Acute type A dissection without intimal tear in arch: Proximal or extensive repair?

ObjectiveFor acute type A dissection without an intimal tear in the arch, the optimal surgical strategy is unknown. The present study was designed to clarify the issue by comparing the early and late outcomes of proximal (PR) and extensive repair (ER).MethodsFrom January 2002 to June 2010, 331 patients with acute type A dissection were treated surgically at our institute. Of these 331 patients, 197 were identified without an arch tear on the preoperative imaging examination and by intraoperative inspection. Of these 197 patients, 74 underwent proximal repair, including the aortic root, ascending aortic, or hemiarch repair, and 88 underwent extensive repair, including proximal repair, total arch replacement and a stented elephant trunk technique. The perioperative variables and late results were statistically analyzed.ResultsNo significant difference was found in the rates of early mortality and morbidity between the 2 groups, despite the shorter duration of circulatory arrest in the PR group. During long-term follow-up (mean, 55.7 ± 33.1 months; maximum, 129), the overall survival rate in the whole cohort was 100%, 90.8%, and 71.1% at 1, 5, and 8 years, respectively. No difference was found in survival between the 2 groups (P > .05). However, complete thrombosis of the false lumen in the proximal descending aorta was achieved in 100% of the ER group and 24.6% of the PR group (P < .001). For patients with a patent false lumen in the PR group, distal anastomosis leakage and unclosed small intimal tears were identified in 53.3% and 35.6% patients, respectively. The reintervention rate was also lower in the ER group than in the PR group (4.9% vs 15.9%, P < .05) during follow-up. Moreover, the reintervention rate for patients with Marfan syndrome was 9.5% in the ER group and 38.5% in the PR group (P < .05).ConclusionsFor patients with acute type A dissection without an intimal tear in the arch, extensive repair could promote the occlusion of distal false lumen and decrease the reintervention rate without increasing the operative risk

Diversity and Complexity of the Large Surface Protein Family in the Compacted Genomes of Multiple Pneumocystis Species

Pneumocystis, a major opportunistic pathogen in patients with a broad range of immunodeficiencies, contains abundant surface proteins encoded by a multicopy gene family, termed the major surface glycoprotein (Msg) gene superfamily. This superfamily has been identified in all Pneumocystis species characterized to date, highlighting its important role in Pneumocystis biology. In this report, through a comprehensive and in-depth characterization of 459 msg genes from 7 Pneurnocystis species, we demonstrate, for the first time, the phylogeny and evolution of conserved domains in Msg proteins and provide a detailed description of the classification, unique characteristics, and phylogenetic relatedness of five Msg families. We further describe, for the first time, the relative expression levels of individual msg families in two rodent Pneumocystis species, the substantial variability of the msg repertoires in P. coda from laboratory and wild rats, and the distinct features of the expression site for the classic msg genes in Pneumocystis from 8 mammalian host species. Our analysis suggests multiple functions for this superfamily rather than just conferring antigenic variation to allow immune evasion as previously believed. This study provides a rich source of information that lays the foundation for the continued experimental exploration of the functions of the Msg superfamily in Pneumocystis biology. IMPORTANCE Pneumocystis continues to be a major cause of disease in humans with immunodeficiency, especially those with HIV/AIDS and organ transplants, and is being seen with increasing frequency worldwide in patients treated with immunode-pleting monoclonal antibodies. Annual health care associated with Pneumocystis pneumonia costs similar to$475 million dollars in the United States alone. In addition to causing overt disease in immunodeficient individuals, Pneumocystis can cause subclinical infection or colonization in healthy individuals, which may play an important role in species preservation and disease transmission. Our work sheds new light on the diversity and complexity of the msg superfamily and strongly suggests that the versatility of this superfamily reflects multiple functions, including antigenic variation to allow immune evasion and optimal adaptation to host environmental conditions to promote efficient infection and transmission. These findings are essential to consider in developing new diagnostic and therapeutic strategies.Peer reviewe

Stem‐Cell Therapy for Esophageal Anastomotic Leakage by Autografting Stromal Cells in Fibrin Scaffold

