibitor wortmannin significantly inhibited Trps1-induced tubular cell proliferation in vitro Trps1 may promote tubular cell proliferation through the Pde4d/phosphatidylinositol 3 kinase/AKT signaling pathway, suggesting Trps1 as a potential therapeutic target for kidney repair after I/R injury.

3D carbon nanosphere and gold nanoparticle-based voltammetric cytosensor for cell line A549 and for early diagnosis of non-small cell lung cancer cells.

An electrochemical cytosensor for the detection of the non-small-cell lung cancer cell line A549 (NSCLC) had been developed. A microwave-hydrothermal method was employed to prepare monodisperse colloidal carbon nanospheres (CNSs). Gold nanoparticles (AuNPs) were placed on the surface of the colloidal CNSs by self-assembly to obtain 3D-structured microspheres of the type CNS@AuNP. The results of an MTT assay show the microspheres to possess good biocompatibility. The CNS@AuNP nanocomposite was then placed, in a chitosan film, on a glassy carbon electrode (GCE). The voltammetric signals and detection sensitivity are significantly enhanced owing to the synergistic effect of CNSs and AuNPs. A cytosensor was then obtained by immobilization of antibody against the carcinoembryonic antigen (which is a biomarker for NSCLC) on the GCE via crosslinking with glutaraldehyde. Hexacyanoferrate is used as an electrochemical probe, and the typical working voltage is 0.2 V (vs. SCE). If exposed to A549 cells, the differential pulse voltammetric signal decreases in the 4.2 × 10-1 to 4.2 × 10-6 cells mL-1 concentration range, and the detection limit is 14 cells mL-1 (at S/N = 3). Graphical abstract Schematic presentation of design strategy and fabrication process of the electrochemical cytosensor for A549 cells. (CNS: carbon nanospheres; GA: glutaraldehyde; PEI: polyethyleneimine; AuNPs: gold nanoparticles; BSA: Bovine serum albumin).

Realization and Technology Acceptance Test of a Wearable Cardiac Health Monitoring and Early Warning System with Multi-Channel MCGs and ECG.

In this work, a wearable smart clothing system for cardiac health monitoring with a multi-channel mechanocardiogram (MCG) has been developed to predict the myo-cardiac left ventricular ejection fraction (LVEF) function and to provide early risk warnings to the subjects. In this paper, the realization of the core of this system, i.e., the Cardiac Health Assessment and Monitoring Platform (CHAMP), with respect to its hardware, firmware, and wireless design features, is presented. The feature values from the CHAMP system have been correlated with myo-cardiac functions obtained from actual heart failure (HF) patients. The usability of this MCG-based cardiac health monitoring smart clothing system has also been evaluated with technology acceptance model (TAM) analysis and the results indicate that the subject shows a positive attitude toward using this wearable MCG-based cardiac health monitoring and early warning system.

A Novel Orthogonal Waveform Separation Scheme for Airborne MIMO-SAR Systems.

In recent years, multi-input multi-output (MIMO) synthetic aperture radar (SAR) systems, which can promote the performance of 3D imaging, high-resolution wide-swath remote sensing, and multi-baseline interferometry, have received considerable attention. Several papers on MIMO-SAR have been published, but the research of such systems is seriously limited. This is mainly because the superposed echoes of the multiple transmitted orthogonal waveforms cannot be separated perfectly. The imperfect separation will introduce ambiguous energy and degrade SAR images dramatically. In this paper, a novel orthogonal waveform separation scheme based on echo-compression is proposed for airborne MIMO-SAR systems. Specifically, apart from the simultaneous transmissions, the transmitters are required to radiate several times alone in a synthetic aperture to sense their private inner-aperture channels. Since the channel responses at the neighboring azimuth positions are relevant, the energy of the solely radiated orthogonal waveforms in the superposed echoes will be concentrated. To this end, the echoes of the multiple transmitted orthogonal waveforms can be separated by cancelling the peaks. In addition, the cleaned echoes, along with original superposed one, can be used to reconstruct the unambiguous echoes. The proposed scheme is validated by simulations.

[Primary culture and identification of mouse renal proximal tubular epithelial cells].

The present study was aimed to establish a modified method for culturing mouse renal proximal tubular epithelial cells (TECs). Renal cortex was isolated from mouse kidney and scissored into pieces. TECs were separated by digesting scissored renal cortex in type II collagenase combined with strainer filtration, and then cultured in DMEM. The morphology of TECs was observed under inverted microscopy. The cell proliferative ability was assessed by flow cytometry, and cell viability was analyzed by CCK-8 assay. The purity of TECs was identified by immunofluorescence. Immunofluorescence observation showed that more than 95% cells were epithelial marker CK18 positive and more than 90% cells expressed renal proximal TECs marker proteins, Villin, AQP1, and SGLT2. The cells could be subcultured for about 5 times. The cell proliferative ability declined following the repeated passage. This study introduced a modified efficient method for culturing highly purified mouse renal proximal TECs.