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.
The following articles have been retracted at the request of the Editors and the Publisher. After conducting a thorough investigation, SAGE found that the submitting authors of a number of papers published in the Journal of the Renin-Angiotensin Aldosterone System ( JRAAS) (listed below) had supplied fabricated contact details for their nominated reviewers. The Editors accepted these papers based on the reports supplied by the individuals using these fake reviewer email accounts. After concluding that the peer review process was therefore seriously compromised, SAGE and the journal Editors have decided to retract all affected articles. Online First articles (these articles will not be published in an issue) Wenzhuang Tang, Tian-Biao Zhou, and Zongpei Jiang Association of the angiotensinogen M235T gene polymorphism with risk of diabetes mellitus developing into diabetic nephropathy Journal of Renin-Angiotensin-Aldosterone System 1470320314563426, first published on December 18, 2014 doi: 10.1177/1470320314563426 Tian-Biao Zhou, Hong-Yan Li, Zong-Pei Jiang, Jia-Fan Zhou, Miao-Fang Huang, and Zhi-Yang Zhou Role of renin-angiotensin-aldosterone system inhibitors in radiation nephropathy Journal of Renin-Angiotensin-Aldosterone System 1470320314563424, first published on December 18, 2014 doi: 10.1177/1470320314563424 Weiqiang Zhong, Zongpei Jiang, and Tian-Biao Zhou Association between the ACE I/D gene polymorphism and T2DN susceptibility: The risk of T2DM developing into T2DN in the Asian population Journal of Renin-Angiotensin-Aldosterone System 1470320314566019, first published on January 26, 2015 doi: 10.1177/1470320314566019 Tian-Biao Zhou, Xue-Feng Guo, Zongpei Jiang, and Hong-Yan Li Relationship between the ACE I/D gene polymorphism and T1DN susceptibility/risk of T1DM developing into T1DN in the Caucasian population Journal of Renin-Angiotensin-Aldosterone System 1470320314563425, first published on February 1, 2015 doi: 10.1177/1470320314563425 Chun-Hua Yang and Tian-Biao Zhou Relationship between the angiotensinogen A1166C gene polymorphism and the risk of diabetes mellitus developing into diabetic nephropathy Journal of Renin-Angiotensin-Aldosterone System 1470320314566221, first published on February 1, 2015 doi: 10.1177/1470320314566221 Chun-Hua Yang and Tian-Biao Zhou Association of the ACE I/D gene polymorphism with sepsis susceptibility and sepsis progression Journal of Renin-Angiotensin-Aldosterone System 1470320314568521, first published on February 3, 2015 doi: 10.1177/1470320314568521 Articles published in an issue Guohui Liu, Tian-Biao Zhou, Zongpei Jiang, and Dongwen Zheng Association of ACE I/D gene polymorphism with T2DN susceptibility and the risk of T2DM developing into T2DN in a Caucasian population Journal of Renin-Angiotensin-Aldosterone System March 2015 16: 165-171, first published on November 14, 2014 doi: 10.1177/1470320314557849 Weiqiang Zhong, Zhongliang Huang, Yong Wu, Zongpei Jiang, and Tian-Biao Zhou Association of aldosterone synthase (CYP11B2) gene polymorphism with IgA nephropathy risk and progression of IgA nephropathy Journal of Renin-Angiotensin-Aldosterone System September 2015 16: 660-665, first published on August 20, 2014 doi: 10.1177/1470320314524011
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 β 1 (TGFβ1) 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.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.We found that the recruited macrophages are polarized to a M2 subtype after renal injury. M2 macrophages released high levels TGFβ1 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.Thus, our study highlights M2 macrophages as a critical target for treating renal fibrosis.
