Face Blindness in Children and Current Interventions.

Children with prosopagnosia, also known as face blindness, struggle to recognize the faces of acquaintances, which can have a negative impact on their social interactions and overall functioning. This paper reviews existing research on interventions for children with prosopagnosia, including compensatory and remedial strategies, and provides a summary and comparison of their effectiveness. However, despite the availability of these interventions, their effectiveness remains limited and constrained by various factors. The lack of a widely accepted treatment for children with prosopagnosia emphasizes the need for further research to improve intervention strategies. Last, three future research directions were proposed to improve interventions for prosopagnosia, including ecological approaches, the social challenges faced by children, and new potential intervention methods.

IFC-305 attenuates renal ischemia-reperfusion injury by promoting the production of hydrogen sulfide (H2S) via suppressing the promoter methylation of cystathionine γ-lyase (CSE).

Renal ischemia-reperfusion (I/R) injury is characterized by elevated expression of homocysteine and decreased production of hydrogen sulfide (H2S). Cystathionine γ-lyase (CSE) is a key factor in the onset of renal I/R injury, while IFC-305 can regulate the expression of CSE via epigenetic modification. Animal and cellular models of I/R were established in this work, followed by H&E staining to evaluate the extent of renal tissue injury under distinct conditions. Several methods, including ELISA, qPCR and Western blot, were used to analyze the levels of creatinine, CSE and H2S in various I/R models. Bisulfite sequencing PCR was used to evaluate the level of DNA methylation. The severity of the renal injury was significantly elevated in I/R rats and alleviated by the IFC-305 treatment. The level of Hcy was increased in the renal tissue and peripheral blood of I/R rats, while the IFC-305 treatment inhibited the expression of homocysteine (Hcy). Mechanistically, the DNA methylation in the CSE promoter was dramatically enhanced in I/R rats and cells, while the IFC-305 treatment reduced the level of DNA methylation in the CSE promoter. Moreover, the IFC-305 increased the concentration of H2S, which was reduced in I/R rats and cells. Finally, I/R rats and cells showed aberrantly high levels of MDA and superoxide, while the IFC-305 treatment reduced the levels of malondialdehyde (MDA) and superoxide. IFC-305, an adenosine derivative, promoted the production of H2S and attenuated renal injury in cellular and animal models of renal I/R by modifying the methylation status of the CSE promoter.

Fortified phosphorus­lowering treatment through administration of lanthanum protects against vascular calcification via regulation of FGF23 in chronic kidney disease.

Phosphorus reduction can prevent against vascular calcification (VC) in chronic kidney disease (CKD), but the mechanisms underlying its actions remain unclear. The aim of the present study was to determine the effect of a fortified phosphorus­lowing treatment on VC in CKD. Serum levels of creatinine, blood urea nitrogen (BUN), fibroblast growth factor 23 (FGF23), calcium and phosphorus, and the plasma levels of parathyroid hormone (PTH) were determined in an animal model of CKD treated with or without lanthanum. Haematoxylin and eosin (H&E) staining was performed to examine the structure of kidney tissues. Western blot analysis was performed to compare the levels of total­ (t­) extracellular signal­related kinase (ERK) and phospho­ (p­)ERK among the different experimental groups to investigate the effect of FGF23 on p­ERK expression. In the animal model, administration of adenine increased the serum levels of creatinine, BUN, FGF23 and phosphorus but decreased the serum levels of calcium. In addition, adenine treatment increased the plasma levels of PTH. H&E staining showed that lanthanum treatment did not alter the severity of renal cortex injury. Furthermore, the levels of t­ERK levels did not notably differ between the Adenine­free, Adenine­vehicle and Adenine­lanthanum groups, whereas the levels of p­ERK and aortic calcium in the Adenine­vehicle group were significantly upregulated. In addition, ectopic overexpression of FGF23 increased the levels of p­ERK, Msx2 and Osx in a dose­dependent manner. Furthermore, a total of 48 patients were enrolled in the present study. In the fortified group, the serum levels of FGF23, phosphorus and PTH were significantly reduced, whereas the serum levels of calcium were significantly increased, indicating an enhanced preventative effect in the fortified group. The results of the present study suggest that FGF23 may be used as a therapeutic target in the management and prevention of VC in CKD.

