From the patient’s perspective， taking the control right of artificial intelligence （AI） in the analysis of pregnant and postpartum women’s health data as the entry point， this paper constructed a patient-centered governance framework for AI medical data control. It defined the different stages and scenarios of applications related to the health data analysis of pregnant and postpartum women， conducted a comparative analysis that combines existing ethical issues concerning AI data control in the medical field， and discussed autonomy issues in health management scenarios from three dimensions， namely， voluntariness， purposiveness， and steadfastness. Based on these discussions， this paper highlighted the reflection on autonomy under the behavioral research paradigm. Starting from the basic actions such as provision， deletion， analysis， triggering， presentation， revision， and response， it regarded technical behaviors as a form of instrumental communication and emphasized ensuring patients’ ample opportunities to participate in interactive links such as “information provision and adoption” “analysis and judgment” “presentation and summarization，” and “feedback and revision.” This will lay a foundation for expanding the existing discussion on medical AI autonomy to the ethical category of information usage.

To improve the targeted therapeutic effect of magnolol (Mag) on neuroblastoma, Mag-loaded mitochondria-targeting immunoliposomes modified by datuximab (aGD2) and triphenylphosphine (TPP) (Mag/aGD2-T-ILN) were prepared, and their physicochemical properties, targeting characteristics and anti-tumor activity were evaluated. Physico-chemical properties showed that the surface of Mag/aGD2-T-ILN was smooth and spherical, with good dispersibility. The particle sizes, PDI and Zeta potentials of Mag/aGD2-T-ILN were measured to be (136.5 ± 5.1) nm, 0.184 ± 0.010 and (27.5 ± 3.6) mV, respectively. Mag/aGD2-T-ILN could release the drug continuously and slowly, and maintain good stability at 4 ℃. Cytotoxicity test exhibited that the IC50 of 2-ME/aGD2-T-ILN was (4.07 ± 0.48) µmol/L, and compared with free Mag, the toxicity of Mag/aGD2-T-ILN to SH-SY5Y cells increased by 6.4 times. Cellular binding and uptake assays suggested that Rho-aGD2-T-ILN could specifically target GD2-positive tumor cells and then further reach their mitochondria. Therapeutic efficacy indicated that Mag/aGD2-T-ILN could better suppress the growth of SH-SY5Y tumor cells in the body with lower toxicity and less side-effects. The results demonstrated that the Mag/aGD2-T-ILN nanoparticles system could achieve intracellular endocytosis through specific binding of antibodies and antigens between the carrier and the surface of tumor cells and electrostatic interaction, then effectively delivered and released the drugs into mitochondria by crossing the mitochondrial phospholipid membrane through TPP, and thus achieving mitochondria-targeting therapy of Mag/aGD2-T-ILN. Through the construction of this active targeting delivery system, the clinical application value of datuximab and Mag is improved, providing a novel approach for the clinical treatment of neuroblastoma.

To report diagnosis and treatment of a patient with rectal cancer and synchronous liver metastases, accompanied by severe coronary artery stenosis and cardiac insufficiency, and to provide a reference for clinical decision-making in such cases through introducing the treatment contradiction, the choice of systemic treatment plan and the timing of operation, and the final outcome. After definitive diagnosis, the patient received systemic therapy with cetuximab＋irinotecan＋oxaliplatin＋raltitrexed, and along with oral medication to improve cardiac function, followed by elective coronary revascularization. After revascularization, the cardiac function of patient was fully improved. And the tumor lesion was effectively controlled after antitumor therapy. Once the cardiac condition of patient stabilized, two-stage surgical resection of the primary rectal cancer and liver metastases was performed, ultimately achieving tumor-free status, and discharged.

Background Microparticles (MPs) are one of the main medium of inflammatory reaction with an important role in atherosclerotic progression. Studies on association of air pollution exposure and levels of peripheral blood MPs are limited among human. Objective To evaluate the effects of short-term exposure to air pollution on levels of peripheral blood MPs. Method A panel of 73 healthy adults was followed with 4 repeated follow-ups in Beijing, China, from November 2014 to January 2016. During each visit, we collected questionnaire information, fasting venous blood, urine, and exposures to fine particulate matter (PM_2.5), black carbon, nitric oxide, nitrogen dioxide, nitrogen oxide, sulfur dioxide, carbon monoxide, and ozone. We used linear mixed-effect models to analyze associations of air pollution exposure with levels of total MPs (TMPs) and MPs derived from various cells. Stratified analysis was conducted by levels of C-reactive protein (CRP) and malondialdehyde (MDA). Results The results showed significant associations between air pollution exposure and peripheral blood TMPs at 2 h-6 d prior to the follow-ups (P<0.05), while no statistical associations were found for MPs derived from different cell types. Significant increases in TMPs of 7.8% (95%CI: 0.7%, 15.3%) and 14.3% (95%CI: 2.8%, 27.2%) were observed with each interquartile range (IQR) increase in PM_2.5 (IQR=64.9 μg·m⁻³) at prior 18 h and NO (IQR=40.5 μg·m⁻³) at prior 48 h. Among participants with low levels of CRP and MDA, significantly positive associations were observed between air pollution exposure and levels of TMPs (P<0.05). Conclusion Short-term exposure to air pollution is significantly associated with increased levels of circulating MPs in healthy adults, and in people with lower systemic inflammation, peripheral blood MPs levels are more easily affected after exposure to air pollutants.

