Objective: To investigate the characteristics and potential risk factors associated with HIV infection among newly reported HIV positive male student cases in Jiangsu Province from 2023 to 2024, so as to provide evidence for targeted intervention strategies. Methods: Data were obtained from the China CDC Surveillance System on newly reported HIV positive male student cases from 2023 to 2024. A survey was conducted to collect information on demographic characteristics, knowledge of AIDS prevention, education and training history, HIV testing history, behavioral and substance use patterns, and other relevant factors prior to HIV diagnosis among 343 newly reported HIV positive male student cases in Jiangsu Province. Multivariate Logistic regression analysis was used to assess the risk factors of HIV infection among male students. Results: Among the HIV positive male student cases, homosexual behavior accounted for 93.88% of transmission routes, while 10.20% involved heterosexual contact, as well as 4.08% for two sexual hehaviors. Awareness of HIV prevention knowledge was 97.08%, and 66.76% had previously undergone HIV testing. Among the respondents, 10.50% had used rush poppers as enhancers, and 72.30% had received HIV prevention education within the past year. Among students cases with homosexual behavior, the median time from first homosexual contact to HIV diagnosis was ≤2 years, with 54.66% of cases falling into this category; the most common way of finding same sex partners was through social software, accounting for 88.20% of cases, while the proportion of those via "Blued" app reached 87.07% ; the proportion of using condoms every time during sexual activity in the past six months was 12.27%. Among the student cases with homosexual behavior, the results of multiple Logistic regression analysis showed that student cases aged 18 to 24 ( OR =4.52) and >24 ( OR = 19.23 ), without receiving education on HIV prevention in the past year ( OR =1.86), having consistent condom use ( OR =2.73) and not using condoms ( OR =2.12) during the last sexual activity were more likely to had the first same sex sexual activity for more than 3 years before being diagnosed as HIV positive cases (all P <0.05). Student cases who were uncertain about their partner s sexual identity ( OR =0.33), and who primarily identified same sex partners through "other" means ( OR = 0.23 ) were more likely to avoid HIV testing; in contrast, student cases with consistent condom use during the last homosexual encounter ( OR =7.20) was significantly associated with increased likelihood of HIV testing (all P <0.05). Conclusions Newly reported HIV positive male student cases in Jiangsu Province exhibit serious discrepancies between knowledge and practice regarding HIV prevention. Measures are needed to accelerate the optimization of campus based HIV prevention education content and delivery methods. Simultaneously, enhanced management of extracurricular male populations is essential to effectively control the spread of HIV.

Objective Objective To analyze the potential spatial factors affecting the genetic differentiation of Oncomelania hupensis robertsoni in Yunnan Province. Methods A total of 13 administrative villages were selected from schistosomiasis-endemic areas of Yunnan Province as O. hupensis snail sampling sites. At least 200 snails were collected in each site, and the spatial variable data of each site were recorded, including longitude, latitude and altitude. Thirty active and Schistosoma japonicum uninfected O. hupensis snails were selected from each sampling site by means of the crawling method and the cercarial shedding method. Genomic DNA was extracted from O. hupensis snails. Following PCR amplification, purification of PCR amplification products and sequencing, the gene sequences of O. hupensis snail samples were spliced and edited using the DNAstar software and the NCBI database to yield the complete mitochondrial sequences of O. hupensis snails at each sampling site, and the mitochondrial genetic distance matrix of O. hupensis robertsoni was calculated at each sampling site. The geographical coordinates of each sampling site were marked using the software ArcGIS 10.2, and the straight-line geographical distance between each sampling site was calculated. The altitude difference, longitude difference and latitude difference between each sampling site were calculated using the Excel software, and the correlation between the mitochondrial genetic distance matrix of O. hupensis robertsoni and each spatial variable matrix was examined by using the Mantel test at 13 sampling sites in Yunnan Province. Results Among the 13 O. hupensis snail sampling sites in Yunnan Province, the largest mitochondrial genetic distance of O. hupensis robertsoni snail populations was seen between Anding Village, Nanjian Yi Autonomous County and Caizhuang Village, Midu County (26.244 2), and the largest geographical distance was seen between Dongyuan Village, Gucheng District and Cangling Village, Chuxiong County (272.64 km). The highest altitude difference was seen between Anding Village, Nanjian Yi Autonomous County and Dongyuan Village, Gucheng District (1 086.10 m), and the largest longitude difference was found between Qiandian Village, Eryuan County and Cangling Village, Chuxiong County (1.86°), while the largest latitude difference was measured between Leqiu Village, Nanjian Yi Autonomous County and Dongyuan Village, Gucheng District (1.81°). In addition, the mitochondrial genetic distance of O. hupensis robertsoni snail populations was positively correlated with altitude at 13 snail sampling sites in Yunnan Province (r = 0.542 8, P < 0.001), and showed no significant correlations with geographical distance (r = 0.093 4, P > 0.05), longitude (r = −0.199 5, P > 0.05) or latitude (r = 0.205 7, P > 0.05). Conclusion Altitude may be a potential spatial factor affecting the genetic differentiation of O. hupensis robertsoni in Yunnan Province.

