Comparison of Cyclosporine A and Cyclosporine A Combined with Corticosteroid in the Treatment of Acquired Pure Red Cell Aplasia / 中国实验血液学杂志

OBJECTIVE@#To evaluate the efficacy, safety and relapse of cyclosporine A (CsA) and CsA combined with corticosteroid (CS) as the frontline therapy for patients with newly diagnosed acquired pure red cell aplasia (aPRCA).@*METHODS@#The clinical features, treatment responses, relapses and clinical outcomes of patients with newly diagnosed aPRCA in Peking Union Medical College Hospital (PUMCH) from January 2015 to May 2020 were analyzed retrospectively. All the enrolled patients had been treated with either CsA or CsA+CS for at least 6 months and had been followed up for at least 12 months, with complete clinical data and consent forms.@*RESULTS@#96 patients including 72 treated with CsA and 24 treated with CsA+CS were enrolled. With comparable baseline characteristics and follow-up periods, patients treated with CsA or with CsA+CS had similar overall response rates (ORRs) and complete response rates (CRRs) at the 3rd, 6th and 12th month and at the end of follow-up (P>0.05). Meanwhile, no significant difference was found between the two groups in the optimal ORR, optimal CRR, time to response or time to complete response. CsA+CS and CsA groups had similar adverse event (AE) rates, but CsA+CS group had higher CS-related infection rate (P <0.05). One patient in CsA+CS group died of multiple infections. As for the relapse, the two groups had compatible relapse rates at different time points, time to relapse, overall relapse rate and relapse-free survival (P>0.05). CsA exposure time, rather than different therapy regimens, was the only influence factor for either ORR or relapse rate (P <0.05).@*CONCLUSION@#CsA monotherapy has similar efficacy, AE rate and relapse rate as compared with CsA+CS for patients with newly diagnosed aPRCA, and shows less CS-related AEs such as infection.

STING1 in sepsis: Mechanisms, functions, and implications / 中华创伤杂志(英文版)

Sepsis is a life-threatening clinical syndrome and one of the most challenging health problems in the world. Pathologically, sepsis and septic shock are caused by a dysregulated host immune response to infection, which can eventually lead to multiple organ failure and even death. As an adaptor transporter between the endoplasmic reticulum and Golgi apparatus, stimulator of interferon response cGAMP interactor 1 (STING1, also known as STING or TMEM173) has been found to play a vital role at the intersection of innate immunity, inflammation, autophagy, and cell death in response to invading microbial pathogens or endogenous host damage. There is ample evidence that impaired STING1, through its immune and non-immune functions, is involved in the pathological process of sepsis. In this review, we discuss the regulation and function of the STING1 pathway in sepsis and highlight it as a suitable drug target for the treatment of lethal infection.

Recombinant Human Thioredoxin-1 Protects Macrophages from Oxidized Low-Density Lipoprotein-Induced Foam Cell Formation and Cell Apoptosis

Oxidized low-density lipoprotein (ox-LDL)-induced macrophage foam cell formation and apoptosis play critical roles in the pathogenesis of atherosclerosis. Thioredoxin-1 (Trx) is an antioxidant that potently protects various cells from oxidative stress-induced cell death. However, the protective effect of Trx on ox-LDL-induced macrophage foam cell formation and apoptosis has not been studied. This study aims to investigate the effect of recombinant human Trx (rhTrx) on ox-LDL-stimulated RAW264.7 macrophages and elucidate the possible mechanisms. RhTrx significantly inhibited ox-LDL-induced cholesterol accumulation and apoptosis in RAW264.7 macrophages. RhTrx also suppressed the ox-LDL-induced overproduction of lectin-like oxidized LDL receptor (LOX-1), Bax and activated caspase-3, but it increased the expression of Bcl-2. In addition, rhTrx markedly inhibited the ox-LDL-induced production of intracellular reactive oxygen species (ROS) and phosphorylation of p38 mitogen-activated protein kinases (MAPK). Furthermore, anisomycin (a p38 MAPK activator) abolished the protective effect of rhTrx on ox-LDL-stimulated RAW264.7 cells, and SB203580 (a p38 MAPK inhibitor) exerted a similar effect as rhTrx. Collectively, these findings indicate that rhTrx suppresses ox-LDL-stimulated foam cell formation and macrophage apoptosis by inhibiting ROS generation, p38 MAPK activation and LOX-1 expression. Therefore, we propose that rhTrx has therapeutic potential in the prevention and treatment of atherosclerosis.

Research progress for antitumor drug treating coronary artery disease / 心血管康复医学杂志

The present article summarizes research progress for anti-tumor drug relating coronary artery disease, reviews domestic and foreign relevant literature about it and makes a review about its research progress. Its mechanism is multi-level and multi-site. Some anti-tumor drug are expected to be new targets of treating coronary artery disease.

