Community-acquired bacterial co-infection predicts severity and mortality in influenza-associated pneumonia admitted patients.

BACKGROUND: Influenza is frequently complicated by bacterial co-infection, causing additional hospitalization and mortality. We determined the incidence, risk factors and outcomes of patients with influenza-associated community-acquired bacterial co-infection. METHOD: This was a retrospective, observational study. Influenza was diagnosed using the polymerase chain reaction. Co-infection had to be confirmed using standard bacteriological tests. The primary endpoint was presence of community-acquired co-infection, and the secondary endpoint was in-hospital mortality. RESULTS: During the 8 influenza seasons from 2010 to 2018, of the 209 influenza-associated pneumonia admitted patients, 41 (19.6%) were identified with community-acquired bacterial co-infections and Staphylococcus aureus was the predominant strain. Compared with patients without co-infection, patients with co-infection had similar demographic characteristics and co-morbidities, obtained a higher APACHE II score and a higher SOFA score, and had higher ratio of sepsis shock, invasive mechanical ventilation, and ICU requirement. In-hospital mortality independently associated with bacterial co-infection (adjusted hazard ratio (aHR) 2.619; 95%CI 1.252-5.480; p = 0.011); in subgroup S. aureus (aHR 6.267; 95%CI 2.679-14.662; p < 0.001) and other pathogens (aHR 2.964; 95%CI 1.160-7.577; p = 0.023); and in subgroup positive findings in bloodstream (aHR 7.420; 95%CI 2.712-20.302; p < 0.001) and positive findings in other site (aHR 3.427; 95%CI 1.514-7.757; p = 0.003). CONCLUSION: Community-acquired bacterial co-infection was frequent in influenza-associated pneumonia, without risk factor identified yet. Bacterial co-infection was likely to predict severity, and was an independent risk factor for in-hospital mortality. Co-infection of Staphylococcus aureus with influenza was identified as a lethal synergism, and should be targeted when developing clinical antibiotic strategies.

Recognition of Latent Fingerprints and Ink-Free Printing Derived from Interfacial Segregation of Carbon Dots.

Carbon dots (CDs) have attracted increasing interest in recent years owing to their desirable properties. Despite the availability of diverse elaborate CDs, the function and application of CDs are far to be fully exploited. Here, biomass-derived carbon dots dispersed in a polymer matrix are found to behave as ink-free patterned substrates, which are demonstrated to be useful for nondestructive collection and recognition of latent fingerprints (LFPs), as well as printing. The coating of CD/poly(vinyl alcohol) solution on a LFP yields a flexible transparent film; a stable fluorescent fingerprint with clear ridge details enabling personal identification is formed on this film. Encouragingly, this method can be applied to nondestructively lift and recognize long-timely exposed LFPs from various surfaces. The mechanism for LFP collection and visualization is proposed, which should be ascribed to the interfacial segregation of CDs in the polymer matrix during the film forming process. This mechanism is further validated by and utilized for application of CD/polymer composites in relief printing, intaglio printing, and micro-trace transferring.

Direct Synthesis of Multicolor Fluorescent Hollow Carbon Spheres Encapsulating Enriched Carbon Dots.

Multicolor fluorescent hollow carbon spheres (HCSs) are fabricated by an easy one-step route of in situ pyrolysis process with the use of natural scales and collagen powders as the precursor. The gas blow forming mechanism and photoluminescence (PL) emission mechanism of HCSs have been thoroughly discussed and proved that HCSs represent the first examples of three-dimensional multicolor fluorescent nanomaterials based on carbon dots (CDs). The HCSs encapsulate enriched carbon dots with high quantum yields (QYs) of 38%, and thus are applied in inkjet printing and sensitized solar cells. This strategy offers a promising avenue for preparing multicolor fluorescent hollow carbon materials on an industrial scale.

Alpha-lipoic acid ameliorates oxidative stress by increasing aldehyde dehydrogenase-2 activity in patients with acute coronary syndrome.

