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.

Objective:To explore the predictive value of preoperative peripheral hematological parameters combined with clinicopathological features for cervical lymph node metastasis（CLNM） in patients with laryngeal squamous cell carcinoma（LSCC）, and to construct and validate a nomogram model for CLNM. Methods:A retrospective analysis was conducted on the clinical data of 264 LSCC patients who underwent surgical treatment and were pathologically confirmed, collected from the Second Affiliated Hospital of Shandong First Medical University and Taian 88 Hospital. Specifically, 161 patients from one hospital were allocated to the training cohort, while 103 patients from another hospital constituted the validation cohort. Based on postoperative pathological results, patients were categorized into CLNM-positive and CLNM-negative groups. The general clinical data, clinicopathological features, and hematological parameters of the two groups were analyzed and compared. A preoperative predictive model for CLNM was developed using logistic regression analysis, followed by validation and sensitivity analysis to evaluate the robustness of the model's predictive performance. Results:The results showed that there were significant differences in tumor location, tumor size, tumor differentiation, neutrophil percentage, lymphocyte count, lymphocyte percentage, c-reactive protein（CRP）, fibrinogen, neutrophil-to-lymphocyte ratio（NLR）, platelet-to-lymphocyte ratio（PLR）, systemic immune-inflammation index（SII）, systemic inflammation response index（SIRI）, and prognostic inflammatory index（PIV） between the CLNM-positive and CLNM-negative groups（P<0.05）. Lasso regression identified tumor location, clinical T stage, tumor size, tumor differentiation degree, red blood cell distribution width（RDW） -coefficient of variation（RDW-CV）, CRP, FIB, D-dimer, NLR, and lymphocyte-to-monocyte ratio（LMR） were the most predictive parameters. Multivariate logistic regression revealed that tumor location, tumor size, tumor differentiation degree, CRP, and NLR were independent risk factors for CLNM in LSCC patients（P<0.05）. A nomogram was constructed based on these five factors. The model demonstrated excellent discrimination, with a C-index of 0.837（95%CI 0.766-0.908） in the training cohort and 0.809（95%CI 0.698-0.920） in the validation cohort. Calibration curves and DCA curves in both cohorts confirmed the clinical utility of the model. Sensitivity analysis further supported the robustness of the results, showing good discrimination and calibration across different age and BMI subgroups. Conclusion:Tumor location, tumor size, tumor differentiation degree, CRP, and NLR were independent risk factors for CLNM in LSCC patients. The nomogram based on these variables exhibits strong discrimination, calibration, and clinical applicability, and may serve as a valuable tool for preoperative risk assessment and individualized treatment planning.
Humans ; Nomograms ; Laryngeal Neoplasms/blood* ; Retrospective Studies ; Lymphatic Metastasis ; Carcinoma, Squamous Cell/blood* ; Lymph Nodes/pathology* ; Male ; Female ; Middle Aged ; Neck ; C-Reactive Protein ; Aged ; Logistic Models ; Neutrophils ; Prognosis

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Objective:To investigate the clinically curative effect of composite dressing of adipose mesenchymal stem cell exosomes and chitosan hydrogel in treating deep Ⅱ burn wound.Methods:A total of 108 patients with superficially deep Ⅱ burns,who admitted to Tangdu Hospital,Air Force Medical University within 48 hours during March 2022 and October 2024,were selected.Patients were randomly divided into conventional treatment group and the combined treatment group by using a random number table,with 54 patients in each group.All patients underwent enzymatic debridement(collagenase ointment)to conduct conventional treatment.The combined treatment group received treatment with composite dressings of adipose-derived mesenchymal stem cell exosomes(ADSCs-Exo)combined with chitosan hydrogel,while the conventional treatment group received treatment with silver sulfadiazine dressings(SSD)on the basis of conventional treatment.The healing rates of wound,Vancouver Scar Scale(VSS)scores,the levels of serum inflammatory factors included interleukin-6(IL-6),interleukin-1β(IL-1β),C-reactive protein(CRP),and tumor necrosis factor-α(TNF-α),as well as curative efficacy rates,and adverse reactions between two groups were compared at different time points after treatment.Results:There was not statistically significant difference in healing rates of wound between the two groups at the 7th day after treatment(P>0.05).At the 14th day and the 21th day after treatment,the average healing rates of wound in the combined treatment group were respectively(67.69±8.57)%and(89.46±7.54)%,which were higher than(59.50±4.93)%and(75.52±9.11)%in the conventional treatment group,and the differences were statistically significant(t=6.087,8.662,P<0.05).The average VSS score was(6.42±1.20)points in the combined treatment group after treatment,which was lower than that in the conventional treatment group(8.94±1.58),and the difference was statistically significant(t=9.33,P<0.05).Before treatment,there were not statistically significant difference in VAS scores and the levels of serum inflammatory factor between the two groups(P>0.05).At the 7th day,the 14th day and the 21th day after treatment,the VAS scores in the combined treatment group were significantly lower than those in the conventional treatment group(t=10.008,12.004,13.899,P<0.05),respectively.At the 21th day after treatment,the levels of IL-6,IL-1β,CRP,and TNF-α of the combined treatment group were significantly lower than those of the conventional treatment group(t=3.400,4.490,7.293,5.900,P<0.05).The efficacy rate of clinical treatment in the combined treatment group was 96.30%,which was higher than 83.33%of the conventional treatment group,with a statistical significance(x2=7.942,P<0.05).The incidence of adverse reaction in the combined treatment group was 14.81%,which was lower than 24.07%of the conventional treatment group,without statistical significance(P>0.05).Conclusion:Compared with conventional silver sulfadiazine dressing,the composite dressing of adipose mesenchymal stem cell exosomes and chitosan hydrogel can quickly promote the re-epithelialization process in treating patients with superficially deep Ⅱ burns at the middle to late stage,and improve the healing rate,and relieve the inflammatory reaction and pain perception of patients for wound,and enhance efficiency and safety.

