Atherosclerosis （AS） is the main pathological basis of cardiovascular diseases and seriously threatens human quality of life. Its prevention and treatment urgently need breakthroughs. The inflammatory response， which runs through the physiological and pathological evolution process of AS， is one of the important mechanisms for AS occurrence. Currently， the treatment methods for AS in Western medicine are relatively mature. However， they have adverse reactions such as abnormal liver and kidney function， drug tolerance， target vessel restenosis， and stent thrombosis， which remain the key bottleneck restricting clinical efficacy. Traditional Chinese medicine （TCM）， characterized by multiple components， multiple targets， and multi-pathway synergy， shows unique clinical application potential and efficacy advantages in the intervention of AS. This article reviewed the research progress of TCM in intervening in AS by regulating inflammatory-related signaling pathways， such as nuclear factor-κB （NF-κB）， Toll-like receptors （TLRs）， mitogen-activated protein kinase （MAPK）， and Janus kinase/signal transducer and activator of transcription （JAK/STAT）， in the past five years. It summarized the combined mechanism of action of TCM monomers， TCM pairs， and compound preparations in inhibiting the inflammatory cascade reaction through multiple targets， regulating lipid metabolism disorders， and improving vascular endothelial dysfunction and the imbalance of the microenvironment. It deepened the research on the molecular mechanism of TCM in anti-AS， so as to provide a scientific basis for the clinical transformation application and related theoretical research of TCM in anti-AS.

Atherosclerosis （AS） is the main pathological basis of cardiovascular diseases and seriously threatens human quality of life. Its prevention and treatment urgently need breakthroughs. The inflammatory response， which runs through the physiological and pathological evolution process of AS， is one of the important mechanisms for AS occurrence. Currently， the treatment methods for AS in Western medicine are relatively mature. However， they have adverse reactions such as abnormal liver and kidney function， drug tolerance， target vessel restenosis， and stent thrombosis， which remain the key bottleneck restricting clinical efficacy. Traditional Chinese medicine （TCM）， characterized by multiple components， multiple targets， and multi-pathway synergy， shows unique clinical application potential and efficacy advantages in the intervention of AS. This article reviewed the research progress of TCM in intervening in AS by regulating inflammatory-related signaling pathways， such as nuclear factor-κB （NF-κB）， Toll-like receptors （TLRs）， mitogen-activated protein kinase （MAPK）， and Janus kinase/signal transducer and activator of transcription （JAK/STAT）， in the past five years. It summarized the combined mechanism of action of TCM monomers， TCM pairs， and compound preparations in inhibiting the inflammatory cascade reaction through multiple targets， regulating lipid metabolism disorders， and improving vascular endothelial dysfunction and the imbalance of the microenvironment. It deepened the research on the molecular mechanism of TCM in anti-AS， so as to provide a scientific basis for the clinical transformation application and related theoretical research of TCM in anti-AS.