Aldehyde dehydrogenase-2 (ALDH2) is the main enzyme responsible for acetaldehyde oxidation in ethanol metabolism and also provides protection against oxidative stress. Alpha-lipoic acid (α-LA), a natural dithiol compound with antioxidant properties, has been reported to increase ALDH2 activity in cultured cells. We analyzed the therapeutic efficacy of α-LA in 63 patients with confirmed acute coronary syndrome (ACS). These patients (52 men and 11 women, with age range 49-72 years) were randomized into two groups: untreated group (n = 30) and α-LA group (n = 33). Patients in the α-LA group were given an intravenous injection of 600 mg α-LA every day for 5 days while the patients in the untreated group were given saline. An isoprostane, 8-iso-prostaglandin F2α (8-iso-PGF2α), one product of arachidonic acid metabolism, was measured as a marker for oxidative stress. The serum levels of 8-iso-PGF2α and ALDH2 activity were determined at admission to the hospital (time 0), and at 24 hours and 1 week after treatment. At 24 hours and 1 week after treatment, ALDH2 activity was significantly higher in the α-LA group than in the untreated group (P < 0.05), whereas the levels of 8-iso-PGF2α were significantly lower in the α-LA group than in the untreated group (all P < 0.05). Importantly, the decrease of 8-iso-PGF2α levels correlated with the increased ALDH2 activity at both 24 hours (r = 0.6234, P < 0.001) and 1 week after treatment (r = -0.3941, P = 0.0014). α-LA may ameliorate oxidative stress through up-regulating ALDH2 activity in patients with ACS.

The polymorphism in aldehyde dehydrogenase-2 gene is associated with elevated plasma levels of high-sensitivity C-reactive protein in the early phase of myocardial infarction.

Aldehyde dehydrogenase-2 (ALDH2) is a key enzyme of alcohol metabolism, catalyzing the conversion of aldehyde to acetic acid. The G-to-A polymorphism in exon 12 of the ALDH2 gene, which causes Glu-to-Lys substitution at codon 504, has been shown to be an independent risk factor for acute myocardial infarction (AMI). We investigated the possible role of the G-to-A polymorphism in the severity of the myocardial damage in the early phase of AMI by measuring plasma levels of inflammatory markers, including high-sensitivity C-reactive protein (hs-CRP). A total of 226 Han Chinese patients with AMI were divided into two groups: subjects without A allele (GG, n = 144) and subjects with A allele (GA and AA, n = 82), and the blood samples were collected within 12 hours after the onset of AMI. The results displayed that high-density lipoprotein cholesterol (HDL-C) was higher in GG group than that in GA and AA group (p < 0.05). The body mass index (BMI) and the concentration of hs-CRP were lower in GG group than that in GA and AA group (p < 0.05). Multivariate logistic regression analysis showed that subjects with the A allele were at an increased risk for the high level of hs-CRP (> 3 mg/L) compared with those with GG genotype (OR = 4.908, 95% CI = 1.57 approximately 20.98). Thus, the A allele in ALDH2 gene is associated with the elevated plasma levels of hs-CRP after the onset of AMI, suggesting a higher susceptibility of the myocardium to ischemic injuries.

Meta-analysis of the role of high-dose statins administered prior to percutaneous coronary intervention in reducing major adverse cardiac events in patients with coronary artery disease.

1. There is considerable evidence regarding the efficacy of statins for the primary and secondary prevention of coronary artery disease (CAD). However, due to lack of sufficient evidence, there is still doubt whether high-dose statin therapy prior to percutaneous coronary intervention (PCI) is beneficial. In the present study, we performed a meta-analysis to evaluate the effect of preoperative high-dose statin therapy on the incidence of major adverse cardiac events (MACE) after successful PCI. 2. Trials were retrieved through Medline (1980-2009) and the reference files limited to English-language articles. Data were abstracted using a standardized protocol and a meta-analysis was performed. 3. Five studies of a total 1789 patients with CAD qualified for analysis. Administration of high-dose statins in CAD patients before PCI was associated with a significant reduction in MACE 30 days after the procedure. The incidence of MACE in the high-dose statin group (6.98%) was significantly lower than that in the placebo group (14.77%), with an odds ratio (OR) of 0.43 (95% confidence interval (CI) 0.31-0.59; P < 0.00001). The incidence of post-PCI increases in creatine kinase MB in the high-dose statin and placebo groups was 9.20%vs 18.83%, respectively (OR 0.43; 95% CI 0.33-0.58; P < 0.00001), whereas the incidence of increases in troponin I was 30.13%vs 44.53%, respectively (OR 0.53; 95% CI 0.43-0.67; P < 0.00001), respectively. 4. In conclusion, high-dose statin therapy before PCI provides a significant benefit over placebo in preventing post-PCI MACE. Findings from the present analysis strongly support a strategy of routine loading of high-dose statins before interventional therapy.