Reappraising the role of chronic inflammatory burden in heart failure.

BACKGROUND: Heart failure (HF) is a clinical syndrome associated with poor quality of life, substantial utilization of health care resources, and premature mortality. It is now considered to be the most urgent unmet medical need in the field of cardiovascular disease. Accumulated evidence suggested that comorbidity-driven inflammation has emerged as a critical component of HF pathogenesis. Although anti-inflammatory therapies have increased in popularity, very few effective treatments are still available. A comprehensive understanding of the interplay between chronic inflammation and its impact on HF will facilitate the identification of future therapeutic targets. METHODS: A two-sample Mendelian randomization study was conducted to assess the association between genetic liability for chronic inflammation and HF. By analyzing functional annotations and enrichment data, we were able to identify common pathophysiological mechanisms. RESULTS: The present study did not provide evidence for chronic inflammation as the cause of HF and the reliability of the results was enhanced by the other three Mendelian randomization analysis methods. Functional annotations of genes and pathway enrichment analyses have indicated that chronic inflammation and HF share a common pathophysiology. CONCLUSIONS: The associations between chronic inflammation and cardiovascular disease from observational studies may be explained by shared risk factors and comorbidities rather than direct effects.

Anatomical and Functional Discrepancy in Diabetic Patients With Intermediate Coronary Lesions　- An Intravascular Ultrasound and Quantitative Flow Ratio Study.

BACKGROUND: Data regarding the performance of computational fractional flow reserve in patients with diabetes mellitus (DM) remain scarce. This study sought to explore the impact of DM on quantitative flow ratio (QFR) and its association with intravascular ultrasound (IVUS)-derived anatomical references.Methods and Results: IVUS and QFR were retrospectively analyzed in 237 non-diabetic and 93 diabetic patients with 250 and 102 intermediate lesions, respectively. Diabetics were further categorized based on adequate (HbA1c <7.0%: 47 patients with 53 lesions) or poor (HbA1c ≥7.0%: 46 patients with 49 lesions) glycemic control. Lesions with QFR ≤0.8 or minimum lumen area (MLA) ≤4.0 mm2and plaque burden (PB, %) ≥70 were considered functionally or anatomically significant, respectively. PB increased, and MLA decreased stepwise across non-diabetics, diabetics with adequate glycemic control and those with poor glycemic control. In contrast, QFR was similar among the 3 groups. PB correlated significantly with the QFR for lesions in non-diabetics, but not for lesions in diabetics. DM was independently correlated with the functionally non-significant lesions (QFR >0.8) with high-risk IVUS features (MLA ≤4.0 mm2and PB ≥70; OR 2.053, 95% CI: 1.137-3.707, P=0.017). When considering the effect of glycemic control, HbA1c was an independent predictor of anatomical-functional discordance (OR 1.347, 95% CI: 1.089-1.667, P=0.006). CONCLUSIONS: Anatomical-functional discordance of intermediate coronary lesions assessed by IVUS and QFR is exacerbated in patients with diabetes, especially when glycemia is poorly controlled.

Hypersensitive C-reactive protein as a potential indicator for predicting left ventricular hypertrophy in elderly community-dwelling patients with hypertension.

