Objective To investigate the characteristics of changes in blood uric acid(UA)and detection rate of hyperuricemia(HUA)among officers and soldiers during long-term maritime missions,as well as their related influencing factors.Methods A total of 100 servicemen were randomly selected from 240 officers and soldiers who will participate in a long-distance voyage mission.Their general information,including age,education level,administrative position,years of service on board,and department,was surveyed.Their annual data of physical examination were retrospectively analyzed and compared with the results of another 335 shore-based servicemen during the same period.On mission day 10(D10)and day 50(D50),the venous blood samples were collected from the participants to synchronously measure blood UA level and body composition indicators(body fat mass,BMI,fat percentage,fat mass,muscle mass,and muscle percentage).Additionally,on D50,Self-Rating Scale of Sleep(SRSS)and Symptom Checklist-90(SCL-90)were employed to survey their conditions.Seventy service members were randomly selected from the 100 participants to engage in aerobic exercise.The changes in UA level and detection rate of HUA among the mission personnel were analyzed,along with their influencing factors.Results The UA level and HUA detection rate in long-term navigation personnel during concurrent annual physical examinations were significantly lower than those in shore-based personnel(P<0.01).Compared to pre-voyage physical examination results,the UA level and HUA detection rate in long-term navigation personnel were significantly increased from mission day D10(P<0.001).Compared to the values at D10,the UA level and HUA detection rate at D50 showed significant decreases(P<0.05),and then essentially returned to pre-mission examination levels(P>0.05).Aged<32 years was an independent risk factor for new-onset HUA at mission D10(P<0.05).<32 years old and aerobic exercise during the voyage were independent influencing factors for HUA outcome(P<0.05).Conclusion Serum UA level and HUA detection rate among officers and soldiers participating in long-term maritime missions are relatively low before departure,but in significant increases during the early stages of the mission,particularly among those aged<32 years.Scientific aerobic exercise during the mission period helps reduce UA level and HUA detection rate,playing a crucial role in guaranteeing physical and mental health.

OBJECTIVE To predict and validate the potential mechanisms of Kaixinsan(KXS)in ameliorating neuroinflammation in Alzheimer's disease(AD).METHODS Network pharmacology was employed to identify core anti-inflammatory components and key inflammatory targets of KXS for AD.Gene ontology(GO)functional annotation,Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment,and molecular docking were performed.Based on these findings,male SD rats were used to establish an AD model via chronic D-galactose induction.The effects of KXS on AD rats were evaluated,including quantitative behavioral score,learning and memory parameters(escape latency,platform crossings,platform quadrant distance and time),organ indexes(heart,liver,spleen,thymus),histopathological alterations in the hippocampus,and expressions of inflammation-related pathway proteins and their upstream/downstream regulators.RESULTS Core anti-inflammatory components of KXS for AD included gomisin B,panaxytriol,gomisin A,enhydrin,vulgarin and panaxydol,while key inflammatory targets involved nuclear factor-kappa B subunit 1(NFKB1),nuclear factor-κB p65(NF-κB p65),interleukin-1β(IL-1β),IL-6,Toll-like receptor 4(TLR4),tumor necrosis factor,nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3(NLRP3)and caspase-1(CASP1).GO and KEGG pathway enrichment involved inflammatory response,phosphorylation and the NF-κB signaling pathway.Molecular docking confirmed strong binding affinities between core components and key targets.Animal experiments demonstrated that,compared to the model group,KXS significantly alleviated histopathological damage(e.g.,neuronal shrinkage,reduced Nissl bodies in hippocampal CA1,CA3,and DG regions),increased organ indexes(except for liver index)and Nissl-stained positive cells,improved learning and memory performance,and reduced behavioral scores(at the 8 and 12 weeks of the experiment)and protein expression of NF-κB p65,phosphorylated NF-κB p65,TLR4,NLRP3,CASP1 and IL-1β.CONCLUSIONS KXS effectively mitigates neuroinflammation,reduces hippocampal neuronal injury,and enhances learning and memory ability in AD rats,potentially through suppressing the NF-κB signaling pathway and its upstream/downstream regulators.

