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Objective:To investigate the diagnostic and early-warning value of laboratory test indicators for sepsis-induced myocardial injury (SIMD).Methods:The clinical data of 183 patients with sepsis admitted to the Department of Emergency and Critical Care Medicine of Guangdong Provincial People's Hospital from August 2016 to October 2020 were collected. The patient's age, gender, past medical history, vital signs and pathogen culture results were extracted. Cardiac function, blood routine, liver function, renal function, inflammatory factors, coagulation function, APACHE Ⅱ and SOFA scores were recorded at enrollment and 72 h after admission. SIMD was defined as cTnT ≥300 pg/mL and NT-proBNP ≥1243 pg/mL twice in 72 h intervals between enrolled cases, and the early-warning factors of patients with SIMD were analyzed. The differences in various indicators between the two groups were compared, and Logistic regression analysis was used to explore the diagnostic efficacy of cTnT and NT-proBNP combined for SIMD, and the correlation between PCT/PLT ratio and the occurrence of SIMD.Results:Among 250 patients, 67 patients were excluded for lack of the main indicators, and 183 patients (including 62 patients with history of cardiac disease) were enrolled finally. Among 183 patients with sepsis, 105 patients (57.38%) with cTNT ≥300 pg/mL and NT-proBNP ≥1 243 pg/mL, were diagnosed as myocardial injury; after excluding 62 patients with history of cardiac disease, 59 patients (48.76%) with cTNT ≥300 pg/mL and NT-proBNP ≥1 243 pg/mL were diagnosed as myocardial injury. Logistic regression analysis showed that increased PCT/PLT ratio ( OR=1.585, 95% CI: 1.124-2.237, P=0.009) was an independent risk factor for early-warning of SIMD. The PCT/PLT ratio ( OR= 1.850, 95% CI: 1.103-3.102, P=0.020) could stably predict the occurrence of SIMD in patients without previous history of heart disease. ROC curve analysis showed that PCT/PLT ratio could effectively predict the occurrence of SIMD (AUC=0.693, 95% CI: 0.617-0.769, P<0.001), the optimal cut-off value was 0.177 (sensitivity: 65.7%, specificity: 66.7%). The PCT/PLT ratio was still effective in predicting the occurrence of SIMD after excluding patients with previous history of heart disease (AUC=0.733, 95% CI: 0.643-0.823, P<0.001), and the optimal cut-off value was 0.429 (sensitivity: 55.9%, specificity: 83.9%). Conclusions:The combination of cTnT and NT-proBNP has certain diagnostic value for SIMD, and the PCT/PLT ratio could warn the occurrence of SIMD.
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Objective:To explore the mechanism of resveratrol on ameliorating the cognitive dysfunction induced by sepsis associated encephalopathy (SAE) in rats.Methods:The 12 weeks old male Sprague-dawley (SD) male rats were randomly divided into sham group, sepsis group and resveratrol group, with 30 rats in each group. The rat model of sepsis was made by injecting LPS (10 mg/kg) into tail vein. The rats in sham group was given the same amount of normal saline (NS). After LPS injection, resveratrol (8 mg·kg -1·d -1) was intraperitoneally injected once daily for 2 days in the resveratrol group; the same amount of NS was given to the sepsis group and sham group. At 24 hours after model establishment, the cognitive function of the experimental rats was assessed by the Morris water maze test. The blood-brain barrier (BBB) permeability was evaluated by the brain water content (BWC) and Evans blue (EB) test. The protein expressions of matrix metalloproteinase 9 (MMP-9), Occludin and Claudin-5 in cortical tissue were detected by Western Blot. Double immunofluorescence was used to verify the co-localization of MMP-9 protein and the marker protein of astrocyte GFAP in the cortical tissue of rats. Results:Compared with the sham group, the escape latency in the sepsis group was significantly longer [48-hour escape latency (s): 56.56±6.43 vs. 36.62±3.32, 72-hour escape latency (s): 57.72±7.23 vs. 26.46±4.24, both P < 0.01], the BWC and extravasation of EB were increased [BWC: (84.56±2.03)% vs. (76.82±2.22)%, EB (μg/g): 17.56±2.28 