Objective: To analyze the prevalence and determinants of comorbid overweight/obesity and elevated blood pressure among primary and secondary school students in Yangzhou City, and to explore the association between sleep patterns, eating behavior and the comorbidity of overweight/obesity and elevated blood pressure, so as to provide reference for developing prevention strategies targeting common comorbidities in students. Methods: By using stratified cluster random sampling, a total of 8 735 primary and secondary school students were selected from 36 schools in six counties of Yangzhou from October to November 2023. Students underwent physical examinations and a questionnaire survey was conducted using the questionnaire on students health status and influencing factors. The Chi square test was used to compare the detection rate of comorbid overweight/obesity and elevated blood pressure in different groups of primary and secondary school students. The Logistic regression model was used to explore the association between sleep and dietary behaviors and their combined effects and coexistence. Results: The detection rate of comorbid overweight/obesity and elevated blood pressure among primary and secondary school students in Yangzhou was 9.85%, which was higher among boys (12.14%) than girls (7.59%)( χ 2=50.86, P <0.01). After controlling for gender, residence, educational stage, parental education, smoking, drinking, and moderate to vigorous exercise, multivariate Logistic regression analysis showed that irregular breakfast consumption and inadequate daily sleep were associated with a higher risk of comorbidities compared with regular breakfast consumption and adequate daily sleep among overall and primary school students (overall: OR =1.52, 95% CI =1.18- 1.96 , primary school students: OR =2.79, 95% CI =1.61-4.82)(both P <0.05). From the perspective of primary school students of different genders, the risk of comorbidities in girls who consumed breakfast irregularly and had inadequate daily sleep was 3.59 times higher than that in girls who consumed breakfast irregularly and had inadequate daily sleep (95% CI =1.65-7.82, P <0.01). Conclusion The sleep patterns and breakfast behaviors of primary and secondary school students are found to be associated with comorbid overweight/obesity and elevated blood pressure, especially in primary school girls.

ObjectiveThe lung mesenchymal stem cells （LMSCs） induced by D-galactose （D-gal） were intervened by Wenfei Huaxian decoction-containing serum to explore the mechanism of Wenfei Huaxian decoction in delaying the senescence of LMSCs through the nicotinamide phosphoribosyltransferase/silent information regulator 1 （NAMPT/SIRT1） signaling pathway. MethodWenfei Huaxian decoction-containing serum was prepared. LMSCs were isolated by gradient density centrifugation， and they were cultured and identified in vitro. The senescence model in vitro was established by stimulating cells via D-gal for 24 h. LMSCs cells were modeled after being treated with different volume fractions （5%， 10%， 20%， 40%， and 80%） of Wenfei Huaxian decoction-containing serum for 24 h， and the cell proliferation level was detected by methyl thiazolyl tetrazolium （MTT） method. The cells were randomly divided into blank serum group， model group， and high， medium， and low dose groups of Wenfei Huaxian decoction-containing serum. Senescence-associated β-galactosidase （SA-β-gal） staining was used to detect the senescence of LMSCs in each group. The content of NAD + was detected by colorimetry. The levels of senescence-associated factors （p16 and p53）， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） in cell culture supernatant were detected by enzyme-linked immunosorbent assay （ELISA）. Western blot was used to detect the relative expression of senescence-associated proteins and NAMPT/SIRT1 signaling pathway-related proteins. ResultCompared with the blank serum group， the proliferation of LMSCs was significantly inhibited after D-gal stimulation for 24 h （P<0.01）. Compared with the model group， the proliferation of LMSCs could be promoted after intervention with the corresponding Wenfei Huaxian decoction-containing serum （P<0.05， P<0.01）. Compared with the blank serum group， the SA-β-gal staining of LMSCs in the model group after D-gal stimulation was enhanced， and the content of NAD⁺ was increased （P<0.01）. The expression levels of senescence factors p16 and p53， as well as SASP pro-inflammatory factors IL-6 and TNF-α in the cell culture supernatant， were significantly increased （P<0.01）. The expression of senescence-associated proteins p16， p21， and p53 increased （P<0.01）， and the protein expression of NAMPT， SIRT1， peroxisome proliferator-activated receptor γ coactivator 1α （PGC-1α）， and forkhead box family transcription factor O1 （FoxO1） decreased （P<0.01）. Compared with the model group， the SA-β-gal staining of LMSCs in each group of Wenfei Huaxian decoction-containing serum was significantly reduced， and the content of NAD⁺ was decreased （P<0.01）. The senescence factors （p16 and p53） and inflammatory factors （IL-6 and TNF-α） in the cell culture supernatant were significantly decreased （P<0.01）. The expression of senescence-associated proteins （P16， P21， and P53） decreased （P<0.05， P<0.01）. The protein expressions of NAMPT， SIRT1， PGC-1α， and FoxO1 were significantly up-regulated （P<0.05， P<0.01）. ConclusionWenfei Huaxian decoction can alleviate senescence and inflammatory response damage of D-gal-induced LMSCs， and its mechanism may be related to the regulation of the NAMPT/SIRT1 signaling pathway.

