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.

[Purpose]To analyze the trends of incidence and age at onset of leukemia in Jiangsu cancer registration areas from 2009 to 2019.[Methods]The continuous monitoring data of leukemia from 2009 to 2019 were collected from 16 cancer registries in Jiangsu Province.All datasets were checked and evaluated based on data quality control criteria and were included in the analysis.Crude incidence rate(CIR),age-standardized incidence rate by Chinese standard population(ASIRC),the average annual percentage change(AAPC),the standardized average age at onset,the changes in the age structure of incidence and the changes in the birth cohort by year were calculated.[Results]The incidence rate of leukemia significantly increased from 5.22/105 in 2009 to 7.88/105 in 2019,with a significant upward trend(for CIR,AAPC=4.95％,95％CI:3.82％～6.09％;for ASIRC,AAPC=2.97％,95％CI:1.52％～4.43％).The incidence rates were in-creased in all age groups and increased with the birth cohort by years.There was a tendency of backward shift for the age composition of the population,with the increasing of composition for those over 60 years old.The mean age at onset increased from 48.62 years old in 2009 to 57.96 years old in 2019,with a backward shift in the mean age(β=0.773,P＜0.001),and the mean age at onset increased with the year only in rural areas after standardization(β=0.428,P=0.017).[Conclusion]Leukemia incidence rate in Jiangsu Province increased from 2009 to 2019,and the age at onset has shifted backwards.It's important to strengthen the early prevention and control of leukemia.

Objective To observe the effects of Hedysarum Polybotrys polysaccharide(HPS)on the glucose metabolism of small intestinal smooth muscle in rats with diabetic gastroparesis(DGP)of spleen qi deficiency syndrome;To explore its mechanism based on AMPK/GLUT4 signaling pathway.Methods Totally 72 male Wistar rats were randomly divided into 12 in the blank group and the remaining 60 rats were assigned to the model group.The DGP spleen qi deficiency syndrome model was replicated by intraperitoneal injection of streptozotocin+irregular feeding with high-fat and high sugar feed combined with swimming exhaustion method.The model rats were randomly divided into model group,metformin group and HPS high-,medium-and low-dosage groups.The metformin group was given 100 mg/kg metformin hydrochloride by gavage,while the HPS high-,medium-and low-dosage groups were given 200,100 and 50 mg/kg HPS by gavage,respectively.The blank group and model group were given purified water by gavage once a day for 8 consecutive weeks.The gastric emptying rate and small intestine propulsion rate in rats were detected,HE staining was used to observe the smooth muscle morphology of gastric antrum and ileal tissue,immunofluorescence staining was used to detect the expression of glucagon like peptide-1(GLP-1)in ileal tissue,ELISA was used to detect the contents of adiponectin(APN),glucagon(Glu)and insulin(INS)in serum,Western blot was used to detect the protein expressions of glucose transporter(GLUT)4,GLUT1,AMP-activated protein kinase(AMPK)and p-AMPK in ileal tissue.Results Compared with the blank group,the model group rats showed significantly increased random blood glucose,significantly decreased body mass,gastric emptying rate and small intestinal propulsion rate(P<0.01);the edema in the submucosal layer,loose arrangement of connective tissue,infiltration of a small number of lymphocytes,granulocytes and macrophages,reduced number of goblet cells in the ileal tissue,shedding of intestinal villous epithelial cells and widening of the gap between the submucosal layer and the lamina propria;the expression of GLP-1 in ileal tissue was significantly decreased(P<0.05),the contents of serum APN and INS were significantly decreased,and the content of Glu significantly increased(P<0.01),the expressions of GLUT4 and p-AMPK/AMPK proteins in ileal tissue were significantly decreased,while the expression of GLUT1 protein significantly increased(P<0.01).Compared with the model group,rats in metformin group and HPS high-dosage group showed a random decrease in blood glucose,an increase in body mass,gastric emptying rate,and small intestine propulsion rate(P<0.05,P<0.01);a more regular arrangement of gastric antral tissue cells,a reduction of shedding cells and edema,the smooth muscle structure of the ileal tissue was relatively intact,with evenly distributed cells and reduced infiltration of inflammatory cells;the expression of GLP-1 in ileal tissue increased,the contents of serum APN and INS increased,and the content of Glu decreased,the expressions of GLUT4 and p-AMPK/AMPK proteins in ileal tissue increased,while the expression of GLUT1 protein decreased(P<0.05,P<0.01).Conclusion HPS may up-regulate GLUT4 and down-regulate GLUT1 expression through activates AMPK,promotes glucose uptake and utilization by small intestinal smooth muscle,and improves glucose metabolism of DGP rats with spleen qi deficiency syndrome.

