BACKGROUND AND OBJECTIVES:Asthma in children is a global epidemic that causes various medical conditions associated with an increased incidence of premature death. This study aims to examine the trends in asthma incidence, prevalence, disability-adjusted life-years (DALYs), and mortality among children, alongside identifying risk factors associated with asthma-related deaths and DALYs, over the period from 1990 to 2021. METHODS:A cross-sectional study was conducted utilizing data from the Global Burden of Diseases (GBD) 2021, encompassing 204 countries and territories. The analysis included children aged 0-14 years diagnosed with asthma. Data analysis was conducted from October 1, 2024, to December 30, 2024. The primary outcomes included incidence, prevalence, all-cause and cause-specific mortality, DALYs, and the corresponding estimated annual percentage changes (EAPCs). These trends were further stratified by region, country, age, sex, and sociodemographic index (SDI). RESULTS:Between 1990 and 2005, there was an overall decline in the global incidence, prevalence, and DALY rates of childhood asthma. However, from 2005 to 2010, these rates experienced an upward trend. Following 2010, the incidence, prevalence, and disability-adjusted life expectancy of childhood asthma resumed a downward trajectory. Throughout the period from 1990 to 2021, both the number of deaths and the mortality rate associated with childhood asthma consistently decreased. Over the past two decades, among the five SDI regions, the high SDI region has generally shown a more pronounced increase in incidence, prevalence, and DALY rates, while concurrently experiencing a greater reduction in mortality rates. Conversely, the low SDI region has demonstrated a more significant decrease in incidence, despite a substantial increase in the number of incident cases. Nonetheless, the current burden remains considerable. Notably, there has been a rapid escalation in the disease burden in certain areas of Central Europe and High-income North America. Central Europe and high-income regions of North America exhibited the most substantial increases in incidence, with EAPC of 1.64 (95% confidence interval [CI], 1.40-1.88) and 0.61 (95% CI, 0.27-0.94), respectively. Among 204 countries, Haiti reported the highest national incidence of childhood asthma in 2021, with a rate of 4422 per 100,000 population (95% uncertainty interval [UI], 3544-5482). Furthermore, Haiti demonstrated the highest asthma-related mortality rate, recorded at 5.33 per 100,000 population (95% UI, 1.48-9.25), and the highest rate of DALYs at 1383.24 per 100,000 population (95% UI, 920.79-1923.12). An analysis of health disparities indicated that the burden of asthma is increasingly concentrated in countries with a low SDI. On a global scale, elevated body mass index and air pollution emerged as significant risk factors influencing the rate of DALYs associated with childhood asthma in 2021. CONCLUSIONS:The burden of childhood asthma continues to be significant. The results of this cross-sectional study suggest that, although there has been a global decrease in incidence, prevalence, mortality rates, and DALYs, the absolute numbers for incidence, prevalence, and DALYs remain high among children with asthma, especially in areas with a low SDI. A more thorough understanding of the epidemiology of childhood asthma could improve strategies for its prevention and management.

This study aimed to investigate the beneficial effects of iron isomaltoside (IIM) on myocardial function and the associated mechanisms in rats with myocardial ischemia/reperfusion (I/R)-induced damage and hypoxia/reoxygenation (H/R)-induced H9C2 cells. Changes in cardiac pathology after myocardial infarction (MI) were analyzed with hematoxylin-eosin staining. Myocardial cell apoptosis in the heart tissues of rats with MI was assessed using TUNEL staining. In H/R-induced H9C2 cells, cell viability and lactate dehydrogenase (LDH) and adenosine 5'-triphosphate levels were detected. Apoptosis and MMP in H9C2 cells were detected with flow cytometry. Our results demonstrated that IIM treatment reduced myocardial injury induced by ischemia-reperfusion (I/R) and suppressed cardiomyocyte apoptosis, inflammation, and autophagy induced by I/R in rats. Moreover, we confirmed that IIM repressed apoptosis and regulated MMP in H9C2 cells exposed to H/R. IIM relieved the inflammatory response and autophagy in H/R-treated H9C2 cells. In addition, IIM inhibited the Krüpple-like factor 4 (KLF4)/NF-κB pathway in H/R-induced H9C2 cells. Interestingly, the function of IIM on apoptosis, MMP, inflammation and autophagy were abolished by KLF4 overexpression in H/R-induced H9C2 cells. In conclusion, IIM could repress cardiomyocyte apoptosis, inflammation and autophagy through the inhibition of the KLF4/NF-κB pathway and thus reduced myocardial injury in vivo and in vitro.

