Long noncoding RNA SNHG9 facilitates growth of glioma stem-like cells via miR-326/SOX9 axis.

BACKGROUND: Glioma stem-like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. METHODS: GSCs were obtained from glioma cells (U87 and U251) and referred to as GSC-87 and GSC-251, respectively. The interactions between miR-326 and SNHG9 or SOX9 were analyzed using luciferase reporter assay. Cell growth of GSCs was evaluated by EdU assay and sphere formation assay. RESULTS: SNHG9 expression was significantly higher in GSC-87 and GSC-251 cells than in U87 and U251 cells. SNHG9 overexpression promoted GSC cell growth, whereas SNHG9 knockdown inhibited GSC cell growth. Mechanistically, SNHG9 acted as a competitive endogenous RNA of miR-326 to elevate the expression of SOX9, a direct target of miR-326. Moreover, transfection with miR-326 inhibitor counteracted SNHG9 knockdown-mediated inhibition of GSC cell growth. CONCLUSIONS: SNHG9 facilitates growth of GSCs via the miR-326/SOX9 axis. This study provides a promising therapeutic target for glioma treatment.

Increase in the efficiency of III-nitride micro LEDs by atomic layer deposition.

The effect of atomic-layer deposition (ALD) sidewall passivation on the enhancement of the electrical and optical efficiency of micro-light-emitting diode (µ-LED) is investigated. Various blue light µ-LED devices (from 5 × 5 µm2 to 100 × 100 µm2) with ALD-Al2O3 sidewall passivation were fabricated and exhibited lower leakage and better external quantum efficiency (EQE) comparing to samples without ALD-Al2O3 sidewall treatment. Furthermore, the EQE values of 5 × 5 and 10 × 10 µm2 devices yielded an enhancement of 73.47% and 66.72% after ALD-Al2O3 sidewall treatments process, and the output power also boosted up 69.3% and 69.9%. The Shockley-Read-Hall recombination coefficient can be extracted by EQE data fitting, and the recombination reduction in the ALD samples can be observed. The extracted surface recombination velocities are 551.3 and 1026 cm/s for ALD and no-ALD samples, respectively.

Oncolytic vaccinia virus as a vector for therapeutic sodium iodide symporter gene therapy in prostate cancer.

Oncolytic strains of vaccinia virus are currently in clinical development with clear evidence of safety and promising signs of efficacy. Addition of therapeutic genes to the viral genome may increase the therapeutic efficacy of vaccinia. We evaluated the therapeutic potential of vaccinia virus expressing the sodium iodide symporter (NIS) in prostate cancer models, combining oncolysis, external beam radiotherapy and NIS-mediated radioiodide therapy. The NIS-expressing vaccinia virus (VV-NIS), GLV-1h153, was tested in in vitro analyzes of viral cell killing, combination with radiotherapy, NIS expression, cellular radioiodide uptake and apoptotic cell death in PC3, DU145, LNCaP and WPMY-1 human prostate cell lines. In vivo experiments were carried out in PC3 xenografts in CD1 nude mice to assess NIS expression and tumor radioiodide uptake. In addition, the therapeutic benefit of radioiodide treatment in combination with viral oncolysis and external beam radiotherapy was measured. In vitro viral cell killing of prostate cancers was dose- and time-dependent and was through apoptotic mechanisms. Importantly, combined virus therapy and iodizing radiation did not adversely affect oncolysis. NIS gene expression in infected cells was functional and mediated uptake of radioiodide both in vitro and in vivo. Therapy experiments with both xenograft and immunocompetent Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) mouse models showed that the addition of radioiodide to VV-NIS-infected tumors was more effective than each single-agent therapy, restricting tumor growth and increasing survival. In conclusion, VV-NIS is effective in prostate cancer models. This treatment modality would be an attractive complement to existing clinical radiotherapy practice.

[Apoptotic mechanism of gecko crude peptides on human liver carcinoma cell line HepG2].

