[(Histamine)(18-crown-6)2][BF4]2 is a high-temperature piezoelectric.

We discovered that [(histamine)(18-crown-6)2][BF4]2 is a high-temperature host-guest inclusion complex that presents decent piezoelectric properties (d33 = 5 pC/N), undergoes a phase transition at 406 K, and also possesses potential ferroelectricity. This work provides a new idea for constructing host-guest inclusion piezoelectrics.

Crown Ether Host-Guest Molecular Ferroelectrics.

In recent years, molecular ferroelectrics have received great attention due to their low weight, mechanical flexibility, easy preparation and excellent ferroelectric properties. Among them, crown-ether-based molecular ferroelectrics, which are typically composed of the host crown ethers, the guest cations anchored in the crown ethers, and the counterions, are of great interest because of the host-guest structure. Such a structure allows the components to occur order-disorder transition easily, which is beneficial for inducing ferroelectric phase transition. Herein, we summarized the research progress of crown ether host-guest molecular ferroelectrics, focusing on their crystal structure, phase transition, ferroelectric-related properties. In view of the small spontaneous polarization and uniaxial nature, we outlook the chemical design strategies for obtaining high-performance crown-ether-based molecular ferroelectrics. This minireview will be of guiding significance for the future exploration of crown ether host-guest molecular ferroelectrics.

The complete mitochondrial genome of Huainan partridge chicken (Gallus gallus).

Huainan Partridge chicken is one of the indigenous chicken breeds in China. In this study, the first complete mitochondrial DNA (mtDNA) sequence of Huainan Partridge chicken had been obtained using PCR amplification, sequencing and assembling. The mitogenome of Huainan Partridge chicken is 16785 bp in length, including a control region (D-loop), 13 protein-coding genes, 22 transfer genes and 2 ribosomal genes. The base composition of the complete mtDNA sequence is 30.27% for A, 23.73% for T, 13.50%for G, 32.50% for C. This study will provide reference for the phylogenetic analysis of Huainan Partridge chicken.

TRIM21-regulated Annexin A2 plasma membrane trafficking facilitates osteosarcoma cell differentiation through the TFEB-mediated autophagy.

Osteosarcoma (OS) is the most common primary malignant bone tumor in children and adolescents, which is characterized by dysfunctional autophagy and poor differentiation. Our recent studies have suggested that the tripartite motif containing-21 (TRIM21) plays a crucial role in regulating OS cell senescence and proliferation via interactions with several proteins. Yet, its implication in autophagy and differentiation in OS is largely unknown. In the present study, we first showed that TRIM21 could promote OS cell autophagy, as determined by the accumulation of LC3-II, and the degradation of cargo receptor p62. Further, we were able to identify that Annexin A2 (ANXA2), as a novel interacting partner of TRIM21, was critical for TIRM21-induced OS cell autophagy. Although TRIM21 had a negligible effect on the mRNA and protein expressions of ANXA2, we did find that TRIM21 facilitated the translocation of ANXA2 toward plasma membrane (PM) in OS cells through a manner relying on TRIM21-mediated cell autophagy. This functional link has been confirmed by observing a nice co-expression of TRIM21 and ANXA2 (at the PM) in the OS tissues. Mechanistically, we demonstrated that TRIM21, via facilitating the ANXA2 trafficking at the PM, enabled to release the transcription factor EB (TFEB, a master regulator of autophagy) from the ANXA2-TFEB complex, which in turn entered into the nucleus for the regulation of OS cell autophagy. In accord with previous findings that autophagy plays a critical role in the control of differentiation, we also demonstrated that autophagy inhibited OS cell differentiation, and that the TRIM21/ANXA2/TFEB axis is implicated in OS cell differentiation through the coordination with autophagy. Taken together, our results suggest that the TRIM21/ANXA2/TFEB axis is involved in OS cell autophagy and subsequent differentiation, indicating that targeting this signaling axis might lead to a new clue for OS treatment.

Astragaloside IV attenuates high glucose-induced EMT by inhibiting the TGF-ß/Smad pathway in renal proximal tubular epithelial cells.