Hypertension is a multifactorial condition influenced by both genetic and environmental factors. Protein disulfide isomerase family A member 3 (PDIA3) is a key endoplasmic reticulum protein which may contribute to increased blood pressure. However, the relationship between PDIA3 polymorphisms and hypertension remain unclear. This study aims to explore the relationship between PDIA3 polymorphisms and hypertension. First, Mendelian randomization (MR) analyses were performed to assess the causal link between PDIA3 and hypertension. Second, key gene polymorphism on PDIA3 was identified using online databases and analyzed with Haploview software. Third, multivariate-adjusted logistic regression analyses were employed to evaluate the associations between PDIA3 rs2788 and hypertension. Finally, stratified analyses were conducted to further assess interactions between PDIA3 rs2788 and antihypertensive medications. MR analyses indicated a causal relationship between PDIA3 and hypertension. The rs2788 gene polymorphism locus on PDIA3 was identified using online databases and Haploview software. Multivariable-adjusted logistic regression analyses revealed that PDIA3 rs2788 was an independent risk for hypertension (OR: 4.603, 95% CI: 2.946-7.194; p < 0.001). Significant interactions were identified between PDIA3 and antihypertensive medications, particularly ACEI/ARB treatments (p = 0.013 for interaction). Similar findings were observed regarding the causal relationship between antihypertensive treatments and hypertension. PDIA3, particularly its rs2788 polymorphisms, may represent a novel biomarker for hypertension. These findings may contribute to the development of targeted screening strategies and personalized treatment approaches for hypertension management.

Background: Postresuscitation cardiac dysfunction is a significant contributor to early death following cardiopulmonary resuscitation (CPR). Therapeutic hypothermia (TH) mitigates myocardial dysfunction due to cardiac arrest (CA); however, the underlying mechanism remains unclear. Sirtuin 3 (Sirt3) was found to affect autophagic activity in recent research, motivating us to investigate its role in the cardioprotective effects of TH in the treatment of CA. Methods: Sprague-Dawley rats were used to establish an in vivo CA/CPR model and treated with a selective Sirt3 inhibitor or vehicle. Survival rate, myocardial function, autophagic flux, and Sirt3 expression and activity were evaluated. H9C2 cells were subjected to oxygen-glucose deprivation/reoxygenation (OGD/R) injury in vitro. The cells were transfected with Sirt3-siRNA and treated with the autophagy inhibitor chloroquine or the PI3K inhibitor LY294002, and cell viability and autophagic flux were assessed. Results: Rats exhibited decreased survival and impaired cardiac function after CA/CPR, which were alleviated by TH. Mechanistically, TH restored Sirt3 expression and autophagic flux, which were impaired by CA/CPR. Sirt3 inactivation diminished the capacity of TH to restore autophagic flux and partially abolished the improvements in myocardial function and survival. An in vitro study further showed that TH-induced restoration of disrupted autophagic flux by OGD/R was attenuated by pretreatment with Sirt3-siRNA, and this attenuation was partially rescued by the inhibition of PI3K/Akt/mTOR signaling cascades. Conclusions: Sirt3 mediates the cardioprotective effect of TH by restoring autophagic flux via the PI3K/Akt/mTOR pathway. These findings suggest the potential of Sirt3 as a therapeutic target for CA.