Background Lead smelting workers are exposed to mixed heavy metals such as lead (Pb) and cadmium (Cd). However, the specific associations and molecular mechanisms by which their combined exposure induces genetic damage remain unclear. Objective To clarify the association between combined Pb-Cd exposure and genetic damage and to explore the possible biological mechanisms through occupational epidemiological investigations and animal experiments. Methods (1) Population study: A cross-sectional study was conducted on 374 lead smelting workers in northern China. Inductively coupled plasma mass spectrometry (ICP-MS) was used to detect urinary levels of 8 metals including Pb and Cd, and graphite furnace atomic absorption spectroscopy (GFAAS) was used to quantify blood levels of Pb and Cd. The cytokinesis-block micronucleus assay (CBMN) was used to assess genetic damage. Poisson regression was used to analyze the association between metal exposure and micronucleus rates. (2) In vivo experiment: Thirty SD rats were randomly assigned to five groups: control (pure water), Pb (300 mg·L⁻¹ lead acetate), Cd (50 mg·L⁻¹ cadmium chloride), combined exposure (Pb + Cd), and resveratrol intervention (Pb + Cd + 50 mg·L⁻¹ resveratrol). After 8 weeks of ad libitum drinking water exposure, liver pathology, oxidative stress indicators [reactive oxygen species (ROS), reduced glutathione (GSH), oxidized glutathione (GSSG), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD)], genetic damage (Comet assay and γ-H2AX) were evaluated. Furthermore, cell cycle distribution, apoptosis rates, and mRNA expression of DNA damage response (DDR), DNA repair, and apoptosis-related genes were measured. Results (1) The geometric mean (GM, 95%CI) of urinary Pb and Cd were 14.69 (13.14, 16.51) µg·L⁻¹ and 2.11 (1.90, 2.33) µg·L⁻¹, respectively; the blood Pb and Cd levels were 117.10 (105.59, 129.87) µg·L⁻¹ and 4.55 (4.23, 4.89) µg·L⁻¹, respectively among the 374 workers. The mean micronucleus rate was (1.64±0.081) ‰, with significantly higher rates in males (1.65±0.083) ‰ than females (1.53±0.334) ‰ (U=4.166, P=0.041). All Pb and Cd biomarkers were positively correlated with micronucleus rate (FR>1, P<0.05), with a significant interaction effect observed between Pb and Cd (FR>1, P<0.05). (2) In rats, co-exposure to Pb and Cd caused liver tissue damage and inflammatory infiltration. Significant increases were observed in lymphocyte ROS; GSSG and MDA in lung tissue increased, while GSH and CAT activity decreased. Comet assay indicators and γ-H2AX levels were significantly elevated. Co-exposure induced S-phase arrest and increased apoptosis. mRNA levels of DDR (ATM, ATR, Chk2, and P53) and pro-apoptotic genes (Bax and Caspase-3) were upregulated, while the anti-apoptotic gene Bcl-2 and DNA repair genes (BRCA1, BRCA2, RAD51, RAD52, and CtIP) were downregulated. Two-way ANOVA confirmed synergistic effects on GSSG, Comet assay indicators, and ATR/Chk2 mRNA expression. Conclusion Occupational co-exposure to Pb and Cd synergistically induces genetic damage. This damage is mediated by oxidative stress and DNA damage, which activates the DDR pathway and inhibits the expression of DNA repair genes, ultimately leading to cell cycle arrest and apoptosis.

Background Lead smelting workers are exposed to mixed heavy metals such as lead (Pb) and cadmium (Cd). However, the specific associations and molecular mechanisms by which their combined exposure induces genetic damage remain unclear. Objective To clarify the association between combined Pb-Cd exposure and genetic damage and to explore the possible biological mechanisms through occupational epidemiological investigations and animal experiments. Methods (1) Population study: A cross-sectional study was conducted on 374 lead smelting workers in northern China. Inductively coupled plasma mass spectrometry (ICP-MS) was used to detect urinary levels of 8 metals including Pb and Cd, and graphite furnace atomic absorption spectroscopy (GFAAS) was used to quantify blood levels of Pb and Cd. The cytokinesis-block micronucleus assay (CBMN) was used to assess genetic damage. Poisson regression was used to analyze the association between metal exposure and micronucleus rates. (2) In vivo experiment: Thirty SD rats were randomly assigned to five groups: control (pure water), Pb (300 mg·L⁻¹ lead acetate), Cd (50 mg·L⁻¹ cadmium chloride), combined exposure (Pb + Cd), and resveratrol intervention (Pb + Cd + 50 mg·L⁻¹ resveratrol). After 8 weeks of ad libitum drinking water exposure, liver pathology, oxidative stress indicators [reactive oxygen species (ROS), reduced glutathione (GSH), oxidized glutathione (GSSG), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD)], genetic damage (Comet assay and γ-H2AX) were evaluated. Furthermore, cell cycle distribution, apoptosis rates, and mRNA expression of DNA damage response (DDR), DNA repair, and apoptosis-related genes were measured. Results (1) The geometric mean (GM, 95%CI) of urinary Pb and Cd were 14.69 (13.14, 16.51) µg·L⁻¹ and 2.11 (1.90, 2.33) µg·L⁻¹, respectively; the blood Pb and Cd levels were 117.10 (105.59, 129.87) µg·L⁻¹ and 4.55 (4.23, 4.89) µg·L⁻¹, respectively among the 374 workers. The mean micronucleus rate was (1.64±0.081) ‰, with significantly higher rates in males (1.65±0.083) ‰ than females (1.53±0.334) ‰ (U=4.166, P=0.041). All Pb and Cd biomarkers were positively correlated with micronucleus rate (FR>1, P<0.05), with a significant interaction effect observed between Pb and Cd (FR>1, P<0.05). (2) In rats, co-exposure to Pb and Cd caused liver tissue damage and inflammatory infiltration. Significant increases were observed in lymphocyte ROS; GSSG and MDA in lung tissue increased, while GSH and CAT activity decreased. Comet assay indicators and γ-H2AX levels were significantly elevated. Co-exposure induced S-phase arrest and increased apoptosis. mRNA levels of DDR (ATM, ATR, Chk2, and P53) and pro-apoptotic genes (Bax and Caspase-3) were upregulated, while the anti-apoptotic gene Bcl-2 and DNA repair genes (BRCA1, BRCA2, RAD51, RAD52, and CtIP) were downregulated. Two-way ANOVA confirmed synergistic effects on GSSG, Comet assay indicators, and ATR/Chk2 mRNA expression. Conclusion Occupational co-exposure to Pb and Cd synergistically induces genetic damage. This damage is mediated by oxidative stress and DNA damage, which activates the DDR pathway and inhibits the expression of DNA repair genes, ultimately leading to cell cycle arrest and apoptosis.