OBJECTIVE: To investigate the effect of Gecko crude peptides (GCPS) on human liver carcinoma HepG2 cells and its mechanism. METHODS: MTT assay was used to analyze the effect of the GCPS on the proliferation of HepG2 Cell; Nucleus change of HepG2 treated with GCP was observed by Hoechst33258 fluorescence staining, and BAX and BCL-2 were detected with western-blot assay. RESULTS: GCPS could inhibit the proliferation of HepG2 Cell in a time and dosage dependent way, and its half-maximal inhibitory concentration (IC50) was 1.2 mg/mL; HepG2 pretreated with GCPS showed apoptotic morphological changes. GCPS (1.6 mg/mL, 0.8 mg/mL) could decrease the expression of BCL-2 protein, and increase the expression of BAX protein. CONCLUSION: GCPS can inhibit the proliferation of HepG2 cell. The mechanism may be related to the induction apoptosis of HepG2.

iRHOM2: A Regulator of Palmoplantar Biology, Inflammation, and Viral Susceptibility.

The palmoplantar epidermis is a specialized area of the skin that undergoes high levels of mechanical stress. The palmoplantar keratinization and esophageal cancer syndrome, tylosis with esophageal cancer, is linked to mutations in RHBDF2 encoding the proteolytically inactive rhomboid protein, iRhom2. Subsequently, iRhom2 was found to affect palmoplantar thickening to modulate the stress keratin response and to mediate context-dependent stress pathways by p63. iRhom2 is also a direct regulator of the sheddase, ADAM17, and the antiviral adaptor protein, stimulator of IFN genes. In this perspective, the pleiotropic functions of iRhom2 are discussed with respect to the skin, inflammation, and the antiviral response.

Decompression with fusion versus decompression in the treatment of lumbar spinal stenosis: A systematic review and meta-analysis.

OBJECTIVE: The goal of this study was to review relevant studies in order to determine the efficacy of decompression with fusion versus decompression in the treatment of lumbar spinal stenosis. METHODS: Using appropriate keywords, we identified relevant studies using PubMed, the Cochrane library, and Embase. Key pertinent sources in the literature were also reviewed, and all articles published through October 2019 were considered for inclusion. For each study, we used odds ratios, mean difference (MD), and 95% confidence interval (95% CI) to assess and synthesize outcomes. RESULTS: We found 13 studies that were consistent with this meta-analysis with a total of 29066 patients. Compared with decompression, decompression with fusion significantly increased the incidence of complications (RR: 1.41, 95%CI: 1.26-1.57), the length of hospital stay (WMD: 1.868, 95%CI: 1.394-2.343), operative time (WMD: 80.399, 95%CI: 44.397-116.401), estimated blood loss (WMD: 309.356, 95%CI: 98.008-520.704) and Zurich claudication questionnaire in symptom severity (WMD: 0.200, 95%CI: 0.006-0.394). The reoperation rate was lower in the decompression with fusion group than the decompression group but without significant difference (RR: 0.91, 95%CI: 0.82-1.00). There was no significant difference between 2 groups in visual analog scale (leg pain and back pain), ODI, Short Form 36 Health Survey physical component summary, Short Form 36 Health Survey mental component summary, and Zurich claudication questionnaire physical function. CONCLUSION: Decompression with fusion has no significant clinical advantages in treatment of lumbar spinal stenosis when compared with decompression.

Heat resistive dielectric multi-layer micro-mirror array in epitaxial lateral overgrowth gallium nitride.

Ta2O5 / SiO2 dielectric multi-layer micro-mirror array (MMA) with 3mm mirror size and 6mm array period was fabricated on c-plane sapphire substrate. The MMA was subjected to 1200 degrees C high temperature annealing and remained intact with high reflectance in contrast to the continuous multi-layer for which the layers have undergone severe damage by 1200 degrees C annealing. Epitaxial lateral overgrowth (ELO) of gallium nitride (GaN) was applied to the MMA that was deposited on both sapphire and sapphire with 2:56 mm GaN template. The MMA was fully embedded in the ELO GaN and remained intact. The result implies that our MMA is compatible to the high temperature growth environment of GaN and the MMA could be incorporated into the structure of the micro-LED array as a one to one micro backlight reflector, or as the patterned structure on the large area LED for controlling the output light.

The functional changes of the perivascular adipose tissue in spontaneously hypertensive rats and the effects of atorvastatin therapy.