Objective To investigate the temporal changes in pathological damage and macrophage polarization in liver and spleen tissues of mice infected with Angiostrongylus cantonensis, and to preliminarily unravel the peripheral immune responses during the early stage of A. cantonensis infection. Methods Forty female BALB/c mice at ages of 6 to 8 weeks were randomly divided into four groups, including the control group and 7-, 14-, and 21-day infection groups, with 10 mice in each group. Each mouse in the infection groups was inoculated with 30 third-stage (L3) larvae of A. cantonensis by oral gavage, and five mice were randomly selected from each infection group on days 7, 14, and 21 post-infection, while mice in the control group were given the same volume of physiological saline and five mice were randomly selected from the control group on the day of oral gavage. Mouse liver and spleen tissues were sampled. The histopathological changes of mouse liver and spleen tissues were observed using hematoxylin and eosin (HE) staining, and the percentage of positive staining area and the co-localization positive rates of the macrophage surface antigens F4/80, CD86, and CD206 were quantified in mouse liver and spleen tissues using immunohistochemical and immunofluorescence staining. In addition, five mice were collected from each infection group on days 7, 14, and 21 post-infection, and five mice were collected from the control group on the day of oral gavage. Mouse liver and spleen tissues were sampled for detection of macrophage markers CD86 and CD206 and macrophage phenotyping using flow cytometry, and the expression of M1 macrophage markers, including inducible nitric oxide synthase (Nos2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and M2 markers, including arginase 1 (Arg1), mannose receptor C-type 1 (Mrc1) and chitinase-like protein 3 (Chil3) was quantified in mouse liver and spleen tissues using real-time quantitative PCR (RT-qPCR) assay. Results Proliferative lesions of the hepatocyte were observed in mouse liver tissues and the follicular structures of the mouse spleen white pulp were disrupted 21 days post-infection with A. cantonensis. Immunohistochemical staining showed that there were significant differences in the percentages of F4/80, CD86 and CD206 positive staining areas in the liver and spleen tissues among the four groups of mice (F = 242.40, 197.14, 183.19, 157.65, 242.35 and 146.24; all P values < 0.001), and the percentages of positive staining in the liver and spleen tissues of mice in the 14-day infection group [(4.45 ± 0.51)%, (3.74 ± 0.67)%, (8.32 ± 0.72)%, (16.56 ± 1.14)%, (11.62 ± 0.52)%, and (8.29 ± 0.72)%, respectively] and the 21-day infection group [(3.70 ± 0.11)%, (3.22 ± 0.43)%, (11.53 ± 1.03)%, (12.59 ± 1.05)%, (9.02 ± 0.83)%, and (11.67 ± 1.10)%, respectively] were higher than in the control group [(0.35 ± 0.16)%, (0.40 ± 0.02)%, (0.93 ± 0.05)%, (2.78 ± 0.26)%, (2.33 ± 0.20)%, and (1.85 ± 0.20)%, respectively] (all P values < 0.05). Immunofluorescence staining showed significant differences in the positive rates of F4/80 co-localization with CD86 and CD206 in mouse liver and spleen tissues among the four groups (F = 24.42, 25.28, 54.51 and 130.55; all P values < 0.001). Flow cytometry detected significant differences in the proportions of CD86⁺ and CD206⁺ macrophages in mouse liver and spleen tissues among the four groups (F = 67.98, 18.41, 29.77, 172.80; all P values < 0.001), and the proportions of CD206⁺ macrophages in the liver and spleen of the 21-day infection group were significantly higher than those in the control group [(9.25 ± 2.55)% vs (3.83 ± 0.72)%, and (4.22 ± 0.56)% vs (0.47 ± 0.18)%, respectively] (both P values < 0.05). In addition, RT-qPCR assay quantified significant differences in the relative mRNA expression of M1 macrophage markers (IL-1β, TNF-α and Nos2) and M2 macrophage markers (Arg1, Chil3 and Mrc1) in mouse liver and spleen tissues among the four groups (F = 41.30, 31.82, 199.33, 19.96, 62.01, 119.76, 23.67, 95.90, 72.27, 82.59, 123.41 and 29.75; all P values < 0.05). Conclusions A. cantonensis infection may cause progressive pathological damage in mouse liver and spleen tissues, accompanied by dynamic temporal changes in macrophage polarization. M1 macrophage polarization predominates at the early stage of A. cantonensis infection and shifts towards M2 polarization at the later stages, suggesting that M2 polarization may participate in immune regulation at late stages of A. cantonensis infection by suppressing excessive inflammatory responses and promoting tissue repair.

