Anomalous aortic origin of the coronary artery(AAOCA) refers to the abnormal initiation, route, or distribution of coronary arteries, which is generally believed to be caused by abnormal or incomplete development of embryonic coronary arteries, and is a rare congenital cardiovascular malformation. It can exist independently without other congenital heart disease. With the development of medical science and people's understanding of AAOCA, more and more AAOCA has been detected, and its clinical significance has attracted more and more attention. Based on abnormal coronary artery opening, malignant or potential contorts can cause long-term blood flow dynamic change, appear abnormal blood vessel hardening of the arteries, at the same time due to walk in the pulmonary artery and the ascending aorta between two vessels, vulnerable to the extrusion of large blood vessels, which caused a temporary blood flow in coronary artery interruption, can cause acute angina pectoris, myocardial infarction, arrhythmia, exercise-induced cardiac syncope. This review focuses on the anatomy, diagnosis and treatment of coronary artery abnormalities arising from aorta.

Objective:To assess the effect of intra-aortic balloon pump (IABP) on in-hospital mortality in patients with cardiac arrest undergoing extracorporeal cardiopulmonary resuscitation (ECPR).Methods:A retrospective study was performed on 696 patients with intra-hospital cardiac arrest undergoing ECPR from Samsung Medical Center in Korea between January 2004 and December 2013. According to whether IABP was used, the patients were divided into ECPR group and ECPR+IABP group. Cox regression and propensity score matching (PSM) were used to examine the correlation between IABP usage and in-hospital mortality, and standardized mean difference ( SMD) was used to check the degree of PSM. Survival analysis of in-hospital mortality was performed by the Kaplan-Meier method, and further analyzed by the Log-Rank test. Using the propensity score as weights, multiple regression model and inverse probability weighting (IPW) model were used for sensitivity analysis. In-hospital mortality, extracorporeal membrane oxygenation (ECMO) withdrawal success rate and neurological function prognosis were compared between the two groups. Results:A total of 199 patients with cardiac arrest undergoing ECPR were included, including 120 males and 79 females, and the average age was (60.0±16.8) years. Thirty-one patients (15.6%) were treated with ECPR and IABP, and 168 patients (84.4%) only received ECPR. The total hospitalized mortality was 68.8% (137/199). The 1 : 1 nearest neighbor matching algorithm was performed with the 0.2 caliper value. The following variables were selected to generate propensity scores, including age, gender, race, marital status, insurance, admission type, service unit, heart rate, mean arterial pressure, respiratory rate, pulse oxygen saturation, white blood cell count. After the propensity score matching, 24 pairs of patients were successfully matched, with the average age of (63.0±12.8) years, including 31 males and 17 females. The in-hospital mortality was 72.6% (122/168) and 48.4% (15/31) in the ECPR group and the ECPR+IABP group [hazard ratio ( HR) = 0.48, 95% confidence interval (95% CI) was 0.28-0.82, P = 0.007]. Multiple regression model, adjusted propensity score, PSM and IPW model showed that the in-hospital mortality in the ECPR+IABP group was significantly lower compared with the ECPR group ( HR = 0.44, 0.50, 0.16 and 0.49, respectively, 95% CI were 0.24-0.79, 0.28-0.91, 0.06-0.39 and 0.31-0.77, all P < 0.05). The combined application of IABP could improve the ECMO withdrawal success rate [odds ratio ( OR) = 8.95, 95% CI was 2.72-29.38, P < 0.001] and neurological prognosis ( OR = 4.06, 95% CI was 1.33-12.40, P = 0.014) in adult cardiac arrest patients. Conclusion:In patients with cardiac arrest using ECPR, the combination of IABP was independently associated with lower in-hospital mortality, higher ECMO withdrawal success rate and better neurological prognosis.

Bivalves are species-rich mollusks with prominent protective roles in coastal ecosystems.Across these ancient lineages,colony-founding larvae anchor themselves either by byssus produc-tion or by cemented attachment.The latter mode of sessile life is strongly molded by left-right shell asymmetry during larval development of Ostreoida oysters such as Crassostrea hongkongensis.Here,we sequenced the genome of C.hongkongensis in high resolution and compared it to reference bivalve genomes to unveil genomic determinants driving cemented attachment and shell asymmetry.Importantly,loss of the homeobox gene Antennapedia(Antp)and broad expansion of lineage-specific extracellular gene families are implicated in a shift from byssal to cemented attachment in bivalves.Comparative transcriptomic analysis shows a conspicuous divergence between left-right asymmetrical C.hongkongensis and symmetrical Pinctada fucata in their expression profiles.Especially,a couple of orthologous transcription factor genes and lineage-specific shell-related gene families including that encoding tyrosinases are elevated,and may cooperatively govern asymmet-rical shell formation in Ostreoida oysters.