In the present study, we examined the molecular mechanism of astragaloside IV (AS-IV) in high glucose (HG)-induced epithelial-to-mesenchymal transition (EMT) in renal proximal tubular epithelial cells (PTCs). NRK-52E cell viability and apoptosis were determined by the cell counting kit-8 (CCK-8) assay and flow cytometric analysis, respectively. Expressions of E-cadherin, N-cadherin, vimentin, and occludin were measured by Western blot, and those of E-cadherin and N-cadherin were additionally measured by immunofluorescence analysis. Transforming growth factor-ß1 (TGF-ß1) and α-smooth muscle actin (α-SMA) expressions were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. The expressions of Smad2, Smad3, phosphorylated-Smad2 (p-Smad2), and p-Smad3 were measured using Western blot. We found that AS-IV could recover NRK-52E cell viability and inhibit HG-induced cell apoptosis. TGF-ß1, α-SMA, Smad2, Smad3, p-Smad2, and p-Smad3 expressions were decreased in the AS-IV-treated groups compared with the HG group. Moreover, the expressions of E-cadherin and occludin were remarkably up-regulated and those of N-cadherin and vimentin were down-regulated in the AS-IV-treated groups compared with the HG group. Interestingly, the TGF-ß1 activator SRI-011381 hydrochloride had an antagonistic effect to AS-IV on HG-induced EMT behavior. In conclusion, AS-IV attenuates HG-induced EMT by inhibiting the TGF-ß/Smad pathway in renal PTCs.

YAP mediates the positive regulation of hnRNPK on the lung adenocarcinoma H1299 cell growth.

Lung cancer is the leading cause of cancer death worldwide, and non-small cell lung cancer (NSCLC) accounts for 80%-85% of diagnostic cases. The molecular mechanisms of NSCLC pathogenesis are not well understood. Heterogeneous nuclear ribonucleoprotein K (hnRNPK) is a multifunctional protein that regulates gene expression and signal transduction and closely associated with tumorigenesis, but its mechanism of action in the pathogenesis of NSCLC is unclear. In this study, we observed that the expression pattern of hnRNPK in H1299 lung adenocarcinoma cells varied depending on the cell density in culture. Moreover, hnRNPK stimulated the ability of proliferation and colony formation of H1299 cells, which is important for the multilayered cell growth in culture. We further investigated whether there is an association between hnRNPK and the elements involved in the cell contact inhibition pathway. By using quantitative reverse transcriptase-polymerase chain reaction assay and a YAP activity reporter system, we found that hnRNPK upregulated the mRNA and protein levels and transcriptional activity of Yes-associated protein 1 (YAP), a master negative regulator of Hippo contact inhibition pathway. Furthermore, YAP knockdown with siRNA abolished the stimulatory effect of hnRNPK on H1299 cell proliferation. These results suggested that YAP could be one of the effectors of hnRNPK. Our data may provide new clues for further understanding the biological functions of hnRNPK, particularly in the context of lung adenocarcinoma oncogenesis.

Genome-wide profiling of mRNA and lncRNA expression in dengue fever and dengue hemorrhagic fever.

Dengue fever (DF) and dengue hemorrhagic fever (DHF) are recurrent diseases that are widespread in the tropics. Here, we identified candidate genes associated with these diseases by performing integrated analyses of DF (GSE51808) and DHF (GSE18090) microarray datasets in the Gene Expression Omnibus (GEO). In all, we identified 7635 differentially expressed genes (DEGs) in DF and 8147 DEGs in DHF as compared to healthy controls (P < 0.05). In addition, we discovered 215 differentially expressed long non-coding RNAs (DElncRNAs) in DF and 225 DElncRNAs in DHF. There were 1256 common DEGs and eight common DElncRNAs in DHF vs DF, DHF vs normal control, and DF vs normal control groups. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis revealed that signal transduction (false discovery rate = 8.33E-10), 'toxoplasmosis', and 'protein processing in endoplasmic reticulum' were significantly enriched pathways for common DEGs. We conclude that the MAGED1,STAT1, and IL12A genes may play crucial roles in DF and DHF, and suggest that our findings may facilitate the identification of biomarkers and the development of new drug design strategies for DF and DHF treatment.

Regulation and related mechanism of GSN mRNA level by hnRNPK in lung adenocarcinoma cells.

