芸豆淀粉理化特性研究

淀粉是芸豆中的主要碳水化合物,其性质直接影响芸豆资源的开发与利用.以花芸豆、小红芸豆、红芸豆、小黑芸豆和小白芸豆等菜豆属芸豆为试验材料,采用湿磨法提取淀粉,以马铃薯淀粉和玉米淀粉为对照,分析芸豆淀粉的颗粒特性与糊化特性.结果表明,5种芸豆淀粉颗粒形貌相似,大淀粉颗粒多为卵圆形或肾形,小颗粒多呈圆形,淀粉颗粒长轴粒径介于玉米淀粉和马铃薯淀粉之间.淀粉颗粒偏光十字多为较粗的“X”形或斜“十”形,较明显.芸豆淀粉溶解度和膨胀度均随温度升高而增大,属限制型膨胀淀粉.芸豆淀粉的透光度明显小于马铃薯淀粉,冻融稳定性不及玉米淀粉和马铃薯淀粉.芸豆淀粉起糊温度、峰值黏度、破损值、最终黏度和回生值分别为76.6 ～ 77.8℃、117.3 ～ 150.9 RVU、5.0 ～ 32.0 RVU、205.1 ～225.2 RVU和91.9～104.2 RVU.芸豆淀粉糊表现出好的热稳定性、抗剪切,易回生.     

Mast Cell Chymase and Kidney Disease

A sizable part (~2%) of the human genome encodes for proteases. They are involved in many physiological processes, such as development, reproduction and inflammation, but also play a role in pathology. Mast cells (MC) contain a variety of MC specific proteases, the expression of which may differ between various MC subtypes. Amongst these proteases, chymase represents up to 25% of the total proteins in the MC and is released from cytoplasmic granules upon activation. Once secreted, it cleaves the targets in the local tissue environment, but may also act in lymph nodes infiltrated by MC, or systemically, when reaching the circulation during an inflammatory response. MC have been recognized as important components in the development of kidney disease. Based on this observation, MC chymase has gained interest following the discovery that it contributes to the angiotensin-converting enzyme’s independent generation of angiotensin II, an important inflammatory mediator in the development of kidney disease. Hence, progress regarding its role has been made based on studies using inhibitors but also on mice deficient in MC protease 4 (mMCP-4), the functional murine counterpart of human chymase. In this review, we discuss the role and actions of chymase in kidney disease. While initially believed to contribute to pathogenesis, the accumulated data favor a more subtle view, indicating that chymase may also have beneficial actions.     

A Role for Human Renal Tubular Epithelial Cells in Direct Allo-Recognition by CD4+ T-Cells and the Effect of Ischemia-Reperfusion

Direct allorecognition is the earliest and most potent immune response against a kidney allograft. Currently, it is thought that passenger donor professional antigen-presenting cells (APCs) are responsible. Further, many studies support that graft ischemia-reperfusion injury increases the probability of acute rejection. We evaluated the possible role of primary human proximal renal tubular epithelial cells (RPTECs) in direct allorecognition by CD4+ T-cells and the effect of anoxia-reoxygenation. In cell culture, we detected that RPTECs express all the required molecules for CD4+ T-cell activation (HLA-DR, CD80, and ICAM-1). Anoxia-reoxygenation decreased HLA-DR and CD80 but increased ICAM-1. Following this, RPTECs were co-cultured with alloreactive CD4+ T-cells. In T-cells, zeta chain phosphorylation and c-Myc increased, indicating activation of T-cell receptor and co-stimulation signal transduction pathways, respectively. T-cell proliferation assessed with bromodeoxyuridine assay and with the marker Ki-67 increased. Previous culture of RPTECs under anoxia raised all the above parameters in T-cells. FOXP3 remained unaffected in all cases, signifying that proliferating T-cells were not differentiated towards a regulatory phenotype. Our results support that direct allorecognition may be mediated by RPTECs even in the absence of donor-derived professional APCs. Also, ischemia-reperfusion injury of the graft may enhance the above capacity of RPTECs, increasing the possibility of acute rejection.     

Kidney Injury Caused by Preeclamptic Pregnancy Recovers Postpartum in a Transgenic Rat Model

Preeclampsia (PE) is characterized by the onset of hypertension (≥140/90 mmHg) and presence of proteinuria (>300 mg/L/24 h urine) or other maternal organ dysfunctions. During human PE, renal injuries have been observed. Some studies suggest that women with PE diagnosis have an increased risk to develop renal diseases later in life. However, in human studies PE as a single cause of this development cannot be investigated. Here, we aimed to investigate the effect of PE on postpartum renal damage in an established transgenic PE rat model. Female rats harboring the human-angiotensinogen gene develop a preeclamptic phenotype after mating with male rats harboring the human-renin gene, but are normotensive before and after pregnancy. During pregnancy PE rats developed mild tubular and glomerular changes assessed by histologic analysis, increased gene expression of renal damage markers such as kidney injury marker 1 and connective-tissue growth factor, and albuminuria compared to female wild-type rats (WT). However, four weeks postpartum, most PE-related renal pathologies were absent, including albuminuria and elevated biomarker expression. Only mild enlargement of the glomerular tuft could be detected. Overall, the glomerular and tubular function were affected during pregnancy in the transgenic PE rat. However, almost all these pathologies observed during PE recovered postpartum.     