ObjectiveTo explore the mechanism by which Yizhi Qingxin prescription improves mitochondrial dysfunction in Alzheimer's disease （AD） through regulating mitochondrial Ca²⁺ homeostasis and kinetic balance based on the protein kinase A （PKA）/calcineurin （CaN） signaling pathway. MethodsSixty three-month-old amyloid precursor protein （APP）/presenilin 1 （PS1） double transgenic mice were randomly divided into a model group， a donepezil group（0.65 mg·kg^-1）， a low-dose Yizhi Qingxin prescription group （YQF-L，2.6 g·kg^-1）， a medium-dose Yizhi Qingxin prescription group （YQF-M，5.2 g·kg^-1）， and a high-dose Yizhi Qingxin prescription group （YQF-H，10.4 g·kg^-1）， with 12 mice in each group. Twelve C57BL/6J mice with the same genetic background served as a normal group. Each treatment group received gavage administration daily， with the model and normal groups receiving equal volume of physiological saline. Intervention continued for 12 consecutive weeks. The learning and memory abilities of the mice were assessed using the novel object recognition （NOR） and Morris water maze （MWM） tests. Hematoxylin-eosin （HE）/Nissl staining was used to observe histopathological changes in the hippocampus. Transmission electron microscopy （TEM） was used to observe mitochondrial ultrastructure. Fluo-4 acetoxymethyl ester （Fluo-4 AM） Ca²⁺ probe was used to measure intracellular Ca²⁺ concentration in brain tissue. Western blot was used to determine the protein expression of PKA， CaN， sodium/calcium/lithium exchanger （NCLX）， mitochondrial calcium uniporter （MCU）， calmodulin （CaM）， dynamin-related protein 1 （Drp1）， and phosphorylated dynamin-related protein 1 （serine 637 site） ［p-Drp1（S637）］ in the hippocampus. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to measure the expression of PKA， CaN， CaM， NCLX， MCU， and Drp1 mRNAs. ResultsCompared with those in the normal group， the recognition index （RI） of the model group decreased （P0.01）， and the number of crossings through the original platform area， the duration of stay in the target quadrant， and the distance were reduced （P0.01）. The protein expression of PKA， NCLX， and p-DRP1 （ser637） significantly decreased （P0.05）， and the mRNA expression of PKA and NCLX significantly decreased （P0.05）. The escape latency （EL） was prolonged （P0.05）， and the intracellular Ca²⁺ level significantly increased （P0.01）. The protein expression of CaN， CaM， MCU， and Drp1， as well as the mRNA expression of CaN， MCU， and Drp1， significantly increased （P0.05）. After intervention with Donepezil and Yizhi Qingxin prescription， compared with that in the model group， the RI of the treatment group significantly increased （P0.05）， and the number of crossings through the platform and the duration of stay in the target quadrant significantly increased （P0.05）. The protein expression of PKA， NCLX， and p-Drp1 （ser637） and the mRNA expression of PKA and NCLX significantly increased （P0.05）. On the 4th and 5th days， the EL was shortened （P0.05）， and the intracellular Ca²⁺ level decreased （P0.05）. The protein expression of CaN， CaM， MCU， and Drp1 and the mRNA expression of CaN， MCU， and Drp1 significantly decreased （P0.05）. ConclusionYizhi Qingxin prescription regulates the PKA/CaN pathway， upregulates the expression of PKA， NCLX， and p-Drp1 （ser637） proteins， reduces the expression of CaN， CaM， MCU， and Drp1 proteins， and regulates Ca²⁺ homeostasis and mitochondrial dynamic balance， thereby enhancing the spatial learning and memory abilities of AD mice.