The aim of this study was to examine the function of perivascular adiposa tissue (PVAT) on vascular relaxation response in spontaneously hypertensive rats (SHR) and the modulatory effects of the atorvastatin therapy on the PVAT functions. We investigated the mechanisms of the perivascular adipocyte-derived relaxation factor (PVRF) by using isolated rat's aortic rings and isometric contraction measurements. We found that contraction of the thoracic aorta induced by phenylephrine was significantly attenuated in the presence of PVAT from normotensive Wistar-Kyoto rats (WKY group) or the spontaneously hypertensive rats treated with atorvastatin (SHR-A group, atorvastatin 50mg/kg/day), whereas this effect was not observed in the thoracic aortic rings from the control SHR (SHR group). Transferring the solution incubated with PVAT-intact thoracic aorta to PVAT-free thoracic aorta, it induced a remarkable relaxation response in the WKY but not in the control SHR. Tetraethylammoniumchloride (TEA) could block the above relaxation. It was also shown that the PVRF function was likely, depending on the extracellular [Ca(2+)]; the anti-contractile effect of PVAT could be reduced by the inhibitor of the adenosine triphosphate (ATP)-dependent potassium channels, glibenclamide, and could be reduced by the inhibitor of cyclooxygenase by indomethacin. We thus infer that the PVAT function was distorted in hypertension rats, and the lipid-lowering treatment with atorvastatin could restore the PVAT function. The function of the PVRF may involve the Ca(2+)-activated potassium channels, the ATP-dependent potassium channels in vascular smooth muscle cell (SMC), and the release of PVRF from PVAT may involve prostaglandins (PGs) and the calcium metabolism. These results provide an insight into the pathological mechanisms of hypertension development, and indicate that the PVAT may be a potential new target for the hypertensive therapy.

Prognostic value of nuclear FBI-1 in patients with rectal cancer with or without preoperative radiotherapy.

Factor that binds to the inducer of short transcripts of the human immunodeficiency virus-1 (FBI-1) represents as a crucial gene regulator in colorectal cancer; however, the correlation between FBI-1 and preoperative radiotherapy (RT) in rectal cancer (RC) has not yet been reported. The aim was to detect FBI-1 expression in patients with RC with or without RT, by immunohistochemistry and quantitative polymerase chain reaction, and to analyze its association with clinicopathological features and response to RT. The results from immunohistochemistry analysis (n=139) and reverse transcription-quantitative polymerase chain reaction (n=55) demonstrated that FBI-1 was overexpressed in patients with RC, whether they had received preoperative RT or not. Subsequently, the association between FBI-1 expression, and the clinicopathological features and response to RT in patients with RC was analyzed. Cytoplasmic FBI-1 was upregulated in non-RT (n=77) and RT (n=62) groups (17.7 vs. 74.0%, P<0.001; 41.1 vs. 69.4%, P=0.002, respectively) of patients with RC compared with normal mucosa. However, nuclear FBI-1 was downregulated (75.8 vs. 22.1%, P<0.001; 83.9 vs. 35.5%, P<0.001, respectively) in both groups. RT had no significant effect on FBI-1 expression in RC tissues. Furthermore, nuclear FBI-1 was positively associated with tumor-node-metastasis stage and distant recurrence (P=0.003 and P=0.010, respectively). In patients with stage I, II or III RC, higher nuclear FBI-1 expression was associated with poorer disease-free survival [hazard ratio (HR)=1.934, 95% confidence interval (CI): 1.055-3.579, P=0.033] and overall survival (HR=2.174, 95% CI: 1.102-4.290, P=0.025), independently of sex, age, growth pattern, differentiation and RT. In addition, FBI-1 was positively correlated with numerous biological factors, including p73 [Spearman's correlation coefficient (rs)=0.332, P=0.007], lysyl oxidase (rs=0.234, P=0.043), Wrap53 (rs=-0.425, P=0.0002) and peroxisome proliferator-activated receptor δ (rs=-0.294, P=0.026). In conclusion, the present study demonstrated that nuclear FBI-1 was an independent prognostic factor in patients with RC and correlated with numerous biological factors, which indicated that it may have multiple roles in RC.

Gorab is a Golgi protein required for structure and duplication of Drosophila centrioles.

