Nitrogen-Doped Porous Carbon Derived from Covalent Triazine Framework for Catalytic Oxidation of Benzyl Alcohol.

The catalytic oxidation of alcohols is an important transformation in the chemical industry. Carbon materials with a large surface area and N doping show great promise as metal-free catalysts for the reaction. In this study, a rich N-containing covalent triazine framework polymerized by cyanuric chloride and p-phenylenediamine was used to synthesize N-doped porous carbon with the assistance of a pore-forming agent-NaCl. First, the mass ratio of the polymer/NaCl was optimized to 1:9. Then, the influence of the pyrolysis temperatures (700-1000 °C) on the materials was studied in detail. It was found that the carbon materials were gradually exfoliated by molten salt at high temperatures. XRD and Raman characterizations showed them with a certain graphitization. The optimal doped carbon CNN-1-9-900 achieved the highest surface area of 199.03 m2g-1 with the largest pore volume of 0.29 cm3g-1. Furthermore, it had a high N content of 9.9 at% with the highest relative proportion of pyridinic/graphitic N. Due to the synergistic effect between the surface area and pyridinic/graphitic N, CNN-1-9-900 showed the best performance for benzyl alcohol oxidation with TBHP at moderate conditions, and the process also worked for its derivatives.

Polypeptides inhibit HIV-1 replication by interfering viral Vpu-mediated tetherin degradation.

Background: HIV-1 Vpu acts by counteracting the tethering function of tetherin and resulting in the release of HIV-1 virion. Disrupting Vpu-tetherin interactions may provide a promising new target for antiretroviral therapy. Methods: Polypeptides that covered the amino acid sequence on the interface of Vpu-tetherin complex were designed. Phenotypic susceptibilities and cellular toxicities to the polypeptides were measured. The mechanisms of the anti-HIV-1 polypeptides were determined by the Western blot analysis and laser confocal scanning. Seven 20-mer polypeptides from wild-type Vpu amino acid sequence were designed. Results: We report the design and identification of 3 novel anti-HIV-1 polypeptides that derived from Vpu sequence which can efficiently inhibit HIV-1 infection. A pilot mechanism study showed that the active polypeptide could counteract Vpu-mediated tetherin downregulation. Laser confocal image scanning study showed that the polypeptides bound on the cell surface with a receptor specific binding manner, which may target tetherin that expressed on cell surface. Conclusion: Our work provided first evidence that counteracting Vpu-mediated tetherin downregulation could be a target for novel anti-HIV-1 drug design. Future works to provide direct evidence of inhibitors interact with tetherin at atomic resolution and the development of small molecules inhibitors targeting Vpu-tetherin interactions may open a new avenue for novel antiretroviral therapy.

Mechanical Properties of Composite Silty Soil Modified with Cement and Zirconia-Based Nanopowder.

This study assessed the modification effects of zirconia-based nanopowder and cement contents and curing age on the mechanical properties of silty soil. The orthogonal test design was applied to derive the best combination of each influencing factor using the lateral unconfined compressive test. Two-dimensional particle flow code (PFC2D) distinct-element modeling software was also used to fit and analyze the test curves, as well as simulate the triaxial test with the derived parameters. The test results reveal the optimal combination of 20% cement, 2% zirconia-based nanopowder, and 28 d curing age. The extreme difference table was used to plot the orthogonal trend diagram, and cement content was found to be the most significant factor controlling the silty soil strength. The maximum peak stress was 2196.33 kPa under the optimum combination of factors, which could be obtained through the index estimation, and these results were experimentally verified. According to the predicted strength envelope, the cohesive force of nanopowder-cement-modified silty soil in the optimal proportion was 717.11 kPa, and the internal friction angle was 21.05°. Nano zirconium dioxide will accelerate the hydration reaction of cement, the flocculent structure produced by the hydration of cement and soil particles connected to each other, play the role of filling and anchoring, and thus increase the strength of the nano-zirconium dioxide, and the optimal dosage of nano-zirconium dioxide is 2%.

Study on the correlation between maternal serum uric acid and foetal birth weight in Naqu, Tibet.