OBJECTIVE To analyze the drug resistance,laboratory indicators and clinical characteristics of blood-stream infections caused by Enterobacter in children,providing references for early empirical treatment.METHODS A retrospective analysis was conducted on the clinical data of 302 children(aged 29 days to 12 years)with bloodstream infections caused by Enterobacter(monomicrobial infections)admitted to the Maternity and Child Health Care of Guangxi Zhuang Autonomous Region from Jan.2017 to Dec.2023.The drug resistance of Enterobacter and major pathogens were analyzed across different age groups of children.Based on prognosis,the children were divided into a favorable prognosis group(266 cases)and a poor prognosis group(36 cases),and their laboratory indicators and clinical characteristics were compared.Multivariate logistic regression was used to analyze the risk factors for poor prognosis.RESULTS The major pathogens causing infections were Salmonella,Escherichia coli and Klebsiella pneumoniae.The distribution difference of major pathogens across age groups(29 days-6 months,＞6 months-1 year,＞1-2 years,＞2 years)was statistically significant(P＜0.001).The drug resistance rates of Salmonella to ampicillin,chloramphenicol and sulfamethoxazole/trimethoprim were 68.61％,54.01％and 44.53％,respectively.E.coli exhibited drug resistance rates of 83.33％,52.22％and 47 78％to ampicillin,sulfamethoxazole/trimethoprim and cefazolin,respectively.K.pneumoniae showed drug resistance rates exceeding 50％to ampicillin/sulbactam,cefuroxime and cefazolin.Hypoalbuminemia(OR=3.319),sepsis(OR=3.122),ventricular purulent encephalitis(OR=5.104)and prior use of penicillin-class anti-bacterial drugs before culture positivity(OR=3.374)were identified as risk factors for poor prognosis of the chil-dren with Enterobacteriaceae bloodstream infections(P＜0.05).CONCLUSIONS Bloodstream infections caused by Enterobacter in children predominantly occur in those under 2 years of age,with Salmonella,E.coli and K.pneumoniae as the major pathogens,exhibiting high drug resistance rates to penicillin and cephalosporin antibacte-rial drugs.Clinical therapeutic regimen should be adjusted early based on laboratory indicators and risk factors to improve prognosis.

BACKGROUND:Polyamines play a crucial role in tissue calcification.Spermidine/spermine N1-acetyltransferase 1(SAT1),as a key rate-limiting enzyme regulating intracellular polyamine metabolism,has been associated with various pathological processes.However,its role in vascular calcification remains unclear.OBJECTIVE:To investigate the role of SAT1 in rat vascular smooth muscle cell calcification.METHODS:(1)Bioinformatics analysis:Differential expression of SAT1 in human carotid atherosclerotic plaques and their surrounding healthy carotid artery tissues were using GEO datasets.PanglaoDB database was used to analyze SAT1 expression abundance and localization across different cell types through single-cell sequencing.(2)Rat vascular smooth muscle cells were divided into three groups:a control group cultured in DMEM medium,a calcification group induced by DMEM medium containing 10 mmol/L β-glycerophosphate sodium and 3 mmol/L calcium chloride,and the 50,100 μmol/L diacetylaminotriazamidine groups treated with the SAT1 inhibitor,diacetylaminotriazamidine,in addition to the calcification medium.After 7-10 days of culture,alizarin red S staining was performed,and cellular calcium content and alkaline phosphatase activity were assessed.Western blot was used to detect the protein expression of Runt-related transcription factor 2,bone morphogenetic protein 2,alpha-smooth muscle actin,and SAT1.Immunofluorescence staining was conducted to examine the expression of Runt-related transcription factor 2 and SAT1.RESULTS AND CONCLUSION:(1)Bioinformatics analysis revealed significantly upregulated expression of SAT1 and Runt-related transcription factor 2(P<0.05)in carotid atherosclerotic plaques compared with healthy carotid tissues(P<0.05).Single-cell sequencing database analysis confirmed SAT1 expression in vascular smooth muscle cells.(2)Compared with the control group,the calcification group showed significantly increased Runt-related transcription factor 2,bone morphogenetic protein 2,SAT1,calcium content,and alkaline phosphatase activity,while alpha-smooth muscle actin expression was significantly decreased(all P<0.05).Compared with the calcification group,the 50 and 100 μmol/L diacetylaminotriazamidine groups showed significantly decreased Runt-related transcription factor 2,bone morphogenetic protein 2,calcium content,and alkaline phosphatase activity,while alpha-smooth muscle actin expression was significantly increased(all P<0.05).(3)Immunofluorescence experiments demonstrated that compared with the calcification group,the expression intensity of Runt-related transcription factor 2 was significantly reduced in the 50 and 100 μmol/L diacetylaminotriazamidine groups.Overall,SAT1 may promote vascular smooth muscle cell calcification by upregulating Runt-related transcription factor 2 expression.

