A Chinese scoring system for predicting successful retrograde collateral traverse in patients with chronic total coronary occlusion.

BACKGROUND: Retrograde approach technique has been challenging in percutaneous coronary interventional treatment of chronic total occlusion (CTO) coronary disease. The present study endeavors to determine a novel Chinese scoring system for predicting successful collateral channels traverse via retrograde approach. METHODS: The demographic characteristics and angiographic characteristics of 309 CTO patient were analyzed by univariable and multivariable analysis for selecting potential predictors. And the nomogram was used to establish the scoring system. Then it was evaluated by the internal and external validation. RESULTS: The predictors of Age, Connections between collateral channels and recipient vessels, and Channel Tortuosity (ACT) were identified with univariable and multivariable analysis and employed to the ACT score system. With acceptable calibrations, the area under curve of the scoring system and the external validation were 0.826 and 0.816 respectively. Based on score, the predictors were divided into three risk categories and it showed a consistent prediction power in the validation cohort. CONCLUSIONS: The novel Chinese ACT score is a reliable tool for predicting successful retrograde collateral traverse.

Retinal honeycomb appearance and its role in patients with X-linked retinoschisis.

BACKGROUND: To investigate the clinical characteristics of retinal honeycomb appearance in a large cohort of patients with X-linked retinoschisis (XLRS) and to determine whether it is associated with complications like retinal detachment (RD) and vitreous hemorrhage (VH). METHODS: A retrospective observational case series. A chart review of medical records, wide-field fundus imaging, and optical coherence tomography (OCT) was performed on 78 patients (153 eyes) diagnosed with XLRS at Beijing Tongren eye center between Dec 2017 and Feb 2022. The chi-square test or Fisher exact test was performed on the 2 × 2 cross-tabulations of honeycomb appearance and other peripheral retinal findings and complications. RESULTS: Thirty-eight patients (48.7%), and 60 eyes (39.2%) had a honeycomb appearance of different areas on the fundus. The supratemporal quadrant was the most commonly affected (45 eyes, 75.0%), followed by the infratemporal (23 eyes, 38.3%), the infranasal (10 eyes,16.7%), and supranasal (9 eyes,15.0%). The appearance was significantly associated with peripheral retinoschisis, inner retinal layer break, outer retinal layer break, RD, and rhegmatogenous retinal detachment (RRD) (p < 0.01, p = 0.032, p < 0.01, p = 0.008, p < 0.01, respectively). All the eyes complicated with RRD had the appearance. None of the eyes without the appearance had RRD. CONCLUSIONS: The data suggest that the honeycomb appearance is not uncommon in patients with XLRS and is more likely to be accompanied by an RRD, and inner and outer layer breaks, thus should be treated with caution and close observation.

[Methods for the evaluation of intestinal mucosal permeability].

The intestinal mucosal barrier (IMB), which consists of mechanical barrier, chemical barrier, biological barrier and immune barrier, plays an important role in the maintenance of intestinal epithelium integrity and defense against invasion of bacteria, endotoxins and foreign antigens. Impaired IMB, characterized by increased intestinal mucosal permeability (IMP) and decreased transmembrane resistance (TR), has been implicated in the pathogenesis of various digestive, urinary, circulatory, neurological and metabolic dysfunctions. Electrophysiological recording of TR in the ex vivo intestinal tissues or cultured epithelial cell monolayers, or biochemical quantification of transepithelial movement of orally-administered molecular probes or specific endogenous protein molecules has frequently been used in the evaluation of IMB. In this paper, the composition and function of IMB will be summarized, with emphasis on the evaluation methods of IMP.

[Fibroblast growth factor 21 plays a protective role in cardiovascular diseases by inducing autophagy].

Fibroblast growth factor 21 (FGF21) is a growth factor with endocrine function in the fibroblast growth factor family. Previous reports have shown that FGF21 is involved in the regulation of energy metabolism and plays a protective role in cardiovascular diseases such as coronary heart disease, diabetes, non-alcoholic fatty liver disease and so on. Recent studies have found that FGF21 can induce autophagy in a variety of tissues and organs, and autophagy is involved in many pathological processes of cardiovascular diseases, including vascular calcification, atherosclerosis, and myocardial ischemia-reperfusion injury. Therefore, FGF21 may play a protective role in a variety of cardiovascular diseases by regulating autophagy. This article reviews the research progress on the protective role of FGF21 in cardiovascular diseases by inducing autophagy.

