BACKGROUND:A large number of articles have reported the effect and mechanism of platelet-rich plasma and hydrogel in the treatment of spinal cord injury,but few articles have summarized their treatment strategies for spinal cord injury. OBJECTIVE:To summarize the pathological process of spinal cord injury and the strategies of repairing spinal cord injury with platelet-rich plasma and hydrogel alone and in combination. METHODS:PubMed and CNKI databases were searched for articles published from inception to March 2024 by computer.The Chinese search terms were"spinal cord injury,platelet-rich plasma,hydrogel."The English search terms were"spinal cord injury,spinal cord,platelet-rich plasma,hydrogel,angiogenesis,neuralgia,combination therapy."Articles were screened according to inclusion and exclusion criteria,and 128 articles were finally included for review and analysis. RESULTS AND CONCLUSION:(1)The classification of platelet-rich plasma is complex and diverse,and the effects of platelet-rich plasma in the repair treatment of spinal cord injury are various,but they all show certain positive effects,that is,they can promote axon regeneration,stimulate angiogenesis,and treat neuropathic pain and so on.(2)The effect of platelet-rich plasma is mainly due to the growth factors contained in platelet-rich plasma.(3)There are many types of hydrogels,which mainly play the role of filling,simulating extracellular matrix,carrying drugs and biological products,and carrying cells as scaffolds in the repair treatment of spinal cord injury.(4)Compared with single therapy,combination therapy of platelet-rich plasma and hydrogel can promote nerve regeneration and spinal cord function recovery more effectively.

Objective To analyze the risk factors for chronic mountain sickness(CMS)in young male migrants living in high-altitude areas and to construct a diagnostic model and evaluate its diagnostic efficacy.Methods From June 10 to December 29,2023,a cross-sectional study was conducted on young male migrants subjected with convenience sampling who had been living in high-altitude areas(4 500～5 000 m)for 6 months or longer.Their demographic data were collected and blood samples were collected for laboratory test.According to the Qinghai Score for Chronic Mountain Sickness,they were divided into CMS group and non-CMS group.Then the participants were randomly divided into a training set and a test set in a ratio of 8∶2.Independent risk factors for CMS occurrence were screened out,through random forest variable importance ranking,univariate and multivariable logistic regression analysis,and a diagnostic model was constructed based on these factors.Receiver operating characteristic(ROC)curve analysis,calibration curve analysis,clinical decision curve analysis,and influence curve analysis were used to comprehensively evaluate the diagnostic performance of the model.Results According to the inclusion and exclusion criteria,308 out of 376 participants were finally subjected,and 17.53%of them were diagnosed with CMS.The major clinical symptoms of the CMS patients were dyspnea or palpitations(79.63%)and sleep disorders(85.19%).Further analysis revealed that creatine kinase-MB/creatine kinase(CK-MB/CK,OR=2.17,95%CI:1.43～3.28),high-altitude residence time(OR=2.44,95%CI:1.08～5.54),and body mass index(BMI,OR=1.62,95%CI:1.05～2.50)were 3 major independent risk factors for CMS.The area under the curve(AUC)value of the CMS diagnostic model in the training set and test set was 0.821(95%CI:0.756～0.886)and 0.821(95%CI:0.700～0.944),the specificity was 66.30%and 73.90%,the sensitivity was 89.50%and 81.20%,respectively,indicating good discrimination ability.Hosmer-Lemeshow goodness-of-fit test showed consistency between predicted results and actual observations(χ2=10.029,P=0.263;χ2=4.477,P=0.812).Clinical decision curve analysis demonstrated that within the threshold probability range from 0.1 to 0.7,the net benefit of the model exceeded both full intervention and no intervention strategies.The influence curve analysis showed high consistency between the model predictions and actual incidence when the threshold probability exceeded 0.4.These two analyses together confirmed the clinical application value of the model.Conclusion CK-MB/CK,high-altitude residence time and BMI are independent risk factors for CMS,and their diagnostic model helps identify potential individuals at risk for CMS.Early intervention can prevent the harm of CMS to the health of young men migrating to high-altitude areas.

