ObjectiveTo develop a classification model based on complete blood count （CBC） parameters combined with clinical factors to predict severe respiratory infections caused by Human adenovirus （HAdV） in pediatric patients. MethodsFrom September 2023 to September 2024， the CBC parameters and related clinical data from pediatric patients diagnosed with HAdV infection were collected. Principal component analysis and random forest models were used to identify potential predictors of severe cases. ResultsA total of 668 pediatric patients were included， with 564 cases assigned to the training cohort and 104 cases to the validation cohort. Severe cases were defined as pneumonia and/or fever lasting ≥5 days （pneumonia or prolonged fever， PorPF）. Principal component analysis and feature importance analysis （Mean Decrease Gini value） identified the monocytosis ratio （PMono）， red blood cell count （RBC）， and platelet count （PLT） as the most critical CBC parameters. Logistic regression analysis revealed that oxygen therapy （OR = 4.367， 95% CI： 1.568–12.161） and increased work of breathing （OR = 3.904， 95% CI： 2.146–7.101） were relative risk factors for PorPF. Meanwhile， higher PMono （OR = 0.696， 95% CI： 0.640–0.757）， RBC （OR = 0.201， 95% CI： 0.124–0.325）， and PLT （OR = 0.990， 95% CI： 0.987–0.994） were protective factors. When PMono was used as a predictive marker for PorPF， the area under the receiver operating characteristic curve （AUC） was 0.648 and 0.705， respectively. A random forest model incorporating four risk factors ［PMono， RBC， PLT， and hematocrit （HCT）］ was constructed to classify PorPF and general cases， achieving AUCs of 0.688 and 0.768， respectively. ConclusionsPMono， RBC， and PLT may serve as characteristic CBC indicators for predicting pneumonia or prolonged fever in children with HAdV infection. A risk factor model built using PMono， RBC， PLT， and HCT offers a relatively simple and accurate approach to predicting severe cases in pediatric HAdV infections.

Objective To study the clinical characteristics and treatment outcome of infants with bacterial meningitis (BM) under 6 months.Methods Seventy-two cases of infants with BM under 6 months were retrospectively analyzed.Among them,the infants of age ranging from 29 days to 30 days were assigned into the 1 month age group,60 days to 179 days infants were assigned into the 2 to 5 months old group.Results The incidence of BM was more common in male (51 cases,70.8％) and infants with the age of 1 month (45 cases,62.5％).The clinical manifestations included fever (71 cases,98.6％),procalcitonin increase (55 cases,76.3％),respiratory tract infection (48 cases,66.6％),peripheral blood WBC count abnormal results (34 cases,47.3％),abnormal blood CRP (20 cases,27.8％) and nervous system abnormalities (18 cases,25％).Among the 1 month old group,12 infants had urinary tract infection (16.6％),and 6 had convulsions (8.3％).There were 4 cases (5.5％) with subdural effusion in the 2 ～ 5 months old group.Compared with the 2 ～ 5 months old group,the 1 month old group was more likely to be caused by urinary tract infection,more prone to seizures,the difference was statistically significant (x2 =3.996,3.927,P＜0.05).Compared with the 1 month old group,the 2 ～ 5 months old group was more prone to subdural effusion,and the peripheral blood white blood ceils was higher,the difference was statistically significant (x2 =7.059,4.295,P＜0.05).Conclusion There is no obvious clinical manifestation or laboratory examination for infants under 6 months old BM,so it is necessary to make early cerebrospinal fluid examination for early diagnosis and early treatment.

OBJECTIVETo examine the effect of phloretin on apoptosis of BEL-7402 cells.

METHODSThe viability changes of BEL- 7402 cells as a result of phloretin-induced toxicity were analyzed using MTT assay, and the cell morphology changes were observed with fluorescence microscope. Flow cytometry was used to analyze the cell cycle and mitochondrial membrane potential changes, and chromogenic substrate assay performed to detect caspase activity.

RESULTSPhloretin induced obvious cytotoxicity against BEL-7402 cells with IC50 of 89.23 microg/mL. The growth curve demonstrated decreased growth of the cells as phloretin concentration increased. Cell apoptosis occurred 24 h after treatment with 40-160 microg/mL phloretin. Morphological, the cells exposed to phloretin exhibited nuclear chromatin condensation and increased fluorescence intensity. The activity of caspase-9 reached the peak level 12 h after phloretin exposure, and leak levels of caspase-6 and caspase-3 activities occurred 18 and 24 h after the exposure, respectively.

CONCLUSIONPhloretin can induce BEL-7402 cell apoptosis though the mitochondrial pathway.

Apoptosis ; drug effects ; Caspase 6 ; metabolism ; Caspase 9 ; metabolism ; Cell Cycle ; drug effects ; Cell Line, Tumor ; Cell Survival ; drug effects ; Dose-Response Relationship, Drug ; Flow Cytometry ; Humans ; Liver Neoplasms ; metabolism ; pathology ; Membrane Potential, Mitochondrial ; drug effects ; Phloretin ; pharmacology