Reduced acetylcholine and elevated muscarinic receptor 2 in duodenal mucosa contribute to the impairment of mucus secretion in 6-hydroxydopamine-induced Parkinson's disease rats.

Patients with Parkinson's disease (PD) have a higher incidence rate of duodenal ulcers. The mucus barrier provides the first line of defense for duodenal mucosal protection. However, it is unknown whether duodenal mucus secretion is affected in PD. In the present study, we used the rats microinjected 6-hydroxydopamine (6-OHDA) into the bilateral substantia nigra to investigate duodenal mucus secretion and potential therapeutic targets in duodenal ulcer in PD. Alcian blue-periodic acid-Schiff, transmission electron microscopy, immunofluorescence, duodenal mucosal incubation, and enzyme-linked immunosorbent assays were used. The 6-OHDA rats exhibited mucin accumulation and retention in duodenal goblet cells. Mucin granules were unable to fuse with the apical membranes of goblet cells, and the exocytosis ratio of goblet cells was significantly reduced. Moreover, decreased acetylcholine and increased muscarinic receptor 2 (M2R) levels were detected in the duodenal mucosa of 6-OHDA rats. Bilateral vagotomy rats were also characterized by defective duodenal mucus secretion and decreased acetylcholine with increased M2R levels in the duodenal mucosa. Application of the cholinomimetic drug carbachol or blocking M2R with methoctramine significantly promoted mucus secretion by goblet cells and increased MUC2 content in duodenal mucosa-incubated solutions from 6-OHDA and vagotomy rats. We conclude that the reduced acetylcholine and increased M2R contribute to the impaired duodenal mucus secretion of 6-OHDA rats. The study provides new insights into the mechanism of duodenal mucus secretion and potential therapeutic targets for the treatment of duodenal ulcers in PD patients.

Case Report: Focal Choroidal Excavation Underlying Combined Hamartoma of the Retina and Retinal Pigment Epithelium.

SIGNIFICANCE: There are few reports of focal choroidal excavation (FCE) in combined hamartoma of the retina and retinal pigment epithelium (CHRRPE). This report documents a case of this rare condition and suggests that there might be a relationship between FCE and CHRRPE. PURPOSE: The purpose of this study was to describe a case of FCE underlying CHRRPE. CASE REPORT: A 6-year-old Chinese boy presented with a 2-month history of decreased vision in his left eye. Fundus examination of the left eye showed an elevated fibrotic mass in the macular area with pigment disturbance. Optical coherence tomography revealed a cup-shaped FCE in the macula with thickening and disorganization of multiple retinal layers and overlying epiretinal proliferation in the left eye. A diagnosis of FCE within CHRRPE was made, and periodic review was recommended. CONCLUSIONS: There may be an association or a causal relationship between CHRRPE and FCE. It is plausible that FCE in the setting of CHRRPE is a developmental abnormality that occurs after birth because of a weakening of the retinal pigment epithelium and thinning of the choroid beneath the tumor. Continued monitoring for FCE progression and potential choroidal neovascularization is indicated.

Association Between Blood Glucose Variability and the Characteristics of Vulnerable Plaque in Elderly Non-ST Segment Elevation Acute Coronary Syndrome Patients.

Blood glucose variability is considered to be one of the risk factors for coronary heart disease, and there is growing evidence that blood glucose fluctuation is closely related to the characteristics of plaques. The aim of the study was to investigate the influence of blood glucose variability on the vulnerability of culprit plaques in elderly non-ST segment elevation acute coronary syndrome (NSTE-ACS) patients.Coronary angiography and VH-IVUS were applied to evaluate the components of culprit plaque in NSTE-ACS patients. CGMS monitoring was performed for 72 hours and blood glucose variability was assessed by glycemic excursions (MAGE), absolute means of daily differences (MODD), postprandial glycemic excursions (PPGE), and the largest amplitude of glycemic excursions (LAGE). An oxidative stress indicator (urinary 8-iso-PGF2α) was also tested.Eighty two elderly NSTE-ACS patients were enrolled in this study. Higher glucose variability was associated with the increased culprit plaque instability. MODD was positively correlated with urinary 8-iso-PGF2α. PPGE and urinary 8-iso-PGF2α were independent risk factors for percent fibrous and necrotic volume in culprit plaques (PPGE: ß = -0.340, P = 0.024; urinary 8-iso-PGF2α: ß = -0.294, P = 0.013).Blood glucose variability is positively related to oxidative stress. With an increase in blood glucose variability, the instability of criminal plaques in elderly NSTE-ACS patients increased.