In high-altitude regions, low birth weight is mainly caused by hypoxia. We aimed to determine whether maternal serum uric acid (SUC) level was associated with decreased foetal birth weight. The relevant data of individual pregnant women who delivered between 37 and 40 weeks in the People's Hospital of Naqu City, Tibet were retrospectively collected. The correlation between maternal SUC and birth weight was examined using multivariate linear regression analysis and subgroup analysis. The results showed that there was a significant negative correlation between SUC and birth weight in pregnant women with proteinuria, female foetuses, and primiparas. Fitting smoothing curve analysis showed that there was a negative linear correlation between SUC and birth weight in primiparas and female foetuses. Maternal SUC is negatively associated with foetal birth weight in a single pregnancy with proteinuria, primipara, or female foetuses in the Naqu region of Tibet, China.IMPACT STATEMENTWhat is already known on this subject? Preeclampsia associated with hyperuricaemia can affect foetal birth weight, foetal birth weight in plains area is negatively correlated with maternal hyperuricaemia.What do the results of this study add? Maternal SUC was negatively correlated with foetal birth weight, especially in primipara, mothers with proteinuria, and pregnant girls.What are the implications of these findings for clinical practice and/or further research? The results suggest that attention should be paid to SUC in pregnant women, especially in primipara, mothers with proteinuria, and pregnant girls, in the prevention of low birth weight infants in Naqu Plateau area of Tibet.

Combinatorial Application of Papain and CD66B for Isolating Glioma- Associated Neutrophils.

BACKGROUND: Stromal cells in the tumor microenvironment play crucial roles in glioma development. Current methods for isolating tumor-associated stromal cells (such as neutrophils) are inefficient due to the conflict between tissue dissociation and cell surface protein protection, which hampers the research on patient-derived stromal cells. Our study aims to establish a novel method for isolating glioma-associated neutrophils (GANs). METHODS: To observe neutrophil-like polymorphonuclear cells, we performed Hematoxylin-Eosin staining on glioma tissues. For isolating single cells from glioma tissues, we evaluated the efficiency of tissue dissociation with FastPrep Grinder-mediated homogenization or proteases (trypsin or papain) digestion. To definite specific markers of GANs, fluorescence-activated cell sorting (FACS) and immunofluorescence staining were performed. FACS and Ficoll were performed for the separation of neutrophils from glioma tissue-derived single-cell or whole blood pool. To identify the isolated neutrophils, FACS and RT-PCR were carried out. RESULTS: Neutrophil-like cells were abundant in high-grade glioma tissues. Among the three tissue dissociation methods, papain digestion produced a 5.1-fold and 1.7-fold more living cells from glioma mass than physical trituration and trypsin digestion, respectively, and it preserved over 97% of neutrophil surface protein markers. CD66B could be adopted as a unique neutrophil surface protein marker for FACS sorting in glioma. Glioma-derived CD66B+ cells specifically expressed neutrophil marker genes. CONCLUSION: A combination of papain-mediated tissue dissociation and CD66B-mediated FACS sorting is an effective novel method for the isolation of GANs from glioma tissues.

Interleukin-6 Downregulates the Expression of Vascular Endothelial-Cadherin and Increases Permeability in Renal Glomerular Endothelial Cells via the Trans-Signaling Pathway.

The pathogenesis of IgA nephropathy (IgAN) is still unknown, but reportedly, interleukin 6 (IL-6) is involved in this process. However, its role in damaging glomerular endothelial cells is still unclear. Therefore, in this study, to clarify the mechanism of the pathogenesis of IgAN, we investigated the effect of IL-6 on the permeability of glomerular endothelial cells. A rat model of IgAN was established, and the animals divided into two groups, namely, the normal and IgAN groups. Glomerular endothelial cell injury was evaluated via electron microscopy. Furthermore, IL-6-induced changes in the permeability of human renal glomerular endothelial cells (HRGECs) were measured via trans-endothelial resistance (TEER) measurements and fluorescein isothiocyanate-dextran fluorescence. Furthermore, vascular endothelial-cadherin (VE-cadherin) was overexpressed to clarify the effect of IL-6 on HRGEC permeability, and to determine the pathway by which it acts. The classical signaling pathway was blocked by silencing IL-6R and the trans-signaling pathway was blocked by sgp30Fc. In IgAN rats, electron microscopy showed glomerular endothelial cell damage and western blotting revealed a significant increase in IL-6 expression, while VE-cadherin expression decreased significantly in the renal tissues. IL-6/IL-6R stimulation also significantly increased the permeability of HRGECs (p < 0.05). This effect was significantly reduced by VE-cadherin overexpression (p < 0.01). After IL-6R was silenced, IL-6/IL-6R still significantly reduced VE-cadherin expression and sgp30Fc blocked the trans-signaling pathway as well as the upregulation of IL-6/IL-6R-induced VE-cadherin expression. This suggests that IL-6 mainly acts via the trans-signaling pathway. IL-6 increased the permeability of HRGECs by decreasing the expression of VE-cadherin via the trans-signaling pathway.