[This corrects the article DOI: 10.1016/j.apsb.2021.07.004.].

Cerebral edema is characterized by fluid accumulation, and the glymphatic system (GS) plays a pivotal role in regulating fluid transport. Using the Tenecteplase system, magnesium salt of salvianolic acid B/ginsenoside Rg1 (SalB/Rg1) was injected intravenously into mice 4.5 h after middle cerebral artery occlusion and once every 24 h for the following 72 h. GS function was assessed by Evans blue imaging, near-infrared fluorescence region II (NIR-II) imaging, and magnetic resonance imaging (MRI). SalB/Rg1 had significant effects on reducing the infarct volume and hemorrhagic transformation score, improving neurobehavioral function, and protecting tissue structure, especially inhibiting cerebral edema. Meanwhile, the influx/efflux drainage of GS was enhanced by SalB/Rg1 according to NIR-II imaging and MRI. SalB/Rg1 inhibited matrix metalloproteinase-9 (MMP-9) activity, reduced cleaved β-dystroglycan (β-DG), and stabilized aquaporin-4 (AQP4) polarity, which was verified by colocalization with CD31. Our findings indicated that SalB/Rg1 treatment enhances GS function and attenuates cerebral edema, accompanying the regulation of the MMP9/β-DG/AQP4 pathway.
Animals ; Ginsenosides/administration & dosage* ; Brain Edema/etiology* ; Male ; Benzofurans/administration & dosage* ; Glymphatic System/diagnostic imaging* ; Mice ; Infarction, Middle Cerebral Artery/drug therapy* ; Aquaporin 4/metabolism* ; Disease Models, Animal ; Mice, Inbred C57BL ; Matrix Metalloproteinase 9/metabolism* ; Neuroprotective Agents/pharmacology* ; Depsides

