Background The coronavirus disease 2019 (COVID-19) has caused a global pandemic, resulting in considerable mortality. The risk factors, clinical treatments, especially comprehensive risk models for COVID-19 death are urgently warranted. Methods In this retrospective study, 281 non-survivors and 712 survivors with propensity score matching by age, sex, and comorbidities were enrolled from January 13, 2020 to March 31, 2020. Results Higher SOFA, qSOFA, APACHE II and SIRS scores, hypoxia, elevated inflammatory cytokines, multi-organ dysfunction, decreased immune cell subsets, and complications were significantly associated with the higher COVID-19 death risk. In addition to traditional predictors for death risk, including APACHE II (AUC = 0.83), SIRS (AUC = 0.75), SOFA (AUC = 0.70) and qSOFA scores (AUC = 0.61), another four prediction models that included immune cells subsets (AUC = 0.90), multiple organ damage biomarkers (AUC = 0.89), complications (AUC = 0.88) and inflammatory-related indexes (AUC = 0.75) were established. Additionally, the predictive accuracy of combining these risk factors (AUC = 0.950) was also significantly higher than that of each risk group alone, which was significant for early clinical management for COVID-19. Conclusions The potential risk factors could help to predict the clinical prognosis of COVID-19 patients at an early stage. The combined model might be more suitable for the death risk evaluation of COVID-19.

While it is common for pregnant women to take anesthesia during surgery, the effects of prenatal anesthesia exposure (PAE) on the long-term neurodevelopment of the offspring remain to be clarified. Preclinical animal research has shown that in utero anesthetic exposure causes neurotoxicity in newborns, which is mainly characterized by histomorphological changes and altered learning and memory abilities. Regional birth cohort studies that are based on databases are currently the most convenient and popular types of clinical studies. Specialized questionnaires and scales are usually employed in these studies for the screening and diagnosis of neurodevelopmental disorders in the offspring. The time intervals between the intrauterine exposure and the onset of developmental outcomes often vary over several years and accommodate a large number of confounding factors, which have an even greater impact on the neurodevelopment of the offspring than prenatal anesthesia itself. This narrative review summarized the progress in prenatal anesthetic exposure and neurodevelopmental outcomes in the offspring from animal experimental research and clinical studies and provided a brief introduction to assess the neurodevelopment in children and potential confounding factors.

All‐trans retinoic acid (ATRA) is the natural and synthetic analogue of vitamin A, playing an essential tumor suppressive role in multiple cancers including the esophageal squamous cell carcinoma (ESCC). Cytochrome P450 family 26 subfamily B member 1 (CYP26B1) exerts a critical regulator of ATRA levels through specific inactivation of ATRA to hydroxylated forms. Our previous exome‐wide analyses revealed a rare missense variant in CYP26B1 significantly associated with ESCC risk in the Chinese population. However, it is still unclear whether there are common variants in CYP26B1 affect the susceptibility of ESCC and the tumor promotion role of CYP26B1 in vivo. In this research, we conducted a two‐stage case‐control study comprised of 5057 ESCC cases and 5397 controls, followed by a series of biochemical experiments to explore the function of CYP26B1 and its common variants in the tumorigenesis of ESCC. Intriguingly, we identified a missense variant rs2241057[A>G] in the fourth exon of CYP26B1 significantly associated with the ESCC risk (combined odds ratio = 1.28; 95% confidence interval = 1.15–1.42; p = 2.96 × 10−6). Through further functional analysis, we demonstrated that ESCC cells with the overexpression of rs2241057[G] had a significant lower level of retinoic acid, compared with the overexpression of rs2241057[A] or the control vector. In addition, the CYP26B1 overexpression and knock‐out ESCC cells affected cell proliferation rate both in vitro and in vivo. These results highlighted the carcinogenicity of CYP26B1 related to the ATRA metabolism in ESCC risk.

During the storage process of hazelnut fresh fruits, browning is easy to occur, which reduces the storage quality. In this study, the method of 60Coγ irradiation was used to dynamically monitor the effects of fresh hazelnuts on storage quality, physiological indicators, and sterilization effect after being irradiated and refrigerated at 4 ± 0.5°C for 3 months. The results showed that irradiation at a dose of 0.25 to 1.0 kGy could preserve the current quality of the product, delay the browning of hazelnut shells, and reduce the activity of polyphenol oxidase. In addition, 0.5 kGy irradiation inhibited the respiration intensity and the accumulation of malondialdehyde in hazelnut fruits at the later stage of storage. Further research found that the content of microorganisms in hazelnut fruits decreased with the increase in irradiation dose. In addition, 0.5 kGy was the best irradiation dose to slow down the transpiration of hazelnut water and delay the reduction of fat, but the irradiation treatment of less than 1.0 kGy was effective for hazelnuts. Fruit peroxide value had no significant effect. At the same time, through the principal component analysis of hazelnut fruits stored for 90 days, the results also show that the 60Coγ irradiation with a dose of 0.5 kGy has the best storage effect and can effectively prolong the shelf life. The results of this study provide an effective theoretical basis and technical support for the preservation of fresh hazelnut fruits and the inhibition of the browning of hazelnut shells during storage. Novelty impact statement In this study, 60Coγ irradiation inhibited the polyphenol oxidase activity of polyphenol oxidase to a certain extent, thus delaying the browning of hazelnut shells. The synergistic effect of irradiation and low temperature prolonged the shelf life of hazelnut. The results showed that treatment with 0.5 kGy had the best effect, which was validated by the results of principal component analysis.

Background: Coronavirus disease 2019 (COVID-19) has spread globally. However, the association between COVID-19 and disseminated intravascular coagulation (DIC) has been scarcely addressed. We aimed to systematically characterize the clinical features and examine risk factors for DIC development in COVID-19 patients.Methods: In this single-centered, retrospective, and observational study, all patients with DIC (N=59) and 270 patients without DIC were matched by propensity score matching based on age, sex, and comorbidities. Demographic data, symptoms, radiological, laboratory examinations, and clinical outcomes were compared between patients with and without DIC. Furthermore, univariable and multivariable logistic regression were used to explore the risk factors associated with DIC development in COVID-19 patients.Results: Higher proportion of patients with DIC and COVID-19 (54 of 59 [91·53%]) developed into death than non DIC patients (58 of 270 [21·48%]). Patients with DIC presented aggravated inflammation responses, liver damage, and especially coagulation dysfunction. Moreover, in addition to previously reported coagulation-related markers, such as FDP, D-dimer, and platelet, we also identified several novel risk factors associated with DIC development, including decreased fibrinogen (OR=0·476, 95%CI=0·380-0·596, P<0·0001) and ALB (0·901, 0·845- 0·961, P=0·0015), and elevated IL-6 (1·010, 1·005-1·015, P=0·00017) and TNF-α (1·053, 1·016-1·091, P=0·0045).Conclusions: Patients with DIC and COVID-19 were predisposed to poor clinical outcomes. These risk factors identified may be helpful for early surveillance of disease progression and making standardized treatment strategies.