BACKGROUND: The aim of this study was to investigate the relationship between Hypersensitive C-reactive protein (hs-CRP) and left ventricular hypertrophy (LVH) in elderly community-dwelling patients with hypertension. METHODS: A cross-sectional study was conducted, involving the recruitment of 365 elderly hypertensive residents ≥ 65 years of age from five communities. The participants were divided into two groups: an LVH group (n = 134) and a non-LVH group (n = 231), based on the left ventricular mass index (LVMI) determined by echocardiography. Spearman correlation analysis was used to assess the relationship between hs-CRP and LVH. Univariate and Multivariate analysis was performed to detect variables associated with LVH. The diagnostic value of hs-CRP for LVH was expressed as the area under the receiver operating characteristic (ROC) curve. RESULTS: The incidence of LVH in elderly hypertension patients in the community was 36.7%. The hs-CRP levels were significantly higher in subjects with LVH compared to those without LVH (1.9 [0.8, 2.9] vs. 0.7 [0.4, 1.4], P = 0.002). Spearman correlation analysis demonstrated a positive correlation between hs-CRP and LVMI (r = 0.246, P < 0.001), as well as with IVST (r = 0.225, P < 0.001) and LVPWT (r = 0.172, P = 0.001). Among elderly hypertensive residents in the community, the cut-off value of hs-CRP for diagnosing LVH was 1.25 mg/L (sensitivity: 57.5%; specificity: 78.4%), and the area under the ROC curve for hs-CRP to predict LVH was 0.710 (95%CI: 0.654-0.766; P < 0.001). In the final model, hs-CRP ≥ 1.25 mg/L (OR = 3.569; 95%CI, 2.153-5.916; P<0.001) emerged as an independent risk factor for LVH. This association remained significant even after adjusting for various confounding factors (adjusted OR = 3.964; 95%CI, 2.323-6.765; P < 0.001). CONCLUSIONS: This community-based cohort of elderly hypertensive individuals demonstrates a strong association between hs-CRP levels and the presence of LVH. The hs-CRP ≥ 1.25 mg/L may serve as an independent predictor for LVH in hypertensive subjects and exhibit good diagnostic efficacy for LVH.

Prevalence and risk factors of osteosarcopenia: a systematic review and meta-analysis.

BACKGROUND: Osteosarcopenia is a syndrome with a concomitant presence of both sarcopenia and osteopenia/osteoporosis. It increases the risk of frailty, falls, fractures, hospitalization, and death. Not only does it burden the lives of older adults, but it also increases the economic burden on health systems around the world. This study aimed to review the prevalence and risk factors of osteosarcopenia to generate important references for clinical work in this area. METHODS: Pubmed, Embase, Cochrane Library, Web of Science, CNKI, Wanfang, CBM, and VIP databases were searched from inception until April 24th, 2022. The quality of studies included in the review was evaluated using the NOS and AHRQ Scale. Pooled effects of the prevalence and associated factors were calculated using random or fixed effects models. Egger's test, Begg's test, and funnel plots were used to test the publication bias. Sensitivity analysis and subgroup analysis were conducted to identify the sources of heterogeneity. Statistical analysis was performed using Stata 14.0 and Review Manager 5.4. RESULTS: A total of 31 studies involving 15,062 patients were included in this meta-analysis. The prevalence of osteosarcopenia ranged from 1.5 to 65.7%, with an overall prevalence of 21% (95% CI: 0.16-0.26). The risk factors for osteosarcopenia were female (OR 5.10, 95% CI: 2.37-10.98), older age (OR 1.12, 95% CI: 1.03-1.21), and fracture (OR 2.92, 95% CI: 1.62-5.25). CONCLUSION: The prevalence of osteosarcopenia was high. Females, advanced age, and history of fracture were independently associated with osteosarcopenia. It is necessary to adopt integrated multidisciplinary management.

Modification of wine phenolic profiles by gibberellic acid application in 'Cabernet Gernischt' grapevines before anthesis.

BACKGROUND: Vitis vinifera L. 'Cabernet Gernischt' grapes from the Yantai wine region of China usually form dense clusters and contain low phenolic content. We applied five concentrations (ranged from 5 to 25 mg L-1 ) of gibberellic acid (GA3 ) to 'Cabernet Gernischt' before anthesis to decrease cluster compactness in two consecutive vintages. Yield indices, grape maturity, and wine phenolic compounds were determined. RESULTS: GA3 application significantly reduced cluster compactness, bunch weight, and yield per vine, but it did not significantly improve fruit ripening. The levels of total phenolics, total tannins, and total anthocyanins in wine were enhanced by GA3 application, with 10 and 15 mg L-1 GA3 treatments consistently producing a significant increase in the concentrations of mavidin, cyanidin, and their derivatives. Specifically, trans-resveratrol was consistently significantly increased by 15 mg L-1 GA3 application. Principal component analysis of phenolic compounds demonstrated the differences among wines produced from GA3 treatment groups and the control. CONCLUSION: Overall, wine phenolic profiles could be significantly modified by application of low concentrations of GA3 before anthesis. Application of high levels of GA3 is not recommended due to significant yield decrease. © 2022 Society of Chemical Industry.

