Clinical characteristics of children with SARS-CoV-2 Omicron variant infection in Kunming / 中华儿科杂志

Objective: To investigate the clinical characteristics of hospitalized children infected with the Omicron variant in Kunming after the withdrawal of non-pharmaceutical interventions (NPI) and analyze the risk factors of severe cases. Methods: Clinical data was retrospectively collected from 1 145 children with SARS-CoV-2 Omicron infection who were hospitalized in six tertiary grade A hospitals in Kunming from December 10th, 2022 to January 9th, 2023. According to clinical severity, these patients were divided into the general and severe SARS-CoV-2 groups, and their clinical and laboratory data were compared. Between-group comparison was performed using t-test, chi-square test and Mann-Whitney U test. Spearman correlation test and multivariate Logistic regression analysis were used to determine the risk factors of severe illness. Results: A total of 1 145 hospitalized patients were included, of whom 677 were male and 468 female. The age of these patients at visit was 1.7 (0.5, 4.1) years. Specifically, there were 758 patients (66.2%) aged ≤3 years at visit and 387 patients (33.8%) aged >3 years. Of these children, 89 cases (7.8%) had underline diseases and the remaining 1 056 cases (92.2%) had no combined diseases. Additionally, of all the patients, 319 cases (27.9%) were vaccinated with one or two doses of SARS-CoV-2 vaccine, 748 cases (65.3%) had acute upper respiratory tract infection (AURTI), and six cases died (0.5%). A total of 1 051 cases (91.8%) were grouped into general SARS-CoV-2 group and 94 cases (8.2%) were grouped into severe SARS-CoV-2 group. Compared with the general cases, the severe cases showed a lower rate of SARS-CoV-2 vaccination and younger median age, lower lymphocyte count, as well as proportions of CD8+T lymphocyte (36 cases (38.3%) vs. 283 cases (26.9%), 0.5 (2.6, 8.0) vs. 1.6 (0.5, 3.9) years, 1.3 (1.0, 2.7) ×109 vs. 2.7 (1.3,4.4)×109/L, 0.17 (0.12, 0.24) vs. 0.21 (0.15, 0.16), respectively, χ2=4.88, Z=-2.21,-5.03,-2.53, all P<0.05). On the other hand, the length of hospital stay, proportion of underline diseases, ALT, AST, creatine kinase isoenzyme, and troponin T were higher in the severe group compared to those in the general group ((11.6±5.9) vs. (5.3±1.8) d, 41 cases (43.6%) vs. 48 cases (4.6%), 67 (26,120) vs. 20 (15, 32) U/L, 51 (33, 123) vs. 44 (34, 58) U/L、56.9 (23.0, 219.3) vs. 3.6 (1.9, 17.9) U/L, 12.0 (4.9, 56.5) vs. 3.0 (3.0, 7.0) ×10-3 pg/L,respectively, t=-20.43, χ2=183.52, Z=-9.14,-3.12,-6.38,-3.81, all P<0.05). Multivariate regression analysis indicated that increased leukocyte count (OR=1.88, 95%CI 1.18-2.97, P<0.01), CRP (OR=1.18, 95%CI 1.06-1.31, P<0.01), ferritin (OR=1.01, 95%CI 1.00-1.00, P<0.01), interleukin (IL)-6 (OR=1.05, 95%CI 1.01-1.08, P=0.012), D-dimer (OR=2.56, 95%CI 1.44-4.56, P<0.01) and decreased CD4+T lymphocyte (OR=0.84, 95%CI 0.73-0.98, P=0.030) were independently associated with the risk of severe SARS-CoV-2 in hospitalized children with Omicron infection. Conclusions: After the withdrawal of NPI, the pediatric inpatients with Omicron infection in Kunming were predominantly children younger than 3 years of age, and mainly manifested as AURTI with relatively low rate of severe SARS-CoV-2 infection and mortality. Elevated leukocyte counts, CRP, ferritin, IL-6, D-dimer, and decreased CD4+T lymphocytes are significant risk factors for developing severe SARS-CoV-2 infection.