Identification of Neural Progenitor Cell-associated Chemoradiotherapy Resistance Gene Set (ARL4C, MSN, TNFAIP6) for Prognosis of Glioma.

BACKGROUND: Glioma is the most common malignant intracranial tumor with high lethality. Despite surgery combined with chemoradiotherapy, the prognosis for patients with glioma remains poor. This is primarily due to acquired chemoradiotherapy resistance. Therefore, to improve the prognosis of glioma, further study into the mechanism of chemoradiotherapy resistance is needed. OBJECTIVE: This study aimed to (1) evaluate the prognosis of patients with glioma by using a prognostic risk score model constructed by chemoradiotherapy resistance genes, (2) provide new targets and directions for precise treatment of glioma, and (3) discuss the tumor heterogeneity of tumor cells. METHODS: According to therapy class and overall survival (OS), we identified 53 genes associated with glioma chemoradiotherapy resistance in The Cancer Genome Atlas Glioblastoma (TCGA GBM) database. Considering the important role of chemoradiotherapy resistance-related genes in the prognosis of glioma, we preliminarily screened and identified vital prognostic factors among these genes by using the Cox regression model of absolute contraction and selection operators in the TCGA GBM lower-grade glioma (TCGA GBMLGG) dataset. Next, the heterogeneity of the chemoradiotherapy resistance-associated genes in different glioma cells was revealed by single-cell sequencing in the GSE117891 cohort. RESULTS: A prognostic risk score model consisting of three genes (ARL4C, MSN, TNFAIP6) was constructed. The expression of this model was high in glioma neural progenitor cells (NPCs) and low in glioma oligodendrocytes. The OS rates were significantly lower in the high- vs. low-risk group. CONCLUSION: Our 3 gene risk score complements the current glioma diagnosis and provides a novel insight into chemoradiotherapy resistance mechanisms for the prognosis of patients with glioma.

The association between skinfold thicknesses and estimated glomerular filtration rate in adolescents: a cross-sectional study.

BACKGROUND: Obesity is one of the causes of glomerular hyperfiltration. Studies on the relationship between body fat content and glomerular hyperfiltration have been limited to special children. Therefore, we aimed to evaluate the correlation between skinfold thickness, which represents body fat content, and estimated glomerular filtration rate (eGFR). METHODS: The cross-sectional study included 6655 participants (3532 boys and 3123 girls; age: 12 - 17.99 years); data was obtained from the National Health and Nutrition Examination Survey (NHANES; 2001-2010). The independent variables were subscapular skinfold thickness and triceps skinfold thickness. The dependent variable was eGFR. We used multivariate linear regression models to evaluate their associations and also performed subgroup analyses. RESULTS: After adjusting for age, standing height, race, family income, blood urea nitrogen and uric acid variables, multivariate regression analysis identified that triceps skinfold thickness and subscapular skinfold thickness were positively correlated with eGFR and glomerular hyperfiltration in boys. In subgroup analyses stratified by age and body mass index, triceps skinfold thickness was also associated with glomerular hyperfiltration in boys. There was a linear relationship between triceps skinfold thickness and eGFR in boys (ß = 0.389, P < 0.001) and girls (ß = 0.159, P = 0.0003). CONCLUSIONS: Triceps skinfold thickness and subscapular skinfold thickness are positively correlated with eGFR and glomerular hyperfiltration in US male adolescents. In all adolescents, there is a linear relationship between triceps skinfold thickness and eGFR.

Identification and Evaluation of Reference Genes for Quantitative PCR Normalization in Alligator Weed Flea Beetle (Coleoptera: Chrysomelidae).