Improvement of LVEF in patients with HFrEF with coronary heart disease after revascularization-A real-world study.

OBJECTIVE: This study aimed to explore the predictive factors for left ventricular ejection fraction (LVEF) improvement after revascularization. METHODS: This real-world study examined 993 patients with ischemic HFrEF who had received revascularization (PCI or CABG), had survived at least 90 days and had undergone an echocardiography review. Based on the change in the LVEF, we divided the patients into two groups. RESULT: We obtained 454 patients with ≥10% improvement and 539 with <10% improvement or deterioration. By Cox regression analysis, we obtained five independent factors for LVEF improvement, including female (P = 0.018, OR 0.726, 95% CI 0.557-0.947), prior MI (P = 0.000, OR 0.590, 95% CI 0.476-0.732), LVEF (P = 0.008, OR 0.967, 95% CI 0.943-0.991), digoxin (P = 0.027, OR 0.708, 95% CI 0.521-0.961), loop diuretic (P = 0.000, OR 1.515, 95% CI 1.208-1.901), and triple-vessel disease (P = 0.000, OR 1.462, 95% CI 1.192-1.792). By multivariate generalized estimation, we obtained seven factors associated with the degree of improvement, namely, low LVEF, short LVESD, short LVEDD, no prior MI, no hyperuricemia, clopidogrel use and triple-vessel disease. CONCLUSIONS: The method of revascularization (PCI vs CABG) had no effect on LVEF improvement. Patients with severely impaired baseline LVEFs, triple-vessel disease, or no history of MI tended to exhibit marked LVEF improvement (≥10%) after revascularization. In addition, LVESD, LVEDD, hyperuricemia, clopidogrel use and loop diuretic affected the degree of improvement.

Assessment of Liver Fibrosis Using Real-time Shear-wave Elastography for Patients with Hepatitis B e Antigen-negative Chronic Hepatitis B and Alanine Transaminase <2 Times the Upper Limit of Normal.

BACKGROUND: We assessed liver fibrosis using real-time shear-wave elastography (SWE) combined with liver biopsy (LB) for patients with hepatitis B e antigen (HBeAg)-negative chronic hepatitis B (CHB) and alanine transaminase < 2 times the upper limit of normal and hepatitis B virus DNA < 2000 IU/ml. METHODS: A total of 107 patients met the inclusion criteria. Real- ime SWE and ultrasoundassisted liver biopsies were consecutively performed. Fibrosis was staged according to the METAVIR scoring system. Analyses of receiver operating characteristic curve were performed to calculate the optimal area under the receiver operating characteristic curve for F0-F1 versus F2-F4, F0-F2 versus F3-F4, and F0-F3 versus F4 for real-time SWE. RESULTS: The most concurrent liver fibrosis degrees were between F1 and F2 for these HBeAg-negative CHB patients. Liver stiffness increased in parallel with the degree of liver fibrosis using SWE measurements. The area under the receiver operating characteristic curves was 0.881 (95% confidence interval [CI]: 0.704-1.000) for SWE (p = 0.004); 0.912 (95% CI: 0.836-0.987) for SWE (p = 0.000); 0.981 (95% CI: 0.956-1.000) for SWE (p = 0.000); 0.974 (95% CI: 0.936-1.000) for SWE (p = 0.000) when comparing F0 versus F1-F4, F0-F1 versus F2-F4, F0-F2 versus F3-F4, and F0-F3 versus F4, respectively. CONCLUSIONS: SWE has the advantage of providing an image of liver stiffness in real-time. As an alternative to LB, the development of all these noninvasive methods for dynamic evaluation of liver fibrosis will decrease the need for LB, making clinical care safer and more convenient for patients with liver diseases.

