Background: Patients with critical illness due to infection with the 2019 coronavirus disease (COVID-19) show rapid disease progression to acute respiratory failure. The study aimed to screen the most useful predictive factor for critical illness caused by COVID-19. Methods: The study prospectively involved 61 patients with COVID-19 infection as a derivation cohort, and 54 patients as a validation cohort. The predictive factor for critical illness was selected using LASSO regression analysis. A nomogram based on non-specific laboratory indicators was built to predict the probability of critical illness. Results: The neutrophil-to-lymphocyte ratio (NLR) was identified as an independent risk factor for critical illness in patients with COVID-19 infection. The NLR had an area under receiver operating characteristic of 0.849 (95% confidence interval [CI], 0.707 to 0.991) in the derivation cohort and 0.867 (95% CI 0.747 to 0.944) in the validation cohort, the calibration curves fitted well, and the decision and clinical impact curves showed that the NLR had high standardized net benefit. In addition, the incidence of critical illness was 9.1% (1/11) for patients aged ≥ 50 and having an NLR < 3.13, and 50% (7/14) patients with age ≥ 50 and NLR ≥ 3.13 were predicted to develop critical illness. Based on the risk stratification of NLR according to age, this study has developed a COVID-19 pneumonia management process. Conclusions: We found that NLR is a predictive factor for early-stage prediction of patients infected with COVID-19 who are likely to develop critical illness. Patients aged ≥ 50 and having an NLR ≥ 3.13 are predicted to develop critical illness, and they should thus have rapid access to an intensive care unit if necessary.

Objectives: In late December 2019, an outbreak of coronavirus disease in Wuhan, China was caused by a novel coronavirus, newly named severe acute respiratory syndrome coronavirus 2. We aimed to quantify the severity of COVID-19 infection on high-resolution chest computed tomography (CT) and to determine its relationship with clinical parameters. Materials and Methods: From January 11, 2020, to February 5, 2020, the clinical, laboratory, and high-resolution CT features of 42 patients (26-75 years, 25 males) with COVID-19 were analyzed. The initial and follow-up CT, obtained a mean of 4.5 days and 11.6 days from the illness onset were retrospectively assessed for the severity and progression of pneumonia. Correlations among clinical parameters, initial CT features, and progression of opacifications were evaluated with Spearman correlation and linear regression analysis. Results: Thirty-five patients (83%) exhibited a progressive process according to CT features during the early stage from onset. Follow-up CT findings showed progressive opacifications, consolidation, interstitial thickening, fibrous strips, and air bronchograms, compared with initial CT (all P < 0.05). Before regular treatments, there was a moderate correlation between the days from onset and sum score of opacifications (R = 0.68, P < 0.01). The C-reactive protein, erythrocyte sedimentation rate, and lactate dehydrogenase showed significantly positive correlation with the severity of pneumonia assessed on initial CT (R range , 0.36-0.75; P < 0.05). The highest temperature and the severity of opacifications assessed on initial CT were significantly related to the progression of opacifications on follow-up CT (P = 0.001-0.04). Conclusions: Patients with the COVID-19 infection usually presented with typical ground glass opacities and other CT features, which showed significant correlations with some clinical and laboratory measurements. Follow-up CT images often demonstrated progressions during the early stage from illness onset.

BackgroundPrimary graft dysfunction (PGD) is the main cause of early morbidity and mortality after lung transplantation. Previous studies have yielded conflicting results for PGD risk factors. Herein, we carried out a systematic review and meta-analysis of published literature to identify recipient-related clinical risk factors associated with PGD development.MethodA systematic search of electronic databases (PubMed, Embase, Web of Science, Cochrane CENTRAL, and Scopus) for studies published from 1970 to 2013 was performed. Cohort, case-control, or cross-sectional studies that examined recipient-related risk factors of PGD were included. The odds ratios (ORs) or mean differences (MDs) were calculated using random-effects modelsResultThirteen studies involving 10042 recipients met final inclusion criteria. From the pooled analyses, female gender (OR 1.38, 95% CI 1.09 to 1.75), African American (OR 1.82, 95%CI 1.36 to 2.45), idiopathic pulmonary fibrosis (IPF) (OR 1.78, 95% CI 1.49 to 2.13), sarcoidosis (OR 4.25, 95% CI 1.09 to 16.52), primary pulmonary hypertension (PPH) (OR 3.73, 95%CI 2.16 to 6.46), elevated BMI (BMI≥25 kg/m2) (OR 1.83, 95% CI 1.26 to 2.64), and use of cardiopulmonary bypass (CPB) (OR 2.29, 95%CI 1.43 to 3.65) were significantly associated with increased risk of PGD. Age, cystic fibrosis, secondary pulmonary hypertension (SPH), intra-operative inhaled nitric oxide (NO), or lung transplant type (single or bilateral) were not significantly associated with PGD development (all P>0.05). Moreover, a nearly 4 fold increased risk of short-term mortality was observed in patients with PGD (OR 3.95, 95% CI 2.80 to 5.57).ConclusionsOur analysis identified several recipient related risk factors for development of PGD. The identification of higher-risk recipients and further research into the underlying mechanisms may lead to selective therapies aimed at reducing this reperfusion injury.

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Both stable negative permittivity and low dielectric loss are observed in silica microsphere templated carbon nanocomposites.

Ethyl acetate-appended nanoporous organic polytriazine (NOP-20 ) displays a high CO2–N2 ideal selectivity of 81 (273 K), which makes it a promising candidate as adsorbent for CO2 capture in fields related to the environment and energy.

ObjectiveDrug‐resistant epilepsy causes great clinical danger and still lacks effective treatments.MethodsHere, we used multifaceted approaches combining electrophysiology, optogenetics, and chemogenetics in a classic phenytoin‐resistant epilepsy model to reveal the key target of subicular pyramidal neurons in phenytoin resistance.ResultsIn vivo neural recording showed that the firing rate of pyramidal neurons in the subiculum, but not other hippocampal subregions, could not be inhibited by phenytoin in phenytoin‐resistant rats. Selective inhibition of subicular pyramidal neurons by optogenetics or chemogenetics reversed phenytoin resistance, whereas selective activation of subicular pyramidal neurons induced phenytoin resistance. Moreover, long‐term low‐frequency stimulation at the subiculum, which is clinically feasible, significantly inhibited the subicular pyramidal neurons and reversed phenytoin resistance. Furthermore, in vitro electrophysiology revealed that off‐target use of phenytoin on sodium channels of subicular pyramidal neurons was involved in the phenytoin resistance, and clinical neuroimaging data suggested the volume of the subiculum in drug‐resistant patients was related to the usage of sodium channel inhibitors.InterpretationThese results highlight that the subicular pyramidal neurons may be a key switch control of drug‐resistant epilepsy and represent a new potential target for precise treatments. ANN NEUROL 2019;86:626–640