Children and adults differ significantly in physiology,biochemistry and immune function,which leads to sig-nificant differences in blood transfusion strategies between children and adults.To guide the clinical transfusion practice of pediatric patients and improve the prognosis of children,the National Health Commission organized the formulation and re-lease of the health industry standard Guideline for Pediatric Transfusion(WS/T 795-2022).This paper will briefly introduce some concepts that help understand of the Standard and the preparation process of the Standard,and explain and interpret the preparation of the"scope","general provisions"and"factors to consider"of the Standard,hoping to contribute to the understanding and implementation of the Standard.

Chronic pancreatitis(CP)is a progressive fibroinflammatory disease characterized by destruction of pancreatic aci-nar cells,infiltration of inflammatory cells,activation of pancreatic stellate cell(PSC),and pancreatic fibrosis.Autophagy partici-pates in the maintenance of cell homeostasis.Recent studies have shown that autophagy closely related to the occurrence and develop-ment of CP.However,several autophagy types in the pancreatic microenvironment play different roles in the progression of CP.The autophagy of acinar cells has a"double-edged sword"effect.PSC autophagy is positively correlated with its activation,while the role of autophagy of inflammatory cells is still unclear.This study focused on some key cells in the CP microenvironment and explored the role and mechanism of autophagy in the progression of CP.

As research delves deeper into the mechanisms of tumor immune responses,studies reveal the importance of microbial com-munities within the tumor microenvironment in tumor progression and their interactions with the host immune system.Intratumoral micro-biota could influence the tumor microenvironment,thereby promoting or inhibiting tumor growth and development.Despite this import-ance,the specific role of intratumoral microbiota impacting cancer immunotherapeutic efficacy remains largely unexplored.A deeper under-standing of the characteristics and biological functions of tumor-specific microbiota heralds a potential revolutionary innovation in cancer treatment.In this review,we introduce the discovery and sources of intratumoral microbiota,also addressing its composition,and discuss tumor tissue characteristics.Moreover,we briefly review the history of cancer immunotherapy development with a particular focus on the research progress concerning the impact of intratumoral microbiota on cancer immunotherapy.Furthermore,we explore emerging strategies that combine targeting intratumoral microbiota with immunotherapy to enhance immune efficacy,inhibit tumor progression,and improve cure rates,anticipating that this approach could represent a new direction for enhancing treatment outcomes and prospects.

Concurrent chemoradiotherapy (CCRT) refers to the simultaneous treatment of chemotherapy and radiotherapy, and the effect of radiotherapy is enhanced with low-dose chemotherapy, which can reduce tumor recurrence and metastasis and improve clinical prognosis of patients. At present, the main factors for the increase of radiosensitivity of concurrent chemotherapy is that concurrent chemotherapy prevents the repair of tumor cells, and chemotherapy and radiotherapy act on different cell cycles and have synergistic effects. However, even for patients with locally advanced cervical cancer (LACC) who have undergone CCRT, the 5-year survival rate is only 60%, which is still not ideal. In order to improve the efficacy, researchers have conducted a series of exploratory studies, which consist of the combination of targeted drugs and immunodrugs, and neoadjuvant regimens before CCRT, etc. Although targeted or immunologic drugs are effective treatment of LACC, in view of the lack of large-scale evidence-based medical evidence, multi-center prospective and randomized phase III clinical trials and high-level articles are needed to improve the level of evidence-based medicine. This consensus summarizes several key evidence-based medical studies published recently, especially the clinical research progress in targeted and immunological therapies, providing reference for domestic peers.