Gelsolin (GSN) is an actin filament-capping protein that plays a key role in cell migration. Here we show that heterogeneous nuclear ribonucleoprotein K (hnRNPK) regulates GSN expression level by binding to the 3'-untranslated region (3'UTR) of GSN mRNA in non-small cell lung cancers (NSCLC) H1299 cells which are highly metastatic and express high level of GSN. We found that hnRNPK overexpression increased the mRNA and protein level of GSN, whereas hnRNPK knockdown by siRNA decreased the mRNA and protein level of GSN in both H1299 and A549 cells, indicating a positive role of hnRNPK in the regulation of GSN expression. Furthermore, hnRNPK knockdown affected the migration ability of H1299 and A549 cells which could be rescued by ectopic expression of GSN in those cells. Conversely, GSN knockdown in hnRNPK-overexpressing cells could abort the stimulatory effect of hnRNPK on the cell migration. These results suggest that hnRNPK function in the regulation of cell migration is GSN-dependent. Taken together, these data unveiled a new mechanism of regulation of the GSN expression by hnRNPK and provides new clues for the discovery of new anti-metastatic therapy.

The effect of high glucose-based peritoneal dialysis fluids on thioredoxin-interacting protein expression in human peritoneal mesothelial cells.

BACKGROUND: It has been demonstrated that thioredoxin-interacting protein (TXNIP) interacted with NACHT, LRR and PYD domains-containing protein 3 (NLRP3) and participated in the NLRP3 inflammasome activation. Our previous study has demonstrated that in human peritoneal mesothelial cells (HPMCs), exposure to high glucose-based peritoneal dialysis (PD) solutions induced mitochondrial reactive oxygen species (ROS) production, activation of NLRP3 inflammasome and IL-1ß expression. This study aimed to investigate the effect of high glucose-based PD fluids on the TXNIP expression and the underlying mechanisms by which TXNIP-NLRP3 interaction mediates the inflammatory injury to HPMCs in high glucose-based PD fluids conditions. METHODS: TXNIP gene and protein expression was detected by real-time polymerase chain reaction (RT-PCR) and immunoblot. Immunoprecipitation was used to evaluate the interaction between TRX1 and TXNIP, TXNIP and NLRP3. ROS production and IL-1ß expression was examined by flow cytometry and immunoblot and enzyme-linked immunosorbent assay (ELISA) respectively. RESULTS: It was identified that high glucose-based PD solutions enhance the level of TXNIP gene and protein in cultured HPMCs and a rat-based PD model. We also found that ROS generation induced by high glucose-based PD solutions disrupts the TRX1-TXNIP association, while promoting the binding of TXNIP to NLRP3 in HPMCs. Furthermore, the application of a ROS inhibitor (APDC) to HPMCs blocked the high glucose-based PD solution-induced TXNIP-NLRP3 binding, in addition to ROS production and IL-1ß expression. CONCLUSION: The results of the present study revealed a novel mechanism underlying high glucose-containing PD-mediated peritoneal inflammatory injury, supporting the attenuation of ROS generation as a potential therapeutic strategy to alleviate such pathology.

Absorption and efflux characteristics of CP-25 in plasma and peripheral blood mononuclear cells of rats by UPLC-MS/MS.

Paeoniflorin-6'-O-benzene sulfonate (code: CP-25), is an active monomer obtained by modifying the structure of paeoniflorin (Pae). CP-25 can alleviate the course of adjuvant arthritis (AA) rats by regulating immune inflammatory response and reducing bone damage. In addition, our research has found that immune cells are important target cells for its anti-inflammatory and immunomodulatory effects. Therefore, it is of great significance to study the pharmacokinetics of CP-25 in immune cells. The aim of this study was to investigate the absorption and efflux of CP-25 in plasma and peripheral blood mononuclear cells (PBMCs) of rats. We established a sensitive ultra-high performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) to rapidly determine CP-25 in plasma and PBMC of rat. We found that the transport amount of CP-25 in PBMC gradually decreased with the increase of time, and reached equilibrium after 1 h. Moreover, there is a certain correlation between the concentration of CP-25 in plasma and the concentration of CP-25 in PBMC. In addition, we used several transporter inhibitors to study their effects on the efflux of CP-25 in PBMC. The efflux of CP-25 in PBMC increased with the increase of time in the first 30 min, and the efflux of CP-25 decreased gradually after 30 min. Furthermore, after multiple administration of 50 mg/kg in rats, concentration of CP-25 in PBMC is similar to the change of concentration of CP-25 in plasma. Our results suggest that CP-25 may enter PBMC by passive transport, and P-glycoprotein (P-gp), multidrug resistance-associated protein 2 (MRP2) and breast cancer resistance protein (BCRP) may be involved in the efflux of CP-25 in PBMC. This research provides a basis and guidance for further study of the clinical application of CP-25.