Objective To explore the content and the psychometric properties of assessment tools used for evaluating functioning and adaptive behavior in school-age children with intellectual and developmental disabilities within educational settings. Methods The most used assessment tools included Vineland Adaptive Behavior Scales(VABS),Supports Intensity Scale for Children(SIS-C),Strengths and Difficulties Questionnaire(SDQ)and Repetitive Behavior Scale-Revised(RBS-R),for assessing functioning and adaptive behavior children with intellectual and developmental disabili-ties.Employing the framework and methods of the International Classification of Functioning,Disability,and Health(ICF),this research encoded and categorized the assessment dimensions and items of the four tools,and explored their psychometric properties. Results VABS's assessment content was solely focused on activities and participation,including speaking(d330),con-versation(d350),toileting(d530),eating(d550),drinking(d560),basic interpersonal interactions(d710),com-plex interpersonal interactions(d720),changing and maintaining body positions(d410-d429),carrying,moving and handing objects(d430-d449),and walking and moving(d450-d469).SIS-C assessed activities and participa-tion,and environmental factors,including washing oneself(d510),caring for body parts(d520),community life(d910),using transportation(d470),school education(d820),basic learning(d130-d159),looking after one's health(d570),basic interpersonal interactions(d710),and products and technology for education(e130).SDQ fo-cused on body functions,and activities and participation,including emotional functions(b152),global psychoso-cial functions(b122),attention functions(b140),and basic interpersonal interactions(d710).RBS-R focused on body functions,and activities and participation,including involuntary movement reaction functions(b755),invol-untary movement functions(b765),looking after one's health(d570),energy and drive functions(b130),under-taking a single task(d210),carrying out daily routine(d230),attention functions(b140),and handling stress and other psychological demands(d240).VABS was characterized by good specificity and excellent sensitivity.SIS-C demonstrated very good internal consistency,reliability and validity.SDQ was good in internal consistency,with excellent credibility and validity.RBS-R showed good internal consistency,reliability and validity. Conclusion SDQ and RBS-R cover both body functions,and activities and participation,SIS-C covers activity and par-ticipation,and environmental factors,while VABS solely assesses activities and participation.In terms of body functions,the assessment items primarily focus on mental functions(b130-b189)and movement functions(b750-b799).For activities and participation,the tools assess content across eight domains of functioning.Regarding en-vironmental factors,the assessment content mainly includes products and technology for education(e130),as well as design,construction and building products and technology of buildings for public use(e150).VABS,SIS-C,SDQ,and RBS-R are all norm-referenced measures,with moderate to excellent internal consistency,and good to excellent reliability and validity.

Objective To explore the intrinsic connectivity alterations of brain-wide functional networks in patient with trigeminal neuralgia(TN)via combining resting-state functional magnetic resonance imaging(rs-fMRI)and graph theory methods.Methods A total of 41 patients with TN(TN group)and 41 healthy controls(HC)(HC group)were recruited,and differences in network topologyat-tributes and correlations with clinical variables were analyzed between the two groups.Results Both groups met the σ standard.The global efficiency(Eg)of TN group was lower than that of HC group(P＜0.05),whereas the λ of TN group was higher than that of HC group(P＜0.05).The node efficiency(Ne)of bilateral rectus gyrus and bilateral pallidum of TN group were significantly higher than those of HC group,while the Ne of left supraparietal gyrus,left angular gyrus,left post-central gyrus,bilateral marginal supraparietal gyrus,and left caudate nucleus of TN group were significantly lower than those of HC group(P＜0.05).The local efficiency(Eloc)of the TN group was negatively correlated with the visual analogue scale(VAS)score(P＜0.05),the clustering coefficient(Cp)of the TN group was negatively correlated with the short-form McGill pain questionnaire(SF-MPQ)sensory score(P＜0.05),and the Ne of right rectus gyrus of the TN group was positively correlated with the disease duration(P＜0.05).Conclusion The TN group retain σ,but the overall information transfer efficiency of the brain is reduced and functional integration is diminished.Several brain regions in the TN group has abnormal Ne,which provide an objective basis for altered brain functional networks in TN.