Increased plasma BMP-2 levels are associated with atherosclerosis burden and coronary calcification in type 2 diabetic patients.

BACKGROUND: Although Bone morphogenetic protein-2 (BMP-2) is a known mediator of bone regeneration and vascular calcification, to date no study has investigated the relationship between BMP-2 and type 2 diabetes mellitus (T2DM) and its possible role in coronary artery disease (CAD). The purpose of this study is to evaluate the relationship of BMP-2 with atherosclerosis and calcification in patients with T2DM. METHODS: 124 subjects were enrolled in this study: 29 patients with T2DM and CAD; 26 patients with T2DM and without CAD; 36 patients with CAD and without T2DMand 34 without T2DM or CAD (control group). Severity of coronary lesions was assessed using coronary angiography and intravascular ultrasound (IVUS). Plasma BMP-2 levels were quantified using a commercially available ELISA kit. RESULTS: Compared to the control group, the mean plasma BMP-2 level was significantly higher in T2DM patients with or without CAD (20.1 ± 1.7 or 19.3 ± 1.5 pg/ml, vs 17.2 ± 3.3 pg/ml, P < 0.001). In a multivariable linear regression analysis, both T2DM and CAD were significantly and positively associated with BMP-2 (Estimate, 0.249; standard error (SE), 0.063; p <0.0001; Estimate, 0.400; SE, 0.06; p < 0.0001). Plasma BMP-2 was also strongly correlated with glycosylated hemoglobin A1c (HbA1c) (Spearman ρ = -0.31; p = 0.0005). SYNTAX score was also significantly associated with BMP-2 (Spearman ρ = 0.46; p = 0.0002). Using the results from IVUS, plasma BMP-2 levels were shown to positively correlate with plaque burden (Spearman ρ = 0.38, P = 0.002) and plaque calcification (Spearman ρ =0.44, P = 0.0003) and to negatively correlate with lumen volume (Spearman ρ =0.31, P = 0.01). CONCLUSIONS: Our study demonstrates that patients with T2DM had higher circulating levels of BMP-2 than normal controls. Plasma BMP-2 levels correlated positively with plaque burden and calcification in patients with T2DM.

Possible role of fibroblast growth factor 21 on atherosclerosis via amelioration of endoplasmic reticulum stress-mediated apoptosis in apoE(-/-) mice.

Fibroblast growth factor 21 (FGF-21) is an endocrine factor that can be secreted into circulation by the liver. FGF-21 takes part in metabolic actions and is thought to be a promising candidate for the treatment of diabetes. However, the role of FGF-21 in atherosclerosis is unknown. In this study, apoE(-/-) mice were fed an atherogenic diet for 4 weeks with and without subcutaneous injections of FGF-21. ApoE(-/-) mice fed an atherogenic diet showed hyperlipidemia, a large plaque area in aortas and increased vessel wall thickness. Plasma FGF-21 content and protein level of FGF receptor 1 (FGFR1) in aortas was greater in apoE(-/-) than C57BL/6J mice. Exogenous FGF-21 treatment significantly ameliorated dyslipidemia in apoE(-/-) mice. FGF-21-treated apoE(-/-) mice showed reduced number of aortic plaques and plaque area as well as reduced number of TUNEL-positive cells. Protein levels of the endoplasmic reticulum stress markers glucose-regulated protein 94, caspase-12 and C/EBP homologous protein were reduced by 34.5, 31.4 and 26.5 %, respectively, in apoE(-/-) mice. Endogenous expression of FGF-21 and its receptor FGFR1 were upregulated in apoE(-/-) mice, and exogenous administration of FGF-21 ameliorated the atherogenic-induced dyslipidemia and vascular atherosclerotic lesions. FGF-21 protecting against atherosclerosis might be in part by its inhibitory effects on endoplasmic reticulum stress-mediated apoptosis.

Inefficient antimicrobial functions of innate phagocytes render infant mice more susceptible to bacterial infection.