YWHAZ Binds to TRIM21 but Is Not Involved in TRIM21-stimulated Osteosarcoma Cell Proliferation.

OBJECTIVE: Osteosarcoma is the most common type of malignant bone tumor in children and adolescents. The role of E3 ligases in tumorigenesis is currently a focus in tumor research. In the present study, we investigated the role of the E3 ligase tripartite motif 21 (TRIM21) in osteosarcoma cell proliferation. METHODS: 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assays were used to assess osteosarcoma cell viability. U2-OS cells stably carrying a recombinant lentivirus expressing tetracycline-regulated TRIM21 were screened. Co-immunoprecipitation was coupled with LCMS/MS analysis to identify novel interacting partners of TRIM21. Co-immunoprecipitation and bimolecular fluorescence complementation (BIFC) were performed to validate the interactions between TRIM21 and its novel partner YWHAZ. A TRIM21-ΔRING construct was generated to test the effects of TRIM21 ligase activity on YWHAZ. RESULTS: TRIM21 positively regulated osteosarcoma cell proliferation. Overexpression of TRIM21 enhanced osteosarcoma cell tolerance toward various stresses. YWHAZ protein was identified as a novel interacting partner of TRIM21 and its expression levels were negatively regulated by TRIM21. The RING domain of TRIM21 was required for TRIM21 negative regulation of YWHAZ expression. However, overexpression of YWHAZ did not affect positive regulation of osteosarcoma cell proliferation by TRIM21. CONCLUSION: Our results further clarify the molecular mechanisms underlying the pathogenesis of osteosarcoma.

PPAR­Î³ agonist rosiglitazone protects rat peritoneal mesothelial cells against peritoneal dialysis solution­induced damage.

Long-term peritoneal dialysis (PD) leads to ultrafiltration failure (UFF). Peritoneal mesothelial cells, which form the innermost monolayer of the peritoneal cavity, have been shown to regulate various responses, including inflammation, in UFF. The present study was designed to investigate the effect of the peroxisome proliferator­activated receptor­Î³ (PPAR­Î³) agonist, rosiglitazone, on peritoneal dialysis solution (PDS)­induced injuries in rat peritoneal mesothelial cells (RPMCs). RPMCs were cultured for different durations and with different concentrations of PDS. The gene expression levels of aquaporin­1 (AQP­1) and zonula occluden­1 (ZO­1) were determined using reverse transcription­quantitative polymerase chain reaction analysis. The protein levels of AQP­1, ZO­1 and PPAR­Î³ were measured using western blot analysis. Interleukin (IL)­6 and IL­8 were detected using ELISA. The RPMCs were damaged by stimulation with 4.25% PDS for 72 h. The expression levels of AQP­1 and ZO­1 were increased, and the secretion of IL­6 and IL­8 were decreased by rosiglitazone. The use of the PPAR­Î³ inhibitor, GW­9662, completely prevented the effects of rosiglitazone. These results indicated that PDS exposure stimulated an inflammatory response in the RPMCs. The PPAR­Î³ activator, rosiglitazone, appeared to relieve the injury by inhibiting inflammation, and regulating the expression of AQP­1 and ZO­1, however further investigations are required to elucidate the potential underlying mechanism.

Atorvastatin alleviates renal ischemia-reperfusion injury in rats by promoting M1-M2 transition.