We demonstrate that a Drosophila Golgi protein, Gorab, is present not only in the trans-Golgi but also in the centriole cartwheel where, complexed to Sas6, it is required for centriole duplication. In addition to centriole defects, flies lacking Gorab are uncoordinated due to defects in sensory cilia, which lose their nine-fold symmetry. We demonstrate the separation of centriole and Golgi functions of Drosophila Gorab in two ways: first, we have created Gorab variants that are unable to localize to trans-Golgi but can still rescue the centriole and cilia defects of gorab null flies; second, we show that expression of C-terminally tagged Gorab disrupts Golgi functions in cytokinesis of male meiosis, a dominant phenotype overcome by mutations preventing Golgi targeting. Our findings suggest that during animal evolution, a Golgi protein has arisen with a second, apparently independent, role in centriole duplication.

Associations of genetic variants in M3 receptor with blood pressure responses to salt and potassium intake / 西安交通大学学报(医学版)

【Objective】 M3 muscarinic acetylcholine receptor(M3 receptor), encoded by CHRM3 gene, is widely distributed in the cardiovascular system and plays an important role in cardiac regulation. The aim of this study was to assess the association of genetic variants in M3 receptor with blood pressure(BP) responses to controlled dietary sodium and potassium interventions. 【Methods】 A total of 333 subjects from 124 families were recruited from the rural areas of northern China. After a three-day baseline observation, they were sequentially on a seven-day low-salt diet, a seven-day high-salt diet, and a seven-day high-salt diet plus potassium supplementation. Thirteen CHRM3 single nucleotide polymorphisms(SNPs) were selected for analysis. 【Results】 SNP rs10802811 of the CHRM3 was significantly associated with diastolic BP(DBP) and mean arterial pressure(MAP) responses to both low-salt and high-salt diets while SNPs rs6429147, rs373288072, rs114677844 and rs663148 showed significant associations with systolic BP(SBP) and MAP responses to high-salt diet. In addition, SNP rs6692904 was significantly associated with SBP, DBP and MAP responses to high-salt diet with potassium supplementation. 【Conclusion】 Genetic variants in M3 receptor are significantly associated with BP responses to sodium and potassium intervention, suggesting that M3 receptor may be mechanistically involved in BP salt and potassium sensitivity.

Association of genetic variants in uromodulin with blood pressure responses to dietary salt and potassium intake / 西安交通大学学报(医学版)

【Objective】 Based on our previously established salt-sensitive hypertension cohort, we aimed to examine the association of genetic variants in uromodulin with blood pressure(BP) responses to dietary interventions of sodium and potassium intake. 【Methods】 In 2004, 514 subjects from 124 families in Mei County, Shaanxi Province, were recruited to establish the salt-sensitive hypertension study cohort. Among them, 333 non-parent subjects were selected and sequentially maintained on a normal-diet for 3 days, low-salt diet for 7 days, then a high-salt diet for 7 days and a high-salt diet with potassium supplementation for another 7 days. Thirteen single nucleotide polymorphisms(SNPs) in the uromodulin gene were genotyped on the MassARRAY platform. 【Results】 BP levels decreased from the baseline to low-salt diet, increased from low-salt to high-salt diet, and decreased again from the high-salt diet to the high-salt plus potassium supplementation intervention. SNPs rs77875418 and rs4997081 of the uromodulin gene were significantly associated with diastolic BP(DBP) and mean arterial pressure(MAP) responses to high-salt diet. In addition, SNPs rs77875418, rs79245268, rs4293393, rs6497476, rs4997081, rs13333226, and rs12917707 were significantly associated with systolic BP(SBP), DBP, and MAP responses to high-salt diet with potassium supplementation. 【Conclusion】 Genetic variants in uromodulin gene are significantly associated with BP responses to sodium and potassium supplementation, suggesting that uromodulin may be mechanistically involved in BP sodium-sensitivity and potassium-sensitivity.