Neonates and infants, due to the immaturity in their adaptive immunity, are thought to depend largely on the innate immune system for protection against bacterial infection. However, the innate immunity-mediated antimicrobial response in neonates and infants is incompletely characterized. Here, we report that infant mice were more susceptible to microbial sepsis than adult mice, with significantly reduced bacterial clearance from the circulation and visceral organs. Infant PMNs exhibited less constitutive expression of the chemokine receptor CXCR2, and bacterial infection caused further reduction of PMN CXCR2 in infant mice compared with adult mice. This correlates with diminished in vitro chemotaxis of infant PMNs toward the chemoattractant CXCL2 and impaired in vivo recruitment of infant PMNs into the infectious site. Furthermore, consistent with the reduced antimicrobial response in vivo, infant macrophages displayed an impaired bactericidal activity with a defect in phagosome maturation after ingestion of either gram-positive or gram-negative bacteria. Thus, infant mice exhibit an increased vulnerability to microbial infection with delayed bacterial clearance, which is associated with the inefficiency in their innate phagocyte-associated antimicrobial functions characterized by defects in PMN recruitment and macrophage phagosome maturation during microbial sepsis.

Prior ischemic stroke is not associated with worse clinical outcomes in patients undergoing percutaneous coronary intervention.

PURPOSE: Cerebrovascular accidents (CVAs) frequently coexist with coronary artery disease (CAD) and adversely affect prognosis in patients with CAD; however, fewer studies have investigated the role of prior ischemic stroke on the outcomes of percutaneous coronary intervention (PCI). The aim of this study was to determine the safety and effectiveness of PCI in patients with a prior ischemic stroke. METHODS: A review of patients who underwent PCI between June 2003 and September 2005 (n=3893) at the Beijing Anzhen Hospital of Capital University of Medical Science, identified 295 PCI patients with a prior ischemic stroke (≥ 3 months) and 3598 patients without a prior stroke. To investigate whether prior history of an ischemic stroke was independently associated with increased risk of adverse PCI outcomes, prognostic parameters were analyzed using univariate analysis and Cox multivariate regression analysis. Propensity score analysis was then used to match the two subgroups of patients based on multiple factors known to impact cardiac outcome. RESULTS: Patients with a prior ischemic stroke had more frequent high-risk baseline characteristics (diabetes, hypertension, hyperlipidemia and prior myocardial infarction). No significant differences were found in the major adverse cardiac and cerebrovascular event (MACCEs) rates between the two groups (1.7% in the stroke group vs. 1.4% in the non-stroke group; p=0.06). Diabetes mellitus, triple vessel CAD, number of diseased vessels, chronic total occlusion and previous myocardial infarction were independent predictors of MACCE in patients with prior stroke undergoing PCI. CONCLUSIONS: This study demonstrates that, in daily clinical practice, PCI can be provided safely and with good results to patients with a prior ischemic stroke (≥ 3 months).

Nonculprit lesion progression in patients with ST elevation myocardial infarction after primary percutaneous coronary intervention.

The majority of cardiovascular events in patients with ST elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary interventions (PPCI) arise from the progression of nonculprit lesions (NCL) during the long-term follow-up period. However, the clinical and angiographic factors related to the progression of nonculprit lesions are unknown.The purpose of the study was to investigate the clinical and angiographic factors related to the progression of nonculprit lesions of patients with STEMI undergoing PPCI.A total of 492 patients with STEMI who underwent PPCI from January 2006 to December 2009 were enrolled. All patients underwent PPCI as a treatment for the culprit lesion. The clinical and angiographic follow-up was performed at 12 months. Primary endpoint: Clinically driven nonculprit lesion PCI. The levels of serum catecholamines [epinephrine (E), norepinephrine (NE)] and C-reactive protein (CRP) were assayed, and the clinical and angiographic features were also analyzed.The clinical and angiographic follow-up was performed in 492 patients, and 45 patients underwent clinically driven nonculprit lesions PCI (study group). A total of 447 patients were free of additional PCI (control group). There were significant differences in the level of catecholamines (E (621.48 ± 79.31) pg/mL versus (268.14 ± 73.26) pg/mL, P < 0.0001), NE (6212.43 ± 822.41) pg/mL versus (3218.34 ± 614.16) pg/mL, P < 0.0001), CRP (3.29 ± 1.31) mg/dL versus (2.51 ± 1.14) mg/dL, P < 0.0001, cTnI peak value (27.27 ± 4.02) ng/mL versus (16.12 ± 3.23) ng/mL, P < 0.0001), thrombotic lesion rate ((62.22% versus 23.04%), P < 0.0001), ≥ 2 vessel lesions rate (80.00% versus 46.09%), P < 0.0001), culprit lesion length ((33.2 ± 2.9 versus 28.1 ± 3.1), P = 0.013), and complex lesion rate ((57.78% versus 36.02%), P = 0.006) between the two groups. Correlation analysis between nonculprit lesion stenosis degree and serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, and complex lesion rate showed that there were significant correlations between serum E, serum NE, serum CRP, cTnI peak value, thrombotic lesion rate, ≥ 2 vessel lesions rate, culprit lesion length, complex lesion rate, and nonculprit lesion stenosis degree. The correlation coefficients were 0.95, 0.97, 0.83, 0.90, 0.81, 0.84, 0.95, and 0.96, respectively, and P < 0.0001, P < 0.0001, P = 0.01, P = 0.01, P = 0.01, P = 0.01, P < 0.0001, and P < 0.0001, respectively.Recurrent PCI was mainly due to nonculprit lesion progression in patients with STEMI after primary PCI. Complex nonculprit lesions may be prone to for additional PCI. Chronic inflammation and sustained stress may be involved in the progression of nonculprit lesions in patients with STEMI.