ObjectiveTo explore the mechanism by which Yizhi Qingxin prescription improves mitochondrial dysfunction in Alzheimer's disease （AD） through regulating mitochondrial Ca²⁺ homeostasis and kinetic balance based on the protein kinase A （PKA）/calcineurin （CaN） signaling pathway. MethodsSixty three-month-old amyloid precursor protein （APP）/presenilin 1 （PS1） double transgenic mice were randomly divided into a model group， a donepezil group（0.65 mg·kg^-1）， a low-dose Yizhi Qingxin prescription group （YQF-L，2.6 g·kg^-1）， a medium-dose Yizhi Qingxin prescription group （YQF-M，5.2 g·kg^-1）， and a high-dose Yizhi Qingxin prescription group （YQF-H，10.4 g·kg^-1）， with 12 mice in each group. Twelve C57BL/6J mice with the same genetic background served as a normal group. Each treatment group received gavage administration daily， with the model and normal groups receiving equal volume of physiological saline. Intervention continued for 12 consecutive weeks. The learning and memory abilities of the mice were assessed using the novel object recognition （NOR） and Morris water maze （MWM） tests. Hematoxylin-eosin （HE）/Nissl staining was used to observe histopathological changes in the hippocampus. Transmission electron microscopy （TEM） was used to observe mitochondrial ultrastructure. Fluo-4 acetoxymethyl ester （Fluo-4 AM） Ca²⁺ probe was used to measure intracellular Ca²⁺ concentration in brain tissue. Western blot was used to determine the protein expression of PKA， CaN， sodium/calcium/lithium exchanger （NCLX）， mitochondrial calcium uniporter （MCU）， calmodulin （CaM）， dynamin-related protein 1 （Drp1）， and phosphorylated dynamin-related protein 1 （serine 637 site） ［p-Drp1（S637）］ in the hippocampus. Real-time quantitative polymerase chain reaction （Real-time PCR） was used to measure the expression of PKA， CaN， CaM， NCLX， MCU， and Drp1 mRNAs. ResultsCompared with those in the normal group， the recognition index （RI） of the model group decreased （P0.01）， and the number of crossings through the original platform area， the duration of stay in the target quadrant， and the distance were reduced （P0.01）. The protein expression of PKA， NCLX， and p-DRP1 （ser637） significantly decreased （P0.05）， and the mRNA expression of PKA and NCLX significantly decreased （P0.05）. The escape latency （EL） was prolonged （P0.05）， and the intracellular Ca²⁺ level significantly increased （P0.01）. The protein expression of CaN， CaM， MCU， and Drp1， as well as the mRNA expression of CaN， MCU， and Drp1， significantly increased （P0.05）. After intervention with Donepezil and Yizhi Qingxin prescription， compared with that in the model group， the RI of the treatment group significantly increased （P0.05）， and the number of crossings through the platform and the duration of stay in the target quadrant significantly increased （P0.05）. The protein expression of PKA， NCLX， and p-Drp1 （ser637） and the mRNA expression of PKA and NCLX significantly increased （P0.05）. On the 4th and 5th days， the EL was shortened （P0.05）， and the intracellular Ca²⁺ level decreased （P0.05）. The protein expression of CaN， CaM， MCU， and Drp1 and the mRNA expression of CaN， MCU， and Drp1 significantly decreased （P0.05）. ConclusionYizhi Qingxin prescription regulates the PKA/CaN pathway， upregulates the expression of PKA， NCLX， and p-Drp1 （ser637） proteins， reduces the expression of CaN， CaM， MCU， and Drp1 proteins， and regulates Ca²⁺ homeostasis and mitochondrial dynamic balance， thereby enhancing the spatial learning and memory abilities of AD mice.

ObjectiveTo evaluate the effect of virtual reality (VR) combined with occupational therapy on upper limb motor function in patients with stroke. MethodsCNKI, VIP, Wanfang data, PubMed, the Cochrane Library and Web of Science were searched for randomized controlled trials investigating the effect of VR combined with occupational therapy on upper limb motor function in patients with stroke. The search covered the period from database inception to April, 2026. The methodological quality of the included studies was assessed using the Cochrane Risk of Bias Tool version 5.1.0 and PEDro scale. Meta-analysis was performed using RevMan 5.4. ResultsA total of 15 studies involving 636 participants were included. The PEDro scores ranged from seven to ten. VR combined with occupational therapy significantly improved scores of Fugl-Meyer Assessment-Upper Extremities (SMD = 0.64, 95%CI 0.28 to 1.01, P < 0.001) and the Action Research Arm Test (SMD = 1.22, 95%CI 0.88 to 1.56, P < 0.001)， while no significant differences were found in Barthel Index/Modified Barthel Index scores (SMD = 0.50, 95%CI -0.07 to 1.07, P = 0.087), Jebsen-Taylor Hand Function Test scores (SMD = 0.32, 95%CI -0.29 to 0.93, P = 0.308), or Box and Block Test scores (SMD = 0.50, 95%CI -0.43 to 1.43, P = 0.289). ConclusionVR combined with occupational therapy may improve the upper limb motor function in patients with stroke; however, its effects on activities of daily living, hand-movement speed, and grasping and object-transfer ability remain uncertain.