Objective:To explore the high-risk factors affecting the severity of neonatal necrotizing enterocolitis (NEC).Methods:This study involved 153 NEC patients admitted to the Neonatology Department of the Children's Hospital of Soochow University from January 1, 2017, to December 30, 2023. Based on the severity of NEC determined by Bell's criteria, these patients were divided into two groups: mild group (Bell stage Ⅱ, n=70) and severe group (Bell stage Ⅲ, n=83). Clinical data including general conditions, clinical treatment and disease status before the onset of NEC, laboratory test results, and perinatal conditions of the mothers were retrospectively collected. Univariate analysis (rank-sum test and Chi-square test) and multivariate analysis (logistic regression analysis) were used to explore the risk factors affecting the severity of NEC. Results:The proportion of infants with gestational age<37 weeks or birth weight<1 500 g, the rate of antibiotic usage, sepsis or shock were higher in the severe group than in the mild group [91.6% (76/83) vs. 75.7% (53/70); 55.4% (46/83) vs. 34.3% (24/70); 85.5% (71/83) vs. 71.4% (50/70); 55.4% (46/83) vs. 17.1% (12/70); 30.1% (25/83) vs. 8.6% (6/70); with χ 2 values of 7.22, 6.84, 4.57, 23.64, and 10.91, respectively, all P<0.05]. Furthermore, the severe group had a late initiation of breastfeeding and longer durations of peripherally inserted central catheter (PICC) placement and parenteral nutrition [2.00 d (1.00-2.00 d) vs. 1.00 d (1.00-2.00 d); 0.00 d (0.00-18.00 d) vs. 0.00 d (0.00-7.50 d); 14.00 d (5.00-21.00 d) vs. 10.50 d (0.00-18.25 d), with Z values of -2.90, -1.98, and -2.09, respectively, all P<0.05]. (2) Within 48 h before the onset, the severe group had higher proportions of infants with decreased white blood cell count, decreased platelet count, electrolyte imbalance, and metabolic acidosis than the mild group [53.0% (44/83) vs. 14.3% (10/70); 49.4% (41/83) vs. 10.0% (7/70); 38.6% (32/83) vs. 14.3% (10/70); 37.3% (31/83) vs. 14.3% (10/70), with χ2 values of 24.94, 27.38, 11.23, and 10.30, respectively, all P<0.05]. Besides, the levels of procalcitonin and C-reactive protein were higher in the severe group than in the mild group [2.31 ng/ml (0.26-11.71 ng/ml) vs. 0.22 ng/ml (0.00-2.19 ng/ml); 58.50 mg/L (14.34-125.25 mg/L) vs. 8.20 mg/L (0.23-34.56 mg/L), with Z values of -3.88 and -5.02, respectively, both P<0.05]. (3) Multivariate logistic regression analysis showed that prolonged duration of PICC placement, decreased platelet count, electrolyte imbalance, metabolic acidosis, and concurrent sepsis were independent risk factors affecting the severity of NEC [ OR (95% CI) values were 1.104 (1.020-1.196), 5.364 (1.667-17.253), 4.047 (1.171-13.986), 4.333 (1.290-14.556), and 3.290 (1.005-10.774), respectively, with all P<0.05]. Conclusions:Prolonged duration of PICC placement, concurrent sepsis, decreased platelet count, electrolyte imbalance, and metabolic acidosis in NEC patients are more likely to lead to severe cases. In clinical practice, attention should be paid to relevant indicators, and abnormal changes should be identified and intervened in a timely manner to reduce the occurrence of severe NEC.