Mechanism of Didangtang in Inhibiting Aortic NLRP3 Inflammasome Cascade of Mice with Diabetic Macrovascular Disease / 中国实验方剂学杂志

Objective:To explore the progression of diabetic macrovascular disease and the effects of Didangtang at different doses on it. Method:Four-week-old male apolipoprotein-E knockout （ApoE^-/-） mice with diabetic macrovascular disease induced by exposure to high-fat diet combined with streptozotocin （STZ） were randomly divided into the model， simvastatin， as well as high-， medium-， and low-dose Didangtang groups. The age-matched ApoE^-/- mice of the same batch only fed with a high-fat diet were classified into the ApoE^-/- （model control） group， and C57BL/6 mice with the same genetic background receiving a regular diet into the normal group. The sampling was conducted at the 8th and 20th weeks of the experiment for observing the pathological characteristics of the aorta and the proportion of plaque area in mice of each group at different time points， followed by the comparison of blood glucose， blood lipid， and oxidized low-density lipoprotein （ox-LDL） levels. The aortic NOD-like receptor protein 3 （NLRP3） and cysteinyl aspartate-specific proteinase-1 （Caspase-1） protein expression was detected by Western blot assay， and the serum interleukin-1<italic>β</italic> （IL-1<italic>β</italic>）， interleukin-18 （IL-18）， interleukin-1<italic>α</italic> （IL-1<italic>α</italic>）， and tumor necrosis factor-<italic>α</italic> （TNF-<italic>α</italic>） levels by enzyme-linked immunosorbent assay （ELISA）. Result:The comparison with the normal group revealed that the proportions of plaque area in the ApoE^-/- group and the model group were increased （<italic>P</italic><0.01）， while the proportion of plaque area in each administration group was significantly reduced in contrast to that of the model group （<italic>P</italic><0.05）. The aortic NLRP3 and Caspase-1 protein expression levels as well as the serum IL-1<italic>β</italic>， IL-18， IL-1<italic>α</italic>， and TNF-<italic>α </italic>levels in the ApoE^-/- group and the model group were significantly higher than those in the normal group （<italic>P</italic><0.01）. Compared with the model group， each administration group exhibited a significant reduction in aortic NLRP3 and Caspase-1 protein expression and serum IL-1<italic>β</italic>， IL-18， IL-1<italic>α</italic>， and TNF-<italic>α</italic> levels （<italic>P</italic><0.05）， with the strongest inhibitory effect detected in the medium-dose Didangtang group （<italic>P</italic><0.05）. Conclusion:Didangtang directly alleviates diabetic macrovascular disease possibly by down-regulating NLRP3 and Caspase-1 protein expression and easing the inflammatory cascade.

Pulmonary ventilation function parameters of children aged 5-14 years in Kunming, China: a comparative analysis of measured values versus predicted values based on Zapletal equation / 中国当代儿科杂志

OBJECTIVE@#To study the percentage of the measured values of the main pulmonary ventilation function parameters in their predicted values based on Zapletal equation among healthy children aged 5-14 years in Kunming, China, and to provide a basis for accurate judgment of pulmonary ventilation function in clinical practice.@*METHODS@#A total of 702 healthy children aged 5-14 years (352 boys and 350 girls) from Kunming were enrolled. The Jaeger spirometer was used to measure the nine indices:forced vital capacity (FVC), forced expiratory volume in one second (FEV1), ratio of forced expiratory volume in one second to forced vital capacity (FEV1/FVC), maximal mid-expiratory flow (MMEF), forced expiratory flow at 25% of forced vital capacity (FEF25), forced expiratory flow at 50% of forced vital capacity (FEF50), forced expiratory flow at 75% of forced vital capacity (FEF75), peak expiratory flow (PEF), and maximal voluntary ventilation (MVV). The values obtained from the Zapletal equation of predicted values provided by the spirometer were used as the predicted values of children, and the percentage of measured values in predicted values was calculated.@*RESULTS@#In the 702 children, the percentages of the measured values of the main pulmonary ventilation function parameters PEF, FVC, FEV1, FEV1/FVC, and MVV in their predicted values fluctuated from 102% to 114%, 94% to 108%, 98% to 113%, 98% to 107%, and 141% to 183% respectively. As for the main airway velocity parameters, the percentages of the measured values of FEF25, FEF50, FEF75, and MMEF in their predicted values fluctuated from 98% to 116%, 85% to 102%, 71% to 98%, and 83% to 100% respectively. The percentages of the measured values of PEF, FVC, FEV1, FEV1/FVC, MVV, FEF25, FEF50, FEF75, and MMEF in their predicted values had the lower limits of normal of 88.2%, 88.4%, 92.0%, 94.4%, 118.5%, 82.9%, 70.0%, 62.1%, and 70.1% respectively.@*CONCLUSIONS@#There are differences between pulmonary ventilation function parameter levels and normal values provided by Zapletal equation in healthy children aged 5-14 years in Kunming. As for the pulmonary ventilation function parameters of PEF, FVC, FEV, FEV1/FVC, MVV, FEF25, FEF50, FEF75, and MMEF in these children, the lower limits of normal of measured values in predicted values may be determined as 88.2%, 88.4%, 92.0%, 94.4%, 118.5%, 82.9%, 70.0%, 62.1%, and 70.1% respectively.

