Abnormal distribution of laminin α2 chain in glomerular basement membrane in membranous nephropathy / 临床与实验病理学杂志

To study the abnormal distribution of type Ⅳ collagen and laminin chains in glomerular basement membrane (GBM) in membranous nephropathy (MN).Methods 52 cases of MN were collected and staged according to electron microscopic morphological characteristics,and 10 cases of kidney tissues of minimal change disease were used as normal GBM control.Distribution pattern of or5 (Ⅳ) chain,laminin α5and β2 chains,and laminin α2 and β1 chains were detected using immunofluorescence method.Results In minimal change disease,α5 (Ⅳ) chain,laminin α5 and β2 chains all showed continuously linear positive expression along GBM,and laminin α2 and β1 chains were negatively expressed in GBM.In stage Ⅰ MN,α5 (Ⅳ) chain,laminin α.5 and β2 chains all showed continuous linear positive expression along GBM.In stage ⅡMN,the expression of α5 (Ⅳ) chain was increased and showed abundant spikes on the basis of continuous linear positive staining along GBM,and the expression of laminin α5 and β2chains was increased,and segmental spikes were seen on the basis of continuous linear positive staining along GBM.In stage ⅢMN,the expression of α5 (Ⅳ),laminin α5 and β2 chains was also enhanced and segmental double tracks were seen.The expression of laminin α2 chain was negative in GBM in stage ⅠMN,but granular positive expression along GBM was seen in stage Ⅱ and stage Ⅲ MN.No positive expression of laminin β1chain was seen in GBM in different stages in MN.Conclusion The GBM thickness in MN originates not only from intrinsic type Ⅳ collagen chains and laminin chains,but also from laminin α2chain,which only exist in glomerulus mesangium in normal condition.

Modeling of electrophysiology and simulation of ECG under ischemic condition in human ventricular tissue / 生物医学工程学杂志

In this paper, to analyze the functional influence of ischemia on cardiac cell electrical activity and subsequently on ventricular electrical wave conduction, a human ventricular ischemic model was developed, which took into account three major pathophysiological components of ischemias hyperkalaemia, acidosis, and anoxia. This model simulated the action potential (AP) propagations of endocardial, midmycardial and epicardial cells with different levels of ischemia, and the influence of each factor on cell AP was analyzed. Finally the ECG waveform under ischemia was quantified by using a 2D model of human left ventricular tissue based on the anatomical structure of human heart. The experimental results showed that under ischemia action potential durations (APD) were reduced. In most cases, the larger the size of ischemic region or the more severe the ischemic level, the more dramatic the changes in the amplitude of ST-T wave were observed. For the three components of ischemia, hyperkalaemia was the dominant contributor to ST-T wave changes, which was in agreement with the results obtained on animal models.