BACKGROUND: Pain and cartilage destruction caused by osteoarthritis (OA) is a major challenge in clinical treatment.Traditional intra-articular injection of hyaluronic acid (HA) can relieve the disease, but limited by the difficulty of longterm maintenance of efficacy. METHODS: In this study, an injectable and self-healing hydrogel was synthesized by in situ crosslinking of N-carboxyethyl chitosan (N-chitosan), adipic acid dihydrazide (ADH), and hyaluronic acid–aldehyde (HA-ALD). RESULTS: This supramolecular hydrogel sustains good biocompatibility for chondrocytes. Intra-articular injection of this novel hydrogel can significantly alleviate the local inflammation microenvironment in knee joints, through inhibiting the inflammatory cytokines (such as TNF-a, IL-1b, IL-6 and IL-17) in the synovial fluid and cartilage at 2- and even 12-weeks post-injection. Histological and behavioral test indicated that hydrogel injection protected cartilage destruction and relieved pain in OA rats, in comparison to HA injection. CONCLUSION This kind of novel hydrogel, which is superior to the traditional HA injection, reveals a great potential for the treatment of OA.

BACKGROUND: Pain and cartilage destruction caused by osteoarthritis (OA) is a major challenge in clinical treatment.Traditional intra-articular injection of hyaluronic acid (HA) can relieve the disease, but limited by the difficulty of longterm maintenance of efficacy. METHODS: In this study, an injectable and self-healing hydrogel was synthesized by in situ crosslinking of N-carboxyethyl chitosan (N-chitosan), adipic acid dihydrazide (ADH), and hyaluronic acid–aldehyde (HA-ALD). RESULTS: This supramolecular hydrogel sustains good biocompatibility for chondrocytes. Intra-articular injection of this novel hydrogel can significantly alleviate the local inflammation microenvironment in knee joints, through inhibiting the inflammatory cytokines (such as TNF-a, IL-1b, IL-6 and IL-17) in the synovial fluid and cartilage at 2- and even 12-weeks post-injection. Histological and behavioral test indicated that hydrogel injection protected cartilage destruction and relieved pain in OA rats, in comparison to HA injection. CONCLUSION This kind of novel hydrogel, which is superior to the traditional HA injection, reveals a great potential for the treatment of OA.

Objective:To establish a nomogram prediction model for the prognosis of patients with septic cardiomyopathy (SCM) based on afterload-corrected cardiac performance (ACP), in order to identify septic patients with poor outcomes and treatment.Methods:The data of patients admitted to the department of critical medicine of the Second Affiliated Hospital of Guangzhou Medical University from June 2016 to June 2019 were analyzed. All patients were monitored by pulse indication continuous cardiac output (PiCCO) monitor more than 24 hours and diagnosed as SCM with ACP less than 80%. The predictors of 30-day death risk of SCM patients were screened by univariate Cox regression analysis. Multivariate Cox regression analysis was used to establish the prediction model for 30-day death risk of SCM patients, which was displayed by the nomogram. Finally, the discrimination and calibration of the model were analyzed by receiver operator characteristic curve (ROC curve) and consistency index (C-index).Results:A total of 102 patients with SCM were included and the 30-day mortality was 60.8% (62 cases). Among 102 patients with SCM, 57 patients (55.9%) had mild impairment of cardiac function (60%≤ACP < 80%), and the 30-day mortality was 43.9% (25/57); 39 patients (38.2%) had moderate impairment of cardiac function (40%≤ACP < 60%), and the 30-day mortality was 79.5% (31/39); 6 patients (5.9%) had severe impairment of cardiac function (ACP < 40%), and the 30-day mortality was 100% (6/6). There was significantly difference in mortality among the three groups (χ 2 = 24.156, P < 0.001). The potential risk factors for 30-day death of SCM patients screened by univariate Cox regression analysis were included in multivariate Cox regression analysis. The results showed that the independent risk factors for 30-day death of SCM patients were acute physiology and chronic health evaluation Ⅱ [APACHEⅡ, risk ratio ( HR) = 1.031, 95% confidence interval (95% CI) was 1.002-1.061, P = 0.039], vasoactive inotropic score (VIS, HR = 1.003, 95% CI was 1.001-1.005, P = 0.012), continuous renal replacement therapy (CRRT; HR = 2.106, 95% CI was 1.089-4.072, P = 0.027), and ACP ( HR = 0.952, 95% CI was 0.928-0.977, P < 0.001). The nomogram model was established based on the above independent risk factors and age, and the area under the curve (AUC) was 0.865 (95% CI was 0.795-0.935), P < 0.001; C-index was 0.797 (95% CI was 0.747-0.847), P > 0.05. Conclusions:The nomogram model based on age, APACHEⅡ score, VIS score, CRRT and ACP has a certain clinical reference significance for the prediction of 30-day mortality of SCM patients. The discrimination and calibration are good, however, further verification is needed.

