Chlamydia psittaci causing severe pneumonia with an initial complaint of massive watery sputum: a case report.

Background: With the widespread application of metagenomic next-generation sequencing (mNGS) in pathogen detection, the reports of severe Chlamydia psittaci (C. psittaci) pneumonia are increasing. It is essential to determine the best management of severe C. psittaci pneumonia. Case Description: This report describes a 51-year-old male patient who presented with symptoms of expectoration, relative bradycardia, and dyspnea. Lung computed tomography (CT) on day 1 (D1) showed consolidation of the left lower lobe. He was intubated and transferred to the intensive care unit (ICU). The symptoms of high fever and progressive dyspnea [the lowest level of arterial partial pressure of oxygen/fractional inspired oxygen (PaO2/FiO2): 52 mmHg] persisted on D3. Meanwhile, he produced a large volume of golden-yellow, watery sputum, due to which endotracheal suction was repeatedly performed to maintain patency of the airway. The repeat radiography showed extensive deterioration of diffuse exudation in bilateral lobes. An early treatment with methylprednisolone was initiated on D3, after which the watery sputum decreased and turned viscous. The mNGS of the bronchoalveolar lavage fluid (BALF) identified C. psittaci on D7, and combined targeted antimicrobial therapy (azithromycin and doxycycline) was subsequently initiated. After 1 week of treatment, the patient was extubated on D14. He was transferred to the respiratory department on D17 and discharged on D25 with oral medications (azithromycin and doxycycline for 2 weeks). The repeat chest CT on D68 showed that the bilateral exudation and left lower lobe consolidation had almost disappeared, without pleural effusion. Conclusions: In severe C. psittaci pneumonia, although the presentations differ, the rapid pathogen identification through BALF mNGS may facilitate the early use of effective antibiotics. Timely and comprehensive treatment is important for improving outcomes in severe C. psittaci pneumonia.

Three-dimensional electronic microfliers inspired by wind-dispersed seeds.

Large, distributed collections of miniaturized, wireless electronic devices1,2 may form the basis of future systems for environmental monitoring3, population surveillance4, disease management5 and other applications that demand coverage over expansive spatial scales. Aerial schemes to distribute the components for such networks are required, and-inspired by wind-dispersed seeds6-we examined passive structures designed for controlled, unpowered flight across natural environments or city settings. Techniques in mechanically guided assembly of three-dimensional (3D) mesostructures7-9 provide access to miniature, 3D fliers optimized for such purposes, in processes that align with the most sophisticated production techniques for electronic, optoelectronic, microfluidic and microelectromechanical technologies. Here we demonstrate a range of 3D macro-, meso- and microscale fliers produced in this manner, including those that incorporate active electronic and colorimetric payloads. Analytical, computational and experimental studies of the aerodynamics of high-performance structures of this type establish a set of fundamental considerations in bio-inspired design, with a focus on 3D fliers that exhibit controlled rotational kinematics and low terminal velocities. An approach that represents these complex 3D structures as discrete numbers of blades captures the essential physics in simple, analytical scaling forms, validated by computational and experimental results. Battery-free, wireless devices and colorimetric sensors for environmental measurements provide simple examples of a wide spectrum of applications of these unusual concepts.

Testosterone antagonizes paraquat-induced cardiomyocyte senescence via the mIGF-1/SIRT1 signaling pathway.

Testosterone has been demonstrated to antagonize doxorubicin-induced cardiomyocyte senescence. However, whether testosterone prevents the paraquat-induced cardiomyocyte senescence is largely unknown. The detection of SA-ß-gal activity was performed using senescence ß-gal staining kit and the reactive oxygen species levels were determined by reactive oxygen species assay kit. The plasmids for insulin-like growth factor 1 shRNA (sh-mIGF-1), sirtuin-1 shRNA (sh-SIRT1), scramble shRNA (sh-NC), overexpressing mIGF-1 (mIGF-1), overexpressing SIRT1 (SIRT1), and negative controls (NC) were obtained for this study. The expression of target genes was detected using quantitative real-time PCR, immunolabeling, and western blot. We found that testosterone significantly delayed the paraquat-induced HL-1 cardiomyocyte senescence as evidenced by decreasing senescence-associated ß-galactosidase activity and reactive oxygen species generation, which were accompanied by the up-regulated expression of mIGF-1 and SIRT1. RNA interference to reduce mIGF-1 and SIRT1 expression showed that testosterone prevented paraquat-induced HL-1 senescence via the mIGF-1/SIRT1 signaling pathway. Furthermore, myocardial contraction was evaluated by expression of genes of the contractile proteins/enzymes, such as α-myosin heavy chain 6 (MHC6), α-myosin heavy chain 7 (MHC7), α-skeletal actin (ACTA-1), and sarco/endoplasmic reticulum calcium ATPase-2 (SERCA2). Testosterone adjusted the above four gene expressions and the adjustment was blocked by mIGF-1 or SIRT1 inhibition. Our findings suggested that the mIGF-1/SIRT1 signaling pathway mediated the protective function of testosterone against the HL-1 cardiomyocyte senescence by paraquat, which provided new clues for the mechanisms underlying the anti-aging role of testosterone in cardiomyocytes.