Influence of Oxygen Management during the Post-Fermentation Stage on Acetaldehyde, Color, and Phenolics of Vitis vinifera L. Cv. Cabernet Sauvignon Wine.

Oxygen exposure is unavoidable and the impact of its management during the post-fermentation stage (PFS) on dry red wine is poorly investigated. This study was dedicated to the variation of acetaldehyde, color and phenolics of Cabernet Sauvignon dry red wine during five discontinuous oxidation cycles of four levels of controlled oxygen supply, which were carried out to simulate probable oxidation during the PFS. Free SO2 disappeared after the first, second and third oxidation cycles in wines with high, medium and low levels of oxygen exposure severally, but subsequent oxygen exposure below or equal to 2 mg O2/L per cycle had little effect while 3-3.9 mg O2/L per cycle dramatically facilitated acetaldehyde accumulation, which was accompanied by an enormous variation in color and pigments, especially when total oxygen consumption was above 10 mg/L. The utilization of clustered heatmap and partial least square regression demonstrated the feasibility of characterization of wine oxidation degree using the chemical parameters measured by UV-spectrophotometry. Oxygen exposure during the PFS should be emphatically controlled, and chemical indexes determined by the UV-spectrophotometric method can be used for a scientific and effective description of wine oxidation degree.

Impact of Arterial Remodeling of Intermediate Coronary Lesions on Long-Term Clinical Outcomes in Patients with Stable Coronary Artery Disease: An Intravascular Ultrasound Study.

BACKGROUND: Treatment of coronary intermediate lesions remains a controversy, and the role of arterial remodeling patterns determined by intravascular ultrasound in intermediate lesion is still not well known. The aim of this study was to investigate the impact of arterial remodeling of intermediate coronary lesions on long-term clinical outcomes. METHODS: Arterial remodeling patterns were assessed in 212 deferred intermediate lesions from 162 patients after IVUS examination. Negative, intermediate, and positive remodeling was defined as a remodeling index of <0.88, 0.88∼1.0, and >1.0, respectively. The primary endpoint was the composite vessel-oriented clinical events, defined as the composition of target vessel-related cardiac death, target vessel-related myocardial infarction, and target vessel revascularization. Quantitative flow ratio was assessed for evaluating the functional significance of intermediate lesions. RESULTS: 72 intermediate remodeling lesions were present in 66 patients, whereas 77 negative remodeling lesions were present in 71 patients, and 63 positive remodeling lesions were present in 55 patients. Negative remodeling lesions had the smallest minimum lumen area (4.16 ± 1.03 mm2 vs. 5.05 ± 1.39 mm2 vs. 4.85 ± 1.76 mm2; P < 0.01), smallest plaque burden (63.45 ± 6.13% vs. 66.12 ± 6.82% vs. 71.17 ± 6.45%; P < 0.01), and highest area stenosis rate (59.32% ± 10.15% vs. 54.61% ± 9.09% vs. 51.67% ± 12.96%; P < 0.01). No significant difference was found in terms of quantitative flow ratio among three groups. At 5 years follow-up, negative remodeling lesions had a higher rate of composite vessel-oriented clinical event (14.3%), compared to intermediate (1.4%, P=0.004) or positive remodeling lesions (4.8%, P=0.06). After adjusting for multiple covariates, negative remodeling remained an independent determinant for vessel-oriented clinical event (HR: 4.849, 95% CI 1.542-15.251, P=0.007). CONCLUSION: IVUS-derived negative remodeling is associated with adverse long-term clinical outcome in stable patients with intermediate coronary artery stenosis.