Aerobic degradation of bisphenol-A and its derivatives in river sediment.

This study investigated the aerobic degradation ofbisphenol-A (BPA) and the derivatives bisphenol-B (BPB), bisphenol-F (BPF), tetrabromobisphenol-A (TBBPA), and tetrachlorobisphenol-A (TCBPA) in river sediment. The degradation rates of BPA and BPF were enhanced by adding brij 30, brij 35, rhamnolipid, surfactin, or crude enzyme; a higher degradation rate was observed with crude enzyme than with the other additives. The degradation rates of BPA and its derivatives (BPAs) in the sediment were BPF > BPA > BPB > TCBPA > TBBPA. Different BPAs affected the changes in the microbial community in the sediment. Sediment fractions with larger particle sizes demonstrated higher degradation rates. Different sediment particle sizes affected the changes in the microbial communities. Pseudomonas sp. may be the dominant bacteria in the process of degradation of BPAs in river sediment.

Genomics-Microbiome Based Assessment of Bidirectional Causality Between Gut Microbiota and Psoriasis.

Background: Traditional observational studies have found a possible risk association of the gut microbiota for psoriasis. Meanwhile, psoriasis may also affect the changes in the gut microbiota. However, the available evidence does not demonstrate a reciprocal relationship between the gut microbiota and psoriasis. This limits our understanding on the role of the gut microbiota in the mechanisms of psoriasis. Methods: To address this question we used Mendelian randomization, a novel epidemiological approach, and acquired the largest current gut microbiota GWAS data from the MiBioGen consortium as well as psoriasis GWAS data from the FinnGen consortium, and performed two-sample bidirectional MR analyses using a multiple MR analysis approach. Finally, the robustness of the results was assessed by sensitivity analysis. Results: Our results indicate that five bacterial genera are causally related to psoriasis and psoriasis is causally related to four bacterial genera. Conclusion: These results suggest a bidirectional causal influence of psoriasis on the gut microbiota. Our results somewhat challenge the causal inferences of previous observational studies. We found that the specific bacterial genera with a risk effect on psoriasis were different from those found to characterize psoriasis in previous observational studies, and that these psoriasis-characterizing genera were inversely associated with psoriasis.

Increased susceptibility of ST2-deficient mice to polymicrobial sepsis is associated with an impaired bactericidal function.

ST2, a member of the Toll/IL-1R superfamily, negatively regulates both TLR2 and TLR4 signaling. In this study, we report that ST2-deficient mice were more susceptible to polymicrobial sepsis than their wild-type littermates, with increased production of proinflammatory cytokines. Bacterial clearance from the circulation and visceral organs following polymicrobial infection was markedly impaired in ST2-deficient mice. This was associated with substantially reduced uptake, phagocytosis, and intracellular killing of both Gram-positive and Gram-negative bacteria by ST2-deficient phagocytes. Consistent with a reduced antimicrobial response, phagocytes lacking ST2 displayed a defect in bactericidal activity in response to bacterial challenges with severely impaired phagosome maturation and NOX2 function. Thus, ST2-deficient mice exhibit an increased susceptibility to polymicrobial infection with impaired bacterial clearance, which is associated with defects in phagosome maturation and NOX2-derived production of reactive oxygen species characterized in ST2-deficient phagocytes.

