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Type 1 diabetes mellitus (T1DM) is an organ-specific autoimmune disease mediated by T cells. Untreated T1DM deteriorate rapidly. Early prediction and diagnosis lead to early treatment and prognosis of patients. Immune system plays an important role in the destruction of β cells in T1DM patients, and the emergence of immunological markers has facilitated the diagnosis and prediction of T1DM. Based on the results of various cohort studies and clinical studies in recent years, this review comprehensively discusses the application of immunological markers in the prediction and diagnosis of T1DM from two aspects: humoral immune markers and cellular immune markers.
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Objective To evaluate the effect of dexmedetomidine on pyroptosis during lung ischemia-reperfusion (I/R) in rats.Methods Adult male Sprague-Dawley rats,weighing 250-320 g,were used in this study.The model of isolated lung perfusion was established using an IL-2 Isolated Perfused Rat or Guinea Pig Lung System after the rats were anesthetized.Thirty lungs in which an ex vivo lung perfusion model was successfully established were divided into 3 groups (n=10 each) by a random number table method:control group (C group),I/R group and dexmedetomidine group (DEX group).The lungs were continuously perfused with K-H solution for 150 min in C group.After 15 min of perfusion,lungs were subjected to 60-min suspension of ventilation and perfusion,followed by 75 min of reperfusion and ventilation to establish the model of lung I/R injury in I/R and DEX groups.In DEX group,dexmedetomidine 10 nmol/L was added to K-H solution at the beginning of reperfusion.Lung tissues were obtained for determina-tion of wet/dry weight ratio (W/D ratio) and for examination of pathological changes (with a light microscope) and ultrastructure (using an electron microscope),and the alveolar damage rate (IAR) was calculated.The expression of pyroptosis-related factors including NOD-like receptor family protein 3 (NLRP3),caspase-1,interleukin-1β (IL-1β),IL-18 and gasdermin D (GSDMD) protein and mRNA was detected by Western blot or by real-time polymerase chain reaction.Results Compared with C group,the W/D ratio and IAR in lung tissues were significantly increased,and the expression of NLRP3,caspase-1,IL-1β,IL-18 and GSDMD protein and mRNA was up-regulated in I/R and DEX groups (P＜0.05).Compared with I/R group,the W/D ratio and IAR in lung tissues were significantly decreased,the expression of NLRP3,caspase-1,IL-1β,IL-18 and GSDMD protein and mRNA was down-regulated (P＜0.05),and the pathological changes were significantly attenuated in DEX group.Conclusion The mechanism by which dexmedetomidine reduces isolated rat lung I/R injury may be related to inhibiting pyroptosis.
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Objective@#To evaluate the effect of dexmedetomidine on pyroptosis during lung ischemia-reperfusion (I/R) in rats.@*Methods@#Adult male Sprague-Dawley rats, weighing 250-320 g, were used in this study.The model of isolated lung perfusion was established using an IL-2 Isolated Perfused Rat or Guinea Pig Lung System after the rats were anesthetized.Thirty lungs in which an ex vivo lung perfusion model was successfully established were divided into 3 groups (n=10 each) by a random number table method: control group (C group), I/R group and dexmedetomidine group (DEX group). The lungs were continuously perfused with K-H solution for 150 min in C group.After 15 min of perfusion, lungs were subjected to 60-min suspension of ventilation and perfusion, followed by 75 min of reperfusion and ventilation to establish the model of lung I/R injury in I/R and DEX groups.In DEX group, dexmedetomidine 10 nmol/L was added to K-H solution at the beginning of reperfusion.Lung tissues were obtained for determination of wet/dry weight ratio (W/D ratio) and for examination of pathological changes (with a light microscope) and ultrastructure (using an electron microscope), and the alveolar damage rate (IAR) was calculated.The expression of pyroptosis-related factors including NOD-like receptor family protein 3 (NLRP3), caspase-1, interleukin-1β (IL-1β), IL-18 and gasdermin D (GSDMD) protein and mRNA was detected by Western blot or by real-time polymerase chain reaction.@*Results@#Compared with C group, the W/D ratio and IAR in lung tissues were significantly increased, and the expression of NLRP3, caspase-1, IL-1β, IL-18 and GSDMD protein and mRNA was up-regulated in I/R and DEX groups (P<0.05). Compared with I/R group, the W/D ratio and IAR in lung tissues were significantly decreased, the expression of NLRP3, caspase-1, IL-1β, IL-18 and GSDMD protein and mRNA was down-regulated (P<0.05), and the pathological changes were significantly attenuated in DEX group.@*Conclusion@#The mechanism by which dexmedetomidine reduces isolated rat lung I/R injury may be related to inhibiting pyroptosis.
