Restenosis after interventional treatment is the major factor infheneing the result of percutaneous transluminal angioplasty, and it is a hot and difficult research in recent years. Endothelial progenitor cells are a class of proliferation and able to differentiate into vascular endothelial precursor cells, and take part in the repair and angiogenesis after endothelial injury-intimate. It is expected to play an important role in the prevention of vascular restenosis after interventional treatment. In this article, we reviewed the endothelial progenitor cell research overview and advances of prevention of restenosis after interventional therapy in recent years.

Objective:To investigate the efficacy and safety of peginterferon alpha-2a plus ribavirin in the treatment of chronic hepatitis C. Methods:Totally 85 patients with chronic hepatitis C were randomly divided into the observation group and the control group. Each patient in the observation group was injected subcutaneously peginterferon alpha-2a with the dose of 180μg once a week plus ribavirin 900-1 200 mg/d, po, and each patient in the control was treated subcutaneously with 5 MU standard interferon alpha-2b three times a week plus the same used ribavirin. After the 48-week treatment, 24-week fellow-up was carried out. HCV RNA and ALT were detected at the baseline, 4th week, 12th week and 48th week during the treatment, and 24th week after the treatment, respective-ly. The rate of rapid virological response ( RVR) , early virological response ( EVR) , end of treatment virological response ( ETVR) , sustained virological response (SVR), ALT normalization and adverse reactions were respectively assessed. Results: The rates of EVR,ETVR and SVR in the observation group were 76. 7%(33/43), 86. 0%(37/43) and 79. 1%(34/43), respectively, which were significantly higher than those in the control group [54. 8%(23/43), 66. 7%(28/43) and 57. 1%(24/43),respectively] (P<0. 05). The ALT normalization rate at 12th and 48th week after the treatment in the observation group was 81. 4% and 90. 7%, re-spectively, which were higher than those in the control group [64. 3% and 71. 4%, respectively](P<0. 05). The rate of white cell counts and platelet underlying (58. 1% and 39. 5%) in the observation group were also higher than those in the control group (35. 7%and 19.0%)(P<0.05). The decreased rate of neutrophil (58.1%) in the observation group was higher than that in the control group(19. 0%)(P<0. 01). The other adverse reactions in the two groups were similar, and there was no new or unique adverse event related to peginterferon. Conclusion:Peginterferon alpha-2a has better effect than the standard interferon alpha-2b in the treatment of patients with chronic hepatitis C with promising tolerance.

Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease. At present, no definite ALS biomarkers are available. In this study, exosomes from the plasma of patients with ALS and healthy controls were extracted, and differentially expressed exosomal proteins were compared. Among them, the expression of exosomal coronin-1a (CORO1A) was 5.3-fold higher than that in the controls. CORO1A increased with disease progression at a certain proportion in the plasma of patients with ALS and in the spinal cord of ALS mice. CORO1A was also overexpressed in NSC-34 motor neuron-like cells, and apoptosis, oxidative stress, and autophagic protein expression were evaluated. CORO1A overexpression resulted in increased apoptosis and oxidative stress, overactivated autophagy, and hindered the formation of autolysosomes. Moreover, CORO1A activated Ca²⁺-dependent phosphatase calcineurin, thereby blocking the fusion of autophagosomes and lysosomes. The inhibition of calcineurin activation by cyclosporin A reversed the damaged autolysosomes. In conclusion, the role of CORO1A in ALS pathogenesis was discovered, potentially affecting the disease onset and progression by blocking autophagic flux. Therefore, CORO1A might be a potential biomarker and therapeutic target for ALS.
Mice ; Animals ; Amyotrophic Lateral Sclerosis/pathology* ; Calcineurin/metabolism* ; Motor Neurons/pathology* ; Microfilament Proteins/metabolism* ; Cytoskeletal Proteins/metabolism*