Effects of the COVID-19 pandemic on reperfusion therapy for acute ischemic stroke patients in Huizhou City, China.

BACKGROUND AND PURPOSE: The COVID-19 pandemic has impacted the reperfusion therapy for acute ischemic stroke (AIS) patients. Huizhou City utilized its experience with the SARS and MERS breakouts to establish a reperfusion treatment program for AIS patients. METHOD: This is a retrospective study on 8 certified stroke hospitals in Huizhou City from January 2020 to May 2020. We analyzed the number of AIS patients with reperfusion therapy, stroke type (anterior/posterior circulation stroke), modes of transport to hospital, NIHSS score, onset to door time (ODT), door to needle time (DNT), and door to puncture time (DPT). The analysis was compared with baseline data from the same time period in 2019. RESULT: In 2020, the number of AIS patients receiving reperfusion therapy decreased (315 vs. 377), NIHSS score increased [8 (4, 15) vs. 7 [ (1, 2)], P = 0.024], ODT increased [126 (67.5, 210.0) vs. 120.0 (64.0, 179.0), P = 0.032], and DNT decreased [40 (32.5, 55) vs. 48 (36, 59), P = 0.003]. DPT did not change. Seventy percent of AIS patients indicated self-visit as their main mode of transport to the hospital. In both periods, mild stroke patients were more likely to self-visit than utilize emergency systems [2019: 152 (57.6%) vs. 20 (45.6%), P = 0.034; 2020: 123 (56.9%) vs. 5 (14.7%), P < 0.001]. The NIHSS score for self-visiting patients was lower for patients who utilized the ambulance system in both years [self-visit: 6.00 (3.00, 12.00), ambulance: 14.00 (9.00, 19.00), P < 0.001]. The volume of reperfusion patients was lower in 2020; however, the decrease was only significant (P = 0.028) in February 2020. CONCLUSION: During the COVID-19 pandemic in 2020, the number of AIS patients receiving reperfusion therapy significantly decreased when compared to the same period in 2019. The patients' condition increased severity, ODT increased, and the DNT decreased. DPT was not significant for self-visiting and ambulance patients. Moderate to severe stroke patients were more likely to utilize ambulance services.

Partial pathogenicity chromosomes in Fusarium oxysporum are sufficient to cause disease and can be horizontally transferred.

In Fusarium oxysporum f.sp. lycopersici, all effector genes reported so far - also called SIX genes - are located on a single accessory chromosome which is required for pathogenicity and can also be horizontally transferred to another strain. To narrow down the minimal region required for virulence, we selected partial pathogenicity chromosome deletion strains by fluorescence-assisted cell sorting of a strain in which the two arms of the pathogenicity chromosome were labelled with GFP and RFP respectively. By testing the virulence of these deletion mutants, we show that the complete long arm and part of the short arm of the pathogenicity chromosome are not required for virulence. In addition, we demonstrate that smaller versions of the pathogenicity chromosome can also be transferred to a non-pathogenic strain and they are sufficient to turn the non-pathogen into a pathogen. Surprisingly, originally non-pathogenic strains that had received a smaller version of the pathogenicity chromosome were much more aggressive than recipients with a complete pathogenicity chromosome. Whole genome sequencing analysis revealed that partial deletions of the pathogenicity chromosome occurred mainly close to repeats, and that spontaneous duplication of sequences in accessory regions is frequent both in chromosome deletion strains and in horizontal transfer strains.

Host-specificity factors in plant pathogenic fungi.

Fortunately, no fungus can cause disease on all plant species, and although some plant-pathogenic fungi have quite a broad host range, most are highly limited in the range of plant species or even cultivars that they cause disease in. The mechanisms of host specificity have been extensively studied in many plant-pathogenic fungi, especially in fungal pathogens causing disease on economically important crops. Specifically, genes involved in host specificity have been identified during the last few decades. In this overview, we describe and discuss these host-specificity genes. These genes encode avirulence (Avr) proteins, proteinaceous host-specific toxins or secondary metabolites. We discuss the genomic context of these genes, their expression, polymorphism, horizontal transfer and involvement in pathogenesis.