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Objective To evaluate the effect of sevoflurane on unfolded protein response-related cell apoptosis during acute lung injury in rats undergoing cardiopulmonary bypass ( CPB) . Methods For-ty-eight clean-grade healthy adult male Sprague-Dawley rats, aged 6-8 weeks, weighing 250-300 g, were allocated into 3 groups ( n=16 each) using a random number table method: sham operation group ( Sham group) , CPB group and sevoflurane group ( Sev group) . Left common carotid artery and right internal jugu-lar vein were only cannulated in group Sham. After establishing CPB, the flow rate was gradually adjusted to the maximum (100 ml·kg-1·min-1) and maintained for 60 min in group CPB. Two percent sevoflurane was inhaled for 30 min, and 15 min later the model of CPB was established in Sev group. Rats were sacri-ficed at 1 h after the end of CPB, lungs were removed and lung tissues were obtained. The pathological changes and ultrastructure of lung tissues were examined with a light microscope and with an electron micro-scope, respectively. The wet to dry weight ratio ( W∕D ratio) , apoptosis in lung cells ( by TUNEL assay) , expression of glucose-regulated protein 78 ( GRP78) , CCAAT∕enhancer-binding protein homologous protein (CHOP), c-Jun N-terminal kinase (JNK) and caspase-12 mRNA was determined by real-time polymerase chain reaction. The expression of GRP78, CHOP, phosphorylated JNK (p-JNK) and caspase-12 was de-tected by Western blot. The index of quantitative assessment of histologic lung injury ( IQA) was measured, and apoptotic index ( AI) was calculated. Results Compared with Sham group, the W∕D ratio, IQA and AI were significantly increased, the expression of GRP78, CHOP, JNK and caspase-12 was up-regulated ( P<0. 05) , and the pathological changes of lung tissues were accentuated in CPB group. Compared with CPB group, the W∕D ratio, IQA and AI were significantly decreased, the expression of GRP78, CHOP, JNK and caspase-12 was down-regulated ( P<0. 05) , and the pathological changes of lung tissues were sig-nificantly attenuated in Sev group. Conclusion The mechanism by which sevoflurane mitigates acute lung injury induced by CPB is related to inhibiting unfolded protein response related cell apoptosis in lung tissues of rats.
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Objective To observe the clinical effects of phosphocreatine treatment on left ventricular function and on amino-terminal pro-brain natriuretic peptide (NT-proBNP) level in elderly patients with chronic heart failure. Methods In our department, the 172 elderly patients with chronic heart failure were randomly divided into treatment group and control group (n= 86, each).The control group received routine anti-heart failure treatment. The treatment group received conventional therapy plus creatine phosphate sodium for 4 weeks. The cardiac function was evaluated and the NT-proBNP level was measured in all subjects. Results Four weeks after treatment, the improvements of left ventricular ejection fraction (LVEF), left ventricular end-systolic diameter (LVESD) and left ventricular end-diastolic dimension (LVEDD) were better in treatment group than in control group (all P＜0.05). The plasma NT-proBNP level decreased significantly in treatment group as compared with control group [before treatment: (956.4 ± 644.2) pmol/L and (973.6 ±639.8) pmol/L; after treatment: (414. 5 ± 163.8 ) pmol/L and ( 719.3 ± 477. 5 ) pmol/L, all P＜0. 05]. Conclusions Phosphocreatine could improve left ventricular function and decrease plasma NT-proBNP level in elderly patients with chronic heart failure.