CGRP 8-37 enhances lipopolysaccharide-induced acute lung injury and regulating aquaporin 1 and 5 expressions in rats

Calcitonin gene-related peptide (CGRP) has been shown to play important roles in biological functions. However, there is very little evidence on the value of CGRP in lipopolysaccharide (LPS)-induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Therefore, this study aimed to investigate the role of CGRP in LPS-induced ALI in rats. In the experiment, Sprague-Dawley (SD) rats were randomized into control, an antagonist of alfa-calcitonin gene-related peptide receptor (CGRP8-37), LPS groups, and CGRP8-37 + LPS groups. ALI model was prepared through retrograde injection of LPS (10 mg/kg). At 6 and 12 h, bronchoalveolar lavage was performed and used to assess total cell count and levels of tumor necrosis factor-alfa, interleukin-1Beta, -6, and -10 by enzyme-linked immunosorbent assay (ELISA). Lung tissue was collected for assessing wet-to-dry (W/D) ratio, hematoxylin and eosin staining. Aquaporin (AQP)-1 and -5 expressions in lung tissues were detected by quantitative PCR and Western blot. The results showed that histological injury, total cell count, and W/D ratio significantly reduced in LPS group after 6 h. The levels of inflammatory cytokines in CGRP8-37 + LPS-treated rats were higher than that in LPS-treated rats (all, P < 0.001). Real-time RT-PCR analysis showed that levels of AQP-1 in rats from CGRP8-37 + LPS group was lower than that in LPS-treated rats (P = 0.005 and P < 0.001). Western blotting analysis showed that AQP-1 protein levels at 6 h significantly decreased in CGRP8-37 + LPS rats. Together, our data suggest that CGRP antagonists, CGRP8-37 could enhance ALI induced by LPS in the rat model, and regulate the expression levels of AQP-1 and AQP-5 by affecting inflammatory cytokines. Thereby, regulating endogenous CGRP may be a potential treatment for ALI/ARDS

CGRP 8-37 enhances lipopolysaccharide-induced acute lung injury and regulating aquaporin 1 and 5 expressions in rats.

Calcitonin gene-related peptide (CGRP) has been shown to play important roles in biological functions. However, there is very little evidence on the value of CGRP in lipopolysaccharide (LPS)-induced acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Therefore, this study aimed to investigate the role of CGRP in LPS-induced ALI in rats. In the experiment, Sprague-Dawley (SD) rats were randomized into control, an antagonist of α-calcitonin gene-related peptide receptor (CGRP8-37), LPS groups, and CGRP8-37 + LPS groups. ALI model was prepared through retrograde injection of LPS (10 mg/kg). At 6 and 12 h, bronchoalveolar lavage was performed and used to assess total cell count and levels of tumor necrosis factor-α, interleukin-1ß, -6, and -10 by enzyme-linked immunosorbent assay (ELISA). Lung tissue was collected for assessing wet-to-dry (W/D) ratio, hematoxylin and eosin staining. Aquaporin (AQP)-1 and -5 expressions in lung tissues were detected by quantitative PCR and Western blot. The results showed that histological injury, total cell count, and W/D ratio significantly reduced in LPS group after 6 h. The levels of inflammatory cytokines in CGRP8-37 + LPS-treated rats were higher than that in LPS-treated rats (all, P < 0.001). Real-time RT-PCR analysis showed that levels of AQP-1 in rats from CGRP8-37 + LPS group was lower than that in LPS-treated rats (P = 0.005 and P < 0.001). Western blotting analysis showed that AQP-1 protein levels at 6 h significantly decreased in CGRP8-37 + LPS rats. Together, our data suggest that CGRP antagonists, CGRP8-37 could enhance ALI induced by LPS in the rat model, and regulate the expression levels of AQP-1 and AQP-5 by affecting inflammatory cytokines. Thereby, regulating endogenous CGRP may be a potential treatment for ALI/ARDS.

Changes of C-Reactive Protein and Von Willebrand Factor in Children with Systemic Inflammatory Response Syndrome Caused by Non-Infective Diseases / 实用儿科临床杂志

Objective To explore the changes of C-reactive protein(CRP) and von willebrand(VW) factor levels on pathogenesis of systemic inflammatory response syndrome(SIRS)caused by non-infective diseases in children.Methods Thirty-two children who attained to SIRS criterias caused by non-infective diseases were selected as study group,who were further divided into multiple organ(fai)-lure(MOF)group and non-MOF group according to whether the patients had MOF.Blood samples were taken to measure VW factor and CRP by ELISA and immune turbidimetry respectively.Twenty health children were as control group.Results Concentrations of blood VW factor(37 mg/L) and CRP[(185.50?27.71)%] were significantly higher in children with SIRS than those in control group(all(P