Platelet function testing guided antiplatelet therapy reduces cardiovascular events in Chinese patients with ST-segment elevation myocardial infarction undergoing percutaneous coronary intervention: The PATROL study.

BACKGROUND: Dual antiplatelet therapy (DAPT) with aspirin and a P2Y12 receptor inhibitor has become the standard of care to reduce thrombotic events in patients with acute coronary syndrome or after percutaneous coronary intervention (PCI). The role of routine platelet function testing (PFT) in patients treated with DAPT after PCI remains controversial and evidence of PFT-guided antiplatelet therapy for patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary PCI is limited. METHODS: We analyzed 1,353 consecutive STEMI patients undergoing primary PCI. PFT was performed 72 hr postprocedure using a vasodilator-stimulated phosphoprotein assay. The primary endpoint of major adverse cardio-cerebral events (MACCEs) was defined as a composite of all-cause death, cardiac death, nonfatal myocardial infarction, target vessel revascularization, and ischemic stroke. Patients with high platelet reactivity (HPR) were randomized to receive an intensified antiplatelet strategy by switching from clopidogrel to ticagrelor (HPR switch group) or to continue on clopidogrel (HPR nonswitch group). One-year clinical outcomes were compared among the groups. RESULTS: The baseline clinical characteristics were comparable across all groups (all p > .05). At the 1-year clinical follow-up, the primary endpoint of MACCE was significantly higher in the HPR nonswitch group than in the non-HPR and HPR switch groups (19.49% vs. 10.20% or 8.57%, p < .05), which was mainly caused by higher mortality (14.87% vs. 4.51% or 5.71%, p < .05). Major bleeding events were comparable across the groups. CONCLUSIONS: In STEMI patients with HPR, identified by vasodilator stimulated phosphoprotein (VASP)-determined PFT, switching clopidogrel to ticagrelor could significantly improve 1-year clinical outcomes without increasing the risk of bleeding.

New anti-neuroinflammatory steroids against LPS induced NO production in BV2 microglia cells by microbial transformation of isorhodeasapogenin.

Microbial transformation of isorhodeasapogenin (1), the major steroidal sapogenin of Tupistra chinensis, was performed with the fungus Syncephalastrum racemosum (AS 3.264). As a result, nine new biotransformation metabolites (2-10) were isolated and their structures were elucidated by spectroscopic analysis. Hydroxylation, oxidation and glycosylation reactions were observed on the B, C, D and F rings of steroidal skeleton. Substrate (1) and its biotransformed metabolites 2-6, 8-10 were evaluated for their anti-neuroinflammatory effect on the NO accumulation induced by LPS in BV-2 cells. All the tested metabolites were found to have more potential anti-neuroinflammatory activity than the substrate. Especially, metabolites 2, 5 and 6 exhibited significant inhibition on NO production after hydroxylation at C-12 or C-15. Moreover, metabolite 2 dose-dependently reduced the LPS-induced protein expression of iNOS and COX-2.

Differential cardiac hypertrophy and signaling pathways in pressure versus volume overload.