Acute kidney injury (AKI) often occurs as a result of ischemia-reperfusion (IR). Previous studies have demonstrated that inflammation is an important contributor to AKI. Atorvastatin (ATO) possesses anti­inflammatory properties and has been demonstrated to exert protective effects against renal IR injury (IRI). However, the underlying mechanism requires further study. In the present study, a rat model of renal IRI was successfully established. Consistent with the results of a previous study, ATO significantly attenuated IRI, which was supported by a decrease in serum creatinine and an increase in creatinine clearance rate, as well as alleviated pathological alterations in renal tubular cells. There are two types of activated macrophages: Proinflammatory M1 and anti­inflammatory M2 macrophages, which have been demonstrated to exert contributory and protective effects on IRI, respectively. The present study demonstrated that treatment with ATO significantly decreased M1 macrophage density and increased M2 macrophage density, as compared with the IR group. In addition, it is well known that M1 macrophages can be induced by T helper 1 cytokines, including tumor necrosis factor (TNF)­α and interferon (IFN)­Î³, whereas M2 macrophages can be induced by peroxisome proliferator-activated receptor (PPAR)­Î³. The present study indicated that ATO treatment significantly decreased the expression levels of TNF­α and IFN­Î³, and increased PPAR­Î³ expression. In conclusion, ATO may ameliorate renal IRI by promoting M1­M2 transition. Furthermore, ATO­mediated macrophage polarization in rats with renal IRI may be associated with the downregulation of TNF­α and IFN­Î³, and the upregulation of PPAR-γ.

Potassium supplementation and long-term outcomes in chronic peritoneal dialysis patients with end-stage renal disease: a propensity score matching study.

OBJECTIVE: In this retrospective matched-cohort study, the association between potassium supplementation and long-term outcomes was determined. METHODS: Chronic peritoneal dialysis (PD) patients, aged ≥ 16 years, being referred to four PD centers in China, with serum potassium levels ≤ 3.5 mEq/L on three consecutive monthly in Q4 2008 and without receiving oral potassium supplementation in the prior three months were included in this study. Patients were divided into two groups, either to receive (test group) or not (control group) oral potassium supplementation in both Q4 2008 and the subsequent follow-up period, until 31 December 2014. The patients from the test group were matched to those from the control group using a propensity score. The clinical outcomes for all-cause and cardiovascular mortality were estimated by Matched Cox regression models during 61.5 months of median follow-up. All patients were also categorized according to serum potassium correction levels (<3.0, 3.0 to <4.0, 4.0 to <5.0 and ≥5.0 mEq/L) after the whole follow-up. The hazard ratios (HRs) were used to assess the relationship between corrected potassium levels and all-cause and cardiovascular mortality in PD patients. Subgroup analysis was used to determine the homogeneity of the associations between potassium supplementation and all-cause mortality. RESULTS: All-cause mortality occurred in 108 patients (605/10,000 person-years) in the test group and 114 patients (677/10,000 person-years) in the control group during 1786- and 1685-year follow-up, respectively [hazard ratio (HR), 0.89; 95% confidence interval (CI), 0.68-1.16; p = 0.38]. Cardiovascular mortality occurred in 97 patients (542/10,000 person-years) in the test group and 101 patients (598/10,000 person-years) in the control group (HR, 0.89; 95% CI, 0.67-1.18; p = 0.43). There were no significant interactions between potassium supplementation and any of the subgroups, except for diabetes mellitus and volume overload. During a median follow-up of 61.5 months, adjusted all-cause mortality hazard ratio (HR) and 95% confidence interval (CI) for corrected serum potassium of <3.0, 3.0 to < 4.0, and ≥5.0 mEq/L, compared with 4.0 to < 5.0 mEq/L (reference), were 2.23 (1.17-3.72), 1.35 (0.89-1.81), and 1.74 (1.05-3.72), respectively. CONCLUSION: The use of potassium supplementation in chronic PD patients is not associated with mortality. While it may be necessary for the correction of hypokalemia or the maintenance of normokalemia, and the consequent reduction of hypokalemia-associated mortality. Additionally, use of aldosterone antagonists may be preferable for the handling of hypokalemia in PD patients.

Involvement of peroxisome proliferator activated receptor-γ in the anti-inflammatory effects of atorvastatin in oxygen-glucose deprivation/reperfusion-stimulated RAW264.7 murine macrophages.