Objective To explore the effect of rotenone exposure on the metabolic homeostasis of nicotinamide adenine dinucleotide(NAD+)in dopaminergic neurons of the rat mid-brain striatum,and investigate the effect of exogenous NAD+intervention on the cellular damage response of dopaminergic neurons induced by rotenone.Methods Male SD rats(8 weeks old,200～250 g)were divided into a control group using a table of random numbers,a rotenone exposure group,an NAD+-intervention group,and an NAD+group.An intoxication model was established in the rotenone exposure group.NAD+(250 mg/kg)was administered simultaneously with rotenone exposure in the NAD+-intervention group.The NAD+group was only given NAD+,while the control group received no intervention.After modeling,open field test was performed to evaluate behavioral changes.After scarification,serum samples and mid-brain striatal tissues were collected.HE staining was used to observe the morphology of dopaminergic neurons in the striatum.The NAD+content in the tissues was detected with NAD+/NADH kit.Western blotting was employed to determine the contents of tyrosine hydroxylase(TH),nicotinamide phosphoribosyltransferase(NAMPT),nicotinamide mononucleotide adenylyltransferase(NMNAT),and solute carrier family 25 member A51(SLC25A51).ELISA was utilized to measure the content of dopamine in the striatal tissues.Immunohistochemical staining was applied to observe the distribution and contents of TH proteins in the striatal tissues of each group.Results Rotenone exposure significantly affected the vital signs and motor abilities of rats,induced disorderly-arranged,atrophy and deformed neurons in the striatal tissue,decreased the content of TH,rate-limiting enzyme for dopamine synthesis,by approximately 29%(P<0.01),the content of dopamine by about 42%,and that of NAD+by almost 50%(P<0.01),while increased the NADH/NAD+ratio(P<0.01).After exposure,the content of NAMPT,an enzyme related to NAD+synthesis,was decreased by 26%(P<0.05),the contents of NMNAT1-3 and SLC25A51,mitochondrial transporters of NAD+by approximately 21%,38%,43%,and 21%,respectively(P<0.01).Exogenous NAD+intervention improved the motor function of exposure rats and the morphology of dopaminergic neurons in the mid-brain striatal tissue,and restored the content of TH in the striatal tissue significantly by 12.8%(P<0.05),and the content of dopamine by 20.9%(P<0.05).Conclusion Rotenone disrupts the NAD+homeostasis in dopaminergic neurons by inhibiting the NAD+synthesis and transport pathways in the mid-brain striatal tissues,while exogenous NAD+intervention can effectively alleviate the dopaminergic neuron damage induced by rotenone exposure.

Hearing loss is the most prevalent disabling disease. Cochlear implantation（CI） serves as the primary intervention for severe to profound hearing loss. This consensus systematically explores the value of genetic diagnosis in the pre-operative assessment and efficacy prognosis for CI. Drawing upon domestic and international research and clinical experience, it proposes an evidence-based medicine three-tiered prognostic classification system（Favorable, Marginal, Poor）. The consensus focuses on common hereditary non-syndromic hearing loss（such as that caused by mutations in genes like GJB2, SLC26A4, OTOF, LOXHD1） and syndromic hereditary hearing loss（such as Jervell & Lange-Nielsen syndrome and Waardenburg syndrome）, which are closely associated with congenital hearing loss, analyzing the impact of their pathological mechanisms on CI outcomes. The consensus provides recommendations based on multiple round of expert discussion and voting. It emphasizes that genetic diagnosis can optimize patient selection, predict prognosis, guide post-operative rehabilitation, offer stratified management strategies for patients with different genotypes, and advance the application of precision medicine in the field of CI.
Humans ; Cochlear Implantation ; Prognosis ; Hearing Loss/surgery* ; Consensus ; Connexin 26 ; Mutation ; Sulfate Transporters ; Connexins/genetics*

Objective To investigate the therapeutic effects and mechanisms of emodin(EMO)on dextran sulfate(DSS)-induced ulcerative colitis(UC)in mice.Methods DSS induced UC mouse model,detection of body weight,colon length and histopathological changes.Enzyme-linked immunosorbent assay(ELISA)was used to measure tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),interleukin-6(IL-6),interleukin-10(IL-10),and myeloperoxidase(MPO)levels.Western blot analysis examined the expression of Toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor κB(NF-κB)signaling pathway-related proteins.Flow cytometry assessed the ratio of helper T cells 17(Th17)to regulatory T cells(Treg).Additionally,16S rDNA sequencing was employed to evaluate gut microbiota composition.Results Compared with the normal group,DSS-treated mice exhibited significant weight loss,shortened colon length,and marked histological damage(P<0.001).EMO intervention,particularly at high doses,demonstrated dose-dependent improvements in body weight and colon injury(P<0.05).ELISA analysis showed EMO reduced TNF-α,IL-1β,and IL-6 levels while increasing IL-10(P<0.05).Western blot results indicated EMO inhibited abnormal activation of the TLR4/MyD88/NF-κB pathway and restored IκB.Conclusion EMO effectively mitigates DSS-induced ulcerative colitis(UC)inflammation and intestinal damage by regulating the TLR4/MyD88/NF-κB pathway,restoring Th17/Treg balance,and maintaining microbial homeostasis,providing theoretical support for its potential as a UC therapeutic agent.

Ornithine transcarbamylase(OTC)is a member of the transcarbamylase protein family,commonly found in the mitochondrial matrix of living organisms.It generally functions in a trimeric form and can catalyze the production of L-ornithine to L-citrulline.OTC is mainly expressed in the liver and intestines of mammals,playing an important role in the urea cycle and amino acid homeostasis.This article introduces the research progress of OTC genes,proteins,physiological functions,the impact of OTC deficiency on body health,and the diagnosis and treatment of OTC deficiency.

