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A study published in the journal Clinical & Translational Medicine examined the relationship between immunoglobulin A nephropathy (IgAN) and immunoglobulin A vasculitis with nephritis (IgAVN) using single-cell RNA sequencing (scRNA-seq) of pediatric renal tissues. The study found similarities and distinctions between the two kidney diseases, providing insights into their pathogenesis, diagnosis, and treatments. The analysis revealed differences in cell type proportions, energy metabolism, and fibrosis levels between IgAN and IgAVN. These findings have the potential to impact future diagnostic approaches, treatment options, and predictive outcomes for patients with these conditions. The study was conducted by a team of researchers from the Children's Hospital, Zhejiang University School of Medicine. [Extracted from the article]

Aims: Diabetic nephropathy (DN) is a leading cause of end‐stage renal disease. BASP1 (brain acid‐soluble protein) is up‐regulated in podocyte‐specific protein phosphatase 2A knockout mice (Pod‐PP2A‐KO) that develop kidney dysfunction. Here, we explore the role of BASP1 for podocytes in DN. Methods: BASP1 was assessed in kidneys from DN patients and DN mouse models, podocyte specific BASP1 knockout mice (Pod‐BASP1‐KO mice) were generated and studied in vivo. Furthermore, podocyte injury and apoptosis were measured after BASP1 knockdown and overexpression in a mouse podocyte cell line (MPC5). Potential signalling pathways involved in podocyte apoptosis were detected. Results: BASP1 expression was up‐regulated in DN patients compared to normal controls. BASP1 specific deletion in podocytes protected against podocyte injury by reducing the loss of expression of slit diaphragm molecules and foot process effacement in the DN model. BASP1 promoted actin cytoskeleton rearrangements and apoptosis in the MPC5 podocyte line. Molecules involved in the p53 pathway were down‐regulated in BASP1 knockdown podocytes treated with high glucose compared to controls. BASP1 promoted podocyte apoptosis and P53 pathway activation through co‐repression with Wilms' tumour 1 transcription factor (WT1). Conclusion: BASP1 activates the p53 pathway through modulation of WT1 to induce podocyte apoptosis in diabetic nephropathy. [ABSTRACT FROM AUTHOR]

Novel palmitic acid–decanoic acid@Ce–Eu/TiO2 (PA–DA@Ce–Eu/TiO2) microspheres with high photocatalysis–thermal–humidity collaborative performance were prepared via a two‐step method. Ce and Eu were used for codoping to modify the TiO2 hollow microspheres to enhance the photocatalytic properties. Furthermore, a eutectic phase change material (PA–DA) was combined with Ce–Eu/TiO2 hollow microspheres to prepare PA–DA@Ce–Eu/TiO2 microspheres. X‐ray diffraction and UV–VIS spectral analyses proved that Ce–Eu codoping enhanced the photocatalytic properties of the PA–DA@Ce–Eu/TiO2 microspheres under solar light; the degradation rate to gaseous formaldehyde at low concentrations reached 54.98% after 5 h. The pore structure, particle size distribution, microstructure, and thermostability of the PA–DA@Ce–Eu/TiO2 microspheres were determined using N2 adsorption isotherms, laser scattering particle size distribution analysis, scanning electron microscopy, and thermogravimetric analysis, respectively. The results showed that the Ce–Eu/TiO2 microspheres had a typical mesoporous structure, concentrated particle size distribution, and rough surface. The porous structure of the PA–DA@Ce–Eu/TiO2 microspheres was conducive to adsorb/desorb moisture, which was recorded to be 0.0575 g/g at 43.16–75.29% relative humidity. The differential scanning calorimeter analysis showed that the phase transition temperature of the PA–DA@Ce–Eu/TiO2 microspheres was 20–22°C and that the PA–DA@Ce–Eu/TiO2 microspheres were stable at 35°C. After 300 thermal cycles, the heat storage capacity of the PA–DA@Ce–Eu/TiO2 microspheres decreased by only 5%. Thus, we concluded that the PA–DA@Ce–Eu/TiO2 microspheres can purify air and control indoor thermal and humidity environments simultaneously and hence can be used as functional building materials to adjust the indoor environment. [ABSTRACT FROM AUTHOR]

Aim: This study aimed to explore the influence of maternal folate and vitamin B12 (B12) status during pregnancy on the incidence of low birthweight (LBW) infants. Methods: A total of 6203 eligible women registered in seven hospitals in southern China, and 230 cases with singleton live births and 382 controls were matched for further analyses. The concentrations of serum folate and B12 were detected with chemiluminescence microparticle immunoassay on ARCHITECT i2000‐1. Conditional logistic regression was used to evaluate the effects of folate and B12 levels on LBW. Results: Maternal serum folate levels increased basically with increasing the period of folic acid supplementation (P trend <0.001). Moreover, maternal serum folate and B12 levels gradually decreased with the increase of gestational age (P < 0.001). Conditional logistic regressions analysis results showed increased odds ratios (OR) for LBW from the fourth to first folate quartiles (P trend <0.01) in the second trimester. Compared with the women in the highest quartile, those in the lowest quartile of serum folate in the second trimester were found with higher risk of LBW (adjusted OR = 1.67, 95% confidence interval [CI]: 1.02–2.73). However, no significant association was observed between serum folate and LBW in the first trimester or third trimester. In addition, serum B12 exhibited no significant association with LBW. Conclusions: Low serum folate levels in the second trimester significantly increases the risk of LBW amongst Chinese women with singleton pregnancies. [ABSTRACT FROM AUTHOR]