vs. 6.25±1.36, both P < 0.01], the expression of MMP-9 protein was increased (MMP-9/β-actin: 0.73±0.01 vs. 0.24±0.01, P < 0.01), the protein expressions of Occludin and Claudin-5 were decreased (Occludin/β-actin: 0.45±0.02 vs. 0.86±0.04, Claudin-5/β-actin: 0.62±0.03 vs. 0.96±0.05, both P < 0.01). At the same time, the co-localization expression of MMP-9 protein and the astrocytes of the cortical were increased [MMP-9 fluorescence intensity (AU): 38.66±4.26 vs. 17.23±3.04, MMP-9 positive cells: (26.92±1.77)% vs. (12.82±1.46)%, both P < 0.01]. Compared with the sepsis group, the escape latency in resveratrol group was significantly shorter [48-hour escape latency (s): 41.42±6.27 vs. 56.56±6.43, 72-hour escape latency (s): 33.46±7.17 vs. 57.72±7.23, both P < 0.01], the BWC and extravasation of EB were decreased [BWC: (77.15±2.27)% vs. (84.56±2.03)%, EB (μg/g): 7.74±1.88 vs. 17.56±2.28, both P < 0.01], the expression of MMP-9 protein was decreased (MMP-9/β-actin: 0.25±0.01 vs. 0.73±0.01, P < 0.01), the protein expressions of Occludin and Claudin-5 were increased (Occludin/β-actin: 0.82±0.03 vs. 0.45±0.02, Claudin-5/β-actin: 0.92±0.04 vs. 0.62±0.03, both P < 0.01). At the same time, the co-localization expression of MMP-9 protein and the astrocytes of the cortical were decreased [MMP-9 fluorescence intensity (AU): 19.44±4.37 vs. 38.66±4.26, MMP-9 positive cells: (13.11±1.29)% vs. (26.92±1.77)%, both P < 0.01]. Conclusion:Resveratrol can inhibit the expression of MMP-9 protein in the astrocytes of the cortical cortex of rats, and then reduce the degradation of tight junction proteins of Occludin and Claudin-5, thereby reducing BBB permeability and eventually ameliorate the cognitive dysfunction induced by SAE.
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Objective To determine the effect of high dose albumin on permeability of blood brain barrier (BBB) in brain of rats after ischemic-reperfusion (IR) in order to explore its possible mechanism.Methods Establishment of brain ischemic reperfusion rat model by using middle cerebral artery occlusion (MCAO).Medicine treatment was given by caudal vein injection after 2 hours of MCAO.Thirty-six healthy male SD rats were then randomly (random number) divided into 6 groups (n =6 in each):6 h and 24 h sham-operation groups (Group Sham:operation without ischemia),6 h and 24 h normal saline groups (Group NS:NS injection 5 ml/kg) and 6 h and 24 h albumin group (Group Alb:25 ％ Alb injection 1.25 g/kg).Six hours and 24 hours after the end of reperfusion,rats were measured by Zea-Longa score (neural function deficit) separately.Serum concentration of S100B was examined by the ELISA kit and Evans blue in brain tissue was detected by spectrophotometer.The level of AQP4 was examined by Western blot and immunohistochemistry.All data were analyzed by one-way analysis of variance (ANOVA),The intergroup comparisons were analyzed by the least-significant-difference (LSD) test by using SPSS version 17.0 software.Differences were considered statistically significant if P ＜ 0.05.Results Zea-Longa score significantly increased in both group NS and group Alb at 6 h and 24 h (P =0.000).However,there was no significant difference in ZEA-LONGA score of 6 h and 24 h between group Alb and group NS (P =1.000).The serum concentration of S100B in group NS 6 h was significantly lower than that in group Alb at 6h (196.67±20.11 vs 160.04±14.00,P=0.000),and at24h (2.45±0.07 vs.2.23±0.07,P=0.000).Furthermore,concentration of Evans blue in brain tissue in group Alb was significantly higher than that in group NS at both 6 h (0.97 ± 0.08 vs.0.74 ± 0.06,P =0.000) and 24 h (2.45 ± 0.07 vs.2.23 ± 0.07,P =0.000).The expression of AQP4 in brain tissue was higher in group Alb than that in group NS at both 6 h (0.72 ±.0.11 vs.0.57 ± 0.06,P ＜ 0.01) and 24 h (0.80 ± 0.03 vs 0.61 ± 0.02,P ＜0.01).Conclusions High dose albumin contribute slightly in improvement of neural deficit in rats after IR.On the contrary,it can also aggravate the IR injury,which increases brain edema then increase the permeability of BBB.The mechanism may be associated with over-expression of AQP4 in brain tissue.
