Objective:To explore the correlation between the methylation of sclerostin (SOST) promoter and glucocorticoid-induced osteoporosis (GIOP) in children.Methods:Children with GIOP ( n=66) were selected as the experimental group. At the same time, children treated with glucocorticoid whose bone mass were selected as the control group ( n=72). The general clinical information of all children was compared, and the data collected by CT were detected by lumbar QCT, and the levels of bone metabolism related indexes were detected by biochemical analyzer. The mRNA expression of SOST was detected by fluorescence quantitative PCR, and the protein content of SOST was detected by enzyme-linked Immunosorbent Assay (ELISA). Methylation status of SOST gene promoter was detected by methylation-specific PCR (MSP), and the risk factors affecting GIOP were compared and analyzed, and the diagnostic and therapeutic value of each index for children with GIOP was evaluated. Results:Compared with the control group, the duration of hormone application and the current dose of hormone in the experimental group were higher, and the expression levels of bone metabolism indexes β-collagen carboxy terminal peptide ( β-CTX) ( t=9.87, P<0.01), typeⅠprocollagenamino-terminal peptide (P1NP) ( t=16.09, P<0.001), osteopontin (OPN) ( t=21.32, P<0.001) and N-MID ( t=15.21, P<0.01) were significantly increased, with statistical significance. However, in terms of bone mineral density, the related level of children in the experimental group was low ( t=22.49, P<0.001), and the expression of SOST mRNA ( t=9.48, P<0.01) and protein content ( t=7.70, P<0.01) was significantly decreased, and the children in the experimental group showed methylation status of SOST. Pearson analysis showed that the level of serum SOST protein in the experimental group was negatively correlated with the levels of β-CTX ( r=-0.16, P=0.012), P1NP ( r=-0.35, P=0.021), OPN ( r=-0.25, P=0.043) and N-MID ( r=-0.09, P=0.036). At the same time, the Logistic regression analysis showed that the high expression of P1NP ( SE=0.35, P<0.001), OPN (S E=0.37, P<0.001) and SOST ( SE=0.33, P<0.001) were risk factors for glucocorticoid-induced osteoporosis in children. The receiver operating characteristic (ROC) curve showed that the area under the curve of SOST was 0.874 (95% CI: 0.824-0.934), with higher sensitivity and specificity. Conclusions:There is a correlation between the methylation of SOST promoter and the GIOP of children. Besides, SOST can be used as a potential diagnostic index of GIOP with high value among many factors affecting children’s GIOP. In this case, the medical industry needs to further strengthen the prevention and treatment of children’s GIOP.

Oxalate is an organic dicarboxylic acid that is a common component of plant foods.The kidneys are essential organs for oxalate excretion,but excessive oxalates may induce kidney stones.Jupiter micro-tubule associated homolog 2(JPT2)is a critical molecule in Ca2+mobilization,and its intrinsic mecha-nism in oxalate exposure and kidney stones remains unclear.This study aimed to reveal the mechanism of JPT2 in oxalate exposure and kidney stones.Genetic approaches were used to control JPT2 expression in cells and mice,and theJPT2 mechanism of action was analyzed using transcriptomics and untargeted metabolomics.The results showed that oxalate exposure triggered the upregulation of JPT2,which is involved in nicotinic acid adenine dinucleotide phosphate(NAADP)-mediated Ca2+mobilization.Tran-scriptomic analysis revealed that cell adhesion and macrophage inflammatory polarization were inhibited by JPT2 knockdown,and these were dominated by phosphatidylinositol 3-kinase(PI3K)/AKT signaling,respectively.Untargeted metabolomics indicated that JPT2 knockdown inhibited the produc-tion of succinic acid semialdehyde(SSA)in macrophages.Furthermore,JPT2 deficiency in mice inhibited kidney stones mineralization.In conclusion,this study demonstrates that oxalate exposure facilitates kidney stones by promoting crystal-cell adhesion,and modulating macrophage metabolism and in-flammatory polarization via JPT2/PI3K/AKT signaling.

Patients with severe trauma require an extremely timely treatment and transfusion plays an irreplaceable role in the emergency treatment of such patients. An increasing number of evidence-based medicinal evidences and clinical practices suggest that patients with severe traumatic bleeding benefit from early transfusion of low-titer group O whole blood or hemostatic resuscitation with red blood cells, plasma and platelet of a balanced ratio. However, the current domestic mode of blood supply cannot fully meet the requirements of timely and effective blood transfusion for emergency treatment of patients with severe trauma in clinical practice. In order to solve the key problems in blood supply and blood transfusion strategies for emergency treatment of severe trauma, Branch of Clinical Transfusion Medicine of Chinese Medical Association, Group for Trauma Emergency Care and Multiple Injuries of Trauma Branch of Chinese Medical Association, Young Scholar Group of Disaster Medicine Branch of Chinese Medical Association organized domestic experts of blood transfusion medicine and trauma treatment to jointly formulate Chinese expert consensus on blood support mode and blood transfusion strategies for emergency treatment of severe trauma patients ( version 2024). Based on the evidence-based medical evidence and Delphi method of expert consultation and voting, 10 recommendations were put forward from two aspects of blood support mode and transfusion strategies, aiming to provide a reference for transfusion resuscitation in the emergency treatment of severe trauma and further improve the success rate of treatment of patients with severe trauma.