Aim Approximately 30-40% of children with steroid sensitive nephrotic syndrome have frequently relapsing nephrotic syndrome ( FRNS) or steroid-dependent nephrotic syndrome ( SDNS). Mycophenolate mofetil ( MMF) and tacrolimus ( TAC) are often alternative treatment choices for these patients. Methods A single-center prospective study was conducted to compare the efficacy of MMF or TAC in reducing relapses and maintaining remission in children with FRNS or SDNS. Of the 72 recruited patients, either MMF (20∼30 mg/kg/d, n = 34) or TAC (0.05∼0.15 mg/kg/d, n = 38) was administered for 12 months. Results The mean 6-month relapse rates decreased from 2.56 episodes before therapy to 0.76 episodes in the first 6 months after therapy (c2 = 44.362, p < 0.001) and 0.67 in the next 6 months (c2 = 37.817, p < 0.001) in the MMF group. In the TAC group, the mean 6-month relapse rates decreased from 2.39 episodes before therapy to 0.41 episodes in the first 6 months after therapy (c2 = 62.242, p < 0.001) and 0.42 in next 6 months (c2 = 67.482, p < 0.001). No significant difference in the relapse rate was found between the groups (before therapy, c2 = 0.902, p = 0.637; first 6 months, c2 = 5.358, p = 0.147; second 6 months, c2 = 4.089, p = 0.252). And there was also no significant difference in cumulative sustained remission and the incidence of adverse events between two groups. Conclusions In combination with low-dose steroids, MMF or TAC presented similar efficacy in maintaining remission in children with FRNS/ SDNS in the present study. Therapy with MMF or TAC is a promising strategy with a moderate risk of side effects in children who are steroid sensitive but have FRNS/ SDNS. [ABSTRACT FROM AUTHOR]

In a PAR shell: Superparamagnetic core–shell materials with Fe3O4 nanoparticle cores and cross ‐ linked polyaryl (PAR) monolayer shells were fabricated by self ‐ assembly of enediyne compound monolayers followed by Bergman cyclization ‐ mediated polymerization. The surface coating with a PAR monolayer was confirmed by TGA, XPS, and Raman analysis. The Fe3O4@PAR composites display a high saturation magnetization and excellent chemical stability, and moreover exhibit a typical ferrofluidic behavior. [ABSTRACT FROM AUTHOR]

Transforming growth factor ( TGFβ)3 is essential for palate development, particularly during the late phase of palatogenesis when the disintegration of the palatal medial edge seam ( MES) occurs resulting in mesenchymal confluence. The MES is composed of medial-edge epithelium ( MEE) of opposite palatal shelves; its complete disintegration is essential for mediating correct craniofacial morphogenesis. This phenomenon is initiated by TGFβ3 upon adherence of opposing palatal shelves, and subsequently epithelial-mesenchymal transition ( EMT) instigates the loss of E- Cadherin, causing the MES to break into small epithelial islands forming confluent palatal mesenchyme; however, apoptosis and cell migration or in combination of all are other established mechanisms of seam disintegration. To investigate the molecular mechanisms that cause this E- Cadherin loss, we isolated and cultured murine embryonic primary MES cells from adhered palates and employed several biological approaches to explore the mechanism by which TGFβ3 facilitates palatal seam disintegration. Here, we demonstrate that TGFβ3 signals by activating both Smad-dependent and Smad-independent pathways. However, activation of the two most common EMT related transcription factors, Snail and SIP, was facilitated by Smad-independent pathways, contrary to the commonly accepted Smad-dependent pathway. Finally, we provide the first evidence that TGFβ3-activated Snail and SIP1, combined with Smad4, bind to the E- Cadherin promoter to repress its transcription in response to TGFβ3 signaling. These results suggest that TGFβ3 uses multiple pathways to activate Snail and SIP1 and these transcription factors repress the cell-cell adhesion protein, E- Cadherin, to induce palatal epithelial seam EMT. Manipulation and intervention of the pathways stimulated by TGFβ3 during palate development may have a significant therapeutic potential. [ABSTRACT FROM AUTHOR]

J Oral Pathol Med (2010) 39 182–187 Background: Candida albicans is the important opportunistic fungal pathogens which can cause oral Candidiasis and even more seriously systemic infection. Apoptosis of C. albicans induced by environmental factor such as weak acid and antifungal drugs were studied recently. Illustrating the phenomenon of apoptosis in C. albicans may help us to discover new antifungal therapy by activating the fungal cells to suicide. Methods: Two oral C. albians clinical isolates which isolated respectively from healthy host [Strain 23C: minimal inhibition concentration (MIC) is 0.125 μg/ml for Amphotericin B (AmB)] and advanced cancer patient (Strain 28A: MIC is 2 μg/ml for AmB), were induced by 1 μg/ml AmB in vitro for 200 min, and then studied the apoptosis markers using terminal deoxynucletidyltransferase-mediated dUTP nick end labeling (TUNEL) (shown by diaminobenzidine and fluorescent isothiocyanate), and the ultrastructure of cell nuclear using transmission electron microscope (TEM), quantitative analysis using flow cytometry for the rapid exposure of phosphatidylserine at the outer membrane and propodium iodide (PI) double staining. C. albicans conference strain YEM30 was used as the control strain. Results: With TUNEL assay and TEM, we detected the typical characteristics of apoptosis. Strain 23C (with low MIC) showed significantly higher percentage of apoptosis (19.92%) compared with Strain 28A (with high MIC) which was isolated from the cancer patient (7.29%) ( P < 0.01). In addition, 7.3% of early apoptosis cells of Strain 23C can form colonies on the plates, while 15% for Strain 28A. None of the PI (+) cells can form colony. Conclusions: Apoptosis of oral C. albicans isolates can be induced by AmB. The feature of antifungal drug susceptibility of the oral C. albicans clinical isolates may associate with the response of apoptosis inducing. [ABSTRACT FROM AUTHOR]