Experience of transcather closure in patients with postinfarction ventricular septal defects / 中华心血管病杂志

<p><b>OBJECTIVE</b>To evaluate the therapeutic effect of transcather closure in patients with postinfarction ventricular septal defects (VSD).</p><p><b>METHODS</b>Transcatheter VSD closure was performed in 12 patients with postinfarction VSD (10 muscular and 2 membranes defects) on top of standard pharmacotherapy and percutaneous transluminal coronary angioplasty (PTCA) as indicated.</p><p><b>RESULTS</b>(1) Percutaneous interventional VSD closure was successful in 9 out 12 patients (75%) and these 9 patients survived post procedure. (2) The medial time between VSD occurrence and closure was (15.5 +/- 9.2) days. Procedure-related complications such as device embolization and malignant arrhythmia occurred in 3 patients (25%). The medial time between procedure and discharge from hospital was (11.3 +/- 5.2) days. (3) Coronary angiography was performed in 2 patients and 4 stents were implanted in diseased lesions.</p><p><b>CONCLUSION</b>Transcatheter closure could be successfully performed in selected patients with postinfarction VSD.</p>

In vitro growth and function of neonatal cardiomyocytes in various transcatheter closure device patches / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the effects of collagen-coating, epidermal growth factor (EGF), Bromodeoxyuridine (BrdU) on growth and function of neonatal ventricular cardiomyocytes in transcatheter closure device patches in vitro.</p><p><b>METHODS</b>Neonatal ventricular cardiomyocytes were cultured with transcatheter closure device patches (1 cm x 2 cm) coated with or without collagen and treated with 10% FBS (control), EGF (20 ng/ml), BrdU (0.1 mmol/L), respectively. In vitro ventricular cardiomyocytes growth and function as well as IGF-I content were determined.</p><p><b>RESULTS</b>(1) The beginning time of ventricular cardiomyocytes beating on patches was similar in collagen-coated and uncoated patches treated with PBS, EGF or BrdU, respectively (P > 0.05). The cell beating time was significantly earlier in Brdu group than in PBS and EGF groups (all P < 0.05). (2) Time of cultured cell covering on patches was significantly earlier in coated patches than those uncoated patches in PBS, EGF and BrdU treated groups (all P < 0.05). The ventricular cardiomyocytes covering time on patches was significantly earlier in EGF group than that in PBS and BrdU groups (all P < 0.05). (3) Ventricular cardiomyocytes types survived on patches included endothelial cells, fibroblasts and myocytes. The highest content of endothelial cells was evidenced in EGF group and the highest content of fibroblasts was found in Brdu group. Myocytes content was similar between PBS and BrdU groups (P > 0.05) and significantly higher than that in EGF group (all P < 0.05). (4) IGF-I peaked at the seventh culture day in all groups (all P < 0.01).</p><p><b>CONCLUSIONS</b>Ventricular cardiomyocytes covering on patches could be enhanced by collagen coating. EGF could promote endothelial cells growth while Brdu could stimulate fibroblasts growth on patches.</p>

Low molecular weight heparin microcapsule coated occluder for atrial-septal defects / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Whether the low molecular weight heparin microcapsule coated occluder is helpful to endothelialization in atrial-septal defect models is uncertain. This study aimed to investigate the best conditions for low molecular weight heparin coated NiTi alloy occluder and provide the evidence of the efficacy and safety of atrial-septal defect occluders in vivo.</p><p><b>METHODS</b>Low molecular weight heparin microcapsules were investigated using gelatin as microcapsule material. The prepared low molecular weight heparin gelatin particles were subjected to nickel and titanium alloy occluder coating by sodium hyaluronate. A dog model of atrial septal defects was established after treatment with low molecular weight heparin microcapsule coated occluder (n = 4) and uncoated occluder (n = 4). Endotheliocytes and fibroblastic cells in occluders were observed. And the rate of endothelialization was detected.</p><p><b>RESULTS</b>When the concentration of gelatin was 1%, the diameters of particles were mostly about 100 microm, and the particle size was uniform. The envelope efficiency of low molecular weight heparin microcapsule was about 80%. The endothelialization of occluder in the model was more obvious in the coated group than in the uncoated group (P < 0.0001).</p><p><b>CONCLUSIONS</b>Low molecular weight heparin can be prepared into microcapsules with their particle size in nanometric grade. The antithrombotic properties are kept in the nickel and titanium alloy occluder successfully coated with sodium hyaluronate. The endothelialization after the interventional occlusion in the coated group is obvious, indicating that low molecular weight heparin is helpful to the growth of endothelial cells in the occlude and the healing after the interventional occlusion.</p>