Objective To compare trunk muscle activation,muscle co-contraction levels and plantar pressure distribution between patients with chronic low back pain(cLBP)and healthy subjects during static standing.Methods From July,2021 to July,2022,17 healthy subjects(healthy control group)and 18 cLBP patients(cLBP group)were recruited from the Department of Rehabilitation Medicine,the First Affiliated Hospital of Sun Yat-sen Uni-versity.Demographic information was collected for both groups,as well as the pain intensity,functional disabili-ty,and center of pressure displacement parameters of the cLBP group in static standing.A plantar pressure plate was used to record plantar pressure distribution in static standing task.Simultaneously,a wireless surface electro-myography(sEMG)system was used to record the activity of the transverse abdominis(TrA),erector spinae(ES)and lumbar multifidus(LM).The activation levels of each muscle and the co-contraction index(CCI)between trunk muscle pairs were analyzed.Results Compared with the healthy control group,the cLBP group showed higher activation levels of the bilateral LM(∣t∣>2.479,P<0.05)and higher lumbar-abdominal muscle CCI of left LM-left TrA(t=2.212,P=0.042),left LM-right TrA(t=2.868,P=0.008)and right LM-right TrA(U=75.000,P=0.009).In the cLBP group,pres-sure decreased in the right big toe region(t=2.825,P=0.009),and increased in the right medial and left lateral heel regions(U<77.000,P<0.05).Conclusions During static standing,patients with cLBP require higher level of trunk muscle activation and co-contrac-tion,with a posterior shift in plantar pressure distribution,which might be due to the adoption of different postur-al compensation strategies to maintain postural stability.

Objective To analyze the adverse reaction reports （ADRs） of drug-induced liver injury in recent ten years, explore the characteristics and related rules of drug-induced liver injury, and provide reference for clinical safe drug use. Methods ADRs in our hospital from 2011 to 2021 which belonged to drug-induced liver injuries were collected, and Pareto analysis was carried on. Results In 259 ADR reports, the most common type of drug-induced liver injury was hepatocellular injury （37.84%）. The age of drug-induced liver injury was mainly over 46 years, totaling 195 （75.28%）. Drugs were mainly distributed in cardiovascular system medicine （44.02%）, anti-infective medicine （23.94%）and anti-tumor medicine （11.58%）. Among the cardiovascular drugs, atorvastatin calcium 40mg and over 40mg were the highest proportion, with 53 cases （46.49%）. The main anti-infectious drugs were cephalosporins （29.03%）, carbapenem （19.35%）， antifungal （17.74%）and quinolones （11.29%）. Adverse reactions occurred within 6 days （69.88%）, the duration of adverse reactions was 1-2 weeks （31.66%）, and most patients were improved （47.88%） or cured （37.07%）. Conclusion For middle-aged and elderly patients, when the application of cardiovascular system drugs, anti-infective drugs or anti-tumor drugs, it is necessary to monitor the liver function changes of patients for at least 6 days. If there are abnormalities, the drugs should be stopped or given treatment in time, to avoid the progress of drug-induced liver injury.