The incidence of coronary heart disease is increasing year by year, seriously threatening human health and interests. Plaque rupture and abnormal activation of platelets are key links in the pathogenesis, and they are also the initiators of coronary heart disease. Therefore, timely and effective inhibition of platelet activation is important in the prevention and treatment of coronary heart disease. Antiplatelet therapy is an important cornerstone of coronary heart disease treatment. It can not only effectively and significantly reduce the incidence of atherosclerotic ischemic events, but also can reduce the risk of complications after stent implantation. Aspirin combined with clopidogrel is the basis of antiplatelet therapy for patients with coronary heart disease, but the new P2Y12 receptor antagonist ticagrelor is superior to clopidogrel for patients with acute coronary syndrome. However, the latest research results show that East Asian patients with coronary heart disease are prone to bleeding after taking ticagrelor. This makes the application of ticagrelor in East Asian patients unclear. In this paper, the current clinical studies on thromboxane A2 inhibitors, P2Y12 receptor antagonists, glycoprotein (GP) Ⅱb/Ⅲa receptor inhibitors, and phosphodiesterase inhibitors were reviewed, and the benefits and risks of oral antiplatelet therapy were analyzed to provide new perspectives and ideas for related clinical treatment.

Objective:To explore the gene mutations of UGT1A1 * 6 and UGT1A1 * 28 in patients with unconjugated hyperbilirubinemia after renal transplantation and understand their clinical significance.Methods:UGT1A1*6 and UGT1A1*28 gene fragments in blood samples of patients with unconjugated hyperbilirubinemia after renal transplantation were detected by digital fluorescent molecular hybridization sequencing.Results:A total of 21 patients with unconjugated hyperbilirubinemia after renal transplantation were examined for UGT1A1*6 and UGT1A1*28 alleles. The results showed that there were 3 UGT1A1*28 and UGT1A1*6 combined heterozygous mutations, 4 UGT1A1*28 gene heterozygous mutations, 2 UGT1A1*6 heterozygous mutations and 4 UGT1A1*6 homozygous mutations. Among them, the mutation rates of UGT1A1*28 gene and UGT1A1*6 gene were 33%(7/21) and 43%(9/21) respectively and the total mutation rate of both was 62%(13/21).Conclusions:UGT1A1 polymorphism is associated with unconjugated hyperbilirubinemiaafter renal transplantation. By detecting the sequence of UGT1A1*6 and UGT1A1*28 gene fragments in blood samples of renal transplant patients, it is helpful to clarify the etiology of unconjugated hyperbilirubinemia after renal transplantation to confirm the diagnosis of Gilbert syndrome and rule out the effect of immunosuppressive drugs on liver function so as to guide the clinical medication of renal transplant patients.

