基于16S rDNA测序研究白酒对大鼠肠道菌群的影响

为探究浓香型白酒对SD大鼠肠道微生态的影响,通过连续8周灌胃适当剂量乙醇,建立SD大鼠慢性酒精性肝损伤模型,同时,灌胃相同剂量的白酒,考察白酒和乙醇对SD大鼠血脂、肝脏指标的影响及造成的肠道菌群变化。结果显示,连续8周灌胃乙醇造成SD大鼠一定程度的酒精性肝损伤,而白酒组的肝损伤程度显著低于乙醇组。多样性分析表明乙醇组SD大鼠肠道菌群丰富度和多样性降低,而白酒的摄入可以回调这种现象。菌群结构分析表明乙醇干预和白酒干预之间存在显著差异,其中白酒干预组物种组成与对照组更加接近。差异性分析筛选出白酒组和乙醇组的3个潜在差异微生物标志物,分别为g＿Eubacterium＿rumminantium＿group、g＿U29-B03和g＿unclassified＿f＿Oscillospiraceae。该研究结果表明白酒可能通过调节肠道微生态来减轻乙醇诱导的轻度肝损伤。     

Organelle Stress and Metabolic Derangement in Kidney Disease

Advanced multiomics analysis has revealed novel pathophysiological mechanisms in kidney disease. In particular, proteomic and metabolomic analysis shed light on mitochondrial dysfunction (mitochondrial stress) by glycation in diabetic or age-related kidney disease. Further, metabolic damage often results from organelle stress, such as mitochondrial stress and endoplasmic reticulum (ER) stress, as well as interorganelle communication, or “organelle crosstalk”, in various kidney cells. These contribute to progression of the disease phenotype. Aberrant tubular mitochondrial lipid metabolism leads to tubular inflammation and fibrosis. This review article summarizes updated evidence regarding organelle stress, organelle crosstalk, and metabolic derangement in kidney disease.     

Human Endothelial Progenitor Cells Protect the Kidney against Ischemia-Reperfusion Injury via the NLRP3 Inflammasome in Mice

Ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI) and progression to chronic kidney disease (CKD). However, no effective therapeutic intervention has been established for ischemic AKI. Endothelial progenitor cells (EPCs) have major roles in the maintenance of vascular integrity and the repair of endothelial damage; they also serve as therapeutic agents in various kidney diseases. Thus, we examined whether EPCs have a renoprotective effect in an IRI mouse model. Mice were assigned to sham, EPC, IRI-only, and EPC-treated IRI groups. EPCs originating from human peripheral blood were cultured. The EPCs were administered 5 min before reperfusion, and all mice were killed 72 h after IRI. Blood urea nitrogen, serum creatinine, and tissue injury were significantly increased in IRI mice; EPCs significantly improved the manifestations of IRI. Apoptotic cell death and oxidative stress were significantly reduced in EPC-treated IRI mice. Administration of EPCs decreased the expression levels of NLRP3, cleaved caspase-1, p-NF-κB, and p-p38. Furthermore, the expression levels of F4/80, ICAM-1, RORγt, and IL-17RA were significantly reduced in EPC-treated IRI mice. Finally, the levels of EMT-associated factors (TGF-β, α-SMA, Snail, and Twist) were significantly reduced in EPC-treated IRI mice. This study shows that inflammasome-mediated inflammation accompanied by immune modulation and fibrosis is a potential target of EPCs as a treatment for IRI-induced AKI and the prevention of progression to CKD.     

盐冻融与干湿作用下沥青混凝土的高低温力学性能分析

制备了沥青混凝土样品,并进行了不同次数的盐冻融干湿循环试验。在此基础上,测试了沥青混凝土的高温车辙深度、动稳定度和低温抗弯拉强度,得到了车辙深度、动稳定度和抗弯拉强度随盐冻融干湿循环次和盐浓度的变化规律,研究了盐冻融与干湿作用下沥青混凝土的高低温力学性能。研究结果表明:(1)沥青混凝土60min车辙深度随盐浓度的增加和冻融循环次数的增多而呈线性增长的趋势;(2)沥青混凝土的抗高温变形能力随盐冻融干湿循环次数的增多而逐渐弱化;(3)沥青混凝土的抗弯拉强度经历9次和15次盐冻融干湿循环后分别下降22%~26.4%和42.6%~51.5%;(4)冻融干湿循环次数一定时,沥青混凝土的抗弯拉强度随盐浓度的增加而缓慢下降,并且当盐浓度达到12%时,沥青混凝土的抗弯拉强度减小就很不明显。     

Rhabdomyolysis-Induced AKI Was Ameliorated in NLRP3 KO Mice via Alleviation of Mitochondrial Lipid Peroxidation in Renal Tubular Cells

