瞬时弹性记录仪Fibroscan在慢性乙型肝炎肝纤维化中的应用价值

目的：探讨瞬时弹性记录仪（FibroScan）对慢性乙型肝炎肝纤维化的临床应用价值。方法：对134例慢性乙型肝炎患者行FibroScan检查,将所检测到的肝硬度值与按照Scheuer系统进行肝组织活检纤维化分级的结果进行比较,用Spearman等级相关系数方法进行统计学分析。结果：134例慢性乙型肝炎患者中,S0期10例、S1期16例、S2期24例、S3期30例、S4期54例。除1例患者因肥胖导致瞬时弹性超声检测失败以外,其余均顺利受检。133例患者的瞬时弹性超声硬度值与其肝纤维化分期有显著相关性（r=0.905,P〈0.01）。轻、中度纤维化组（S0、S1、S2期）与重度纤维化组（S3、S4期）的瞬时弹性超声硬度值相比,t=-16.671,P〈0.01,差异有统计学意义。结论：FibroScan可以较准确地估计慢性乙型肝炎患者的纤维化程度,在乙型肝炎纤维化程度的长期随访与疗效评估中有着较好的应用价值。     

Oxigenación con membrana extracorpórea en la disfunción primaria del injerto en trasplante bipulmonar pediátrico: a propósito de un caso

Primary graft dysfunction is a leading cause of morbimortality in the immediate postoperative period of patients undergoing lung transplantation. Among the treatment options are: lung protective ventilatory strategies, nitric oxide, lung surfactant therapy, and supportive treatment with extracorporeal membrane oxygenation (ECMO) as a bridge to recovery of lung function or re-transplant.We report the case of a 9-year-old girl affected by cystic fibrosis who underwent double-lung transplantation complicated with a severe primary graft dysfunction in the immediate postoperative period and refractory to standard therapies. Due to development of multiple organ failure, it was decided to insert arteriovenous ECMO catheters (pulmonary artery-right atrium). The postoperative course was satisfactory, allowing withdrawal of ECMO on the 5 th post-surgical day. Currently the patient survives free of rejection and with an excellent quality of life after 600 days of follow up.     

Atrial fibrillation: A progressive atrial myopathy or a distinct disease?

Atrial fibrillation is a complex arrhythmia with multiple possible mechanisms. A lot of experimental and clinical studies have shed light on the pathophysiological mechanisms of arrhythmia, especially on molecular basis. Electrical, contractile and structural remodeling, calcium handling abnormalities, autonomic imbalance and genetic factors seem to play a crucial role in atrial fibrillation initiation and maintenance. However, the exact pathophysiological mechanisms of atrial fibrillation are not completely understood and whether atrial fibrillation is an unclassified cardiomyopathy or a distinct disease still remains to be answered. This review highlights proarrhythmic and pathophysiological mechanisms of atrial fibrillation and approaches the molecular basis underlying atrial fibrillation susceptibility.     

Expression and cellular distribution of TLR4, MyD88, and NF-κB in diabetic renal tubulointerstitial fibrosis, in vitro and in vivo

Aim

Inflammation and extracellular matrix hyperplasia are crucial in the pathogenesis of tubulointerstitial fibrosis (TIF) involved in diabetic nephropathy (DN). Macrophage accumulation plays a major role, but whether immune factors contribute to DN pathogenesis is not well understood. This study aimed to investigate TLR4-MyD88-NF-κB-dependent pathway's involvement in TIF pathogenesis.

Methods

STZ-induced diabetic rats and rat renal tubular epithelial NRK-52E cells cultured under high glucose conditions were used as in vivo and in vitro models, respectively. Real-time RT-PCR, western blot, immunohistochemistry and immunofluorescence were performed to examine the mRNA and protein levels of TLR4, MyD88, NF-κB, MCP-1, and α-SMA.

Results

Compared with 5.5 mmol/L glucose, treatment of NRK-52E cells with 25 and 50 mmol/L d-glucose resulted in significantly increased TLR4 and MyD88 mRNA and protein levels (P < 0.05). TLR4 and MyD88 were detected in the cytoplasm of most NRK-52E cells cultured under high glucose. Pronounced damage in the renal tubulointerstitium was observed in diabetic rats (scores: 3.82 ± 0.65 vs. 0.38 ± 0.08, P < 0.01). Compared with the normal controls, a sharp upregulation of TLR4, MyD88, NF-κB p65, MCP-1, and α-SMA mRNA and protein levels was observed in diabetic rat kidneys (P < 0.05). In diabetic animals, TLR4 and MyD88 were strongly expressed in the cytoplasm, while NF-κB p65 was widely expressed in cytoplasm and nuclei of renal tubular epithelial cells.

Conclusion

The inflammatory reaction and epithelial-mesenchymal transformation observed in renal tubulointerstitium may be the result of overactivation of the TLR4-MyD88-NF-κB-dependent innate immunity under high glucose, and may be involved in DN occurrence and progression.     

虫草多糖对平阳霉素诱导的肺纤维化小鼠的影响

目的 研究虫草多糖抗小鼠肺纤维化的作用。方法 采用气管注射平阳霉素制作小鼠肺纤维化模型,酶联免疫吸附法测定血清白介素1受体抑制剂（interleukin-1 receptor antagonist,IL-1RA）含量,碱水解法测定肺组织中羟脯氨酸（hydroxyproline,Hyp）含量,Masson染色法观察肺组织胶原沉积情况。结果 与肺纤维化模型组相比,虫草菌粉组、虫草总多糖组和虫草多糖[分子量（molecular mass,MW）<2×10⁵]组血清中IL-1RA水平明显升高,肺组织中Hyp含量明显降低;虫草总多糖组和虫草多糖（MW<2×10⁵）组肺组织纤维化面积明显减小。结论 虫草多糖具有明显的抗小鼠肺纤维化作用。     

S-allyl-l-cysteine attenuates bleomycin-induced pulmonary fibrosis and inflammation via AKT/NF-κB signaling pathway in mice

Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal lung disease characterized by inflammation, multifocal fibrotic lesions and excessive collagen deposition with limited therapies. As a major bioactive compound in garlic, S-allyl-l-cysteine (SAC) is a neuroprotective drug candidate to prevent cognitive decline, however, its anti-pulmonary fibrotic activity remains unknown. Here, we investigated whether SAC could attenuate bleomycin (BLM)-induced pulmonary fibrosis and inflammation in mice. Our results showed that SAC dose-dependently reduced the infiltration of inflammatory cells, pulmonary lesions and collagen deposition in BLM treated mice with downregulated mRNA expression levels of fibrotic genes including alpha smooth muscle actin (α-SMA), fibronectin, collagen I and collagen III as well as the protein level of α-SMA. In addition, SAC could also reduce the mRNA expression of inflammatory mediators such as TNF-α and iNOS. Furthermore, higher phosphorylation of AKT and NF-κB p65 in IPF patient samples and murine samples was verified by immunohistochemistry while SAC could decrease the phosphorylation level of AKT and NF-κB p65 in mice stimulated with BLM. These findings, for the first time, indicate that SAC might mediate AKT/NF-κB signaling pathway to inhibit BLM-induced pulmonary fibrosis and support the potential role of SAC as an anti-pulmonary fibrosis agent.