Background Previous studies on the pneumonia outbreak caused by the 2019 novel coronavirus disease (COVID-19) were mainly based on information from adult populations. Limited data are available for children with COVID-19, especially for infected infants. Methods We report a 55-day-old case with COVID-19 confirmed in China and describe the identification, diagnosis, clinical course, and treatment of the patient, including the disease progression from day 7 to day 11 of illness. Results This case highlights that children with COVID-19 can also present with multiple organ damage and rapid disease changes. Conclusions When managing such infant patients with COVID-19, frequent and careful clinical monitoring is essential.

Abstract. The present study aimed to investigate genetic and environmental factors involved in the pathogenesis of congenital heart disease (CHD). A total of 61 familial pedigrees with CHD were analyzed, and 134 patients out of 761 family members had a diagnosis of CHD confirmed. The present study revealed that the prevalence of CHD in first-degree relatives (55/249, 22.0%) was significantly higher than that in second-degree relatives (18/526, 3.4%). Additionally, the recurrence rate of CHD in families in which the patient's mother (12/61) or sister (15/61) had CHD were significantly higher than in cases with the father (6/61) or brother (4/61) having CHD. The subtypes of CHD with increased risk of recurrence were ventricle septal defect (VSD) and atrial septal defect (ASD), followed by patent ductus arteriosus and tetralogy of fallot (TOF). In the 21 sets of twins among the 61 familial pedigrees analyzed, the concordance of both twins affected by CHD in identical and dizygotic twins was 94.4% (17/18) and 33.3% (1/3), respectively. Identical subtypes of CHD were identified in 10 out of 21 sets of twins. Of note, the following pattern was identified in three sets of the twins: One twin had TOF, while the other one had VSD. A risk factor survey revealed that threatened abortion in early pregnancy was associated with familial CHD. In conclusion, genetic factors may have important roles in the development of CHD, and TOF and VSD may have similar molecular mechanisms. Threatened abortion in early pregnancy is a novel environmental factor that may be specific in Chinese females with CHD.

IntroductionSustained neutrophilic infiltration is known to contribute to organ damage, such as acute lung injury (ALI). CXC chemokine receptor 2 (CXCR2) is the major receptor regulating inflammatory neutrophil recruitment in acute and chronic inflamed tissues. The purpose of this study was to investigate the functional relevance of the CXCR2 inhibitor SB225002 in LPS-induced acute lung injury.Material and methodsMale C57BL/6 mice were randomly divided into the following four experimental groups (n = 10 per group): untreated group (control group, Ctr); LPS-treated ALI group (LPS group, LPS); LPS + PBS-treated group (LPS + PBS); and SB225002-treated ALI group (LPS + SB225002). Twenty-four hours after treatment, the blood, bronchoalveolar lavage fluid (BALF), and lung tissue were collected and wet/dry ratio, protein concentration, myeloperoxidase (MPO) activity, neutrophil infiltration, and inflammatory cytokine secretion in lung tissue were measured. The pathologic changes in the lungs were examined using optical microscopy. Survival rates were recorded at 120 h in all four groups, in other experiments.ResultsHistology findings revealed that the SB225002-treated group had significantly milder lung injury compared to the LPS-induced ALI and the PBS-treated control groups. Treatment with SB225002 significantly attenuated LPS-induced lung injury and suppressed the inflammatory responses in damaged lung tissue. Compared to the PBS-treated control group, treatment with SB225002 dramatically decreased the lung wet/dry ratio, protein concentration, and infiltration of neutrophils in lung tissue. Therefore, SB225002 treatment appeared to inhibit the production of inflammatory cytokines and increase survival time compared to the PBS-treated control group.ConclusionsTogether, these data demonstrated that inhibition of CXCR2 signaling by SB225002 could ameliorate LPS-induced acute lung injury, by reducing neutrophil recruitment and vascular permeability. SB225002 may be further developed as a potential novel treatment for LPS-induced ALI.