The Application and Functional Progress of γ-Poly-Glutamic Acid in Food: A Mini-Review.

γ-Poly-glutamic acid (γ-PGA) is a naturally occurring homo-polyamide produced by various strains of Bacillus. As a biopolymer substance, γ-PGA possesses a few predominant features containing good water solubility, biocompatibility, degradability and non-toxicity. Based on this, γ-PGA can be used in pharmaceutical, such as drug carrier/deliverer, vaccine adjuvant, and coating material for microencapsulation, etc. Moreover, it has also been applied in a broad range of industrial fields including food, medicine, bioremediation, cosmetics, and agriculture. Especially, γ-PGA is an extremely promising food ingredient. In this mini-review, our aim is to review the function and application progress of γ-PGA in the food industry: e.g., improving taste and flavor, enhancing physical property, and promoting health.

Long noncoding RNA MANTIS relieved the protein-bound uremic toxin-induced injury on human umbilical vein endothelial cells in chronic kidney disease and end-stage renal disease.

This study aimed to explore the role of long, noncoding RNA MANTIS in regulating the protein-bound, uremic toxin-induced injury on human umbilical vein endothelial cells (HUVECs) in chronic kidney disease (CKD) and end-stage renal disease (ESRD). The MANTIS expression in patients with normal kidney function, stage 3 CKD, stage 4 CKD and ESRD was detected. In addition, HUVECs were stimulated with various concentrations of HSA-bound P-cresol (20, 40 and 80 µg/ml) and then transfected with pcDNA-MANTIS, sh-MANTIS and their controls to further investigate the effects of MANTIS overexpression and knockdown on HSA-bound P-cresol-induced HUVECs injury. Furthermore, the regulatory relationships between MANTIS and Sox18, as well as between MANTIS and p38 MAPK or p65 NF-κB pathways were elucidated. MANTIS expression was down-regulated in patients with CKD and ESRD and might be associated with disease severity. In addition, HSA-bound P-cresol induced HUVECs injury and decreased MANTIS expression. Overexpression of MANTIS relieved HSA-bound P-cresol induced HUVECs injury by increasing HUVECs viability, migration and invasion, and inhibiting cell autophagy. Moreover, the effects of MANTIS on HSA-bound P-cresol induced HUVECs injury were through positive regulation of Sox18. Besides, MANTIS overexpression markedly inhibited the activation of p38 MAPK and p65 NF-κB pathways in HSA-bound P-cresol-stimulated HUVECs, which were reversed after overexpression of MANTIS and knockdown of Sox18 synchronously. Our findings reveal that lncRNA MANTIS may relieve the protein-bound uremic toxins-induced HUVECs injury in CKD and ESRD via positive regulation of Sox18 and inhibition of p38 MAPK and p65 NF-κB pathways.

Regulation of renal fibrosis by macrophage polarization.

BACKGROUND/AIMS: Since renal fibrosis always predisposes end-stage renal disease, elucidation of the molecular mechanisms that underlie the progression of renal fibrosis may substantially improve the understanding and treatment for renal failure. Previous studies have highlighted an important counteraction between transforming growth factor ß 1 (TGFß1) and bone morphogenic protein 7 (BMP7) in the epithelial-to-mesenchymal transition (EMT) of renal tubular epithelial cells during chronic renal injury. Macrophages are also believed to play a critical role in renal fibrosis. However, the relationship between macrophages and EMT is unknown. METHODS: Here, we used a mouse unilateral ureteral obstruction (UUO) model to address to these questions, and analyzed macrophage and its subpopulations purified by flow cytometry. RESULTS: We found that the recruited macrophages are polarized to a M2 subtype after renal injury. M2 macrophages released high levels TGFß1 to suppress BMP7 to enhance EMT-induced renal fibrosis. Depletion of M2 macrophages, but not of M1 macrophages, specifically inhibited EMT, and subsequently the renal fibrosis. Adoptive transplantation of M2 macrophages deteriorated renal fibrosis. CONCLUSION: Thus, our study highlights M2 macrophages as a critical target for treating renal fibrosis.