Objective To explore the pharmacodynamic substances of Simiao Wan for the treatment of hyperuricemia and gout.Methods The pharmacological model of hyperuricemia was established.The chemical components in vivo and in vitro of Simiao Wan were analyzed by UPLC-Q-Exactive-MS.Based on the components absorbed in blood,the"active ingredient-target-pathway"network of Simiao Wan for regulating hyperuricemia and gout was constructed by network pharmacology method.The key ingredients were used for molecular docking with key targets[uricogenase(XDH),uric acid transporter(ABCG2,GLUT9,OAT1,URAT1)and inflammatory targets(PTGS2,TLR2,TLR4)]of hyperuricemia and gout.Finally,experimental verification was conducted according to the results of molecular docking.Our aim is to identify the key pharmacodynamic substances of Simiao Wan for the treatment of hyperuricemia and gout.Results Eighty-nine components of Simiao Wan were identified by UPLC-Q-Exactive-MS analysis,including 74 components absorbed in blood,which were confirmed as candidate ingredients.Network pharmacology was used to constructed"components absorbed in blood-target-pathway"network,and components absorbed in blood were matched with 116 targets of hyperuricemia and 173 targets of gout.It is involved in the regulation of biological processes,such as glucose and lipid metabolism,oxidative stress,inflammatory response,ERK1 and ERK2 cascade,MAPK cascade,PI3K signal transduction.Moreover,Simiao Wan plays a role in regulating the network of hyperuricemia and gout through regulating blood lipids and atherosclerosis,apoptosis,AGE-RAGE,TNF,PI3K-Akt,MAPK,TLRs,JAK-STAT,NF-κB and other signaling pathways.Molecular docking studies showed that berberine,phellodendrine,magnoflorine,jatrorrhizine,palmatine,obacunone,limonin,atractylodin,taxifolin,atractylenolide Ⅲ and β-ecdysterone had good affinity with uric acid synthase,uric acid transporter and inflammatory targets.Western Blot test showed that taxifolin negatively regulates the expression of URAT1.The above-mentioned compounds were the main pharmacodynamic substances of Simiao Wan for the treatment of hyperuricemia and gout.Conclusion This article describes the main pharmacodynamic substances of Simiao Wan in the regulation of hyperuricemia and gout,which can provides a scientific basis for the clinical application,improvement in quality evaluation and standard of Simiao Wan.

Spinal surgical site infection (SSI), especially deep SSI after internal fixation is difficult in treatment, with long course of disease and poor prognosis. At present, there are many controversies in the diagnosis and treatment of spinal SSI, with unsatisfactory overall efficacy of its diagnosis and treatment. Besides, no diagnosis and treatment guideline based on evidence-based medicine has been in existence. To this end, the Spinal Infection Group of the Orthopedic Branch of the Chinese Medical Doctor Association and the Spinal Infection Group of the Spinal Surgery Branch of the Chinese Rehabilitation Medicine Association jointly organized relevant experts to formulate Evidence-based clinical guideline for the diagnosis and treatment of surgical site infection in spinal trauma ( version 2024) based on an evidence-based approach. A total of 10 recommendations were proposed on the diagnosis and treatment of spinal SSI, so as to provide a clinical reference for the diagnosis and treatment of spinal SSI.

Spinal surgical site infection (SSI), especially deep SSI after internal fixation is difficult in treatment, with long course of disease and poor prognosis. At present, there are many controversies in the diagnosis and treatment of spinal SSI, with unsatisfactory overall efficacy of its diagnosis and treatment. Besides, no diagnosis and treatment guideline based on evidence-based medicine has been in existence. To this end, the Spinal Infection Group of the Orthopedic Branch of the Chinese Medical Doctor Association and the Spinal Infection Group of the Spinal Surgery Branch of the Chinese Rehabilitation Medicine Association jointly organized relevant experts to formulate Evidence-based clinical guideline for the diagnosis and treatment of surgical site infection in spinal trauma ( version 2024) based on an evidence-based approach. A total of 10 recommendations were proposed on the diagnosis and treatment of spinal SSI, so as to provide a clinical reference for the diagnosis and treatment of spinal SSI.