Objective:To evaluate the safety and efficacy of secondary transport on extracorporeal membrane oxygenation (ECMO) for critically ill children.Methods:This was a retrospective cohort study. Data from 222 pediatric patients who underwent ECMO transport from May 2019 to May 2024 at 5 ECMO centers and Chinese Database of Pediatric Extracorporeal Life Support Organization were collected. The cases were divided into primary and secondary transport groups by nature of transport. The clinical data, including demographics, ECMO indications, transport distance, pre-transport lab results, prognosis and complications were analyzed. Two independent samples t-test, Wilcoxon test, and χ2 test or Fisher′s exact probability method were used to compare the differences between 2 groups and evaluate the safety and efficacy of secondary transport. Results:Among the 222 children transported with ECMO, there were 135 males and 87 females, with an age of 3.0 (0.2, 7.0) years. There were 202 cases in the primary transport group and 20 cases in the secondary transport group. All secondary transport patients had failed attempts at weaning ECMO before transfer. The patients in the secondary transport group were older, had higher rates of surgical cannulation, circulatory support, and pre-ECMO lactate levels compared to the primary transport group (7.0 (2.8, 10.0) vs. 3.0 (0.2, 6.0) years old, 55.0% (11/20) vs. 3.6% (7/202), 80.0% (16/20) vs. 41.6% (84/202), (10±4) vs. (7±6) mmol/L, Z=3.41, χ 2=66.31, 10.99, t=2.24, all P<0.05). In the secondary transport group, the vasoactive-inotropic scores of patients on circulatory support and the oxygenation index for patients requiring respiratory support were higher than those in the primary transport group (83±33 vs. 82±68, 51.0±1.8 vs. 37.4±10.2, t=2.36, 2.63, respectively; both P<0.05). There were no statistically significant differences between the 2 groups in sex, transport distance, pre-ECMO creatinine, arterial blood gas BE values, and ECMO duration (all P>0.05). No life-threatening complications occurred during the transport in either group. Two patients in the secondary transport group underwent heart transplantation, and 1 patient underwent radiofrequency ablation. The overall survival rate between the 2 groups showed no statistically significant difference (45.0% (9/20) vs. 55.4% (112/202), χ2=1.15, P>0.05). Conclusions:Secondary ECMO transport for critically ill children don't increase mortality or life-threatening complications during transport. ECMO patients who cannot receive effective treatment locally can benefit from secondary transport to an advanced ECMO center provides further treatment opportunities.

Objective:To evaluate the safety and clinical efficacy of enteral nutrition (EN) initiated within 24 h after heart transplantation in pediatric patients.Methods:A retrospective cohort study was conducted. Clinical data from 16 pediatric heart transplant recipients at the Seventh Medical Center of the Chinese People′s Liberation Army General Hospital between October 2022 and October 2024 were collected, including demographics, anthropometric measurements, biochemical markers, cytokine levels, and clinical outcomes. Based on the timing of EN initiation, the patients were divided into EN-initiated within 24 h and EN-initiated after 24 h 2 groups. Demographic data, preoperative extracorporeal membrane oxygenation (ECMO) support, physical examination indicators, laboratory parameters, and cytokine levels were compared between groups using independent samples t-test, Mann-Whitney U test, Fisher′s exact probability test. Results:The cohort comprised 16 patients (10 males and 6 females) with an age of (12.5±1.9) years. The EN-initiated within 24 h group comprised 6 cases, and the EN-initiated after 24 h group comprised 10 cases. No significant difference was observed between the two groups in age, preoperative body mass index Z-score, preoperative ECMO support, physical examination indicators, laboratory parameters (total protein, albumin, hemoglobin), or cytokine levels (all P>0.05). Compared to the EN-initiated after 24 h group, the EN-initiated within 24 h group exhibited a shorter intensive care unit stay ( t=2.65, P<0.05) and shorter mechanical ventilation duration ( t=2.23, P<0.05) than EN-initiated after 24 h group. Total hospitalization length had no significant difference ( P>0.05). At 72 h post-transplant, the EN-initiated within 24 h group had a lower interleukin-12 P70 ( t=2.46, P<0.05) and interferon-γ levels ( t=2.55, P<0.05) than EN-initiated after 24 h group. Prior to discharge, the EN-initiated within 24 h group has a lower mean skinfold thickness ( t=2.49, P<0.05) and lower mid-upper arm circumference ( t=2.36, P<0.05) compared with the EN-initiated after 24 h group. Conclusions:Initiating EN within 24 h postoperatively is safe and feasible in pediatric heart transplant recipients. Early EN may shorten the length of intensive care unit stay and mechanical ventilation while attenuating postoperative release of inflammatory cytokine.