Objective To investigate the changes in eosinophil counts and the activation of microglial cells in the brain tissues of mice at different stages of Angiostrongylus cantonensis infection, and to examine the role of microglia in regulating the progression of angiostrongyliasis and unravel the possible molecular mechanisms. Methods Fifty BALB/c mice were randomly divided into the control group and the 7-d, 14-d, 21-day and 25-d infection groups, of 10 mice in each group. All mice in infection groups were infected with 30 stage III A. cantonensis larvae by gavage, and animals in the control group was given an equal amount of physiological saline. Five mice were collected from each of infection groups on days 7, 14, 21 d and 25 d post-infection, and 5 mice were collected from the control group on the day of oral gavage. The general and focal functional impairment was scored using the Clark scoring method to assess the degree of mouse neurological impairment. Five mice from each of infection groups were sacrificed on days 7, 14, 21 d and 25 d post-infection, and 5 mice from the control group were sacrificed on the day of oral gavage. Mouse brain tissues were sampled, and the pathological changes of brain tissues were dynamically observed using hematoxylin and eosin (HE) staining. Immunofluorescence staining with eosinophilic cationic protein (ECP) and ionized calcium binding adaptor molecule 1 (Iba1) was used to assess the degree of eosinophil infiltration and the counts of microglial cells in mouse brain tissues in each group, and the morphological parameters of microglial cells (skeleton analysis and fractal analysis) were quantified by using Image J software to determine the morphological changes of microglial cells. In addition, the expression of M1 microglia markers Fcγ receptor III (Fcgr3), Fcγ receptor IIb (Fcgr2b) and CD86 antigen (Cd86), M2 microglia markers Arginase 1 (Arg1), macrophage mannose receptor C-type 1 (Mrc1), chitinase-like 3 (Chil3), and phagocytosis genes myeloid cell triggering receptor expressed on myeloid cells 2 (Trem2), CD68 antigen (Cd68), and apolipoprotein E (Apoe) was quantified using real-time quantitative reverse transcription PCR (RT-qPCR) assay in the mouse cerebral cortex of mice post-infection. Results A large number of A. cantonensis larvae were seen on the mouse meninges surface post-infection, and many neuronal nuclei were crumpled and deeply stained, with a large number of bleeding points in the meninges. The median Clark scores of mouse general functional impairment were 0 (interquartile range, 0), 0 (interquartile range, 0.5), 6 (interquartile range, 1.0), 14 (interquartile range, 8.5) points and 20 (interquartile range, 9.0) points in the control group and the 7-d, 14-d, 21-d and 25-d groups, respectively (H = 22.45, P < 0.01), and the median Clark scores of mouse focal functional impairment were 0 (interquartile range, 0), 2 (interquartile range, 2.5), 7 (interquartile range, 3.0), 18 (interquartile range, 5.0) points and 25 (interquartile range, 6.5) points in the control group and the 7-d, 14-d, 21-d and 25-d groups, respectively (H = 22.72, P < 0.01). The mean scores of mice general and focal functional impairment were all higher in the infection groups than in the control group (all P values < 0.05). Immunofluorescence staining showed a significant difference in the eosinophil counts in mouse brain tissues among the five groups (F = 40.05, P < 0.000 1), and the eosinophil counts were significantly higher in mouse brain tissues in the 14-d (3.08 ± 0.78) and 21-d infection groups (5.97 ± 1.37) than in the control group (1.00 ± 0.28) (both P values < 0.05). Semi-quantitative analysis of microglia immunofluorescence showed a significant difference in the counts of microglial cells among the five groups (F = 17.66, P < 0.000 1), and higher Iba1 levels were detected in mouse brain tissues in 14-d (5.75 ± 1.28), 21-d (6.23 ± 1.89) and 25-d infection groups (3.70 ± 1.30) than in the control group (1.00 ± 0.30) (all P values < 0.05). Skeleton and fractal analyses showed that the branch length [(162.04 ± 34.10) μm vs. (395.37 ± 64.11) μm; t = 5.566, P < 0.05] and fractal dimension of microglial cells (1.30 ± 0.01 vs. 1.41 ± 0.03; t = 5.266, P < 0.05) were reduced in mouse brain tissues in the 21-d infection group relative to the control group. In addition, there were significant differences among the 5 groups in terms of M1 and M2 microglia markers Fcgr3 (F = 48.34, P < 0.05), Fcgr2b (F = 55.46, P < 0.05), Cd86 (F = 24.44, P < 0.05), Arg1 (F = 31.18, P < 0.05), Mrc1 (F = 15.42, P < 0.05) and Chil3 (F = 24.41, P < 0.05), as well as phagocytosis markers Trem2 (F = 21.19, P < 0.05), Cd68 (F = 43.95, P < 0.05) and Apoe (F = 7.12, P < 0.05) in mice brain tissues. Conclusions A. cantonensis infections may induce severe pathological injuries in mouse brain tissues that are characterized by massive eosinophil infiltration and persistent activation of microglia cells, thereby resulting in progressive deterioration of neurological functions.