Mechanical overload can be classified into pressure overload and volume overload, causing concentric and eccentric cardiac hypertrophy, respectively. Here, we aimed to differentiate the load-mediated signaling pathways involved in pressure versus volume overload cardiac hypertrophy. Pressure or volume overload was imposed on C57BL/6J mice by transverse aortic constriction (TAC) or aortic regurgitation (AR), respectively. After surgery (2 wk), left ventricular structure and function were evaluated by echocardiographic, hemodynamic, and histological analyses. Signaling pathways related to hypertrophy, fibrosis, angiogenesis, and apoptosis were studied by histological analysis, RT-PCR, and Western blot analysis. Although mean wall stress was similar in both TAC and AR mice, systolic wall stress was significantly increased in TAC and diastolic wall stress was mainly elevated in AR. TAC or AR induced concentric or eccentric compensated hypertrophy, respectively. TAC was associated with more significant fibrosis and apoptosis, whereas AR was associated with more significant angiogenesis. MAPK kinase family, ß-arrestin-2, Akt, and Ca2+-related signaling pathways were markedly activated in TAC but mildly upregulated or unchanged in AR. Pressure overload and volume overload induce different phenotypic and molecular adaptations in cardiac hypertrophy. Most load-related signaling pathways assessed in this study predominate in pressure but not volume overload. The stimulus-specific heterogeneity in the signaling pathways requires distinct manipulations for further mechanistic and pharmacological studies. NEW & NOTEWORTHY Using the transverse aortic constriction mouse model and the newly developed aortic regurgitation mouse model, we delineated the prominent differences between concentric and eccentric cardiac hypertrophy on morphological, functional, and molecular levels. Our findings are important for the precise diagnosis and treatment of these two types of cardiac hypertrophy. Listen to this article's corresponding podcast at http://ajpheart.podbean.com/e/chinese-english-language-podcast-on-differential-cardiac-remodeling-in-tac-vs-ar/ .

Loss of P53 regresses cardiac remodeling induced by pressure overload partially through inhibiting HIF1α signaling in mice.

The tumor suppressor p53 is recognized as the guardian of the genome in cell cycle and cell death. P53 expression increases as cardiac hypertrophy worsens to heart failure, suggesting that p53 may play important role in cardiac remodeling. In the present study, deletion of p53 in the mice heart would ameliorate cardiac hypertrophy induced by pressure overload. The role of p53 on heart was investigated using in vivo models. Cardiac hypertrophy in mice was induced by transverse aortic banding surgery. The extent of cardiac hypertrophy was examined by echocardiography, as well as pathological and molecular analyses of heart tissue. Global knockout of p53 in the mice reduced the hypertrophic response and markedly reduced cardiac apoptosis, and fibrosis. Ejection fraction of heart was also improved in hearts without p53 in response to pressure overload. Protein determination further suggested loss of p53 expression markedly increased Hypoxia-inducible factor 1-alpha (HIF1α) and vascular endothelial growth factor (VEGF) expression. The study indicated p53 deteriorated cardiac functions and cardiac hypertrophy, apoptosis, and fibrosis by partially inhibition of HIF1α and VEGF.

Downregulation of MiR-199b-5p Inducing Differentiation of Bone-Marrow Mesenchymal Stem Cells (BMSCs) Toward Cardiomyocyte-Like Cells via HSF1/HSP70 Pathway.

BACKGROUND Bone-marrow mesenchymal stem cells (BMSCs) are pluripotent stem cells with potent self-renewal and differentiation ability that are widely used in transplantation of cell therapy. But the mechanism on microRNA (miRNA) regulating stem cell differentiation is complicated and unclear. The aim of this study was to investigate whether miR-199b-5p is involved in differentiation of cardiomyocyte-like cells and identify potential signal pathways in BMSCs. MATERIAL AND METHODS Mouse BMSCs were treated with 5-azacytidine and transfected by miR-199b-5p mimic and inhibitor, respectively. qRT-PCR was used to detect the expression of miR-199b-5p in BMSCs, 5-azacytidine treated BMSCs, and neonatal murine cardiomyocytes. The expression of cardiac specific genes and the HSF1/HSP70 signal pathway were examined by qRT-PCR or western blotting. The proliferation and migration of BMSCs were evaluated by CCK-8 assay and wound-healing assay. RESULTS The expression of miR-199b-5p decreased gradually in the process of differentiation of BMSCs toward cardiomyocyte-like cells. The expression of cardiac specific genes and HSF1/HSP70 were increased in the miR-199b-5p inhibitor group; however, the miR-199b-5p mimic group presented an opposite result. Both the miR-199b-5p inhibitor group and the miR-199b-5p mimic group had no influence on BMSCs proliferation and migration. Using lentivirus vectors bearing HSF1 shRNA to silence HSF1 and HSP70, the anticipated elevated expression effect of cardiac specific genes induced by miR-199b-5p inhibitor was suppressed. CONCLUSIONS Downregulation of miR-199b-5p induced differentiation of BMSCs toward cardiomyocyte-like cells partly via the HSF1/HSP70 signaling pathway, and had no influence on BMSCs proliferation and migration.