Brain edema could be secondary to cerebral lesion caused by a variety of reasons, severe cases may result in brain herniation or even death. Accurate real-time monitoring of cerebral edema, rational application of dehydrating drugs, and timely treatment of cerebral edema were very important for patients. However, there were defects in the monitoring methods commonly used in clinical practice. Noninvasive brain-edema monitoring was a new method, which can quantify the degree of brain edema by electromagnetic disturbance and directly reflect the state of brain edema. This article reviews the application of noninvasive brain-edema monitoring in the treatment of in critically ill patients with traumatic brain injury.

Background This study aimed to explore the relationship between the Sirtuin 3 (SIRT3) gene and endothelial cell dysfunction, contributing to the progression of coronary atherosclerosis driven by hyperglycemia. Methods We measured serum SIRT3 levels using enzyme-linked immunosorbent assay in 95 patients with type 2 diabetes mellitus (T2DM) who underwent diagnostic coronary angiography. The patients were divided into two groups according to the presence (n = 45) or absence (n = 50) of coronary artery disease (CAD). Human aortic endothelial cells (HAECs) grown in vitro in a medium with various concentrations of glucose (5.5, 11, 16.5, 22, 27.5, 33, and 38.5 mM) for 24 h were assessed for protein expression of SIRT3, peroxisome proliferator-activated receptor alpha (PPAR-alpha), endothelial nitric oxide (NO) synthase (eNOS), and inducible NO synthase (iNOS) using Western blot analysis. HAECs were subjected to SIRT3 overexpression or inhibition through SIRT3 adenovirus and siRNA transfection. Results Serum SIRT3 levels were significantly lower in T2DM patients with CAD than in those without CAD (p = 0.048). The in vitro results showed that HG significantly increased SIRT3, PPAR-alpha, and eNOS protein expression in a concentration-dependent manner. Moreover, iNOS expression was decreased in HAECs in response to HG. Reduced PPAR-alpha and eNOS levels and increased iNOS levels were observed in SIRT3 silenced HAECs cells. In contrast, SIRT3 overexpression significantly improved PPAR-alpha and eNOS expression and suppressed iNOS expression. Conclusion SIRT3 was associated with the progression of atherosclerosis in T2DM patients through upregulation of PPAR-alpha and eNOS and downregulation of iNOS, which are involved in endothelial dysfunction under hyperglycemic conditions.

为了解医学生对慕课的认识、接受程度及存在问题,采用问卷调查法对在山东大学第二医院进行临床学习的山东大学医学院大四和大五学生进行问卷调查.结果显示:学生对慕课的总体学习体验感到满意,学生的慕课学习完成率高;但对慕课的学习兴趣在男女生之间存在差异;学生之间和师生之间互动以及临床技能等方面尚存在不足.慕课作为一种新的教学方式,在医学教育基础课程的教学改革中发挥了重要作用.

Human cartilage glycoprotein 39 (YKL-40) is related with presence and extent of atherosclerosis, which can be a new biomarker of inflammation and endothelial dysfunction. The relationship between YKL-40 and endothelial dysfunction in patients with essential hypertension (EH) has not been intensively investigated. The relationship between serum level of YKL-40 and endothelial dysfunction was evaluated in 60 EH subjects and 50 normal control (NEH) subjects. Enzyme-linked immunosorbent assay (ELISA) was used to measure serum levels of YKL-40. Brachial artery flow-mediated vasodilation (FMD) was used to measure endothelial-dependent nitric oxide-mediated vasodilatory capacity as the function of endothelial index. This study demonstrated that YKL-40 expression was significantly increased ( p < 0.05) in EH subjects compared with NEH subjects. The FMD was significantly impaired in EH subjects compared with NEH subjects. YKL-40 was not only negatively correlated with FMD, but also with carotid artery intima-media thickness (IMT). Multiple liner regression analysis identified that YKL-40 was independent of FMD development. The level of YKL-40 was elevated in EH patients and inversely related with FMD and may be independent of endothelial dysfunction in EH.