Objective To explore the diagnostic value of soluble C5b-9 (sC5b-9) for delayed graft function (DGF) following kidney transplantation. Methods Clinical data of 49 kidney transplant recipients who underwent sC5b-9 detection at the Second People’s Hospital of Shanxi Province between January 2024 and December 2025 were retrospectively analyzed. Recipients were divided into the DGF group (n=25) and the non-DGF group (n=24) according to the occurrence of DGF. Baseline characteristics and serum sC5b-9 levels were compared between the two groups. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic efficacy of sC5b-9 for DGF. A restricted cubic spline model was adopted to investigate the association between sC5b-9 and DGF. Results Among the 49 recipients, DGF occurred in 25 patients. Compared with the non-DGF group, the DGF group presented a higher proportion of male patients, a higher incidence of adverse transplant outcomes, and elevated final serum creatinine levels (all P<0.05). Within 30 days after transplantation, sC5b-9 concentrations were significantly higher in the DGF group than those in the non-DGF group (P<0.001). ROC analysis revealed that the area under the curve (AUC) of sC5b-9 for diagnosing DGF was 0.81, with a 95% confidence interval (CI) of 0.68-0.92, and the optimal cutoff value was 265.7 ng/mL. Recipients with elevated sC5b-9 (≥265.7 ng/mL) had a significantly higher incidence of DGF than those with low sC5b-9 levels (<265.7 ng/mL) (P<0.001). Recipients with adverse outcomes exhibited significantly higher sC5b-9 levels than those without adverse outcomes (P<0.001), and the AUC of sC5b-9 for identifying adverse outcomes was 0.82 (95%CI 0.63-0.95). A significant nonlinear correlation was observed between sC5b-9 and final serum creatinine (P<0.001). Conclusions Elevated sC5b-9 is correlated with the development of DGF after kidney transplantation and exhibits favorable diagnostic performance. It may serve as a potential biomarker for predicting early allograft dysfunction and adverse outcomes in kidney transplant recipients.

ObjectiveTo observe the clinical efficacy and safety of Shenshuai Guanchang prescription in improving the intestinal barrier function，reducing non-indole uremic toxins，ameliorating micro-inflammatory state，and delaying renal function progression in non-dialysis patients with chronic kidney disease （CKD） stage 4-5. MethodsA total of 80 patients with CKD stage 4-5 who did not receive dialysis replacement therapy and were diagnosed with the syndrome of spleen and kidney deficiency，blood stasis and dampness turbidity were randomly assigned into a control group and a treatment group，with 40 patients in each group. The control group received conventional basic treatment and Western medicine symptomatic treatment，while the treatment group received combined intervention with Shenshuai Guanchang prescription through retention enema in addition to the treatment of the control group. Both groups had a treatment course of 4 weeks. The two groups were compared regarding the changes in urine toxin indicators ［p-cresyl sulfate （PCS） and trimethylamine oxide （TMAO）］，intestinal barrier indicators ［D-lactic acid （D-LA），lipopolysaccharide （LPS），and intestinal fatty acid-binding protein （I-FABP）］，renal function indicators ［serum creatinine （SCr），blood urea nitrogen （BUN），and estimated glomerular filtration rate （eGFR）］，and micro-inflammatory state indicators ［interleukin-6 （IL-6），tumor necrosis factor-α （TNF-α），and neutrophil-to-lymphocyte ratio （NLR）］ before and after treatment. The therapeutic effects were evaluated from three aspects：The efficacy regarding traditional Chinese medicine （TCM） symptom scores，the efficacy regarding laboratory indicators，and comprehensive efficacy. The safety of the clinical research drugs used by both groups of patients was also observed. ResultsA total of 37 cases in the treatment group and 38 cases in the control group completed the observation. After treatment，the treatment group showed declined levels of PCS，TMAO，D-LA，SCr，TNF-α，and NLR，spleen and kidney deficiency symptom score，blood stasis and dampness symptom score，and total symptom score （P<0.05），and increased eGFR （P<0.05）. Moreover，the treatment group had lower levels of PCS，TMAO，D-LA，I-FABP，IL-6，and TNF-α，spleen and kidney deficiency symptom score，blood stasis and dampness symptom score，and total symptom score （P<0.05），higher response rate regarding TCM symptoms （χ²=6.68，P<0.05），and higher comprehensive efficacy （χ²=4.08，P<0.05） than the control group. No significant abnormalities were observed in the safety indicators of the two groups of patients. During the treatment period，adverse reactions were reduced after symptomatic treatment，and no serious adverse reactions occurred. ConclusionShenshuai Guanchang prescription can alleviate the clinical symptoms，improve the intestinal barrier function，reduce non-indole-type uremic toxins，alleviate the micro-inflammatory state，and has good clinical application safety of non-dialysis patients with CKD stage 4-5.