Stably expressed reference genes are critical internal standards for the quantification of gene transcription levels using quantitative real-time PCR. Housekeeping genes are commonly used as reference genes but their expressions were variable depending on experimental conditions in many insect species studied. Here we report the identification and evaluation of 10 housekeeping genes in alligator weed flea beetle, Agasicles hygrophila Selman & Vogt (Coleoptera: Chrysomelidae), a biocontrol agent of alligator weed. The 10 housekeeping genes are: beta-actin (Actin), ribosomal protein L13A (PRL13a), succinate dehydrogenase complex subunit A (SDHA), ribosomal protein S20 (RPS20), ribosomal protein S13 (RPS13), glyceraldehyde phosphate dehydrogenase (GAPDH), TATA-box-binding protein (TBP), ribosomal protein L32 (RPL32), tubulin alpha-1 chain (TUBULIN), and elongation factor-1 alpha (ELF). Five programs, geNorm, NormFinder, BestKeeper, ΔCt method, and RefFinder, were used to evaluate the expression stability of the 10 genes among various A. hygrophila body parts and with different nutrient types (starvation, diet types). The expression stability analysis showed that RPS32 and RPL13a were reliable reference genes for the study of gene transcription in different body parts; Actin and RPL13a were optimal reference genes for different nutrient types. The selections of reference genes were validated using a CarE gene (GeneBank No: KX353552). The results of this study provide useful bases for studies of gene expression in various aspects relating to A. hygrophila.

The Clinical Significance and Potential Role of Cathepsin S in IgA Nephropathy.

Objective: Cathepsin S (CTSS) is an important lysosomal cysteine protease. This study aimed at investigating the clinical significance of CTSS and underlying mechanism in immunoglobulin A nephropathy (IgAN). Methods: This study recruited 25 children with IgAN and age-matched controls and their serum CTSS levels were measured by enzyme-linked immunosorbent assay (ELISA). Following induction of IgAN in rats, their kidney CTSS expression, IgA accumulation and serum CTSS were characterized by immunohistochemistry, immunofluorescence, and ELISA. The impact of IgA1 aggregates on the proliferation of human mesangial cells (HMCs) was determined by Cell Counting Kit-8 and Western blot analysis of Ki67. Results: Compared to the non-IgAN controls, significantly up-regulated CTSS expression was detected in the renal tissues, particularly in the glomerular mesangium and tubular epithelial cells of IgAN patients, accompanied by higher levels of serum CTSS (P < 0.05), which were correlated with the levels of 24-h-urine proteins and microalbumin and urine erythrocytes and grades of IgAN Lee's classification in children with IgAN (P < 0.01 for all). Following induction of IgAN, we detected inducible IgA accumulation and increased levels of CTSS expression in the glomerular mesangium and glomerular damages in rats, which were mitigated by LY3000328, a CTSS-specific inhibitor. Treatment with LY3000328 significantly mitigated the Ki67 expression in the kidney of IgAN rats (P < 0.01) and significantly minimized the IgA1 aggregate-stimulated proliferation of HMCs and their Ki67 expression in vitro (P < 0.01). Conclusions: CTSS promoted the proliferation of glomerular mesangial cells, contributing to the pathogenesis of IgAN and may be a new therapeutic target for intervention of aberrant mesangial cell proliferation during the process of IgAN.

Exosome-Derived LncRNA TCONS_00072128 Mediated Osteogenic Differentiation and Inflammation by Caspase 8 Regulation.

Postmenopausal osteoporosis (PMOP) is a systemic metabolic bone disease in postmenopausal women. It has been known that long non-coding RNAs (lncRNAs) play a regulatory role in the progression of osteoporosis. However, the mechanism underlying the effects of exosome-derived lncRNA on regulating the occurrence and development of PMOP remains unclear. Exosomes in the serum of patients PMOP were collected and identified. RNA sequencing was performed to obtain the expression profile of exosome-derived lncRNAs in the serum of PMOP patients. RNA sequencing identified 26 differentially expressed lncRNAs from the exosomes between healthy people and PMOP patients. Among them, the expression of TCONS_00072128 was dramatically down-regulated. A co-location method was employed and searched its potential target gene caspase 8. TCONS_00072128 knockdown notably decreased the expression of caspase 8, while the osteogenic differentiation of BMSCs was also reduced. Reversely, TCONS_00072128 overexpression enhanced caspase 8 expression and osteogenic differentiation of BMSCs. Moreover, the continuous expression of caspase 8 regulated by TCONS_00072128 significantly activated inflammation pathways including NLRP3 signaling and NF-κB signaling. Simultaneously, RIPK1 which has emerged as a promising therapeutic target for the treatment of a wide range of human neurodegenerative, autoimmune, and inflammatory diseases, was also phosphorylated. The results of the present study suggested that exosome-derived lncRNA TCONS_00072128 could promote the progression of PMOP by regulating caspase 8. In addition, caspase 8 expression in BMSCs was possible to be a key regulator that balanced cell differentiation and inflammation activation.