Abstract Esophageal anastomotic leakage (EAL) is a devastating complication for esophagectomy but the available therapies are unsatisfactory. Due to the healing effects of mesenchymal stromal cells (MSCs) and supporting capability of fibrin scaffold (FS), we evaluated the efficacy of a stem‐cell therapy for EAL by engrafting adult and autologous MSCs (AAMSCs) in FS and investigated the potential mechanism. Twenty‐one rabbits were assigned to AAMSC/FS group (n = 12) and control group (n = 9). After harvested, AAMSCs were identified and then labeled with lenti.GFP. To construct EAL model, a polyethylene tube was indwelled through the anastomosis for 1 week. A total of 2 × 106 AAMSCs in 0.2 ml FS were engrafted onto the EAL for the AAMSC/FS group, whereas FS was injected for control. Magnetic Resonance Imaging (MRI) examination was performed after 5 weeks. Esophageal tissues were harvested for macroscopic, histological analyses, Western blot, and immunohistochemistry at 8 weeks. The animal model of EAL was established successfully. MRI scanning revealed a decreased inflammation reaction in AAMSC/FS group. Accordingly, AAMSC/FS group presented a higher closure rate (83.3% vs. 11.1%, p = .02) and lower infection rate (33.3% vs. 88.9%, p = .02). Histological analyses showed the autografted MSCs resided in the injection site. Furthermore, milder inflammation responses and less collagen deposition were observed in AAMSC/FS group. Western blot and immunohistochemistry studies suggested that the therapeutic effect might be related to the secretions of IL‐10 and MMP‐9. Engrafting AAMSCs in FS could be a promising therapeutic strategy for the treatment of EAL by suppressing inflammation response and alleviating fibrosis progression. Stem Cells Translational Medicine 2019;8:548–55

Meta-Analysis of <em>RAGE</em> Gene Polymorphism and Coronary Heart Disease Risk

<div><h3>Background</h3><p>Recent data from human and animal studies have shown an upregulated expression of advanced glycosylation end product–specific receptor (RAGE) in human atherosclerotic plaques 1 and in retina, messangial, and aortic vessels, suggesting an important role of RAGE in the pathogenesis of atherothrombotic diseases. In the past few years, the relationship between <em>RAGE</em> polymorphisms (−429T/C, −374T/A, and G82S) and coronary heart disease (CHD) has been reported in various ethnic groups; however, these studies have yielded contradictory results.</p> <h3>Methods</h3><p>PubMed, ISI web of science, EMBASE and the Chinese National Knowledge Infrastructure databases were systematically searched to identify relevant studies. Data were abstracted independently by two reviewers. A meta-analysis was performed to examine the association between <em>RAGE</em> polymorphisms and susceptibility to CHD. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated.</p> <h3>Results</h3><p>A total of 17 studies including 4343 patients and 5402 controls were involved in this meta-analysis. Overall, no significant results were observed for −429T/C (OR  = 1.01, 95% CI: 0.92–1.12, P  = 0.78), −374T/A (OR  = 1.11, 95% CI: 0.98–1.26, P  = 0.09) and G82S (OR  = 1.12, 95% CI: 0.86–1.45, P  = 0.41) polymorphism. In the stratified analyses according to ethnicity, sample size, CHD endpoint and Hardy-Weinberg status, no evidence of any gene-disease association was obtained.</p> <h3>Conclusions</h3><p>This meta-analysis demonstrates that there is no association between the RAGE −429T/C, −374T/A and G82S polymorphisms and CHD.</p> </div

Characteristics of the studies included in the meta-analysis.

<p>NA: not available; MI: myocardial infarction; CAD: coronary artery disease; CHD: coronary heart disease; IHD: ischemic heart disease; PB: population based; HB: hospital based; WHO: world health organization.</p

Meta-analysis of the <i>RAGE</i> polymorphism on coronary heart disease risk.

<p>NA: not available.</p

Forest plot from the meta-analysis of coronary heart disease and <i>RAGE</i> −429T/C polymorphism.

<p>Forest plot from the meta-analysis of coronary heart disease and <i>RAGE</i> −429T/C polymorphism.</p

Forest plot from the meta-analysis of coronary heart disease and <i>RAGE</i> −374T/A polymorphism.

<p>Forest plot from the meta-analysis of coronary heart disease and <i>RAGE</i> −374T/A polymorphism.</p