The fatality rate of traumatic cardiac arrest (TCA) is extremely high, and it is very different from that of non-traumatic cardiac arrest (NTCA) in resuscitation strategy. Only when the standard resuscitation process is combined with rapid treatment of various reversible causes can the mortality rate of patients be decreased. In this paper, the key factors leading to TCA are reviewed, such as hypovolemic shock, asphyxia, tension pneumothorax, pericardial tamponade, crush syndrome, craniocerebral injury, cerebral hernia, and the control measures are elaborated respectively, so as to provide references for clinical treatment of patients with severe trauma, and reduce TCA incidence and mortality.

Fetal dermal mesenchymal stem cells (FDMSCs), isolated from fetal skin, are serving as a novel MSC candidate with great potential in regenerative medicine. More recently, the paracrine actions, especially MSC-derived exosomes, are being focused on the vital role in MSC-based cellular therapy. This study was to evaluate the therapeutic potential of exosomes secreted by FDMSCs in normal wound healing. First, the in vivo study indicated that FDMSC exosomes could accelerate wound closure in a mouse full-thickness skin wound model. Then, we investigated the role of FDMSC-derived exosomes on adult dermal fibroblast (ADFs). The results demonstrated that FDMSC exosomes could induce the proliferation, migration, and secretion of ADFs. We discovered that after treatment of exosomes, the Notch signaling pathway was activated. Then, we found that in FDMSC exosomes, the ligands of the Notch pathway were undetectable expect for Jagged 1, and the results of Jagged 1 mimic by peptide and knockdown by siRNA suggested that Jagged 1 may lead the activation of the Notch signal in ADFs. Collectively, our findings indicated that the FDMSC exosomes may promote wound healing by activating the ADF cell motility and secretion ability via the Notch signaling pathway, providing new aspects for the therapeutic strategy of FDMSC-derived exosomes for the treatment of skin wounds.

Myocardial infarction (MI) is the leading cause of morbidity and mortality worldwide. Nanoparticle systems carrying drugs have already been developed to treat MI. To improve the efficiency of tanshinone (TAN), and to achieve the synergistic effect of TAN and puerarin (PUE), PUE-prodrug and TAN co-loaded solid lipid nanoparticles (SLN) was structured and utilized for MI treatment in the present research. PUE-prodrug was synthesized by an esterification reaction. PUE-prodrug and TAN co-loaded SLN (PUEp/TAN-SLN) were prepared by a single emulsification followed by a solvent evaporation method. The physicochemical properties of SLN were characterized and the in vivo infarct therapy effects were evaluated in MI rats. PUE-prodrug and TAN contained SLN showed a size of 112.6 ± 3.1 nm. The SLN encapsulation reduced the cytotoxicity of drugs and was a safer system. PUEp-SLN exhibited a 1.7-fold increase in comparison to PUE-SLN (21.2 ± 2.1 versus 12.5 ± 1.5 mg/L), in the mean time a 3.4-fold increase compared with free PUE in heart drug concentration (21.2 ± 2.1 versus 6.3 ± 0.9 mg/L). In vivo infarct therapy efficiency of double drugs loaded PUEp/TAN-SLN (17 ± 1.9%) was significantly better than the single drug loaded PUEp-SLN (31 ± 1.6%) and TAN-SLN (40 ± 2.2%). PUE-prodrug contained, double drugs co-loaded SLN can be utilized as promising candidate delivery system for cardioprotective drugs in treatment of myocardial infarction.