Objective Explore the correlation among difference of skin temperature(ΔT)between proximal and distal ends,peripheral serum indicators and cardiac function,to screen the influencing factors of the main syndrome of"reverse coldness of limbs"in Sini decoction.Methods The clinical data of 134 critically ill patients who visited the emergency department of the Second Affiliated Hospital of Tianjin University of Traditional Chinese Medicine from January 2022 to September 2023 were collected,including echocardiographic indicators[ejection fraction(EF),anterior-posterior diameter of the aortic sinus,left atrial anterior-posterior diameter,right ventricle left-right diameter,right atrial left-right diameter,left ventricular diastolic end anterior-posterior diameter,interventricular septum thickness,left ventricular posterior wall thickness,left ventricular posterior wall movement amplitude,main pulmonary artery inner diameter,pulmonary artery valve flow velocity,aortic valve flow velocity,mitral valve flow velocity,pulmonary artery systolic pressure],blood routine[white blood cell count(WBC),red blood cell count(RBC),platelet count(PLT),hemoglobin(Hb)],myocardial markers[troponin(cTnI,cTnT),MB isoenzyme of creatine kinase(CK-MB),myoglobin(MYO),N-terminal pro-brain natriuretic peptide(NT-proBNP)],D-dimer,blood gas analysis[pH value,arterial oxygen partial pressure(PaO2),arterial partial pressure of carbon dioxide(PaCO2),lactic acid(Lac),arterial oxygen saturation(SaO2)],coagulation function indicators[prothrombin time(PT),activated partial thromboplastin time(APTT),thrombin time(TT),international normalized ratio(INR),fibrinogen(Fib)],infection indicators[C-reactive protein(CRP),procalcitonin(PCT)],biochemical indicators[K+,Na+,Cl-,Ca2+,P3+,total protein(TP),albumin(Alb),aspartate aminotransferase(AST),creatine kinase(CK),α-hydroxybutyrate dehydrogenase(α-HBDH),lactate dehydrogenase(LDH),urea,creatinine(Cr),uric acid(UA)],mean arterial pressure(MAP),and the top 10 disease types.These data were used as independent variables,and the ΔT value was used as the dependent variable for univariate linear regression analysis.Variables with statistically significant differences in the univariate analysis were subjected to multivariate linear regression analysis to identify the influencing factors causing an increase in the ΔT value.Results The univariate analysis analysis showed that variables such as shock,MAP,WBC,MYO,Lac,PT,APTT,TT,CRP,K+,P3+,Alb,urea,Cr,right ventricular left-right diameter,left ventricular posterior wall motion amplitude,main pulmonary artery diameter,pulmonary artery valve velocity,and aortic valve velocity were all risk factors influencing the increase of ΔT between the left axilla and the left hand in critically ill patients(all P<0.05);shock,respiratory failure,MAP,WBC,cTNI,MYO,Lac,PT,APTT,TT,CRP,Ca2+,P3+,Alb,urea,Cr,right ventricular left-right diameter,interventricular septum motion amplitude,left ventricular posterior wall motion amplitude,and main pulmonary artery inner diameter were all risk factors influencing the increase of ΔT between the left axilla and the left foot in critically ill patients(all P<0.05).Multivariate linear regression analysis showed that APTT,Lac,right ventricular left and right diameters,and urea were independent risk factors for the increase of ΔT in the left axilla and left hand[95%confidence interval(95%CI)was 0.016-0.036,0.024-0.095,-0.031 to-0.003,0.002-0.029,respectively;P values were 0.000,0.001,0.015,0.028,respectively],while PT,right ventricular left and right diameters,interventricular septal motion amplitude,and MYO were independent risk factors for the increase of ΔT left axilla and left foot(95%CI was 0.023-0.178,-0.103 to-0.019,0.031-0.245,0.000-0.002,respectively;P values were 0.012,0.006,0.013,0.015,respectively).Conclusion APTT,PT,Lac,MYO,urea,the right ventricular diameter and interventricular septal motion amplitude are key factors affecting the ΔT value of critically ill patients,which can cause reverse coldness of limbs.