[Association of drug resistance of Mycoplasma pneumoniae with DNA load and genotypes in children with Mycoplasma pneumoniae pneumonia].

OBJECTIVE: To investigate the association of drug resistance of Mycoplasma pneumoniae (MP) with DNA load and genotypes in children with MP pneumonia. METHODS: A total of 230 children who were hospitalized and diagnosed with MP pneumonia between January 2012 and December 2016 were enrolled. Throat swabs were collected from the 230 children, and a rapid drug sensitivity assay was used to determine the sensitivity of clinical isolates of MP to nine commonly used antibacterial agents. Quantitative real-time PCR was used to measure MP-DNA load in throat swabs. PCR sequencing was used to determine the genotype of 2063 locus of the MP 23S rRNA V domain. RESULTS: Of the 230 children, 86 (37.4%) had genotype A in 2063 locus, 134 (58.3%) had genotype G, 8 (3.5%) had genotype C, and 2 (0.9%) had genotype T. Mutant strains (genotype G+C+T) had a significantly higher MP-DNA load than wild-type strains (genotype A) (P<0.05). The strains resistant to erythromycin, azithromycin, clarithromycin, and clindamycin had a significantly higher MP-DNA load than non-resistant strains (P<0.05). MP had a high drug resistance rate to macrolide antibiotics. More than 60% of the cases with resistance to macrolides were found to have A2063G mutations. MP was rarely resistant to quinolones (less than 2%). CONCLUSIONS: Mutations in 2063 locus of the MP 23S rRNA V domain may result in the resistance of MP to macrolides and the change in DNA load and can be used as a basis for selecting drugs for MP.

[Application of Mycoplasma pneumoniae antibody and load index in the diagnosis of Mycoplasma pneumoniae pneumonia in children].

OBJECTIVE: To study the role of Mycoplasma pneumoniae (MP) load and antibody measurements in the diagnosis of MP pneumonia. METHODS: A total of 115 children with MP pneumonia and 400 healthy children were enrolled. The MP load and total antibody level were measured at different stages, and the MP load index (MPLI) was calculated. RESULTS: The cut-off value of MPLI for MP infection was 6.12. MPLI and total antibody titer increased during the course of the disease, while MP-DNA decreased rapidly. Within the same time of blood collection, the group with a higher MP load had a significantly higher total antibody titer than the group with a lower MP load (P<0.05). Within 2 weeks of the course of the disease, the negative antibody group had a significantly higher MPLI than the positive antibody group (P<0.05). CONCLUSIONS: MPLI provides a standardized quantitative value of MP-DNA and plays an important role in the early diagnosis of MP infection.

[Association between CHI3L1 SNPs and susceptibility to childhood asthma].

OBJECTIVE: To investigate the association between CHI3L1 single nucleotide polymorphisms (SNPs) and the susceptibility to childhood asthma. METHODS: A total of 316 children diagnosed with asthma between January 2011 and October 2013 and 297 healthy children were selected as asthma group and control group respectively. Peripheral blood samples were collected from all subjects. Chemiluminescence and flow cytometry were applied to measure total IgE level and the percentage of eosinophils. ELISA was used to measure YKL-40 level. Genomic DNA was extracted from peripheral blood hemocytes, and the genotype and allele frequencies at CHI3L1 SNPs rs4950928, rs10399805, and rs883125 were determined by MALDI-TOP mass spectrometry. RESULTS: The total IgE and YKL-40 levels were significantly higher in the asthma group than in the control group (P<0.05), while the percentage of eosinophils showed no significant difference between the two groups (P>0.05). The frequency of GG genotype at rs883125 in the asthma group was significantly higher than that in the control group (P<0.05). For rs4950928, the asthma group had a significantly lower frequency of CC genotype (P<0.05) but a significantly higher frequency of CG genotype (P<0.05) compared with the control group. In the asthma group, the patients with GG and CG genotypes at rs4950928 had significantly increased total IgE and YKL-40 levels compared with those with CC genotype at this locus (P<0.05). CONCLUSIONS: YKL-40 is a potential molecular biomarker for the primary diagnosis of childhood asthma. CHI3L1 SNPs rs4950928 and rs883125 may be associated with childhood asthma. G allele at rs4950928 may increase the risk of childhood asthma.