OBJECTIVE To investigate whether gas-trodin(GAS)plays a neuroprotective role by activating PI3K/Akt/BACH1 signaling axis to improve glycolytic func-tion.METHODS HT22 cells were treated with Aβ25-35 for 24 h to establish cell damage model.GAS pretreated HT22 cells for 2 h,and Akt agonist SC79,Akt inhibitor MK2206,PI3K inhibitor LY294002 were added 0.5 h before GAS treatment to detect their protective mecha-nisms.Pharmacodynamic research of GAS in this model were divided into six groups:control group,GAS group(GAS 10 μmol·L-1),model group(Aβ25-35 20 μmol·L-1),model +GAS 2.5,5 and 10 μ mol·L-1 group).Mecha-nism research of GAS in this model was divided into 6 groups:control group,Aβ25-35 20 μmol·L-1 group,Aβ25-35 20 μmol·L-1 + GAS 10 μmol·L-1 group,Aβ25-35 + SC79 group(Aβ25-35 20 μmol·L-1 +SC79 10 μmol·L-1),Aβ25-35+MK2206+GAS group(A β 25-35 20 μ mol·L-1 +MK2206 10 μmol·L-1+GAS 10 μmol·L-1),Aβ25-35+LY294002+GAS group(Aβ25-35 20 μmol·L-1+LY294002 10 μmol·L-1+GAS 10 μmol·L-1).Cell viability was detected by MTT,mor-phological changes of cells were observed by micro-scope,ATP content was detected by chemilumines-cence,and pyruvate(PA)content was detected by colo-rimetry.Western blotting was used to detect the protein levels of transcription factor BACH1,key glycolysis enzyme hexokinase(HK1)and PI3K/Akt signaling path-way related proteins PI3K,p-PI3K,Akt and p-Akt.RESULTS The results showed that compared with the control group,the cell morphology of HT22 cells damaged by Aβ25-35 was damaged,the number of cells decreased,the cell body became smaller,the number of dead cells increased,the cell survival rate,ATP and PA contents decreased significantly,and the protein expressions of p-PI3K,p-Akt,BACH1 and HK1 were significantly down-regulated.GAS treatmentcansignificantlyimprovethemor-phology of HT22 cells damaged by Aβ25-35,increase cell survival rate,ATP and PA contents,and up-regulate the expression of p-PI3K,p-Akt,BACH1 and HK1 proteins.SC79 also significantly increased cell survival rate,ATP content,protein expression of BACH1 and HK1.However,the above ameliorative effect of GAS on HT22 cell dam-age induced by Aβ25-35 was antagonized by LY294002 and MK2206.CONCLUSION GAS exerts a neuroprotec-tive effect on Aβ25-35-induced HT22 cell injury by improv-ing glycolytic function through activating PI3K/Akt/BACH1 signaling axis.