Objective:To explore the risk factors related to delayed pleural effusion in multiple trauma patients.Methods:A retrospective cohort study was conducted to analyze the clinical data of 145 multiple trauma patients admitted to the First Affiliated Hospital of Soochow University from January 2022 to October 2023, including 99 males and 46 females, aged 18-81 years [56.0(46.5, 64.5)years]. Based on whether delayed pleural effusion developed after injury, the patients were divided into delayed pleural effusion group ( n=66) and non-delayed pleural effusion group ( n=79). The clinical data of the patients in both groups were collected, including gender, age, underlying disease (diabetes mellitus and hypertension), cause of injury (traffic injury, blow injury, fall from height, and others), comorbid injuries (traumatic brain injury, maxillofacial fracture, clavicular fracture, scapular fracture, sternal fracture, spinal fracture, multiple rib fracture, pneumothorax, lung contusion, and pelvic fracture), severity of injury [injury severity score (ISS) and abbreviated injury scale (AIS) score for the chest], location and number of rib fractures, vital signs at admission (body temperature, heart rate, respiration, systolic blood pressure, diastolic blood pressure), and clinical test indices [white blood cells (WBC), hemoglobin (Hb), platelets (PLT), total protein (TP), albumin (ALB), C-reactive protein (CRP), procalcitonin (PCT), fibrinogen (FIB), fibrin degradation product (FDP), D-dimer (D-D), aspartate transaminase (AST), alanine transferase (ALT), and creatinine (Cr)]. Univariate analysis was conducted to assess the correlation between the forementioned factors and the development of delayed pleural effusion after multiple traumas. Multivariate Logistic regression analysis was used to determine the independent risk factors for the development of delayed pleural effusion after multiple traumas. Results:The results of univariate analysis showed that multiple rib fracture, pneumothorax, pulmonary contusion, chest AIS score, posterior rib fracture, number of rib fractures, TP, ALB, CRP, PCT and FDP were correlated with delayed pleural effusion in multiple trauma patients ( P<0.05 or 0.01); whereas gender, age, underlying disease, cause of injury, sternal fracture, spinal fracture, clavicular fracture, scapular fracture, pelvic fracture, maxillofacial fracture, traumatic brain injury, anterior rib fracture, ISS, vital signs at admission, WBC, Hb, PLT, FIB, D-D, AST, ALT, and Cr were not correlated with delayed pleural effusion in multiple trauma patients ( P>0.05). The results of multivariate Logistic regression analysis revealed that lung contusion ( OR=3.96, 95% CI 1.59, 9.85, P<0.01), ALB ( OR=0.79, 95% CI 0.66, 0.94, P<0.01), and CRP ( OR=1.02, 95% CI 1.01, 1.03, P<0.01) were significantly correlated with delayed pleural effusion in multiple trauma patients. Conclusion:Lung contusion, ALB, and CRP are the independent risk factors for delayed pleural effusion in multiple trauma patients.

Background/Aims: The histological characteristics and natural history of precirrhotic primary biliary cholangitis (PBC) with portal hypertension (PH) are unclear. Our aim was to clarify the prevalence, risk factors, and histological characteristics of precirrhotic PBC patients with PH. Methods: This retrospective study compared the clinical features, histological characteristics, and response to ursodeoxycholic acid (UDCA) between the PH and non-PH groups of precirrhotic PBC patients. Results: Out of 165 precirrhotic PBC patients, 40 (24.2%) also had PH. According to histological stage 1, 2 and 3 disease, 5.3% (1/19), 17.3% (17/98), and 45.8% (22/48) of patients also had PH, respectively. Precirrhotic PBC with PH was significantly positively correlated with bile duct loss, degree of cytokeratin 7 positivity, and degree of fibrosis in the portal area, but significantly negatively correlated with lymphoid follicular aggregation. Compared to the non-PH group, patients in the PH group showed a higher prevalence of obliterative portal venopathy, incomplete septal fibrosis, portal tract abnormalities and non-zonal sinusoidal dilatation (p<0.05). In addition, patients with PH were more likely to present with symptoms of jaundice, ascites, epigastric discomfort, a poorer response to UDCA, and more decompensation events (p<0.05). High alkaline phosphatase levels, low white blood cell counts, high Mayo scores, and high FIB-4 index values were risk factors for precirrhotic PBC with PH. Conclusions Approximately 24.2% of precirrhotic PBC patients have PH, which is histologically related to the injury of bile ducts. High alkaline phosphatase levels, low white blood cell counts, high Mayo scores, and high FIB-4 index values are associated with increased risk of precirrhotic PBC with PH.

Objective:To investigate the value of ultrasound in the diagnosis of secondary loss of response in children with Crohn′s disease at maintenance stage treated with Infliximab.Methods:From January 2017 to December 2021, 51 children with Crohn′s disease who received Infliximab treatment and clinical response in the Beijing Children′s Hospital Affiliated to Capital Medical University were retrospectively analyzed, and whether there was secondary loss of response during the maintenance period was observed. The ultrasound examination results at the 14th week of treatment were collected to understand the correlation between ultrasound examination of intestinal wall and peri-intestinal healing and secondary loss of response.Results:A total of 15 out of 51 patients (29.4%) experienced secondary loss of response during treatment follow-up up to 54 weeks. Compared to children with continuous response, children with secondary loss of response had a thicker intestinal wall at week 14 of treatment [5.0 (3.8, 6.0)mm compared to 3.0 (2.0, 4.0)mm, P<0.001], and a higher proportion of intestinal wall stratified structure disappearance [8/15 (53.33%) compared to 3/36 (8.33%), P<0.001]. When intestinal wall thickness>3.0 mm, the sensitivity was 0.955, and the specificity was 0.483. The sensitivity and specificity of clear diagnosis of secondary loss of response in intestinal wall stratification were 0.727 and 0.825, respectively. The sensitivity and specificity of combined diagnosis for secondary loss of response were 0.933 and 0.611, respectively. Conclusions:At the 14th week of treatment with Infliximab in children with Crohn′s disease, the thickness of intestinal wall measured by ultrasound being more than 3.0 mm and the disappearance of intestinal wall statified structure provide important information for the diagnosis of secondary loss of response.