Acute Kidney Injury in COVID-19

COVID-19 is mainly considered a respiratory illness, but since SARS-CoV-2 uses the angiotensin converting enzyme 2 receptor (ACE2) to enter human cells, the kidney is also a target of the viral infection. Acute kidney injury (AKI) is the most alarming condition in COVID-19 patients. Recent studies have confirmed the direct entry of SARS-CoV-2 into the renal cells, namely podocytes and proximal tubular cells, but this is not the only pathomechanism of kidney damage. Hypovolemia, cytokine storm and collapsing glomerulopathy also play an important role. An increasing number of papers suggest a strong association between AKI development and higher mortality in COVID-19 patients, hence our interest in the matter. Although knowledge about the role of kidneys in SARS-CoV-2 infection is changing dynamically and is yet to be fully investigated, we present an insight into the possible pathomechanisms of AKI in COVID-19, its clinical features, risk factors, impact on hospitalization and possible ways for its management via renal replacement therapy.     

硫酸吲哚酚在慢性肾病并发症中的作用

慢性肾病（chronic kidney disease, CKD）是全球性公共卫生问题,其发生发展与体内尿毒症毒素暴露密切相关。硫酸吲哚酚（indoxyl sulfate, IS）是一种肠源性的蛋白结合型尿毒症毒素,由于CKD患者肾脏排泄功能被破坏,IS在CKD患者体内蓄积。IS不仅促进CKD进展,还诱导其他组织器官病变,进而引起CKD相关的并发症。本文综述了IS对CKD患者血管、肌肉、骨骼以及大脑的影响及其相应的机制,并总结通过清除IS治疗CKD的方法。     

Activin A and Cell-Surface GRP78 Are Novel Targetable RhoA Activators for Diabetic Kidney Disease

Diabetic kidney disease (DKD) is the leading cause of kidney failure. RhoA/Rho-associated protein kinase (ROCK) signaling is a recognized mediator of its pathogenesis, largely through mediating the profibrotic response. While RhoA activation is not feasible due to the central role it plays in normal physiology, ROCK inhibition has been found to be effective in attenuating DKD in preclinical models. However, this has not been evaluated in clinical studies as of yet. Alternate means of inhibiting RhoA/ROCK signaling involve the identification of disease-specific activators. This report presents evidence showing the activation of RhoA/ROCK signaling both in vitro in glomerular mesangial cells and in vivo in diabetic kidneys by two recently described novel pathogenic mediators of fibrosis in DKD, activins and cell-surface GRP78. Neither are present in normal kidneys. Activin inhibition with follistatin and neutralization of cell-surface GRP78 using a specific antibody blocked RhoA activation in mesangial cells and in diabetic kidneys. These data identify two novel RhoA/ROCK activators in diabetic kidneys that can be evaluated for their efficacy in inhibiting the progression of DKD.     

细胞模型在临床营养研究中应用现状

传统临床营养研究多停留在人群和动物试验阶段,随着临床营养研究的深入发展,细胞模型试验也逐渐成为临床营养研究中的重要方式。本文主要综述了临床营养中的细胞模型试验常用的细胞系,详细阐述了细胞模型在临床营养中的应用现状,涉及动脉粥样硬化性心脑血管疾病、肌肉衰减综合征、肾脏疾病、肿瘤、胃肠疾病、肝损伤、过敏性炎症、烧伤等领域,就我国居民死因排名靠前的4种疾病做了重点阐述,分别指出各种疾病临床营养研究中常用细胞模型、细胞模型试验的应用优势及其科学意义,以及细胞模型发展应用趋势(三维细胞、细胞组、微流控、高通量高内涵),总结了临床营养中传统细胞模型试验的局限性,并对细胞模型试验中新技术新方法的应用前景进行展望。     

干巴菌多糖对急性酒精损伤小鼠的抗氧化作用

目的:研究干巴菌多糖（Refined polysaccharide from Thelephora ganbajun,RPTG）对急性酒精损伤小鼠心脏、脾脏及肾脏的保护作用。方法:经超声波辅助热水浸提及去蛋白得到干巴菌多糖。将小鼠随机分为空白对照组、模型组、阳性对照组、RPTG各剂量组,建立小鼠急性酒精肝损伤模型。取小鼠心脏、脾脏及肾脏,测定其丙二醛（malondialdehyde,MDA）、还原型谷胱甘肽（glutathione,GSH）含量;超氧化物歧化酶（superoxide dismutase,SOD）、谷胱甘肽过氧化物酶（glutathione peroxidase,GSH-Px）及过氧化氢酶（catalase,CAT）活性。结果:与模型对照组相比,RPTG高、中、低剂量组均可以显著或极显著提高心脏、脾脏和肾脏的GSH含量、SOD活性、GSH-Px活性、CAT活性（p<0.05或p<0.01）;均可以显著或极显著降低心脏、脾脏和肾脏的MDA含量（p<0.05或p<0.01）。结论:RPTG对酒精性肝损伤小鼠心脏、脾脏及肾脏具有明显的抗氧化作用。