RIP2 promotes glioma cell growth by regulating TRAF3 and activating the NF­κB and p38 signaling pathways.

Receptor­interacting protein 2 (RIP2) has recently been reported to be involved in tumor infiltration and cancer metastasis. However, the function of RIP2 in human astrocytoma remains unclear. In the present study, we showed that the expressions of RIP2 and Bcl­xL were positively correlated with the malignant grade in 28 cases of astrocytoma of various grades and 6 cases of normal human tissues. In addition, increased activity of the NF­κB and p38 signaling pathways in astrocytoma tissue was observed. Cytological experiments indicated that RIP2 promoted human glioblastoma cell proliferation by inducing expression of Bcl­xL, and knockdown of endogenous RIP2 promoted cell apoptosis. Mechanistically, knockdown of RIP2 suppressed downstream events including the canonical and alternative NF­κB pathway as well as the mitogen­activated protein kinase (p38) pathway. In addition, the present study also demonstrated that tumor necrosis factor receptor­associated factor 3 (TRAF3), as a novel RIP2 binding partner, was downregulated in glioma tissues and functionally was a negative regulator involved in RIP2­induced glioma cell growth. Taken together, the present study established a negative link between RIP2 and TRAF3 proteins and identifies a new pathway for regulating astrocytoma progression.

Frequency of Polycythemia and Other Abnormalities in a Tibetan Herdsmen Population Residing in the Kham Area of Sichuan Province, China.

INTRODUCTION: The Kham Tibetans are one of several Tibetan ethnic subgroups living in the Kham area of China. Because studies on the high-altitude adaptation of the Kham people are scant, the main aim of this study is to investigate whether the response to hypoxia, especially polycythemia status, in the Kham Tibetans is different from other Tibetan ethnic subgroups. METHODS: The primary investigation was conducted on 346 native Kham Tibetan adults (268 men and 78 women) from 3 herdsmen villages located in Hongyuan County situated at an altitude of greater than 3600 m. The participants were aged 46.2±14.1 (21-82; mean±SD with range) years. Anthropometric measurements such as weight, height, waist circumference, body mass index, and blood pressure, as well as laboratory blood tests such as glycosylated hemoglobin, hemoglobin, total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and uric acid were analyzed. RESULTS: The concentrations of hemoglobin were 171.3±12.9 (66-229) mg·L-1 and 151.4±16.4 (86-190) mg·L-1 in men and women, respectively. The frequency of polycythemia was found to be 25.5 and 21.8% in men and women, respectively. Polycythemia was found to be significantly associated with glycosylated hemoglobin concentrations, hypertension, and hyperuricemia (P=0.002, 0.023, and 0.009, respectively). CONCLUSIONS: There is a higher frequency of polycythemia in the Kham Tibetans when compared with reported studies from other Tibetan ethnic subgroups living on the Qinghai-Tibet plateau.

SCCmec-associated psm-mec mRNA promotes Staphylococcus epidermidis biofilm formation.

Biofilm formation is considered the major pathogenic mechanism of Staphylococcus epidermidis-associated nosocomial infections. Reports have shown that SCCmec-associated psm-mec regulated methicillin-resistant Staphylococcus aureus virulence and biofilm formation. However, the role of psm-mec in S. epidermidis remains unclear. To this purpose, we analysed 165 clinical isolates of S. epidermidis to study the distribution, mutation and expression of psm-mec and the relationship between this gene and biofilm formation. Next, we constructed three psm-mec deletion mutants, one psm-mec transgene expression strain (p221) and two psm-mec point mutant strains (pM, pAG) to explore its effects on S. epidermidis biofilm formation. Then, the amount of biofilm formation, extracellular DNA (eDNA) and Triton X-100-induced autolysis of the constructed strains was measured. Results of psm-mec deletion and transgene expression showed that the gene regulated S. epidermidis biofilm formation. Compared with the control strains, the ability to form biofilm, Triton X-100-induced autolysis and the amount of eDNA increased in the p221 strain and the two psm-mec mutants pM and pAG expressed psm-mec mRNA without its protein, whereas no differences were observed among the three constructed strains, illustrating that psm-mec mRNA promoted S. epidermidis biofilm formation through up-regulation of bacterial autolysis and the release of eDNA. Our results reveal that acquisition of psm-mec promotes S. epidermidis biofilm formation.