Objective:To investigate the relationship between 1-hour lactate (1 h Lac) and 30-day mortality in critical care patients in intensive care unit (ICU).Methods:A retrospective, observational cohort study was performed with adult critical patients (age ≥ 16 years old) having lactate records within 1 hour after ICU admission from Medical Information Mart for Intensive Care-Ⅲ database (MIMIC-Ⅲ). According to the 1 h Lac level, the patients were divided into three groups: < 2 mmol/L, 2-4 mmol/L, and > 4 mmol/L groups. The baseline characteristics were analyzed. Multivariable Logistic regression analysis was performed to assess the association between 1 h Lac and 30-day mortality. The receiver operating characteristic (ROC) curve was used to analyze the predictive value of 1 h Lac for 30-day mortality, and Kaplan-Meier survival curve was performed according to the best cut-off value. In addition, sensitivity analysis was carried out for each classification variable.Results:A total of 3 969 ICU patients were included, with 673 died in 30 days, and the total mortality was 16.95%. There were 1 664, 1 588, 717 patients in Lac < 2 mmol/L, 2-4 mmol/L and > 4 mmol/L group, respectively. There were significant differences in age, ICU duration, ICU type, heart rate, leukocyte count, hemoglobin, creatinine, sequential organ failure score (SOFA), ventilator application, vasoactive drug use and main diagnosis among the three groups. Multivariable Logistic regression analysis showed that a 1 mmol/L increment in Lac was associated with 0.24 times higher risk of 30-day mortality [odds ratio ( OR) = 1.24, 95% confidence interval (95% CI) was 1.19-1.29, P < 0.000 1]. ROC curve analysis showed that the area under ROC curve (AUC) of 1 h Lac for predicting 30-day mortality of severe patients was 0.694 (95% CI was 0.669-0.718). The cut-off value was 3.35 mmol/L with sensitivity of 0.499 and specificity of 0.779, whilst positive likelihood ratio was 2.260, and negative likelihood ratio was 0.643. According to the cut-off value of 1 h Lac, the patients were divided into high lactate group (≥ 3.35 mmol/L) and low lactate group (< 3.35 mmol/L). In the two subgroups, 30-day mortality was 31.58% (336/1 064) and 11.60% (337/2 905), respectively. The Kaplan-Meier survival curve showed that the 30-day cumulative survival rate of high lactate group was significantly lower than that of low lactate group (Log-rank test: χ 2 = 247.72, P < 0.000 1). Multiple Logistic regression analysis showed that the 30-day mortality rate of high lactate group was 2.34 times that the level of low lactate group ( OR = 2.34, 95% CI was 1.90-2.88, P < 0.000 1), after the adjustment of age, time of admission, type of ICU, hemoglobin, leukocyte count, use of vasopressor, use of ventilator and main diagnosis of patients. Stratified analysis showed that the relationship between 1 h Lac and 30-day mortality was stable. Conclusions:1 h Lac is associated with 30-day mortality in critical care patients. The risk of death was significantly increased in critically ill patients with 1 h Lac higher than 3.35 mmol/L.

Objective To evaluate the relationship between cholinergic anti-inflammatory pathway and autophagy during liver injury in septic mice.Methods SPF healthy male 32 C57BL/6 mice,aged 6-8 weeks,weighing 18-22 g,were divided into 4 groups (n=8 each) using a random number table method:sham operation group (group Sham),sepsis group (group Sep),α7nAChR agonist GTS-21 plus sepsis group (GTS-21+Sep group),and α7nACh antagonist α-BGT plus sepsis plus GTS-21 group (α-BGT+Sep+GTS-21 group).Sepsis was induced by cecal ligation and puncture.GTS-21 4 mg/kg was intraperitoneally injected immediately after operation in group GTS-21 +Sep.α-BGT 1 mg/kg was intraperitoneally injected at 15 min before operation,and GTS-21 4 mg/kg was intraperitoneally injected immediately after operation in group α-BGT+Sep+GTS-21.Blood samples were obtained at 6 h after surgery for determination of serum aspartate transaminase (AST) and alanine transaminase (ALT) concentrations by enzyme-linked immunosorbent assay.Liver tissues were obtained for determination of the expression of microtubule-associated protein-1 light chain 3-Ⅱ (LC3 Ⅱ) and sequestosome-1/p62 (by Western blot) and for examination of the number of autophagosomes in liver cells (under a transmission electron microscope).Results Compared with Sham group,the expression of LC3 Ⅱ and sequestosome-1/p62 was significantly up-regulated,the number of autophagosomes was increased,and the serum AST and ALT concentrations were increased in Sep group (P＜0.05).Compared with Sep group,the expression of LC3 Ⅱ was significantly up-regulated,the expression of sequestosome-1/p62 was down-regulated,the number of autophagosomes was increased,and the serum AST and ALT concentrations were decreased in GTS-21 +Sep group (P＜0.05).Compared with GTS-21 +Sep group,the expression of LC3 Ⅱ was significantly down-regulated,the expression of sequestosome-1/p62 was up-regulated,the number of autophagosomes was decreased,and the serum AST and ALT concentrations were increased in α-BGT+Sep+GTS-21 group (P＜0.05).Conclusion Activation of the cholinergic anti-inflammatory pathway can enhance the level of autophagy in liver cells and is involved in the endogenous protective mechanism of sepsis-induced liver injury in septic mice.