Tumor angiogenesis is a core pathological driver of malignant growth, invasion, and metastasis, and represents a major obstacle to effective anticancer therapy. Conventional antiangiogenic agents, including neutralizing monoclonal antibodies and small-molecule tyrosine kinase inhibitors, are constrained by drug resistance, on-target toxicity, and the compensatory activation of alternative pro-angiogenic pathways. Targeted protein degradation (TPD) has emerged as a promising strategy that may overcome these limitations. Unlike traditional inhibitors that operate through an occupancy-driven mechanism, degraders function through an event-driven catalytic mechanism in which a single degrader molecule can catalytically promote the ubiquitination and subsequent proteasomal or lysosomal degradation of multiple molecules of the same target protein, thereby eliminating the target protein together with all of its functions rather than merely blocking a single active site. This review systematically delineates the pathophysiological basis of tumor angiogenesis, encompassing the angiogenic switch driven by hypoxia-inducible factor-1α (HIF-1α), the aberrant structural and functional features of the tumor vasculature, and the self-reinforcing vicious cycles that sustain malignant progression. We then categorize the principal TPD modalities, with particular emphasis on proteolysis-targeting chimeras (PROTACs) and lysosome-targeting chimeras (LYTACs), and describe their design principles and mechanisms of action. PROTACs recruit E3 ubiquitin ligases to direct intracellular targets to the ubiquitin-proteasome system for degradation, whereas LYTACs engage lysosome-targeting receptors to route extracellular and membrane proteins to the lysosome, thereby expanding the degradable target space beyond the intracellular proteome. We further summarize recent advances in the application of TPD to antiangiogenic intervention at four distinct levels. First, at the signaling initiation level, degradation of vascular endothelial growth factor (VEGF) and its receptor vascular endothelial growth factor receptor 2 (VEGFR2) by aptamer-engineered PROTACs, antibody-based LYTACs, and small-molecule VEGFR2 degraders blocks the upstream trigger of the angiogenic cascade. Second, at the signal transduction level, degradation of focal adhesion kinase (FAK), B-Raf proto-oncogene serine/threonine kinase (BRAF), phosphodiesterase 4 (PDE4), and bromodomain-containing protein 4 (BRD4) interrupts intracellular signaling cascades and transcriptional responses. Third, at the microenvironment level, degradation of proviral integration site for Moloney murine leukemia virus (PIM) kinases curtails the pro-angiogenic signals secreted by tumor-associated macrophages. Fourth, multi-target synergistic strategies, exemplified by bispecific degraders that simultaneously target human epidermal growth factor receptor 2 (HER2) and VEGF-A, represent a preliminary exploration of cooperative intervention. Representative degraders reviewed herein elicit diverse antiangiogenic phenotypes, ranging from the direct inhibition of endothelial cell proliferation, migration, and tube formation to reductions in microvessel density and the suppression of vasculogenic mimicry. Finally, we discuss the major challenges that remain, including the precise matching of degradation kinetics with the vascular normalization window, target selectivity and tissue specificity, and the activation of compensatory networks and the emergence of resistance. Since the application of TPD in this setting remains at an early stage, the clinical translation of these approaches will require careful optimization of degradation efficiency, spatiotemporal control, and delivery strategies. We also envision future directions toward immunotherapy-based combination regimens and precision-degradation approaches guided by single-cell and spatial transcriptomics. In our view, TPD should not be regarded merely as a substitute for conventional antiangiogenic drugs, but rather as a molecular tool capable of systematically remodeling the tumor vascular microenvironment. When precise control of degradation efficiency and spatiotemporal regulation are integrated with a thorough understanding of the heterogeneity and compensatory capacity of tumor vessels, the full clinical potential of this strategy can be realized.