Direct common gram-negative bacterial identification from positive blood culture bottles by SELDI-TOF MS.

A protein database was constructed and validated with identification rate over 90% for the 4 most common Gram-negative bacteria on agar plates. By protein masses comparison, 120 bacteria of the 4 species from blood culture bottles were identified. The concordance was high (Kappa=0.906) between our method and conventional approach.

Reduction of preanalytical errors in clinical laboratory through multiple aspects and whole course intervention measures.

OBJECTIVE: Errors in preanalytical phase decrease the accuracy of reports from clinical laboratory department. Considering the disqualified rate of preanalytical sample in our hospital, we performed several intervention measures to improve the situation. METHODS: The disqualified sample types and major causes of errors in the preanalytical phase were investigated in clinical laboratory department from September 2008 to August 2009. In the following year, we utilized multiple measures to properly intervene the key points of whole sample collection process, and the preanalytical errors were reanalyzed trimonthly, then the disqualification rate of total, major disqualified sample types and different test groups were calculated to evaluate the effects of the intervention measures. RESULTS: The total disqualification rate in the preanalytical phase obtained from September 2008 to August 2009 was 1.36%, and the major types of disqualified samples were coagulation of anticoagulant sample, sample inadequacy, sample container error, sample information error and sample type error. After one year intervention through key points of whole preanalytical sample collection process, the total disqualification rate dropped to 0.94%, and the disqualification rate of coagulation of anticoagulant sample, sample inadequacy, sample container error, sample information error, and sample type error decreased by 20.45%, 28.00%, 25.00%, 76.92%, and 66.66%, respectively. As for test groups, the decreasing amplitude of biochemical, routine, immunological, microbiological and emergency test group was 47.36%, 33.33%, 20.00%, 50.00%, and 21.43%, respectively. CONCLUSIONS: The overall effect of the interventions is very good, and the disqualification rate of the main causes decreases to various degrees.

Possible formation of mitochondrial-RNA containing chimeric or trimeric RNA implies a post-transcriptional and post-splicing mechanism for RNA fusion.

Human cells are known to express many chimeric RNAs, i.e. RNAs containing two genes' sequences. Wondering whether there also is trimeric RNA, i.e. an RNA containing three genes' sequences, we wrote simple computer code to screen human expression sequence tags (ESTs) deposited in different public databases, and obtained hundreds of putative trimeric ESTs. We then used NCBI Blast and UCSC Blat browsers to further analyze their sequences, and identified 61 trimeric and two tetrameric ESTs (one EST containing four different sequences). We also identified 57 chimeric, trimeric or teterameric ESTs that contained both mitochondrial (mt) RNA and nuclear RNA (nRNA), i.e. were mtRNA-nRNA fusions. In some trimeric ESTs, the downstream partner was fused to the poly-A tail of the upstream partner, which, together with the mtRNA-nRNA fusions, suggests a possible new mechanism for RNA fusion that occurs after both transcription and splicing have been terminated, and possibly outside the nucleus, in contrast to the two current hypothetical mechanisms, trans-splicing and transcriptional-slippage, that occur in the nucleus. The mt-sequences in the mtRNA-nRNA fusions had pseudogenes in the nucleus but, surprisingly, localized mainly in chromosomes 1 and 5. In some mtRNA-nRNA fusions, as well as in some ESTs that were derived only from mtRNA, the mt-sequences might be cis- or trans-spliced. Actually, we cloned a new cis-spliced mtRNA, coined as 16SrRNA-s. Hence, mtDNA may not always be intron-less. Fusion of three or more RNAs to one, fusion of nRNA to mtRNA, and cis- or trans-splicing of mtRNA should all enlarge the cellular RNA repertoire, in turn enlarging the cellular functions. Therefore, future experimental verification of the existence of these novel classes of fusion RNAs and spliced mtRNAs in human cells should significantly advance our understanding of biology and medicine.

Paired box 2 induces epithelial-mesenchymal transition in normal renal tubular epithelial cells of rats.