To assess whether methylenetetrahydrofolate reductase(MTHFR) gene C677T polymorphism is associated with neural tube defects and preeclampsia.Twenty- four mothers who had given birth to normal children, 27 mothers who had given birth to NTDs children, 120 normal women, and 57 women who had suffered from preeclampsia were genotyped for C677T polymorphism by using PCR/RFLP method.(1) VV genotype frequency in the normal mothers group it was 0.13, while in the NTDs mothers group it was 0.33; mothers with VV genotype were at 3 times increased risk to have a NTDs child, compared with the normal mothers. (2) In the normal women group VV genotype frequency was 0.15, while in the preeclampsia women group it was 0.31; women with VV genotype were at 2.5 times increased risk to have preeclampsia, compared with the normal women.The authors believe that MTHFR VV genotype is associated with the development of NTDs and preeclampsia.
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.
Objective To compare different blood purification techniques on cardiovascular stability in patients with chronic renal failure (CRF) and its inherent possible mechanism. Methods 90patients with CRF were randomly divided into 3 groups. Group A (HD Group) was applied 3 times per week hemodialysis (HD) treatment; Group B (HDF group) 2 times a week routine standard hemodialysis (HD)treatment and 1 time a week hemodiafiltration (HDF) treatment; Group C (HP group) 2 times a week routine standard blood dialysis (HD) treatment and 1 time a week hemoperfusion (HP) combined with hemodialysis (HD) treatment. The treatment time in every group is 10 weeks, after that there was an interval of 2 weeks with a Fresenius F6 or F8 routine HD treatment , the total time was 6 months. The incidence of cardiovascular complications in the three groups during dialysis, and parathyroid hormone (iPTH), plasma renin (RA),angiotensin Ⅱ (Ang Ⅱ ) changes after 6 months of treatment were compared. Results During dialysis,patients of groups B and C compared with group A significantly reduced cardiovascular complications( group B is 11.3%, group C is 10.9%, but group A is 20.4% ), after treatment plasma iPTH, renin (RA),angiotensin Ⅱ (Ang Ⅱ ) were also decreased significantly compared with group A, but the groups B and C had no significant difference. Conclusion Patients with Hemodialysis or hemoperfusion treatment have better cardiovascular stability, This may be associated with the effective removal of plasma RA, Ang Ⅱ , parathyroid hormone (iPTH) and other middle molecule toxins, both treatments have an equal effect due to simple operation and low equipment requirements, hemoperfusion is much easier to be carried out universally.
Key words:
Cardiovascular complications; Hemodiafiltration HDF; Hemoperfusion; Parathyroid hormone; Renin; Angiotensin Ⅱ (Ang Ⅱ )
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 phosphorus‑lowing 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 signal‑related kinase (ERK) and phospho‑ (p‑)ERK among the different experimental groups to investigate the effect of FGF23 on p‑ERK 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 t‑ERK levels did not notably differ between the Adenine‑free, Adenine‑vehicle and Adenine‑lanthanum groups, whereas the levels of p‑ERK and aortic calcium in the Adenine‑vehicle group were significantly upregulated. In addition, ectopic overexpression of FGF23 increased the levels of p‑ERK, Msx2 and Osx in a dose‑dependent 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.
Zinc deficiency rat model was made by feeding zinc deficiency diet. The level of bone calcium of the zinc deficiency rats was significantly lower than that of the control rats. Their bone cortex was thinner and bone density decreased. The counts of their cartilage cells and hypertrophic cells of epiphyseal plate were less frequent, and the diameter of their hypertrophic cells was smaller than that of the controls. It suggested that zinc deficiency caused defective bone calcification which was similar to that in vitamin D deficiency. Zinc deficiency seemed to hinder the linear growth of long bone and might be the cause of dwarf.
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.
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.
'/%3e%3cuse xlink:href='%23a' transform='rotate(23.036 .093 25.536)'/%3e%3cuse xlink:href='%23a' transform='rotate(45.87 1.273 16.18)'/%3e%3cuse xlink:href='%23a' transform='rotate(69.945 .996 12.078)'/%3e%3cuse xlink:href='%23a' transform='rotate(20.66 -19.689 31.932)'/%3e%3c/svg%3e)
'/%3e%3cuse xlink:href='%23a' transform='rotate(144 450 300)'/%3e%3cuse xlink:href='%23a' transform='rotate(216 450 300)'/%3e%3cuse xlink:href='%23a' transform='rotate(288 450 300)'/%3e%3c/svg%3e)