Establishment of risk prediction model and risk score for in-hospital mortality in patients with AECOPD.

OBJECTIVE: Risk stratification for patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) may help clinicians choose appropriate treatments and improve the quality of care. METHODS: A total of 695 patients hospitalized with AECOPD from January 2015 to December 2017 were considered. They were assigned to a death and a survival cohort. The independent prognostic factors were determined by multivariate logistic regression analysis. Meanwhile, we also compared the new scale with three other scores and tested the new scale internally and externally. RESULTS: A new risk score was created, made up of six independent variables: age, D-dimer, albumin, cardiac troponin I, partial pressure of carbon dioxide and oxygenation index. The area under the receiver operator characteristic curve (AUROC) for the model was 0.929, and the other three CURB-65, DECAF and BAP-65 models were 0.718, 0.922 and 0.708. The Cohen's kappa coefficient between the new scale and DECAF was calculated to be 0.648, suggesting that there is a substantial consistency between the two. In the internal and external validation cohorts, 490 and 500 patients were recruited with a total mortality rate of 5.15%. The AUROC for in-hospital mortality was 0.937 in the internal cohort and 0.914 in external cohort, which was significantly better than the scores for CURB-65 and BAP-65, but it was not significantly different from the DECAF. CONCLUSIONS: The new scale may help to stratify the risk of in-hospital mortality of AECOPD. The DECAF performed as well as the new instrument, and it appears to be valid in Chinese patients.

Testosterone antagonizes paraquat-induced cardiomyocyte senescence via the mIGF-1/SIRT1 signaling pathway

Testosterone has been demonstrated to antagonize doxorubicin-induced cardiomyocyte senescence. However, whether testosterone prevents the paraquat-induced cardiomyocyte senescence is largely unknown. The detection of SA-β-gal activity was performed using senescence β-gal staining kit and the reactive oxygen species levels were determined by reactive oxygen species assay kit. The plasmids for insulin-like growth factor 1 shRNA (sh-mIGF-1), sirtuin-1 shRNA (sh-SIRT1), scramble shRNA (sh-NC), overexpressing mIGF-1 (mIGF-1), overexpressing SIRT1 (SIRT1), and negative controls (NC) were obtained for this study. The expression of target genes was detected using quantitative real-time PCR, immunolabeling, and western blot. We found that testosterone significantly delayed the paraquat-induced HL-1 cardiomyocyte senescence as evidenced by decreasing senescence-associated β-galactosidase activity and reactive oxygen species generation, which were accompanied by the up-regulated expression of mIGF-1 and SIRT1. RNA interference to reduce mIGF-1 and SIRT1 expression showed that testosterone prevented paraquat-induced HL-1 senescence via the mIGF-1/SIRT1 signaling pathway. Furthermore, myocardial contraction was evaluated by expression of genes of the contractile proteins/enzymes, such as α-myosin heavy chain 6 (MHC6), α-myosin heavy chain 7 (MHC7), α-skeletal actin (ACTA-1), and sarco/endoplasmic reticulum calcium ATPase-2 (SERCA2). Testosterone adjusted the above four gene expressions and the adjustment was blocked by mIGF-1 or SIRT1 inhibition. Our findings suggested that the mIGF-1/SIRT1 signaling pathway mediated the protective function of testosterone against the HL-1 cardiomyocyte senescence by paraquat, which provided new clues for the mechanisms underlying the anti-aging role of testosterone in cardiomyocytes.