Objective:To compare the clinical utility of 18F-fibroblast activating protein inhibitor (FAPI)-42 and 18F-fluorodeoxyglucose (FDG) PET/CT imaging in newly diagnosed lung cancer patients. Methods:From May 2020 to September 2021, the images of 43 lung cancer patients (32 males, 11 females, age: 37-80 years) who pathologically confirmed and received 18F-FDG and 18F-FAPI-42 PET/CT within 2 weeks in the First Affiliated Hospital of Guangzhou Medical University were prospectively analyzed. The maximum standardized uptake value (SUV max) of 18F-FDG and 18F-FAPI-42 and the number of lesions detected by 2 imaging methods were compared by using paired t test and Wilcoxon rank sum test. Results:The 43 newly diagnosed lung cancer patients included 35 adenocarcinoma, 2 squamous cell carcinoma, 4 small cell lung cancer, and 2 high-grade neuroendocrine tumors. 18F-FAPI-42 had a very high tumor uptake (SUV max: 12.24±3.97) and lesion detection rate (positive rate: 100%(37/37)) in primary lung adenocarcinoma and squamous cell carcinoma. The uptake of 18F-FAPI-42 in lymph node (10.13±5.43), pleura (6.75(4.96, 8.58)) and bone lesion (7.18(4.33, 9.66)) were significantly higher than those of 18F-FDG (6.35±3.30, 2.69(1.81, 5.00), 4.38(2.96, 6.36); t=12.19, z values: 5.47, 5.79, all P<0.001). In lung adenocarcinoma and squamous cell carcinoma, although the uptake of 18F-FAPI-42 in brain metastases was significantly lower than that of 18F-FDG (0.72(0.15, 1.82) vs 6.53(4.65, 9.34); z=6.42, P<0.001), the tumor/background (T/B) ratio was significantly higher than that of 18F-FDG (3.54(1.15, 14.88) vs 0.96(0.77, 1.04); z=6.05, P<0.001). In lung adenocarcinoma and squamous cell carcinoma, the number of lesions detected by 18F-FAPI-42 PET/CT was significantly more than that of 18F-FDG (lymph node: 6.0(2.3, 11.5) vs 4.5(2.0, 10.8); brain: 2.0(1.0, 3.0) vs 0.0(0.0, 0.0); pleura: 6.0(2.8, 10.0) vs 4.0(0.8, 5.5); z values: 2.16, 3.10, 2.04, all P<0.05). However, in high-grade neuroendocrine tumors and small cell lung cancer, the SUV max of 18F-FAPI-42 in primary lesions (8.05±2.60), lymph node lesions (5.98±2.21) and brain lesions (0.44(0.13, 0.82)) were lower than those of 18F-FDG (16.28±5.17, 12.30±5.47, 4.94(4.84, 6.25); t values: 3.58, 7.52, z=3.06, all P<0.05). Conclusions:In lung adenocarcinoma and squamous cell carcinoma, 18F-FAPI-42 has a very high tumor uptake and lesion detection rate in primary tumor. In addition, compared with 18F-FDG PET/CT, 18F-FAPI-42 PET/CT shows clearer tumor contours and more lesions. Therefore, 18F-FAPI-42 is more suitable for preliminary staging of lung adenocarcinoma and squamous cell carcinoma than 18F-FDG, while the opposite is true in small cell lung cancer and high-grade neuroendocrine tumors.

OBJECTIVE: To investigate the effects of ribonucleotide reductase catalytic subunit M1 (RRM1) gene silencing on drug resistance of human breast cancer cell line MCF-7/R. METHODS: We established a paclitaxel-resistant breast cancer MCF-7 cell line (MCF-7/R) by exposing the cells to high-concentration paclitaxel in a short time. Small interfering RNAs (siRNAs) targeting RRM1 were designed to silence RRM1 expression in human breast cancer MCF-7/R cells. MTT assay was used to detect the IC values and the sensitivity to paclitaxel in the cells with or without siRNA transfection. The changes in the proliferative activity of MCF7 and MCF-7/R cells following RRM1 gene silencing were evaluated using EdU assay. Flow cytometry was used to analyze the cell apoptosis and cell cycle changes. We assessed the effect of RRM1 gene silencing and paclitaxel on the tumor growth in a nude mouse model bearing subcutaneous xenografts with or without siRNA transfection. RESULTS: We detected significantly higher expressions of RRM1 at both the mRNA and protein levels in the drug-resistant MCF- 7/R cells than in the parental MCF-7 cells ( < 0.01). Transfection with the specific siRNAs significantly reduced the expression of RRM1 in MCF-7/R cells ( < 0.05), which showed a significantly lower IC value of paclitaxel than the cells transfected with the negative control siRNA ( < 0.05). RRM1 silencing significantly inhibited the proliferation ( < 0.01) and enhanced the apoptosis-inducing effect of paclitaxel in MCF-7/R cells ( < 0.001); RRM1 silencing also resulted in obviously reduced Akt phosphorylation, suppressed Bcl-2 expression and promoted the expression of p53 protein in MCF-7/R cells. In the tumor-bearing nude mice, the volume of subcutaneously transplanted tumors was significantly smaller in MCF-7/R/siRNA+ PTX group than in the other groups ( < 0.001). CONCLUSIONS RRM1 gene silencing can reverse paclitaxel resistance in human breast cancer cell line MCF-7/R by promoting cell apoptosis.
Animals ; Apoptosis ; Breast Neoplasms ; Drug Resistance, Neoplasm ; Gene Silencing ; Humans ; MCF-7 Cells ; Mice ; Mice, Nude ; Paclitaxel ; RNA, Small Interfering ; Ribonucleotide Reductases ; Tumor Suppressor Proteins