Ischemia­reperfusion (I/R) injury is important in the pathogenesis and/or progression of various diseases, including stroke, cardiovascular disease and acute renal injury. Increasing evidence indicates that atorvastatin exerts protective effects in I/R injury­associated diseases; however, the underlying mechanisms remain to be fully elucidated. In the present study, oxygen­glucose deprivation (OGD)/reperfusion­stimulated. RAW264.7 murine macrophages served as a model of I/R injury. The knockdown of peroxisome proliferator activated receptor­Î³ (PPARγ) expression in these cells increased OGD/reperfusion­induced expression of inducible nitric oxide synthase (iNOS), tumor necrosis factor­α (TNF­α) and interferon­Î³ (IFN­Î³), and enhanced OGD/reperfusion­induced downregulation of the expression of cluster of differentiation (CD) 206, at the mRNA and protein levels. Conversely, overexpression of PPARγ significantly attenuated OGD/reperfusion­induced alterations in the expression of iNOS, TNF­α, IFN­Î³ and CD206 at the mRNA and protein levels. Notably, atorvastatin inhibited OGD/reperfusion­induced iNOS expression and reversed OGD/reperfusion­induced downregulation of the expression of CD206 and PPARγ at the mRNA and protein levels. The results of the present study indicate that atorvastatin exhibits significant anti­inflammatory effects in OGD/reperfusion­stimulated RAW264.7 cells, possibly via PPARγ regulation. The findings of the present study may reveal a novel mechanism underlying the protective effects of atorvastatin in I/R injury­associated diseases.

Levels of vitamin D receptor and CYP24A1 in patients with end-stage renal disease.

OBJECTIVE: This study was performed to detect the expression of vitamin D receptor (VDR) and cytochrome P450, family 24, subfamily A, polypeptide 1 (CYP24A1) in 24 end stage renal disease (ESRD) patients and 24 healthy controls. METHOD: In this study, 24 ESRD patients and 24 healthy controls were included. RESULTS: In our study, the levels of VDR in patients with ESRD were reduced when compared with those from healthy controls (5.20±0.32 vs 8.59±1.03; P<0.01). However, the levels of CYP24A1 in ESRD patients were increased than those from healthy controls (50.18±21 vs 7.78±1.31; P<0.01). Correlation analysis showed that VDR levels were negatively correlated with CYP24A1 (r=-0.723; P<0.01). CONCLUSION: VDR levels were reduced and CYP24A1 levels were increased in patients with ESRD, and VDR levels were negatively correlated with CYP24A1.

Knockdown of elF3a inhibits collagen synthesis in renal fibroblasts via Inhibition of transforming growth factor-ß1/Smad signaling pathway.

Renal fibrosis is characterized by an exacerbated accumulation of deposition of the extracellular matrix (ECM). The eukaryotic translation initiation factor (eIF) 3a is the largest subunit of the eIF3 complex and has been involved in pulmonary fibrosis. However, the role of eIF3a in rental fibrosis is still unclear. Therefore, in this study, we investigated the role of eIF3a in rental fibrosis and explored the underlying mechanism. Our study found that eIF3a was up-regulated in renal fibrotic tissues and transforming growth factor (TGF)-ß1-treated HK-2 cells. In addition, knockdown of eIF3a significantly inhibited TGF-ß1-induced expression levels of α-smooth muscle actin (α-SMA) and collagen I. Furthermore, knockdown of eIF3a attenuated TGF-ß1-induced Smad3 activation in HK-2 cells. Taken together, these results suggest that knockdown of eIF3a inhibits collagen synthesis in renal fibroblasts via inhibition of TGF-ß1/Smad signaling pathway, and eIF3a may be a potential molecular target for the treatment of renal fibrosis.

Rosiglitazone, a Peroxisome Proliferator-Activated Receptor (PPAR)-γ Agonist, Attenuates Inflammation Via NF-κB Inhibition in Lipopolysaccharide-Induced Peritonitis.