Objective To investigate the effects of high-frequency repetitive transcranial magnetic stimulation(rTMS)combined with aerobic exercise training on motor function,walking ability and activity of daily living(ADL)in patients with mild to moderate Parkinson's disease(PD).Methods A total of 54 PD patients admitted in our department from March 2021 to January 2023 were recruited and randomly divided into conventional treatment group(n=27,aerobic exercise training for 2 weeks)and combination treatment group[n=27,aerobic exercise training plus high-frequency(10 Hz)rTMS in the bilateral primary motor cortex].Unified Parkinson's Disease Rating Scale-Ⅲ and ADL scale were applied in two groups before treatment(T0)and 1 h(T1)and 4 weeks(T2)after 2 weeks of treatment to compare the differences in motor score,gait pa-rameters(pace,stride length and stride frequency)and ADL score between them.Results At T1 and T2,the combination treatment group obtained significantly lower UPDRS-Ⅲ score(23.30±3.36 vs 26.22±4.04,24.04±3.45 vs 27.19±3.41,P＜0.01),but higher gait speed and longer stride length when compared with the conventional treatment group(P＜0.05,P＜0.01).In the combi-nation treatment group,the UPDRS-Ⅲ and ADL scores at T1 and T2 were decreased,stride speed and stride amplitude were increased when compared with the levels at T0(P＜0.05),and the ADL score was decreased at T1 than T2(P＜0.05).In the conventional treatment group,the UPDRS-Ⅲ and ADL scores at T1 were decreased than those at T0 and T2,and the step speed and stride length were increased at T1 than T0 and T2(P＜0.05).No statistical difference was found in step frequency between the two groups at different time points(P＞0.05).Conclusion High-frequency rTMS in the M1 area bilaterally combined with aerobic exercise training is superior to aerobic exercise training alone in improving PD motor symptoms and gait parameters(gait speed,and stride length),and its efficacy can last up to 4 weeks after treatment.

Objective:To explore the mechanism of exacerbating chronic graft versus host disease (GVHD) in mice with inflammatory status and enhancing immune injury in mice with PD-1.Method:Bone marrow and spleen cells of DBA/2 mice were injected into BALB/C mice pretreated with chemotherapy regimen (Flu+Bu) for constructing a chronic GVHD model. The animals were assigned into two groups of zymosan (100M SPL+10M BM+Zymosan) and control (100M SPL+10M BM+ PBS). After transplantation, two groups of mice were observed for weight changes, survival status and chronic GVHD manifestations. Target organ tissues were harvested for pathological scoring. Flow cytometry was employed for detecting cell subpopulations and surface co-stimulatory molecules in target organs. PD-1 monoclonal antibody was injected into inflammatory murine model. Mice were observed and target organ cells were harvested for subsets and co-stimulatory factors.Result:In in vivo experiments, zymosan group showed more significant changes of chronic GVHD with higher mortality rate, faster weight loss and more severe symptoms of GVHD. At Week 2 post-transplantation, hematoxylin-eosin stain of target organ tissue was performed for pathology examination. Zymosan group showed more lymphocyte infiltration, more severe inflammation and more significant tissue injury with higher GVHD pathological score. The proportion of M2 in liver/lung of zymosan group was significantly lower than that of control group ( P<0.05) and no significant difference existed in the proportion of M1. In in vivo experiments, M1 ratio of splenic cell spiked markedly in zymosan group as compared to control group while M2 ratio declined greatly. The secretions of IL-4 and IL-10 dropped significantly while co-stimulatory molecules CD80 and CD86 rose obviously. Conclusion:The worsening graft-versus-host disease in inflammatory mice with anti-PD1 treatment is associated with a decline of Treg proportion.

In recent years, the prevalence of gestational diabetes mellitus (GDM) has significantly increased, leading to various adverse outcomes for mothers and their offspring. Early diagnosis and good blood glucose control can significantly improve pregnancy outcomes. Currently, the diagnosis of GDM mainly relies on the oral glucose tolerance test (OGTT), but there are many limitations in clinical application. The new biological marker glycosylated CD59 is a glycosylation product of complement regulatory proteins that can stably exist in body fluids and is linearly related to blood glucose levels, which has the advantages of simple testing and good reproducibility, and has been developed into a stable reagent kit. It has shown good value in the early diagnosis, standard diagnosis, and prediction of pregnancy outcomes of GDM.