Objective:To investigate the alterations in voxel-mirrored homotopic connectivity (VMHC) of brain regions, association loop connectivity, and white matter microstructure in patients with white matter hyperintensities (WMH) of presumed vascular origin, and analyze the pathological basis of cognitive impairment in WMH patients.Methods:A prospective study was performed; 75 WMH patients (WMH group) admitted to Jiangsu Shengze Hospital Affiliated to Nanjing Medical University from January 2023 to September 2024 and 67 volunteers without obvious brain diseases (control group) recruited during the same period were enrolled. General data of these participants, and scores of neuropsychological scales such as mini-mental state examination (MMSE), frontal assessment battery (FAB), and trail making test (TMT) were compared between the two groups. Resting-state functional magnetic resonance imaging (rs-fMRI) and diffusion tensor imaging (DTI) data of all participants were collected; rs-fMRI data were then analyzed using VMHC algorithm to calculate and conform the brain regions with significantly different VMHC between the two groups, and these regions were used as seed points to perform functional connectivity with the whole brain; Pearson correlation analyses of VMHC and functional connectivity in these brain regions with scores of neuropsychological scales were performed. DTI data were processed using tract-based spatial statistics (TBSS) method to calculate and conform the brain regions with significantly different diffusion parameters of fiber tracts between the two groups; Pearson correlation analyses of diffusion parameters of the fiber tracts in these brain regions with scores of neuropsychological scales were performed.Results:(1) Comparison of general data and neuropsychological scale scores: proportion of participants with hypertension history was significantly different between the two groups ( P<0.05); scores of TMT-A, TMT-B, and Stroop C scales in the WMH group were significantly higher than those in the control group ( P<0.05). (2) Comparison of VMHC and seed point functional connectivity: compared with that in the control group, the VMHC in bilateral middle occipital gyrus, visual cortex, medial occipitotemporal gyrus, insula, and postcentral gyrus of the WMH group were statistically lower ( P<0.05). Compared with that in the control group, functional connectivity of right visual cortex with right middle temporal gyrus, bilateral precuneus, and right dorsolateral superior frontal gyrus in the WMH group was significantly weakened, and functional connectivity of right postcentral gyrus with right medial occipitotemporal gyrus, left middle temporal gyrus, left visual cortex, and left postcentral gyrus was statistically weakened ( P<0.05). In the WMH group, the VMHC of bilateral insula was negatively correlated with TMT-B score ( r=-0.381, P<0.001), and functional connectivity between right visual cortex and right dorsolateral superior frontal gyrus was negatively correlated with Stroop C score ( r=-0.401, P<0.001). (3) TBSS results: the diffusion parameters of the anterior corona radiata, superior corona radiata, corpus callosum, superior longitudinal fasciculus, and posterior thalamic radiation were statistically significant between the two groups ( P<0.05). In the WMH group, the fractional anisotropy in the genu of the corpus callosum was positively correlated with Stroop C score ( r=0.426, P<0.001), radial diffusivity was negatively correlated with Stroop C score ( r=-0.376, P<0.001), and mean diffusivity of the left anterior corona radiata was negatively correlated with TMT-A score ( r=-0.443, P<0.001). Conclusion:WMH patients have decreased coordination in homotopic brain regions and weakened functional connectivity of association loops, with widely distributed white matter microstructure damages, which may be involved in the neuropathological process of cognitive impairment.