We assessed the anti-inflammatory effect of peroxisome proliferator-activated receptor (PPAR)-γ agonist, rosiglitazone, in a lipopolysaccharide (LPS)-induced peritonitis rat model. LPS was intraperitoneally injected into rats to establish peritonitis model. Male Sprague-Dawley (SD) rats were assigned to normal saline (the solvent of LPS), LPS, rosiglitazone plus LPS, and rosiglitazone alone. A simple peritoneal equilibrium test was performed with 20 ml 4.25 % peritoneal dialysis fluid. We measured the leukocyte count in dialysate and ultrafiltration volume. Peritoneal membrane histochemical staining was performed, and peritoneal thickness was assessed. CD40 and intercellular adhesion molecule-1 messenger RNA (ICAM-1 mRNA) levels in rat visceral peritoneum were detected by reverse transcription (RT)-PCR. IL-6 in rat peritoneal dialysis effluent was measured using enzyme-linked immunosorbent assay. The phosphorylation of NF-κB-p65 and IκBα was analyzed by Western blot. LPS administration resulted in increased peritoneal thickness and decreased ultrafiltration volume. Rosiglitazone pretreatment significantly decreased peritoneal thickness. In addition to CD40 and ICAM-1 mRNA expression, the IL-6, p-p65, and p-IκBα protein expressions were enhanced in LPS-administered animals. Rosiglitazone pretreatment significantly decreased ICAM-1 mRNA upregulation, secretion of IL-6 protein, and phosphorylation of NF-κB-p65 and IκBα without decreasing CD40 mRNA expression. Rosiglitazone has a protective effect in peritonitis, simultaneously decreasing NF-κB phosphorylation, suggesting that NF-κB signaling pathway mediated peritoneal inflammation induced by LPS. PPAR-γ might be considered a potential therapeutic target against peritonitis.

Frequencies of apolipoprotein E alleles in depressed patients undergoing hemodialysis--a case-control study.

OBJECTIVE: To explore the relation between the frequencies of apolipoprotein E (ApoE) alleles and the occurrence of depression in patients undergoing hemodialysis in a Chinese population. METHODS: We examined the ApoE alleles in a sample of 288 subjects: 72 patients with depression under hemodialysis, 74 patients without depression under hemodialysis, 75 patients with depression under nondialytic treatment and 67 patients without depression under nondialytic treatment. The depression state was assessed using the Center for Epidemiological Studies Depression (CES-D) scale. Associations between the occurrence of depression and the frequencies of ApoE alleles were examined using multinomial logistic regression models with adjustment of relevant covariates. Information about sociodemographics, clinical data, vascular risk factors and cognitive function was also collected and evaluated. RESULTS: The frequencies of ApoE-ɛ2 were significantly different between depressed and non-depressed patients irrespective of dialysis (p < 0.05), but no significant difference was found in the frequencies of ApoE-ɛ4 (p > 0.05). Serum ApoE levels were significantly different between depressed and non-depressed patients in the whole sample (p < 0.05). Multinomial logistic regression models showed significant association between the frequency of ApoE-ɛ2 and the occurrence of depression in the Chinese population after control of relevant covariates, including age, sex, educational level, history of smoking and drinking, vascular risk factors and cognitive function. CONCLUSIONS: No association between the frequency of ApoE-ɛ4 and the occurrence of depression was found in patients undergoing hemodialysis. Further research is needed to find out if ApoE-ɛ2 acts as a protective factor in Chinese dialysis population since it might decrease the prevalence of depression and delay the onset age.

Association of vitamin D receptor BsmI (rs1544410) gene polymorphism with the intact parathyroid hormone (iPTH) level among patients with end-stage renal disease.

Association of vitamin D receptor (VDR) BsmI (rs1544410) gene polymorphism with the intact parathyroid hormone (iPTH) level among patients with end-stage renal disease (ESRD) from the published reports is still conflicting. This meta-analysis was performed to evaluate the relationship between VDR BsmI (rs1544410) gene polymorphism and the iPTH level among patients with ESRD. The association studies were identified from PubMed, and Cochrane Library on 1 March 2014, and eligible investigations were included and synthesized using meta-analysis method. Six reports were recruited into this meta-analysis for the association of VDR BsmI gene polymorphism with iPTH level among patients with ESRD. In this meta-analysis, the iPTH level in ESRD patients carrying BsmI Bb genotype was higher than that in ESRD patients carrying bb genotype in overall populations (Bb versus bb: OR = 61.40, 95% CI: 19.65-103.16, p = 0.004). However, the iPTH level in ESRD patients carrying BB genotype was not significant different from that in ESRD patients with Bb genotype and bb genotype in overall populations (BB versus Bb: OR = -18.30, 95% CI: -126.28-89.69, p = 0.74; BB versus bb: OR = 22.85, 95% CI: -70.81-116.51, p = 0.63). Furthermore, the results for Caucasians were similar to those in overall populations. In conclusion, the iPTH level in ESRD patients carrying BsmI Bb genotype was higher than that in ESRD patients carrying bb genotype in overall populations and in Caucasians. However, more studies should be conducted to confirm it.