Association of genetic variants in NEDD4L with blood pressure responses to dietary salt and potassium intake / 西安交通大学学报(医学版)

【Objective】 4-like protein with down-regulated expression and development in neural precursor cells (NEDD4L) plays an important role in blood pressure (BP) regulation and sodium homeostasis by regulating epithelial sodium channel protein. In this study, we aimed to explore the relationship of NEDD4L gene polymorphisms with BP responses to sodium and potassium intake. 【Methods】 In 2004, 514 subjects from 124 families in Meixian County, Shaanxi Province, were recruited to establish a salt-sensitive hypertension study cohort. All the subjects received a 3-day baseline survey, a 7-day low-salt diet, a 7-day high-salt diet, and finally a 7-day high-salt and potassium supplementation. Their BP was measured and peripheral blood samples were collected at different intervention periods. The 14 gene polymorphisms of NEDD4L gene were genotyped and analyzed by MassARRAY platform. 【Results】 BP decreased on a low-salt diet, and significantly increased on a high-salt diet, and decreased again after potassium supplementation. NEDD4L SNPs rs74408486 were significantly associated with systolic BP, diastolic BP and mean arterial pressure responses to the low-salt diet. SNPs rs292449 and rs2288775 were significantly associated with pulse pressure response to the high-salt diet. In addition, SNPs rs563283 and rs292449 were significantly associated with diastolic BP, mean arterial pressure, and pulse pressure responses to high-salt and potassium supplementation diet. 【Conclusion】 NEDD4L gene polymorphisms were significantly associated with BP responses to sodium and potassium intake, suggesting that NEDD4L gene may be involved in the development of salt sensitivity and potassium sensitivity.

Associations of genetic polymorphisms in Corin with blood pressure responses to salt and potassium intake / 西安交通大学学报(医学版)

【Objective】 Corin, a transmembrane serine protease that can cleave atrial natriuretic peptide precursor (pro-ANP) into atrial natriuretic peptide with smaller bioactive molecules, participates in the pathophysiological process of hypertension and cardiac hypertrophy. The purpose of this study was to explore the relationship of Corin gene variation with blood pressure responses to sodium and potassium dietary interventions. 【Methods】 In 2004, we recruited 514 participants from 124 families in 7 villages of Baoji, Shaanxi Province, China. All the subjects received a 3-day normal diet, a 7-day low-salt diet, a 7-day high-salt diet, and finally a 7-day high-salt and potassium supplementation. Fifteen single nucleotide polymorphisms (SNPs) of Corin gene were selected for final analysis. 【Results】 SNPs rs12509275 were significantly associated with diastolic blood pressure (DBP) response to low-salt diet, while rs3749584 was associated with pulse pressure (PP) response to low-salt diet.SNP rs3749584 and rs10517195 were significantly associated with PP response to high-salt diet. In addition,rs17654278 were significantly associated with systolic blood pressure (SBP) response to high-salt and potassium supplementation, rs2271037 was significantly correlated with DBP responses to high-salt and potassium supplementation, and rs4695253, rs12509275, rs2351783, rs36090894 were significantly associated with PP response to high-salt and potassium supplementation. 【Conclusion】 Corin gene polymorphisms were associated with blood pressure response to sodium and potassium, suggesting that Corin gene may be involved in pathophysiological process of salt sensitivity and potassium sensitivity.

Association between residual cholesterol and the risk of subclinical renal damage / 西安交通大学学报(医学版)

【Objective】 Dyslipidemia has shown to be associated with cardiovascular, metabolic and renal diseases. This study aimed to investigate the association between residual cholesterol and the risk of subclinical renal damage (SRD). 【Methods】 A total of 2 342 participants were recruited from the previously established Hanzhong Adolescent Hypertension Study cohort. According to estimated glomerular filtration rate(eGFR) and urinary albumin-to-creatine ratio(uACR), the subjects were divided into SRD group and non-SRD group. The associations of residual cholesterol with eGFR, uACR, and the risk of SRD were analyzed by multiple linear and Logistic regression analyses. 【Results】 Residual cholesterol was positively correlated with uACR(r=0.081, P<0.001) but negatively correlated with eGFR (r=-0.091, P<0.001). Multiple linear regression analysis revealed that residual cholesterol was an influencing factor of uACR (β=0.075, P<0.001) and eGFR (β=-0.027, P<0.001) after adjustment for gender, age, smoke, alcohol, exercise, BMI, hypertension, diabetes and serum uric acid. In addition, Logistic regression analysis revealed that residual cholesterol was significantly associated with the risk of SRD independently of potential confounders [OR(95% CI)=1.387 (1.113-1.728), P<0.001]. Further subgroup analysis showed that residual cholesterol was significantly associated with the risk of SRD in women but not in men. 【Conclusion】 Residual cholesterol is a contributing factor in the risk of subclinical renal damage with gender-specific association.