Objective To establish an animal model of osteoporosis combined with liver cirrhosis and conduct preliminary investigation into the effect of liver cirrhosis on bone loss in mice and the underlying mechanisms.Methods The experimental animals were 25 6-week-old female C57BL/6 mice with a body weight of approximately 20-22 g.A comorbidity model of liver cirrhosis and osteoporosis was established in the mice by ovariectomy combined with carbon tetrachloride(CCl4)induction.The mice were randomly assigned to 4 groups(n=5 in each group),including a control group,a liver cirrhosis group,an osteoporosis group,and a cirrhosis and osteoporosis comorbidity group.Pathological changes in the liver were observed via HE staining,Sirius Red staining,and serum liver function indicators.Bone mass and morphological changes were assessed using micro-CT and HE staining.ELISA,Western blot,and immunohistochemistry were performed to assess the expression of insulin-like growth factor-1(IGF-1)in serum and liver tissues.An additional IGF-1 intervention group was established to investigate the potential role of IGF-1 in the comorbidity of liver cirrhosis and osteoporosis,and changes in bone mass and morphology were analyzed via micro-CT and HE staining.Results Compared with the control and osteoporosis groups,the liver cirrhosis and cirrhosis-osteoporosis comorbidity groups exhibited significant inflammatory cell infiltration and collagen fiber deposition in liver tissues,along with markedly increased serum levels of alanine aminotransferase(ALT),aspartate aminotransferase(AST),and total bilirubin(TBIL)(P＜0.05).According to the Micro-CT and HE staining results,the cirrhosis-osteoporosis comorbidity group showed reduced bone mass and decreased trabecular numbers in the distal femur compared to those in the osteoporosis group,with the differences being statistically significant(P＜0.05).ELISA,Western blot,and immunohistochemistry demonstrated significantly reduced expression of IGF-1 in the liver and serum of the cirrhosis-osteoporosis comorbidity group(P＜0.05).Notably,exogenous IGF-1 treatment restored bone mass in mice with liver cirrhosis combined with osteoporosis(P＜0.05).Conclusion Through ovariectomy combined with CCl4 induction,a mouse model of liver cirrhosis combined with osteoporosis was successfully established.IGF-1 may serve as a potential molecular mechanism and therapeutic target mediating the liver cirrhosis-osteoporosis comorbidity.

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.

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.

Objective To explore the effects and mechanisms of bone marrow mesenchymal stem cells(BMSCs)in regulating microglial polarization on neuropathic pain in rats with sciatic nerve branch-selective injury(SNI).Methods Fifty SD rats were randomly divided into five groups with ten rats in each group;sham group(rats only exposed sciatic nerve without ligation),SNI group(SNI model was estab-lished),BMSCs group[rats were injected with BMSCs(1×106)through the sheath for 3 days after SNI modeling],BMSCs+sh-NC group[rats were intrathecally injected with BMSCs(1×106)and intrathecally injected with knock-down control(adenovirus 2.5×107 IU)for 3 days after SNI modeling],and BMSCs+sh-YY1 group[rats were intrathecally injected with BMSCs(1×106)and intrathecally injected with YY1 knockdown adenovirus(2.5×107 IU)for 3 days after SNI modeling].Neuropathic pain was assessed using paw withdrawal threshold(PWT)and paw withdrawal thermal latency(PWTL)following mechanical stimulation.Immunofluorescence was used to detect the expression of CD86,CD206,iNOS,and Arg1 in the rat spinal cord tissues.Western blotting was used to measure the expression of YY1 and KLF4 in spinal cord tissue.Results Compared with sham group,the values of PWTL and PWT in the SNI group significantly reduced(both P<0.05).In spinal cord tissue,the positive rates of iNOS and CD86 protein increased,whereas the positive rates of CD206 and Arg1 protein and the expression of YY1 and KLF4 decreased(all P<0.05).Compared with the SNI group,the values of PWTL and PWT in the BMSCs and BMSCs+sh-NC groups increased(all P<0.05),the positive rate of CD86 protein in the spinal cord decreased,whereas the positive rate of CD206 protein and the expression of YY1 and KLF4 increased(all P<0.05).Also,the positive rate of iNOS protein in the spinal cord tissue decreased and the positive rate of Arg1 increased in the BMSCs group(all P<0.05).Compared with the BMSCs and BMSCs+sh-NC groups,the PWTL and PWT values in the BMSCs+sh-YY1 group decreased(all P<0.05).The positivity rate of CD86 protein increased,the positivity rate of CD206 protein decreased,and the expression of YY1 and KLF4 decreased in the spinal cord tissue(all P<0.05).Conclusion Intrathecal injection of BMSCs promotes M2 polarization of microglia in the spinal cord and relieves neuropathic pain in rats with SNI,and its mechanism may be related to the upregulation of KLF4 expression mediated by YY1.