After the outbreak of 2019 novel corona virus infection in China, we have the outbreak of disease in Iran and until March 05, 2020 have been reported a total number of confirmed cases more than 3500 and approximately 3.3% deaths. The corona virus disease 2019 (COVID-19) infection as a newly emerging disease in East Asia has caused a great challenge in managing the patients and controlling the disease especially in children. This algorithm is based on the standard diagnosis and treatment strategies for pediatric viral infections and available strategies to prevention of COVID-19 infection. It is hoped that with international cooperation , this global dilemma will end with the least burden of disease. Due to the lack of scientific evidences in children, this algorithm is essential for decision making.

Objective. Current study was designed to investigate the association of metabolic syndrome (MetS) with depression, anxiety, psychological distress, and quality of life (QoL). Design. Two hundred and fifteen contributors with MetS and 253 participants without MetS were randomly selected from 2151 participants of Isfahan Cohort Study who were residents of Isfahan city. Measurements consisted of fasting blood samples, anthropometrics, and self-reported data of 12-item General Health Questionnaire, Hospital Anxiety and Depression Scale, and European Quality of Life-5 Dimension. Binary logistic regression analysis was used to find the association between MetS and four psychological factors. Results. Participants mean age was 56.3 ± 9.8 years. Male/female ratio was 0.86 (217/251). Mean score of depression (P = 0.003), anxiety (P = 0.018), distress (P = 0.047), and QoL (P ≤ 0.001) was significantly higher in MetS group. There were significant increasing relationships between depression (OR 1.10, 95% CI 1.03–1.22), anxiety (OR 1.03, 95% CI 1.05–1.11), and QoL (OR 1.13, 95% CI 1.05–1.23) and MetS when associations were adjusted for other risk factors, but it was not the case for distress (OR 1.03, 95% CI 0.99–1.08). Conclusion. It might be better to consider MetS as a combination of biological and psychological risk factors. Thus, a person with metabolic disease should be recognized as a patient with these factors and be screened for all of them.

Overall, we found a trend toward the effectiveness of citalopram in the treatment of children with FAP. Trials with longer treatment duration in larger samples of patients are required in this regard.

We herein describe a case series of children with SARS-CoV-2 infection (COVID-19) complicated with acute intracardiac thrombosis. The diagnosis of COVID-19 was confirmed through the reverse transcription-polymerase chain reaction (RT-PCR). Transthoracic echocardiography of patients revealed large intracardiac mobile masses resected successfully via cardiac surgery. The underlying mechanisms of this thrombus in the COVID-19 infection may be attributed to the hypercoagulation and inflammatory state of the disease incurred by the SARS-CoV-2 virus.

Human cells homozygous for rare loss-of-expression (LOE) TYK2 alleles have impaired, but not abolished, cellular responses to IFN-α/β (underlying viral diseases in the patients) and to IL-12 and IL-23 (underlying mycobacterial diseases). Cells homozygous for the common P1104A TYK2 allele have selectively impaired responses to IL-23 (underlying isolated mycobacterial disease). We report three new forms of TYK2 deficiency in six patients from five families homozygous for rare TYK2 alleles (R864C, G996R, G634E, or G1010D) or compound heterozygous for P1104A and a rare allele (A928V). All these missense alleles encode detectable proteins. The R864C and G1010D alleles are hypomorphic and loss-of-function (LOF), respectively, across signaling pathways. By contrast, hypomorphic G996R, G634E, and A928V mutations selectively impair responses to IL-23, like P1104A. Impairment of the IL-23–dependent induction of IFN-γ is the only mechanism of mycobacterial disease common to patients with complete TYK2 deficiency with or without TYK2 expression, partial TYK2 deficiency across signaling pathways, or rare or common partial TYK2 deficiency specific for IL-23 signaling.