BACKGROUND:Cardiac dysfunction due to spinal cord injury is an important factor of death in patients with spinal cord injury;however,the specific mechanism is still not clear.Therefore,revealing the mechanism of cardiac dysfunction in spinal cord injury patients is of great significance to improve their quality of life and survival rate. OBJECTIVE:To investigate the mechanism of luteolin in improving serum-induced myocardial cell death in spinal cord injury rats. METHODS:Allen's impact instrument was used to damage the spine T9-T11 of male SD rats to establish a spinal cord injury model meanwhile a sham operation group was set as the control group.The serum of rats of each group was collected.H9c2 cells were divided into a blank control group,a sham operated rat serum group,a spinal cord injury rat serum group and a luteolin pretreatment group.The cells in blank control group were only cultured with ordinary culture medium.The cells in the sham operated rat serum group were treated with medium containing 10%serum from sham operated rat.The cells in the spinal cord injury rat serum group were treated with medium containing 10%serum from spinal cord injury rat.The cells in the luteolin pretreatment group were precultured with a final concentration of 20 μmol/L luteolin for 4 hours and then changed to a medium containing 10%rat serum from spinal cord injury rat.After 24 hours of culture,the survival rate of each group of H9c2 cells was measured by CCK-8 assay.Western blot assay was used to detect the expression of autophagy related protein LC3 and p62 in H9c2 cells in each group. RESULTS AND CONCLUSION:Compared with the blank control group,there was no significant change in cell survival rate in the sham operated rat serum group(P>0.05).Compared with the sham operated rat serum group,the cell survival rate(P<0.01)and the expression of LC3 protein(P<0.05)in spinal cord injury rat serum group was significantly reduced,and the expression of p62 protein was significantly increased(P<0.05).Compared with the spinal cord injury rat serum group,the survival rate of cells in the luteolin pretreatment group significantly increased(P<0.000 1);the expression of LC3 protein significantly increased(P<0.05),and the expression of p62 protein significantly decreased(P<0.05).The results indicate that luteolin may improve myocardial cell death induced by serum from rats with spinal cord injury by promoting autophagy.

Background: and Purpose This study aimed to investigate the association between residual inflammatory risk (RIR) and vulnerable plaques using high-resolution magnetic resonance imaging (HRMRI) in symptomatic intracranial atherosclerotic stenosis (ICAS). Methods: This retrospective study included 70%–99% symptomatic ICAS patients hospitalized from January 2016 to December 2022. Patients were classified into four groups based on high-sensitivity C-reactive protein (hs-CRP) and low-density lipoprotein cholesterol (LDL-C): residual cholesterol inflammatory risk (RCIR, hs-CRP ≥3 mg/L and LDL-C ≥2.6 mmol/L), RIR (hs-CRP ≥3 mg/L and LDL-C <2.6 mmol/L), residual cholesterol risk (RCR, hs-CRP <3 mg/L and LDL-C ≥2.6 mmol/L), and no residual risk (NRR, hs-CRP <3 mg/L and LDL-C <2.6 mmol/L). Vulnerable plaque features on HRMRI included positive remodeling, diffuse distribution, intraplaque hemorrhage, and strong enhancement. Results: Among 336 included patients, 21, 60, 58, and 197 were assigned to the RCIR, RIR, RCR, and NRR groups, respectively. Patients with RCIR (adjusted odds ratio [aOR], 3.606; 95% confidence interval [CI], 1.346–9.662; P=0.011) and RIR (aOR, 3.361; 95% CI, 1.774–6.368, P<0.001) had higher risks of strong enhancement than those with NRR. Additionally, patients with RCIR (aOR, 2.965; 95% CI, 1.060–8.297; P=0.038) were more likely to have intraplaque hemorrhage compared with those with NRR. In the sensitivity analysis, RCR (aOR, 2.595; 95% CI, 1.201–5.608; P=0.015) exhibited an additional correlation with an increased risk of intraplaque hemorrhage. Conclusion In patients with symptomatic ICAS, RIR is associated with a higher risk of intraplaque hemorrhage and strong enhancement, indicating an increased vulnerability to atherosclerotic plaques.