Studies on the preparative isolation and stability of seven main anthocyanins from Yan 73 grape.

BACKGROUND: [corrected] Seven anthocyanin monomers of Yan 73 grape were separated using preparative HPLC and identified by UPLC-ESI-MS/MS. The stabilities of the seven isolated anthocyanins to light, temperature and pH were also investigated. RESULTS: Seven anthocyanin monomers were successfully isolated with an Xbridge Prep C18 column on a preparative scale. The pigments delphinidin-3-O-glucoside, malvidin-3-O-acetylglucoside and malvidin-3-O-coumarylglucoside were yielded in a one-step separation by preparative HPLC, with purities up to 99.9%, 91.7% and 95.5%, respectively. The pigments cyanidin-3-O-glucoside, petunidin-3-O-glucoside, peonidin-3-O-glucoside, and malvidin-3-O-glucoside were further purified with another elution method and their purities were all improved up to 99.9%. Monomeric anthocyanin degradation fitted a first-order reaction model. The seven isolated anthocyanins were significantly more stable in the dark than under light. High temperature was also unfavourable for the stability of anthocyanins. The anthocyanins were more stable at lower pH than at higher pH. In addition, among these anthocyanins, delphinidin-3-O-glucoside, malvidin-3-O-acetylglucoside and malvidin-3-O-coumarylglucoside were more susceptible to light, heat, and pH than the others. CONCLUSION: A simple and clean isolation method of seven anthocyanin monomers from Yan 73 grape was established. The stabilities of the seven anthocyanin monomers to light, temperature and pH were different, but the trends in changes were similar.

The association between O2-pulse slope ratio and functional severity of coronary stenosis: A combined cardiopulmonary exercise testing and quantitative flow ratio study.

Background: The role of cardiopulmonary exercise testing (CPET) parameters in evaluating the functional severity of coronary disease remains unclear. The aim of this study was to quantify the O2-pulse morphology and investigate its relevance in predicting the functional severity of coronary stenosis, using Murray law-based quantitative flow ratio (µQFR) as the reference. Methods: CPET and µQFR were analyzed in 138 patients with stable coronary artery disease (CAD). The O2-pulse morphology was quantified through calculating the O2-pulse slope ratio. The presence of O2-pulse plateau was defined according to the best cutoff value of O2-pulse slope ratio for predicting µQFR ≤ 0.8. Results: The optimal cutoff value of O2-pulse slope ratio for predicting µQFR ≤ 0.8 was 0.4, with area under the curve (AUC) of 0.632 (95 % CI: 0.505-0.759, p = 0.032). The total discordance rate between O2-pulse slope ratio and µQFR was 27.5 %, with 13 patients (9.4 %) being classified as mismatch (O2-pulse slope ratio > 0.4 and µQFR ≤ 0.8) and 25 patients being classified as reverse-mismatch (O2-pulse slope ratio ≤ 0.4 and µQFR > 0.8). Angiography-derived microvascular resistance was independently associated with mismatch (OR 0.07; 95 % CI: 0.01-0.38, p = 0.002) and reverse-mismatch (OR 9.76; 95 % CI: 1.47-64.82, p = 0.018). Conclusion: Our findings demonstrate the potential of the CPET-derived O2-pulse slope ratio for assessing myocardial ischemia in stable CAD patients.