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Background: SARS-CoV-2 is described to cause mild to moderate symptoms in children. To date, clinical data and symptoms of the Delta variant in pediatric patients are lacking. Aim: To describe clinical characteristics and outcomes of infants admitted in the pediatric intensive care unit (PICU) during the period of Delta variant predominance. Methods: We performed a retrospective study, between June 23, 2021 and August 16, 2021. We included children aged under 15 years, admitted to PICU with severe and critical form of SARS-CoV-2 infection as confirmed by RT-PCR. We reviewed medical records for all patients. Results: During the study period, 20 infants were included. The median age was 47 days (IQR: 26.5–77). The sex ratio was 0.8 (9 males). No underlying medical conditions were noted. Parents were not vaccinated. Respiratory involvement was the main feature to be observed in our cohort. Eleven patients had pediatric acute respiratory distress (PARDS) with a median oxygen saturation index (OSI) of 9 (IQR: 7–11). PARDS was mild in 4 cases, moderate in 5 cases and severe in 2 cases. Hemodynamic instability was observed in 4 cases. The main radiological finding was ground glass opacities in 11 cases. Seventeen patients were mechanically ventilated and 3 of them were escalated to high-frequency oscillatory ventilation. The median duration of mechanical ventilation was 6 days (IQR 2.5–12.5). The remaining patients were managed with high flow nasal cannula. Four patients died. Conclusion: We report herein a case series of very young infants, with no comorbidities, and with a life-threatening illness due to SARS-CoV-2 Delta variant.

Abstract We report herein a case series of infants, with no comorbidities, who developed a life‐threatening illness due to the SARS‐CoV‐2 Delta variant. We retrospectively reviewed the medical records of children, aged under 15 years, admitted to PICU, during the peak of Delta infection, between June 23 and August 16 2021, with severe and critical forms of SARS‐CoV‐2 infection, confirmed by RT‐PCR. Twenty infants were included, the median age was 47 days (IQR: 26.5–77) and sex ratio was 0.8. No underlying medical conditions were noted. Parents were not vaccinated. Respiratory involvement was the main feature observed. Eleven patients had paediatric acute respiratory distress (PARDS) with a median oxygen saturation index (OSI) of 9 (IQR: 7–11). PARDS was mild in four, moderate in five, and severe in two cases. Hemodynamic instability was observed in 4 cases. The main radiological finding was ground glass opacities in 11 cases. Seventeen patients were mechanically ventilated, and three of them were escalated to high‐frequency oscillatory ventilation. The median duration of mechanical ventilation was 6 days (IQR 2.5–12.5). The remaining patients were managed with high‐flow nasal cannula. Four patients died.

In this paper, we focus on the (μ 1 , μ 2) -pseudo-asymptotically τ -periodicity and its applications. Then, the problems of existence, uniqueness and global exponential stability of (μ 1 , μ 2) -pseudo-asymptotically τ -periodic solutions for neural networks with delay are considered. Finally, three examples are given to illustrate the validity of the theoretical results [ABSTRACT FROM AUTHOR]

Congenital hypogonadotropic hypogonadism (CHH) and its anosmia-associated form (Kallmann syndrome [KS]) are genetically heterogeneous. Among the >15 genes implicated in these conditions, mutations in FGF8 and FGFR1 account for ~12% of cases; notably, KAL1 and HS6ST1 are also involved in FGFR1 signaling and can be mutated in CHH. We therefore hypothesized that mutations in genes encoding a broader range of modulators of the FGFR1 pathway might contribute to the genetics of CHH as causal or modifier mutations. Thus, we aimed to (1) investigate whether CHH individuals harbor mutations in members of the so-called "FGF8 synexpression" group and (2) validate the ability of a bioinformatics algorithm on the basis of protein-protein interactome data (interactome-based affiliation scoring [IBAS]) to identify high-quality candidate genes. On the basis of sequence homology, expression, and structural and functional data, seven genes were selected and sequenced in 386 unrelated CHH individuals and 155 controls. Except for FGF18 and SPRY2, all other genes were found to be mutated in CHH individuals: FGF17 (n = 3 individuals), IL17RD (n = 8), DUSP6 (n = 5), SPRY4 (n = 14), and FLRT3 (n = 3). Independently, IBAS predicted FGF17 and IL17RD as the two top candidates in the entire proteome on the basis of a statistical test of their protein-protein interaction patterns to proteins known to be altered in CHH. Most of the FGF17 and IL17RD mutations altered protein function in vitro. IL17RD mutations were found only in KS individuals and were strongly linked to hearing loss (6/8 individuals). Mutations in genes encoding components of the FGF pathway are associated with complex modes of CHH inheritance and act primarily as contributors to an oligogenic genetic architecture underlying CHH.