Epithelial­mesenchymal transition (EMT) is considered to be a crucial stage of renal fibrosis. Previous studies have indicated that paired box 2 (PAX2) affects renal fibrosis, likely by regulating EMT. Therefore, we examined whether PAX2 directly induces normal renal tubular EMT in vitro. Recombinant PAX2 plasmid was transfected into a renal tubular epithelial cell line (NRK52E) derived from normal rats. The optimal time­point was evaluated through fluorescence detection, western blotting and real-time polymerase chain reaction (PCR). Morphological alterations were examined using phase­contrast microscopy. At the optimal time­point of transfection, the expression of E-cadherin, α-smooth muscle actin (α-SMA), fibronectin and snail was analyzed by western blotting and real-time PCR. PAX2 expression in NRK52E cells transfected with PAX2 plasmid reached its peak at 72 h post­transfection. The transfected cells became elongated. PAX2 transfection induced a fibrotic phenotype of NRK52E cells with increased expression of α-SMA, fibronectin and snail as well as decreased expression of E-cadherin. The optimal time-point for transfection efficiency was 72 h. In conclusion, PAX2 induces renal tubular mesenchymal transition in vitro.

Transient receptor potential vanilloid 2 (TRPV2), a potential novel biomarker in childhood asthma.

BACKGROUND: The presence of transient receptor potential vanilloid 2 (TRPV2) in human peripheral blood cells may suggest a role under pathological conditions. The aim of this study was to explore the relationship between the expression profile of TRPV2 gene and childhood asthma in the north of China. The effects of allergens exposure on the expression of TRPV2 gene were also investigated. METHODS: Sixty asthmatics children confirmed by physician diagnosis and 60 healthy children as a control group were recruited. Serum total IgE and specific IgE were measured. Using quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR), TRPV2 was detected in total RNA extracted from peripheral blood lymphocytes. Student's t-test and chi-square test were used to analyze the relationship between TRPV2 transcript and different parameter variables on susceptibility of childhood asthma. Multiple logistic regression was used to analyze the associations between TRPV2 gene and allergens. RESULTS: The expression level of TRPV2 gene was increased 2.6 times in asthmatic children compared with controls (p < .01). The up-regulation of TRPV2 gene and sensitization to one of three the allergens-spring pollen, dust mite, and dog and cat hair-were correlated with childhood asthma. In addition, the hypersensitivity to spring pollen, cockroach, and dust mite and up-regulation of TRPV2 gene expression may be the risk factors for the childhood asthma in Beijing. CONCLUSIONS: The increased expression of TRPV2 gene in peripheral lymphocytes is closely correlated with childhood asthma in the north of China. This study provides a potential new biomarker of childhood asthma and lays the basis for further clarification of the pathogenesis underlying asthma.

Elevated serum myeloperoxidase activities are significantly associated with the prevalence of ACS and High LDL-C levels in CHD patients.

AIM: Recent researches have shown that myeloperoxidase (MPO) is a potential inflammatory risk factor for coronary heart disease (CHD). In the present study, the possible associations of MPO with acute coronary syndrome (ACS), low density lipoprotein cholesterol (LDL-C) and other risk factors in CHD patients were investigated. METHODS: Five hundred thirty-six CHD patients [363 ACS and 173 stable angina pectoris (SAP)] and 181 non-CHD patients confirmed by coronary angiography were enrolled in this study. The association study was performed by logistic regression analysis. RESULTS: ACS patients had significantly higher MPO activities than SAP and non-CHD patients (p < 0.001). The area under the receiver operating characteristic (ROC) curve of MPO for diagnosing ACS was 0.84 (95% CI: 0.80-0.88, p < 0.001). The optimal cut-off value (sensitivity; specificity) of MPO was 164.77 ng/mL (79.1% and 82.1%). LDL-C (III versus I tertile, OR: 3.24, 95% CI: 1.67-6.29, p = 0.001) and ACS (yes versus no, OR 2.74, 95% CI: 1.71-4.39, p < 0.001) were significantly associated with elevated serum MPO activities, which had the highest odds ratio in quantitative and qualitative variables, respectively. There were significant increase trends in the prevalence of ACS and high LDL-C levels from I to III MPO tertile, which were 46.4% and 8.9% for I, 68.0% and 31.5% for II, 88.8% and 59.8% for III tertile, respectively (p < 0.001). CONCLUSION: The present study provides epidemiological evidence that elevated serum MPO activities are significantly associated with the prevalence of ACS and high LDL-C levels in CHD patients, and MPO may be a potential early warning marker for ACS.