Objective:To report a Charcot-Marie-Tooth disease type 2 (CMT2) patient with SORD gene mutations, aiming to enhance the understanding of SORD gene-associated peripheral neuropathy. Methods:A CMT2 patient with SORD gene mutations was identified through whole exome sequencing in the Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology in January 2024, and the patients′ clinical features were elaborated in detail. 31-Phosphorus magnetic resonance spectroscopy ( 31P-MRS) was employed to assess the phosphorus profile of the limbs, and real-time quantitative reverse transcription polymerase chain reaction was utilized to detect peripheral blood SORD gene mRNA expression levels in the patient, the family members, and the normal control. Additionally, the genetic and clinical characteristics of SORD gene mutation-related CMT2 and distal hereditary motor neuropathy (dHMN) were reviewed by searching the CNKI and PubMed databases. Results:The male CMT2 patient was 15 years old, presented with early-onset lower limb muscle weakness and atrophy, hypoesthesia, reduced tendon reflexes, and flat feet. 31P-MRS examination indicated that the pH of the patient′s leg was lower than that of the upper limb. Whole exome sequencing showed the patient carrying complex heterozygous mutations c.757delG (p.Ala253GlnfsTer27) and c.218C>T (P.Ser73Leu) in the SORD gene. The mRNA expression of the SORD gene of the patient′s mother [0.623(0.614, 0.645)] was lower than that of the patient′s father [0.961(0.888,1.020), H=13.330, P=0.007] and normal people [1.001(0.917, 1.092), H=14.830, P=0.002]. Through literature review, it is found that 31 SORD gene mutations have been reported worldwide, among which c.757delG (p.Ala253GlnfsTer27) was found to be a hotspot mutation, and all patients exhibited an autosomal recessive inheritance pattern. Conclusions:A patient with CMT2 caused by a compound heterozygous mutation c.757delG/c.218C>T in the SORD gene, with the main clinical symptoms of bilateral lower limb weakness, atrophy, sensory disturbance and reduced tendon reflexes is reported. Furthermore, 31P-MRS of the extremities is anticipated to both early and sensitively detect muscle lesions in patients with hereditary peripheral neuropathy.

Objective: To investigate the status and influencing factors of influenza vaccination among the elderly, so as to provide insights into improving the strategies for influenza vaccination among the elderly. Methods: Elderly people aged 60 years and above were recruited from one community each in five sub-districts of Shihezi City, Xinjiang Uygur Autonomous Region using a random sampling method. Demographic information, knowledge about influenza and influenza vaccines, vaccine literacy and influenza vaccination status in the past year were collected through questionnaire surveys. Factors affecting influenza vaccination among the elderly were analyzed using a multivariable logistic regression model. Results: Totally 1 121 valid questionnaires were recovered, with an effective recovery rate of 95.08%. There were 417 males (37.20%) and 704 females (62.80%). The majority were aged 60-<81 years, accounting for 80.37% (901 individuals). The awareness of knowledge about influenza and influenza vaccines was 78.86%. Low vaccine literacy was observed in 786 individuals, representing 70.12%. The influenza vaccination rate was 20.96%. Multivariable logistic regression analysis showed that age (71-<81 years, OR=1.607, 95%CI: 1.041-2.479; ≥81 years, OR=1.719, 95%CI: 1.040-2.842), educational level (middle school/technical secondary school, OR=0.616, 95%CI: 0.416-0.911), medical expense payment (employee medical insurance, OR=6.531, 95%CI: 2.030-21.010; resident medical insurance, OR=3.385, 95%CI: 1.095-10.466; public expense, OR=4.828, 95%CI: 1.700-13.712), vaccination willingness (yes, OR=6.237, 95%CI: 3.277-11.871), influenza vaccination history (yes, OR=14.600, 95%CI: 8.733-24.408) and vaccine literacy (medium and above, OR=2.412, 95%CI: 1.636-3.555) were associated with influenza vaccination among the elderly. Conclusion The influenza vaccination rate among the elderly was relatively low, and was mainly affected by age, educational level, medical expense payment, vaccination willingness, influenza vaccination history and vaccine literacy.