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Objective To explore whether hypertonic saline would partake in regulating Notch signaling in microglia in experimentally induced cerebral ischemic rats.Methods Male SD rats were randomly divided into sham group, cerebral ischemia group, normal saline group ( NS group ) , 10%hypertonic saline group (10%HS group) , the model of cerebral ischemia were established in all rats except the sham group by using middle cerebral artery occlusion ( MCAO) .After 2 hours of MCAO, the rats were through reperfusion for 24 h.In addition, rats in the normal saline group and 10% HS group were respectively treated with a continuous intravenous injection of normal saline (0.3 mL/h) and 10%HS (0.3 mL/h) by tail vein for 24 h.Immunofluorescence methods, RT-PCR and Western blot were used to detect the expression of Notch1 and intracellular Notch receptor domain ( NICD) .All data was analyzed by one-way analysis of variance ( ANOVA) , The intergroup comparisons were analyzed by the least-significant-difference (LSD) tests.Differences were considered statistically significant if P<0.05.Results Immunofluorescence showed that the expression of Notch1 and NICD were significantly increased in the microglia around peri-ischemia area in cerebral ischemia group and normal saline group compared to sham group;the expression of Notch1 and NICD in the microglia around peri-ischemia area were significantly reduced in 10% HS group compared to ischemia group and NS group.RT-PCR showed that the mRNA expression of Notch1 was significantly increased in ischemia group and NS group compared to sham group ( sham group: 1.000 ± 0.076; ischemia group: 2.203 ±0.283; NS group: 1.616 ±0.185; P <0.01 ); however, it was significantly reduced in 10% HS group compared to ischemia group and NS group ( ischemia group:2.203 ±0.283; NS group: 1.616 ±0.185; 10%HS group: 1.202 ±0.177; P <0.05 ) .Western blot showed that the protein expression of Notch1 was significantly increased in ischemia group and NS group compared to sham group ( sham group: 0.290 ±0.079; ischemia group: 0.750 ±0.029; NS group:0.765 ±0.182;P<0.01);but was significantly reduced in 10%HS group compared to ischemia group and NS group ( ischemia group:0.750 ±0.029; NS group:0.765 ±0.182;10%HS group:0.390 ±0.195;P<0.05 ) .The protein expression of NICD was significantly increased in ischemia group and NS group compared to sham group ( sham group: 0.401 ±0.196; ischemia group: 0.906 ±0.359; NS group:0.847 ±0.153;P<0.01);but was significantly reduced in 10%HS group compared to ischemia group and NS group ( ischemia group:0.906 ±0.359; NS group:0.847 ±0.153;10%HS group:0.561 ±0.165;P<0.05 ) .Conclusion Our results suggest that HS markedly suppresses Notch signaling in microglia around the ischemia tissue area in experimental induced cerebral ischemic rats.
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Objective To evaluate (1,3)-β-D-glucan (BG) assay as an aid for invasive fungal infection (IFI) diagnosis in severe pneumonia patients (diagnosis followed 2007 American Thoracic Society (ATS) and Infectious Disease Society of America (IDSA) severe pneumonia standard).Methods BG antigenemia was measured by BG Assay Box.IFIs was classified according to the blood fungal laboratory reports.Results 558 patients (185 females,373 males,mean age 64.7) were included.41 patients were proven to be fungal infected to be classified in exposure group.BG assay mean value in exposure group and unexposure group were (568.53 ±796.57) pg/mL,(51.4 ±63.27) pg/mL,respectively.Patients in the exposure group had significantly higher BG assay value than patients in the unexposure group (P ＜0.05).For the cutoff 100 pg/mL recommended by manufacturer,the sensitivity,specificity,positive predict value and negative predict value of the BG assay were 92.7％,92.5％,49.4％ and 0.6％,respectively.Conclusion BG assay has positive clinical value in invasive fungal infection diagnosis in severe pneumonia patients.