目的 探讨高敏C反应蛋白(hs-CRP)与急性ST段抬高型心肌梗死(STEMI)患者经皮冠状动脉介入(PCI)术后非靶病变进展之间的关系.方法 行初始PCI的STEMI患者286例,采集入院初始、PCI术后24、48 h、随访期血样标本,测定hs-CRP及血清生化指标,并收集入院初始和随访期冠状动脉造影和PCI临床资料.比较介入治疗前后上述指标的变化情况,并应用Pear-son相关和Logistic回归分析其与非靶病变进展的关系.结果 与非进展组相比,进展组hs-CRP水平在入院初始、PCI术后24、48 h均显著升高(P均<0.01);随访期,进展组低密度脂蛋白胆固醇(LDL-C)显著增高(P<0.01)及冠脉复杂病变发生率明显增高(P<0.05).多因素Logistic回归分析显示住院初始hs-CRP、PCI术后24、48 h hs-CRP、LDL-C均是急性心肌梗死(AMI)患者初次PCI术后非靶病变进展的预测因素.结论 CRP水平与STEMI患者PCI术后非靶病变的进展密切相关.

Objective To determine if high fasting blood glucose (FBG) level is an independent predictor of serious coronary lesions in patients with coronary artery disease (CAD). Methods We enrolled 64 patients who had symptoms of chest discomfort and who underwent coronary angiography. FBG was determined from blood samples and the extent of coronary artery lesions was analyzed according to Gensini score. We examined the relationships among diabetes, FBG, and coronary artery severity. Results Diabetes and FBG were significantly and positively related to Gensini score. Diabetes, but not FBG, was independently correlated with the occurrence of a Gensini score >41. However, FBG was significantly associated with Gensini score >41 in non-diabetic patients. Conclusion Hyperglycemia is an independent predictor of severe CAD in non-diabetic patients. Clinicians should be aware of this and should carry out appropriate early interventions.

Trastuzumab is a molecular targeted drug for Her2-positive breast cancer patients.In this paper,we reported one case of right breast cancer presenting with left ventricular dysfunction after single use of trastuzumab once every 3 weeks.After the second time of use of trastuzumab,she gradually developed breath-lessness which aggravated in a supine position,accompanied with cough,abdominal distension and bilateral lower extremity edema.During hospitalization in the Department of Cardiology,she was diagnosed with left ventricular dysfunction by echocardiography and PET/CT.Before the treatment of trastuzumab,the left ventric-ular ejection fraction (LVEF)of the patient was 0.66 which decreased to 0.29 after usage of trastuzumab.She reported no medical history of hypertension,diabetes mellitus and coronary heart disease.Hence,the inci-dence of left ventricular dysfunction was probably correlated with the use of trastuzumab.Left ventricular dys-function was recovered after trastuzumab withdrawal and 40-day symptomatic treatment.The diagnosis and treatment of this case hinted that standard use of medication should be implemented.Adverse events should be intimately monitored according to the manufacturers'instructions to avert the incidence of severe consequences.

Objective To explore the effect of empty-nest on prevalence and treatment status of hypertension in the elderly and pro-vide scientific evidences for improving the level of hypertension management in community empty-mest elderly. Methods 2057 community elderly were enrolled by cluster sampling from 8 communities in Hekou district, Dongying city. Prevalence, awareness, treatment and control of hypertension and related factors were investigated in all elderly. Loneliness and depression symptom were assessed by using University of California at Los Angels ( UCLA) loneliness scale and Geriatric Depression Scale ( GDS) , respectively. Results Among 2057 community elderly, 653 (31. 75%) were empty-nest elderly. The prevalence, awareness, treatment and control of hypertension were 56. 0%, 88. 8%, 81. 1%, and 6. 0%, respectively. The prevalence of hypertension in empty-nest elderly was significantly higher, and awareness, treatment and control hypertension were markedly lower than those in non-empty-nest elderly (P<0. 001). Multinomial Logistic regression analysis showed that empty-nest was an important factor for prevalence, awareness, treatment, and control of hypertension in the elderly. UCLA was a crucial factor for prevalence, awareness, and control of hypertension in the elderly. GDS was an important factor for prevalence and treat-ment of hypertension in the elderly. The prevalence of hypertension in empty-nest elderly was 2. 630 folds higher respect to non-empty-nest elderly. The awareness, treatment, and control of hypertension in empty-nest elderly were 2. 036, 1. 680, and 1. 958 folds lower respect to non-empty-nest elderly. Conclusions There are significant impact of empty-nest on the prevalence, awareness, treatment, and control of hypertension in the elderly. Psychological counseling and spiritual care may be one of the important means for hypertension management in empty elderly.