Objective To analyze the mechanism of action of seaweed-kunbu in the treatment of breast cancer through network pharmacology. Methods The active ingredients and their targets of seaweed-kunbu were retrieved through the TCMSP database. Relevant targets for breast cancer were obtained through the GeneCards and OMIM databases, and "drug-disease target" network diagram was constructed using Cytoscape software. Protein-protein interaction (PPI) network analysis was performed using the String platform. Gene Ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed using R language. Molecular docking technology was used to verify the binding ability of key compounds to targets, and functional verification was carried out through in vitro experiments. Results A total of 11 effective compounds were obtained from seaweed-kunbu in this study, among which 10 were related to breast cancer. There were 150 highly relevant intersecting targets between seaweed-kunbu and breast cancer, and 10 core genes including Serine/threonine kinase 1 (AKT1), p53 tumor protein (TP53), tumor necrosis factor (TNF), interleukin6 (IL6), vascular endothelial growth factor A (VEGFA), JUN, caspase 3 (CASP3), interleukin1B (IL1B), MYC and human epidermal growth factor receptor (EGFR) were screened out. GO analysis indicated that these compounds may be involved in biological processes such as signal transduction, apoptosis, cell proliferation, and inflammatory response. KEGG pathway analysis showed that the main enriched signaling pathways were PI3K/Akt, MAPK and TNF. Molecular docking and in vitro experimental results demonstrated that fucosterol, the main chemical component of seaweed-kunbu, had an antiproliferative effect on triple-negative breast cancer BT-549 cells. Conclusion Seaweed-kunbu may treat breast cancer through multiple targets and pathways, and its main chemical component fucosterol can effectively inhibit the proliferation activity of BT-549 cells.

Objective To investigate the impact of the Shared Medical Appointment (SMA) model on blood glucose levels and self-management behaviors in patients with gestational diabetes mellitus (GDM). Methods A total of 87 pregnant women diagnosed with GDM at the Obstetrics and Gynecology and Endocrinology Outpatient Departments of the Affiliated Suqian Hospital of Xuzhou Medical University from October 2021 to October 2022 were enrolled and divided into treatment group (n=44) and control group (n=43). The treatment group received SMA-based GDM management, while the control group underwent routine outpatient follow-up. Baseline data, flash glucose monitoring (FGM)-related indicators before and after treatment, and self-management behavior scale scores were compared between the two groups. Results No statistically significant differences were observed between the two groups in age, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), fasting blood glucose (FBG), blood urea nitrogen (BUN), creatinine (Cr), uric acid (UA), triglycerides (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and glycated hemoglobin (HbA1c) (P>0.05). After treatment, the time in range (TIR) of glucose was higher in the treatment group than that in the control group, while mean amplitude of glycemic excursions (MAGE), standard deviation of blood glucose (SDBG), coefficient of variation (CV), and mean blood glucose (MBG) were lower in the treatment group (P < 0.05). Within the treatment group, post-treatment TIR was higher, and MAGE, CV, SDBG, and MBG were lower than pre-treatment levels (P < 0.05). In the control group, post-treatment TIR was higher, and SDBG and MBG were lower than pre-treatment levels (P < 0.05). After treatment, the total score and scores for dietary management, exercise management, medication management, and blood glucose monitoring management in the self-management behavior scale were significantly higher in the treatment group than in the control group (P < 0.05). In the treatment group, post-treatment scores for all self-management behaviors were higher than pre-treatment levels, while post-treatment total scores and scores for medication management and blood glucose monitoring management in the control group were higher than pre-treatment levels (P < 0.05). Conclusion SMA management model can comprehensively improve blood glucose levels and enhance self-management behavior capabilities in GDM patients.

Colorectal tumors often create an immunosuppressive microenvironment that prevents them from responding to immunotherapy.Cannabidiol(CBD)is a non-psychoactive natural active ingredient from the cannabis plant that has various pharmacological effects,including neuroprotective,antiemetic,anti-inflammatory,and antineoplastic activities.This study aimed to elucidate the specific anticancer mechanism of CBD by single-cell RNA sequencing(scRNA-seq)and single-cell ATAC sequencing(scATAC-seq)technologies.Here,we report that CBD inhibits colorectal cancer progression by modulating the suppressive tumor microenvironment(TME).Our single-cell transcriptome and ATAC sequencing results showed that CBD suppressed M2-like macrophages and promoted M1-like macrophages in tumors both in strength and quantity.Furthermore,CBD significantly enhanced the interaction between M1-like macrophages and tumor cells and restored the intrinsic anti-tumor properties of macrophages,thereby preventing tumor progression.Mechanistically,CBD altered the metabolic pattern of macro-phages and related anti-tumor signaling pathways.We found that CBD inhibited the alternative acti-vation of macrophages and shifted the metabolic process from oxidative phosphorylation and fatty acid oxidation to glycolysis by inhibiting the phosphatidylinositol 3-kinase-protein kinase B signaling pathway and related downstream target genes.Furthermore,CBD-mediated macrophage plasticity enhanced the response to anti-programmed cell death protein-1(PD-1)immunotherapy in xenografted mice.Taken together,we provide new insights into the anti-tumor effects of CBD.