Retracted: Association of ACE I/D gene polymorphism with T2DN susceptibility and the risk of T2DM developing into T2DN in a Caucasian population.

BACKGROUND AND OBJECTIVE: The association of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism with type-2 diabetic nephropathy (T2DN) susceptibility and the risk of type-2 diabetes mellitus (T2DM) developing into T2DN in Caucasian populations is still controversial. A meta-analysis was performed to evaluate the association of ACE I/D gene polymorphism with T2DN susceptibility and the risk of T2DM developing into T2DN in Caucasian populations. METHOD: A predefined literature search and selection of eligible relevant studies were performed to collect data from electronic databases. RESULTS: Sixteen articles were identified for the analysis of the association of ACE I/D gene polymorphism with T2DN susceptibility and the risk of T2DM developing into T2DN in Caucasian populations. ACE I/D gene polymorphism was not associated with T2DN susceptibility and the risk of patients with T2DM developing T2DN in Caucasian populations. Sensitivity analysis according to sample size of case (<100 vs. ≥100) was also performed, and the results were similar to the non-sensitivity analysis. CONCLUSIONS: ACE I/D gene polymorphism was not associated with T2DN susceptibility and the risk of patients with T2DM developing T2DN in Caucasian populations. However, more studies should be performed in the future.

Relationship between PPARγ Pro12Ala gene polymorphism and type 2 diabetic nephropathy risk in Asian population: results from a meta-analysis.

The relationship between peroxisome proliferator-activated receptor gamma (PPARγ) Pro12Ala gene polymorphism and type 2 diabetic nephropathy (T2DN) risk in Asians is still unclear. This study was performed to evaluate if there was an association between the PPARγ Pro12Ala gene polymorphism and T2DN risk in Asians using meta-analysis. The relevant reports were searched and identified from PubMed, Cochrane Library and CBM-disc (China Biological Medicine Database) on 1 October 2013, and eligible studies were included and synthesized. Ten reports were recruited into this meta-analysis for the association of the PPARγ Pro12Ala gene polymorphism with T2DN risk. The Pro12Ala gene polymorphism in the Asian population was shown to be not associated with T2DN risk (Ala/Ala: OR = 0.67, 95% CI: 0.22-2.00, p = 0.47; Pro/Pro: OR = 1.77, 95% CI: 0.82-1.65, p = 0.39; Ala allele: OR = 0.74, 95% CI: 0.47-1.16, p = 0.19). In the sensitivity analysis according to Hardy-Weinberg equilibrium (HWE), the control source from hospital, the control source from population, the genotyping methods using PCR-RFLP, the genotyping methods using Taqman, sample size of case (≥ 100), the association of the PPARγ Pro12Ala gene polymorphism with T2DN risk was also not found. Interestingly, in the sensitivity analysis according to sample size of case (<100), Ala allele was associated with T2DN risk, but not the Pro/Pro genotype. However, the sample size for sensitivity analysis according to sample size of case (<100) was relatively small and therefore, the results should be interpreted with care. In conclusion, the PPARγ Pro12Ala gene polymorphism was not associated with T2DN risk in Asians. However, Ala allele was associated with T2DN risk when the sample size of case was less than 100. Nonetheless, additional studies are required to firmly establish a correlation between the PPARγ Pro12Ala gene polymorphism and T2DN risk in Asians.