Objective To investigate obesity type and the association of obesity with arterial stiffness in community populations aged 35-70 years in Ji'nan area,Shandong province.Methods From June 2011 to July 2013,10 079 permanent residents aged 35-70 years were recruited from 24 communities in Ji'nan area of Shandong province using random cluster sampling.Waist circumference (WC),height,weight,carotid-femoral pulse wave velocity (cfPWV),and fasting blood lipids were measured in all the participants and body mass index (BMI) and plasma induced arterial stiffness index (PAI) were calculated.Results The values of cfPWV and PAl were 9.15 ± 1.62 m/s and 2.27 ± 0.96 for the participants with BMI ＜ 28 kg/m2 and non-abdominal obesity (AO),9.82 ± 1.78 rm/s and 2.56 ± 1.18 for those with BMI ＜28 kg/m2 and AO,9.45 ± 1.82 m/s and 2.44 ± 1.19 for BMI≥28 kg/m2 and non-AO,and 10.99 ± 1.91 m/s and 3.21 ± 1.71 for BMI≥28 kg/m2 and AO,respectively.Compared to those with BMI ＜28 kg/m2 and non-AO,the cfPWV and PAl were significantly increased in the participants with BMI ＜ 28 kg/m2 and AO,BMI≥28 kg/m2 and non-AO,and BMI≥28 kg/m2 and AO (P ＜0.05 for all).Compared to those with BMI ＜28 kg/m2 and AO,the cfPWV was significantly increased in the participants with BMI ≥ 28 kg/m2 and non-AO (P ＜ 0.05).Compared to those with BMI≥28 kg/m2 and non-AO,the cfPWV and PAI were significantly increased in the participants with BMI≥28 kg/m2 and AO (both P ＜ 0.05).Significant joint effect of WC and BMI on cfPWV and PAl were observed (F =61.366 and 42.682,both P ＜ 0.001).Compared to those with BMI ＜ 28 kg/m2 and non-AO,the participants with BMI ≥ 28 kg/m2 and non-AO presented significantly increased risks of PAl ＞4 (odd ratios[OR] =1.649,95％ confidence interval[95％ CI]:1.154-2.144) and cfPWV ＞ 10m/s (OR =1.551,95％ CI:1.117-1.985) (both P ＜ 0.001);the participants with BMI ＜ 28 kg/m2 and AO had significantly increased risks of PAl ＞ 4 (OR =1.764,95 ％ CI:1.370-2.158) and cfPWV ＞ 10m/s (OR =1.577,95％ CI:1.264-1.890) (both P ＜ 0.001);and the participants with BMI ≥ 28 kg/m2 and AO had significantly increased risks of PAI ＞4 (OR =5.666,95％ CI:3.726-7.606) and cfPWV ＞ 10rn/s (OR =4.631,95％ CI:2.615-6.647) (both P ＜0.001),after adjusting for age,gender,systolic blood pressure,diastolic blood pressure,and fasting plasma glucose.Conclusion Both simple obesity and abdominal obesity are independent risk fac-tors for arterial stiffness and there is a synergistic effect of WC and BMI on arterial stiffness in populations aged 35-70 years in Ji'nan area of Shandong province.

[Summary] SIRT3 is a member of the silent information regulator 2 ( Sir2) family, located in the inner mitochondrial membrane, with a strong effect of deacetylation. SIRT3 not only modulates energy metabolism, cell apoptosis, tumor growth, anti-aging etc. , but also plays an important role in the field of cardiovascular diseases. In this review, we summarize recent findings related to SIRT3 with metabolic syndrome and cardiac hypertrophy, to provide a theoretical basis for the further study on the potential role of SIRT3 in cardiovascular diseases.