Objective To investigate how the transcription factor MYB activates cathepsin F(CTSF)and affects gastric cancer cell proliferation and stemness through glutamine metabolism and to explore the underlying mechanisms.Methods We used the TCGA and KnockTF databases to analyze CTSFexpression in gastric cancer tissues and predict MYB as the transcription factor of CTSFand analyze MYB expression in gastric cancer,respectively.We performed dual-luciferase and ChIP assays to verify this binding relationship.We assessed CTSFand MYB expression using real-time PCR.We investigated cell proliferation using CCK-8 and colony formation assays.The cell spheroidal ability was detected using a sphere formation assay.We examined stem cell surface marker(OCT4,NANOG,and SOX2)and glutamine transporter(SLC1A5)expression using Western blotting.We used corresponding kits to measure the glutamine,glu-tamic acid,and α-ketoglutaric acid content as well as the NADPH/NADP+ratio,GSH/GSSG ratio,and aspartic and oxaloacetic acid levels.Results We detected low CTSFexpression levels in gastric cancer tissues and cells.CTSFoverexpression could inhibit gastric cancer cell stemness and proliferation.CTSFknockdown significantly increased the glutamine,glutamate acid,andα-ketoglutaric acid contents,NADPH/NADP+and GSH/GSSG ratios,and aspartic and oxaloacetic acid levels,and promoted cell proliferation and stemness.MYB was highly expressed in gastric cancer tissues and cells.Our bioinformatic prediction combined with ChIP and dual-luciferase experiments confirmed MYB as a transcription factor for CTSF.Conclusion The results of our study indicated that the transcription factor MYB acti-vated CTSFto promote gastric cancer cell proliferation and stemness through glutamine metabolism.

Traumatic supraorbital fissure syndrome (TSOFS) is a symptom complex caused by nerve entrapment in the supraorbital fissure after skull base trauma. If the compressed cranial nerve in the supraorbital fissure is not decompressed surgically, ptosis, diplopia and eye movement disorder may exist for a long time and seriously affect the patients′ quality of life. Since its overall incidence is not high, it is not familiarized with the majority of neurosurgeons and some TSOFS may be complicated with skull base vascular injury. If the supraorbital fissure surgery is performed without treatment of vascular injury, it may cause massive hemorrhage, and disability and even life-threatening in severe cases. At present, there is no consensus or guideline on the diagnosis and treatment of TSOFS that can be referred to both domestically and internationally. To improve the understanding of TSOFS among clinical physicians and establish standardized diagnosis and treatment plans, the Skull Base Trauma Group of the Neurorepair Professional Committee of the Chinese Medical Doctor Association, Neurotrauma Group of the Neurosurgery Branch of the Chinese Medical Association, Neurotrauma Group of the Traumatology Branch of the Chinese Medical Association, and Editorial Committee of Chinese Journal of Trauma organized relevant experts to formulate Chinese expert consensus on the diagnosis and treatment of traumatic supraorbital fissure syndrome ( version 2024) based on evidence of evidence-based medicine and clinical experience of diagnosis and treatment. This consensus puts forward 12 recommendations on the diagnosis, classification, treatment, efficacy evaluation and follow-up of TSOFS, aiming to provide references for neurosurgeons from hospitals of all levels to standardize the diagnosis and treatment of TSOFS.