Identification of key genes and pathways associated with dilated cardiomyopathy development by bioinformatics analysis / 西安交通大学学报(医学版)

【Objective】 To explore the potential biomarkers and related enrichment pathways of dilated cardiomyopathy （DCM） by bioinformatics methods. 【Methods】 The data sets related to DCM in GEO database were searched， and microarray data sets GSE42955 and GSE1869 of human cardiomyocytes were extracted. Then， the differentially expressed genes （DEGS） were analyzed using R language， and the protein-protein interaction network was analyzed to identify the core genes and core modules of differential expression. The gene ontology database （GO） enrichment and Kyoto Gene and Genome Encyclopedia （KEGG） pathway analyses were performed. The data sets related to DCM in ArrayExpress database were searched， and the human cardiomyocytes microarray data set E-TABM-480 was extracted to verify the expressions of core genes and modules. 【Results】 We identified 10 DEGS， namely， DZIP3， FBXO32， BTBD6， FBXL5， ASB8， COMMD1， LTN1， FBXO21， RCHY1 and ARIH2， and the core DEG was DZIP3. After GO and KEGG analyses， the GO and KEGG of the above DEGS were mainly related to the ubiquitin-proteasome system. 【Conclusion】 Bioinformatics analysis shows that the ubiquitin-proteasome system plays an important role in the pathogenesis of DCM， and the mechanism remains to be further studied.

Relationship between hypoadiponectinemia and hypertension in young individuals with normal renal function: Hanzhong adolescent hypertension study / 西安交通大学学报(医学版)

【Objective】 To explore the relationship between plasma adiponectin levels and hypertension based on the Hanzhong adolescent hypertension cohort. 【Methods】 A total of 361 young individuals with normal renal function， aged 32 to 41 years old， were taken as the research subjects. We collected or measured data including general characteristics， blood pressure （BP）， height， weight， pulse rate， and biochemistry indexes such as fasting glucose， blood lipid and plasma hs-CRP. The concentration of plasma adiponectin was determined by ELISA method. Binary logistic regression was performed to analyze the relationship between plasma adiponectin and hypertension. 【Results】 The plasma adiponectin level in patients with hypertension was significantly lower than that in normotensive patients ［3.56 （2.57-5.02）） μg/mL vs. 4.82 （3.19-6.89） μg/mL， P=0.012］. Partial correlation analysis showed a weak correlation of plasma adiponectin level with systolic BP and diastolic BP （r=-0.155， P=0.003 and r=-0.144， P=0.006）. Binary logistic regression analysis showed that after adjusting for confounding factors such as age， BMI， and high-sensitivity C-reactive protein， the risk of hypertension was 2.46 times higher in patients with plasma adiponectin in the lowest gender-specific tertile than those in the highest tertile （OR=2.46， 95% CI: 1.22-4.99）. 【Conclusion】 Hypoaponectinemia is an independent risk factor for hypertension in young individuals with normal renal function.

Effects of salt intake serum and urinary uromodulin levels in Chinese adults / 西安交通大学学报(医学版)