Monotropein is a compound classified into iridoid which is found in herbaceous plants Morindae officinalis. It possesses anti-inflammatory, antioxidant, and anti-osteoarthritic activities. Previous study indicates that monotropein may have the potential to combat cardiovascular disease, although the related mechanism remains unclear. In this study, we constructed the model of atherosclerosis by oxidized low density lipoprotein-induced vascular smooth muscle cells and LDLR –/–mice given high-fat diet to investigate the effects of monotropein on atherosclerosis.Our results showed that monotropein treatment significantly reduced the area of atherosclerotic plaques and necrotic cores in mice, inhibited the proliferation and migration of vascular smooth muscle cells, and reduced inflammatory responses and oxidative stress, which in turn alleviated atherosclerosis. In addition, we found that monotropein reduced the expression levels of P-NF-κB and P-AP-1. In conclusion, our data suggest that monotropein inhibited the proliferation and migration of vascular smooth muscle cells by mediating the activity of NF-κB, AP-1, reducing the level of inflammation and oxidative stress, and thus resisting the development of atherosclerosis. These findings demonstrate the efficacious therapeutic impact of monotropein on atherosclerosis and elucidate its specific target.

Objective To explore the effects of CDP-diacylglycerol synthase 1(CDS1)on autophagy and amyloid deposition in hippocampal neurons of mice and the related mechanism.Methods Congo red and immunohistochemical staining were used to observe the amyloid deposition in hippocampus of amyloid precursor protein(APP)/presenilin 1(PS1)double-transgenic mice.Lentivirus-mediated overexpression of APP was induced in HT22 cells,and Congo red staining was used to observe the amyloid deposition in HT22 cells.The protein expression levels of microtubule-associated protein 1 light chain 3(LC3)-Ⅱ and P62 in the hippocampus of APP/PS1 double-transgenic mice and APP-overexpressed HT22 cells were detected by Western blotting.The differential protein CDS1 was screened based on the hippocampal proteomics results of APP/PS1 double-transgenic mice.The expression of CDS1 protein in hippocampal tissue of APP/PS1 transgenic mice and APP-overexpressed HT22 cells was detected by Western blotting.After lentivirus-mediated APP overexpression in HT22 cells,CDS1 was overexpressed,and the protein expression levels of LC3-Ⅱ and P62 were detected by Western blotting.Results β-amyloid protein(Aβ)was deposited in the hippocampus of APP/PS1 mice and in HT22 cells overexpressing APP.The levels of LC3-Ⅱ and P62 protein in the hippocampus of APP/PS1 double-transgenic mice and APP-overexpressed HT22 cells were significantly increased.A differential metabolic pathway,glycerophospholipid metabolic pathway,was screened by Kyoto Encyclopedia of Genes and Genomes pathway analysis in the proteomic results of APP/PS1 double-transgenic mice,and the differential protein CDS1 was obtained.Compared with wild-type C57BL/6 mice,APP/PS1 double-transgenic mice exhibited a significantly decrease in CDS1 protein expression in the hippocampus(0.46±0.07 vs 1.00±0.25,P＜0.01).Similarly,lentivirus-mediated overexpression of APP in HT22 cells resulted in decreased CDS1 protein levels compared to cells infected with empty viral vector controls(0.68±0.18 vs 1.00±0.13,P＜0.01).The autophagy flow of nerve cells was significantly restored after the CDS1 overexpression in APP-overexpressed HT22 cells(LC3-Ⅱ:1.00±0.15 vs 0.21±0.05,P＜0.01;P62:1.00±0.16 vs 0.67±0.10,P＜0.01),and Aβ deposition was significantly decreased.Conclusion Downregulation of CDS1 expression can induce dysfusion of autophagosome and lysosome,promoting amyloid deposition in hippocampus of mice with Alzheimer's disease.