Introduction: A recent study showed that early renal tubular injury is ameliorated in Nod-like receptor pyrin domain-containing protein 3 (NLRP3) KO mice with rhabdomyolysis-induced acute kidney injury (RIAKI). However, the precise mechanism has not been determined. Therefore, we investigated the role of NLRP3 in renal tubular cells in RIAKI. Methods: Glycerol-mediated RIAKI was induced in NLRP3 KO and wild-type (WT) mice. The mice were euthanized 24 h after glycerol injection, and both kidneys and plasma were collected. HKC-8 cells were treated with ferrous myoglobin to mimic a rhabdomyolytic environment. Results: Glycerol injection led to increase serum creatinine, aspartate aminotransferase (AST), and renal kidney injury molecule-1 (KIM-1) level; renal tubular necrosis; and apoptosis. Renal injury was attenuated in NLRP3 KO mice, while muscle damage and renal neutrophil recruitment did not differ between NLRP3 KO mice and WT mice. Following glycerin injection, increases in cleaved caspase-3, poly (ADP-ribose) polymerase (PARP), and a decrease in the glutathione peroxidase 4 (GPX-4) level were observed in the kidneys of mice with RIAKI, and these changes were alleviated in the kidneys of NLRP3 KO mice. NLRP3 was upregulated, and cell viability was suppressed in HKC-8 cells treated with ferrous myoglobin. Myoglobin-induced apoptosis and lipid peroxidation were significantly decreased in siNLRP3-treated HKC-8 cells compared to ferrous myoglobin-treated HKC-8 cells. Myoglobin reduced the mitochondrial membrane potential and increased mitochondrial fission and reactive oxygen species (ROS) and lipid peroxidation levels, which were restored to normal levels in NLRP3-depleted HKC-8 cells. Conclusions: NLRP3 depletion ameliorated renal tubular injury in a murine glycerol-induced acute kidney injury (AKI) model. A lack of NLRP3 improved tubular cell viability via attenuation of myoglobin-induced mitochondrial injury and lipid peroxidation, which might be the critical factor in protecting the kidney.     

高钠血症对颅脑损伤患者预后的影响

目的探讨各种颅脑损伤的患者病程中出现高钠血症后对其预后的影响。方法分析247例各种颅脑损伤患者的临床资料,记录血钠的测定值,治疗及预后的情况,并对所得数据进行统计学处理与分析。结果高钠血征的出现与疾病种类无关;高钠血症患者的死亡率明显高于正常血钠者;同时持续性高钠血征的纠正与否均不改善预后。结论持续性高钠血症的出现暗示着颅脑损伤病情的加重,预后不佳。     

Inhibition of Toll-Like Receptor 4 Signaling Mitigates Microvascular Loss but Not Fibrosis in a Model of Ischemic Acute Kidney Injury

The development of chronic kidney disease (CKD) following an episode of acute kidney injury (AKI) is an increasingly recognized clinical problem. Inhibition of toll-like receptor 4 (TLR4) protects renal function in animal models of AKI and has become a viable therapeutic strategy in AKI. However, the impact of TLR4 inhibition on the chronic sequelae of AKI is unknown. Consequently, we examined the chronic effects of TLR4 inhibition in a model of ischemic AKI. Mice with a TLR4-deletion on a C57BL/6 background and wild-type (WT) background control mice (C57BL/6) were subjected to bilateral renal artery clamping for 19 min and reperfusion for up to 6 weeks. Despite the acute protective effect of TLR4 inhibition on renal function (serum creatinine 1.6 ± 0.4 mg/dL TLR4-deletion vs. 2.8 ± 0.3 mg/dL·WT) and rates of tubular apoptosis following ischemic AKI, we found no difference in neutrophil or macrophage infiltration. Furthermore, we observed significant protection from microvascular rarefaction at six weeks following injury with TLR4-deletion, but this did not alter development of fibrosis. In conclusion, we validate the acute protective effect of TLR4 signal inhibition in AKI but demonstrate that this protective effect does not mitigate the sequential fibrogenic response in this model of ischemic AKI.     

玻璃钢复合材料在海洋环境下的抗冻耐久性能研究

采用1 000次冻融循环试验研究了189不饱和聚酯玻璃钢和MFE–2,MFE–711,MFE–W1环氧乙烯基酯玻璃钢在海水中的抗冻耐久性能。结果表明,1 000次冻融循环试验后,189不饱和聚酯玻璃钢和MFE–711环氧乙烯基酯玻璃钢的树脂基体在冻融循环产生的应力作用下发生开裂破坏,弯曲强度保留率降低至30%左右,渗入189不饱和聚酯玻璃钢和MFE–711环氧乙烯基酯玻璃钢包覆的混凝土试样表层的氯离子质量分数分别为0.08%和0.12%;MFE–2和MFE–W1环氧乙烯基酯玻璃钢在750次冻融循环后,弯曲强度保留率降至最低值65%,且不再随冻融循环次数增加而降低,1 000次冻融循环后,在MFE–2和MFE–W1环氧乙烯基酯玻璃钢包覆的混凝土试样表层未检测到氯离子渗入,它们的树脂基体在冻融循环产生的应力作用下未发生开裂破坏,具有较好的抗冻耐久性能。玻璃钢复合材料的冻融破坏是缓慢累积的过程,至少需要1 000次的冻融循环试验才能区分其抗冻耐久性能的优劣。     

轴承振动信号中调幅特征的奇异值分解提取方法

滚道损伤会在轴承振动中引起调幅现象,但当损伤较轻微或者噪声干扰较严重时,这种特征难以显现出来.提出利用奇异值分解(Singular value decomposition,SVD)来提取这种调幅特征.在Hankel矩阵方式下,SVD可将信号分解为一系列分量信号的简单线性叠加.利用这一特件,对轴承振动信号构造Hankel...     

引气剂稳泡机理及其改善混凝土冻融耐久性能的研究

利用膜天平对比了两种引气剂YQJ和改性松香R在空气-水界面的单分子膜的强度，考察了掺加这两种引气剂的新拌混凝土性能和硬化混凝土的冻融耐久性能。结果表明，引气剂在空气-水界面上的单分子膜的强度直接决定了引气剂的稳泡性能。稳泡性能优异的高性能引气剂，可显著提高混凝土的冻融耐久性能。