[Effects of preoperative uses of aspirin and clopidogrel on patients undergoing coronary artery bypass graft surgery].

OBJECTIVE: To analyze the effects of preoperative uses of aspirin and clopidogrel on perioperative blood loss and blood transfusion requirements and complication in patients undergoing off-pump coronary artery bypass graft (CABG). METHODS: At our hospital from October 2011 to October 2012, a total of 480 patients underwent off-pump CABG performed by the same surgical team. Among them, 198 patients continued aspirin (discontinued clopidogrel at least 5 days) through operation (aspirin group, 1), 53 had aspirin and clopidogrel until 3 days before surgery (aspirin and clopidogrel group, 2) and 229 discontinued antiplatelet therapy 5 more days before surgery (control group, 3). RESULTS: No significant difference of basic clinical characteristics existed among three groups (P > 0.05). Group 2 was associated with a greater volume of chest tube drainage than other groups (827 ± 216 vs 416 ± 135 vs 265 ± 85 ml, P < 0.05). There was no significant difference between groups 1 and 3, even though chest tube drainage volume of group 1 was greater (827 ± 216vs 265 ± 85 ml, P > 0.05). There was no instance of stroke, myocardial infarction or post-operative mortality. CONCLUSION: Preoperative clopidogrel exposure within 5 days of surgery increases perioperative blood loss. And the pre-operative use of aspirin results in no difference in postoperative perioperative blood loss and cardiovascular outcomes.

A high triglyceride-glucose index associated with adverse cardiovascular events in patients with type 2 diabetes mellitus and chronic total occlusion after percutaneous coronary intervention.

Triglyceride-glucose index (TyG index) is a reliable surrogate marker of insulin resistance, associated with morbidity and prognosis of cardiovascular disease. However, its predictive value for cardiovascular events in patients with type 2 diabetes mellitus (T2DM) and chronic total occlusion (CTO) after percutaneous coronary intervention (PCI) has not been studied. Here, we retrospectively enrolled 681 patients with T2DM and CTO after PCI. Patients were divided into two groups based on a median TyG index of 9.02. The TyG index was calculated as ln [fasting triglyceride (mg/dL) × fasting glucose (mg/dL)/2]. The primary observational end point was the composite of overall death, nonfatal myocardial infarction, and unplanned revascularization. The Multivariate Cox hazards regression analysis showed that the TyG index was significantly correlated with the primary end point (hazard ratio = 1.699, 95% confidence interval 1.254-2.303, p = 0.001). The addition of TyG to a baseline risk model had an incremental effect on the predictive value for the primary end point (area under the curve: TyG index vs baseline model, 0.693 vs 0.663, comparison p = 0.040; integrated discrimination improvement = 0.049, p = 0.020). The TyG index might be a predictor of adverse cardiovascular events. Moreover, adding the TyG index into a baseline risk model had a cumulative effect on the predictive potential for the primary end point.

Hepatic inflammatory myofibroblastic tumor: A case report.

BACKGROUND: Hepatic inflammatory myofibroblastic tumor (HIMT) is a rare type of hepatic tumor. It is always misdiagnosed and mistreated because it is primarily found with no obvious specific manifestation, and its imaging findings are diverse. CASE SUMMARY: Here, we report a case of HIMT that was initially diagnosed as liver malignancy but was confirmed as HIMT by histopathology after hepatectomy. Mostly, HIMTs are infiltrated with plasma cells and stain positively for anaplastic lymphoma kinase on immunohistochemistry as well as for some other kinases. CONCLUSION: HIMT can be treated with single nonsteroidal anti-inflammatory drugs and without surgery when it is diagnosed accurately. Because the etiology of HIMT is unknown and the diagnosis is difficult, the pathogenesis and clinical process need to be further studied.