Ulinastatin exhibits anti-inflammatory activity and protects the heart from ischemia/reperfusion injury. However, whether ulinastatin has a protective effect in diabetic cardiomyopathy is yet to be elucidated. The aim of the present study was to investigate the protective effects of ulinastatin against diabetic cardiomyopathy and its underlying mechanisms. A C57/BL6J mice model of diabetic cardiomyopathy was used and mice were randomly assigned to three groups: Control group, diabetes mellitus (DM) group and DM + ulinastatin treatment group. Cardiac function was assessed using echocardiography and the level of inflammatory cytokine high mobility group box 1 (HMGB1) expression was measured using histopathological examination and reverse transcription-quantitative polymerase chain reaction. The levels of tumor necrosis factor (TNF)-α and interleukin (IL)-6 were measured using western blotting and ELISA. The apoptosis rate in the myocardium was assessed by TUNEL assay. Caspase-3 activation, expression of B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated × (Bax) were measured using western blotting, as was the activity of the mitogen activated protein kinase (MAPK) signaling pathway. The results indicated that ulinastatin significantly improved cardiac function in mice with DM. Ulinastatin treatment significantly downregulated HMGB1, TNF-α and IL-6 expression (P<0.05) and significantly reduced the percentage of apoptotic cardiomyocytes (P<0.05) via reduction of caspase-3 activation and the ratio of Bax/Bcl-2 in diabetic hearts (P<0.05). In addition, ulinastatin attenuated the activation of the MAPK signaling pathway. In conclusion, ulinastatin had a protective effect against DM-induced cardiac dysfunction in a mouse model. This protective effect may be associated with the anti-inflammatory and anti-apoptotic abilities of ulinastatin via the MAPK signaling pathway.

Sirt3 is a kind of nicotinamide adenine dinucleotide (NAD+)-dependent deacetylases.Sirt3 is localized in mitochondria and has been involved in a wide range of mitochondrial biological functions, such as nutrient oxidation、ATP generation, reactive oxygen species (ROS) detoxification and mitochondrial homeostasis.Sirt3 plays an important role in the occurrence and development of cardiovascular diseases.Increased expression of Sirt3 gene has been associated with extended lifespan of humans.

A number of studies have suggested that interleukin 6 (IL-6) and interferon-gamma (IFN-gamma) have pathophysiologic roles in cardiovascular diseases. In view of recent evidence that serum IL-6 and IFN-gamma may serve as inflammatory mediators in patients with enhanced inflammation, we hypothesize both IL-6 and IFN-gamma have diagnostic and prognostic value in patients with acute coronary syndrome (ACS) and type 2 diabetes (T2D). Patients with ACS and T2D (n=29), patients with ACS but without T2D (n=33), and patients with T2D but without ACS (n=42) were selected for the study. Thirty volunteers without ACS or T2D served as controls. Serum IL-6 and IFN-gamma were measured, coronary angiography and echocardiography were performed, and Gensini scores were calculated. Higher serum IL-6 and IFN-gamma levels existed in patients with ACS and T2D than patients with ACS or T2D alone (P<0.05); however, no significant differences existed between the T2D and control groups (P>0.05). Of the 29 ACS patients with T2D, the serum levels of IL-6 and IFN-gamma in single-, double-, and triple-vessel lesion groups were higher than the control group (P<0.05), whereas the differences among the triple-vessel lesion groups were not significant. Gensini scores were positively correlated with serum IL-6 and IFN-gamma in ACS patients. Based on stepwise regression analysis, increased serum IL-6 and IFN-gamma were strong independent predictors of the Gensini score. These results indicate that elevated values of IL-6 and IFN-gamma are associated with more intense inflammatory activity in patients with coronary instability. The inflammatory activity is even more intense in patients with T2D.