【Objective】 To explore the effects of dietary salt intake on serum and urinary levels through the chronic salt loading intervention. 【Methods】 Eighty adults （18 to 65 years old） were screened from two villages in Liquan and Lantian counties to participate in a 2-week chronic salt intervention， including a 3-day baseline survey， a 7-day low-salt diet， and a 7-day high-salt diet. Uromodulin levels in serum and urine were determined by enzyme-linked immunosorbent assay （ELISA） kits. According to the baseline blood pressure levels， all subjects were divided into normotensive and hypertensive groups. Pearson or Spearman correlation analyzed the associations of 24 h urinary sodium excretions with serum and urinary levels of uromodulin. 【Results】 At the baseline， serum uromodulin in hypertensive subjects was significantly lower than that in normotensive subjects （26.7±9.9 vs. 57.9±9.7 ng/mL， P=0.033）. Serum uromodulin levels were significantly lower on a high-salt diet than on a baseline diet ［（54.9±8.8 vs. 28.3±4.5） ng/mL， P=0.007］. In addition， daily urinary excretions of uromodulin were lower on a high-salt diet ［（28.4±6.6） ng/mL］ than on a baseline diet ［（282.1±70.0） ng/mL］ and on a low-salt diet ［（154.1±21.3） ng/mL］. The 24 h urinary sodium excretions were inversely correlated with urinary uromodulin excretions （r=-0.40， P<0.001） on both low-salt and high-salt diets， but not correlated with serum uromodulin levels. 【Conclusion】 Variations in dietary salt intake significantly affect plasma and urine uromodulin levels.

Association between body mass index trajectories in children and adolescents of Hanzhong city of Shanxi province and subclinical renal damage in adulthood: a 30-year longitudinal follow-up study / 中华肾脏病杂志

Objective:To investigate the association between body mass index (BMI) trajectories in children and adolescents and subclinical renal damage (SRD) in adulthood.Methods:4 623 participants aged 6-18 years old were recruited from the ongoing cohort of Hanzhong adolescent hypertension study in 1987, and the subjects were followed up in 1989, 1992, 1995, 2005, 2013 and 2017, respectively. Group-based trajectory modeling was used to identify distinct BMI trajectories in longitudinal analysis. Generalized linear model was applied to examine the association between different BMI trajectories and SRD incidence in adulthood.Results:A total of 2 678 subjects from childhood to adulthood were enrolled in this study. All subjects were divided into three groups according to three distinct BMI trajectories: low-increasing BMI group ( n=1 017), moderate-increasing BMI group ( n=1 353), and high-increasing BMI group ( n=308). Over follow up for 30 years, a total of 248 participants (9.3%) developed SRD. Urinary albumin-to-creatinine ratio (uACR) in low to high-increasing BMI group was 0.9(0.6, 1.4), 1.0(0.7, 1.7), 1.6(0.8, 3.2), respectively ( P trend<0.001), and estimated glomerular filtration rate was 98.5(87.6, 111.6) , 96.2(86.4, 109.7), 95.3 (87.5, 125.0) ml·min -1·(1.73 m 2) -1, respectively ( P trend=0.025). The generalized linear model analysis showed that uACR was increased linearly from low to high-increasing BMI group [ β=3.16(95% CI 1.02-5.31), Ptrend=0.004]. There was no correlation or linear trend between BMI trajectory and estimated glomerular filtration rate [ β=-2.30(95% CI-5.18-0.57), Ptrend=0.117]. Compared with the low-increasing BMI group, the high-increasing BMI group had greater odds of experiencing SRD in adulthood after adjusting for multiple confounders such as age, gender, medical history and lifestyle ( OR=2.83, 95% CI 1.84-4.36, Ptrend<0.001). Conclusions:Higher BMI trajectorie is correlated with higher level of uACR and risk of SRD in middle age. Identifying long-term BMI trajectorie from early age may assist in predicting individuals′ renal function in later life.

Conserved molecular interactions in centriole-to-centrosome conversion.

Centrioles are required to assemble centrosomes for cell division and cilia for motility and signalling. New centrioles assemble perpendicularly to pre-existing ones in G1-S and elongate throughout S and G2. Fully elongated daughter centrioles are converted into centrosomes during mitosis to be able to duplicate and organize pericentriolar material in the next cell cycle. Here we show that centriole-to-centrosome conversion requires sequential loading of Cep135, Ana1 (Cep295) and Asterless (Cep152) onto daughter centrioles during mitotic progression in both Drosophila melanogaster and human. This generates a molecular network spanning from the inner- to outermost parts of the centriole. Ana1 forms a molecular strut within the network, and its essential role can be substituted by an engineered fragment providing an alternative linkage between Asterless and Cep135. This conserved architectural framework is essential for loading Asterless or Cep152, the partner of the master regulator of centriole duplication, Plk4. Our study thus uncovers the molecular basis for centriole-to-centrosome conversion that renders daughter centrioles competent for motherhood.