Aim Krüppel-like factor(KLF)2 and 4 are two core transcription factors closely related to vascular homeostasis,with multiple protective effects such as anti-inflammatory,anti-calcification and anti-thrombotic.The aim of this study is to elucidate and validate the vascular homeostasis related gene profile co-regulated by KLF2 and KLF4 in endo-thelial cells.Methods Human umbilical vein endothelial cells(HUVEC)were treated with adenovirus(Ad-KLF2 or Ad-KLF4)and control virus(Ad-NC)for 24 h,RNA was extracted from the cells and analyzed by transcriptomic sequen-cing.The sequencing results of overexpressed KLF2 and KLF4 were superimposed with the sequencing results of reported KLF2/KLF4 double-gene knockout mice.The selected differential expression genes were verified by real-time fluorescence quantitative PCR in HUVEC treated with Ad-KLF2 or Ad-KLF4,and in HUVEC treated with atorvastatin or resveratrol.Results Transcriptomic superposition revealed 256 differential expression genes were up-regulated by KLF2 and KLF4,and KEGG analysis showed that differential expression genes were enriched in hypertrophic cardiomyopa-thy,arrhythmogenic right ventricular cardiomyopathy,dilated cardiomyopathy,ECM-receptor interaction and focal adhesion;there were 145 differential expression genes down-regulated by KLF2 and KLF4,and KEGG analysis showed that differential expression genes were enriched in microRNA of cancer,mineral absorption,glycosaminoglycan biosynthesis-chondroitin sulfate/dermatan sulfate,p53 signaling pathway and biosynthesis of amino acids.Finally,six novel genes regulated by KLF2 and KLF4 were obtained.Conclusion FGFR3,SEMA4B,SEMA6A,PTX3,FABP4 and FABP5 may be novel genes that regulate vascular homeostasis in endothelial cells by the transcription factors KLF2 and KLF4.

Objective To review the application of intelligent robots in the pain intervention of children,and identify the elements of the intervention,so as to guide future research and practice.Methods A literature search was performed in the PubMed,Cochrane Library,Embase,Web of Science,CINAHL,CNKI,Wanfang database,and CBM.Following the methodology of the scoping review,the retrieval time was from the establishment of the database to November 2023.The included studies were summarized and analyzed.Results A total of 10 articles were included,including 7 randomized controlled trials,2 quasi-experimental studies,and 1 mixed method research study.The working principles of intelligent robots in pain intervention for pediatric patients include distraction and pain empathy.Functions of intelligent robots included verbal interaction,limb motion,facial expression,and haptic recognition.Interventions included pre-intervention preparation,intervention content,and intervention duration,of which the intervention content included question-and-answer conversations,breathing exercises,recreation,and verbal encouragement,and the duration of the intervention ranged from 3 to 11 minutes.The outcome indicators included pain level,negative emotions,and feasibility.The results showed the positive feasibility of the application of intelligent robots in pain intervention for children,which may help to reduce the level of pain and improve children's negative emotions such as anxiety and distress.Conclusion Intelligent robots in the field of pain intervention of children present preliminary effects and feasibility.It is recommended that researchers should enrich the functions of intelligent robots,enhance human-robot interaction,carry out personalized interventions,and add physiological indexes as effect evaluation indexes to further validate its application effects.

Objective To explore the effect of urine mixing degree on 24-hour urinary total protein(24 h UTP)in patients with chronic kidney disease(CKD).Methods From October 1,2023 to December 31,2023,30 hospitalized patients who needed to complete 24 h UTP testing in Zhongshan Hospital,Fudan University were selected.A 5 L unified container was used to collect urine for 24 hours.After collection and one hour's standing,the urine sample was divided into upper,middle,and lower equal parts according to volume,which was defined as direct-sampling group.Then,the urine samples were fully mixed with a magnetic stirrer and sampled again according to the above-mentioned three-equal sampling method,which was defined as mixed-sampling group.The generalized estimating equation was used to compare the urinary protein concentration before and after mixing and at different sampling location.Results The results of generalized estimating equation showed that after controlling the variable"sampling position",there was no significant difference in urinary protein concentration between the direct-sampling group and the mixed-sampling group.After controlling the variable"mixing method",there was still no significant difference in urinary protein concentration at different sampling positions.After adjusting the covariates such as age,gender,and estimated glomerular filtration rate(eGFR),the results were consistent.Conclusions With standard protocol,the entire 24-hour urine sample is a relatively even-distributed solution.After the total urine collection is completed,the temporary sample can be directly extracted from any level of the original urine within 1 hour,and the urine protein concentration of the sample multiplied by the urine volume can reflect the 24 h UTR.