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 investigate the effect of PPAR-γon the proliferation of human large cell lung cancer(NCI-H460)cells in a high-glucose microenvironment and to explore the associated molecular mechanism.Methods NCI-H460 cells were treated with normal-glucose(blank group),hypertonic(control group),and high-glucose(30 mmol/L;high-glucose group)media.The effects of a high-glucose microenvironment on the proliferation of NCI-H460 cells were analyzed using Cell Counting Kit 8(CCK-8)and colony-for-mation assays.The specific PPAR-γactivator,rosiglitazone,was used to treat NCI-H460 cells in a high-glucose microenvironment,and the expression of NLRP3-inflammasome-related proteins was detected by Western blotting.The effect of PPAR-γon the proliferation of NCI-H460 cells in a high-glucose microenvironment was analyzed by CCK-8 and clony-formation assays.The NLRP3 inflammasome agonist,NSS,combined with rosiglitazone,were used to treat NCI-H460 cells in a high-glucose microenvironment.CCK-8 and clony-formation assays were used to analyze whether the NLRP3 inflammasome was involved in the inhibitory effect of PPAR-γon the proliferation of NCI-H460 cells in a high-glucose microenvironment.Results A high-glucose microenvironment significantly induced the proliferation of NCI-H460 cells,increased the activity of the NLRP3 inflammasome,and reduced the expression levels of PPAR-γprotein.Rosiglitazone effectively inhibited NLRP3 inflammasome activity and NCI-H460 cell proliferation,and this effect was reversed by NLRP3 inflammasome agonist.Conclusion PPAR-γinhibits the proliferation of NCI-H460 cells in a high-glucose microenvironment by down-regulating the activity of the NLRP3 inflammasome.

Objective:To observe the stoichiometry of vascular endothelial growth factor receptor 2 (VEGFR2) on the retinal vascular endothelial cell membrane by single-molecule fluorescence imaging.Methods:Rhesus monkey retinal vascular endothelial cells (RF/6A) were divided into blank control group (normal culture) and plasmid transfection group [transfected with VEGFR2-green fluorescent protein (GFP) recombinant plasmid]. The expression of GFP in the plasmid transfected group was observed by confocal microscope, and the expression of VEGFR2 in the cells was detected by real-time fluorescent quantitative polymerase chain reaction (qPCR) and Western blot. The fluorescence intensity distribution and bleaching steps of single VEGFR2-GFP molecule on the cell membrane were recorded by single-molecule imaging. The distribution of fluorescence intensity and the number of fluorescence bleaching steps of GFP were recorded.Results:GFP green fluorescence was observed in the transfected cells 12 hours after transfection. qPCR results showed that the expression of VEGFR2 and GFP mRNA in the plasmid transfected group was significantly higher than that in the blank control group ( t=11.240, 12.330; P<0.001, 0.001). Western blot results showed that the expression of VEGFR2 protein in the plasmid transfected group was significantly higher than that in the blank control group ( t=8.346, P<0.01). The results of single-molecule imaging showed that the fluorescence intensity distribution of VEGFR2-GFP on the surface of RF/6A cell membrane without ligand stimulation was bimodal, in which monomer and dimer were 86.0% and 14.0% respectively. By counting the steps of GFP fluorescence bleaching, the proportions of receptor monomer, dimer, trimer, and tetramer were 81.4%, 12.9%, 5.5%, and 0.3% respectively. Conclusion:In the absence of ligands, VEGFR2 coexists in the form of monomers and dimers on the surface of RF/6A cell membrane, and monomers are dominant.

Neovascularization is a characteristic manifestation of a variety of retinal diseases. Vascular endothelial growth factor (VEGF) mainly regulates the proliferation and migration of endothelial cells. VEGF receptor 2 (VEGFR2) is the main receptor to mediate this effect. The activation of downstream signals requires the binding of VEGF and VEGFR2, followed by receptor dimerization and autophosphorylation. Blocking this process and inhibiting neovascularization is very attractive treatment ideas. Monoclonal antibodies and fusion protein drugs currently used in ophthalmology can bind free VEGF. In addition, there are also macromolecular antibodies binding VEGFR2 and small molecule tyrosine kinase inhibitors, which is expected to further expand into the field of ophthalmology. Although anti-VEGFR2 therapy is a revolutionary method to inhibit neovascularization, there are no sufficient clinical evidences at present. In-depth understanding of the application status and progress of anti-VEGFR2 in the treatment of retinal neovascular diseases has important clinical significance.