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BACKGROUND: Anatomic variations of the patent foramen ovale (PFO) are commonly observed, yet limited research has investigated their impact on clinical outcomes following transcatheter closure. We aimed to explore the association between PFO morphology and clinical outcomes. METHODS: Consecutive patients with cryptogenic stroke who underwent PFO closure were prospectively enrolled at a single center from September 2019 to April 2023. Patients were categorized into simple and complex groups based on PFO morphology. Composite events were compared between the two groups during a median follow-up of 24 months, including all-cause mortality, recurrent stroke, residual moderate or severe shunt, and symptomatic atrial fibrillation. RESULTS: A total of 247 patients were enrolled, with a mean age of 41.9 ± 13.0 years and 45.3% males. Ninety-one (36.8%) patients had complex PFO. These individuals were older (45.4 ± 12.5 years vs. 39.9 ± 12.9 years; P = 0.001), more males (56.0% vs. 39.1%; P = 0.010), had longer procedure times (54 ± 32 min vs 46 ± 29 min; P = 0.044), and had a higher rate of using delivery sheath-assisted crossing of the PFO (22.0% vs 12.8%; P = 0.040) than those with simple PFO. The estimated event rates were 27.9% and 11.3% (P = 0.006) in the complex and simple PFO groups, respectively (12.9 events and 5.2 events per 100 person-years; P = 0.001). After adjusting for age, sex, hypertension, diabetes, smoking, device type, and left atrial diameters, complex PFO remained independently associated with composite events (HR 2.10, 95%CI 1.06-4.17, P = 0.034). CONCLUSIONS: Patients with complex PFO may suffer from a higher risk of adverse events following transcatheter PFO closure.

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Objective: To investigate the impact of CYP2C19 gene polymorphism on clopidogrel reactivity and its association with long-term clinical outcome in patients with coronary heart disease (CHD) undergoing percutaneous coronary intervention (PCI). Methods: In total, 675 patients were enrolled. Based on the platelet inhibition rate, patients were categorized into two groups: clopidogrel low responsiveness (CLR) and normal clopidogrel responsiveness (NCR). The CLR group was divided into ticagrelor and clopidogrel group based on the antiplatelet drugs used in the follow-up treatment. Patients were classified into three groups (normal metabolizer, intermediate metabolizer, and poor metabolizer) based on the CYP2C19 genotype. We aimed to evaluate the impact of CYP2C19 gene polymorphism on clopidogrel reactivity. The cumulative rates of 12-month all-cause deaths, major adverse cardiovascular events (MACCEs), and bleeding events were calculated. Results: CLR was observed in 44.4% of the overall population. Significant differences were observed in the platelet inhibition rate of clopidogrel among the three metabolic genotypes (P < 0.05). At the 12-month follow-up, 13 patients (1.9%) died and 96 patients (14.2%) experienced MACCEs. Patients with CLR (9.6% vs. 11.7% vs. 22.1%, P < 0.05) or poor metabolizer (10.7% vs. 16.4% vs. 22.6%, P = 0.026) experienced a higher rate of MACCEs. A MACCEs risk score between zero and two was calculated. The highest incidence of MACCEs significantly increased with the 2-positive results, and the area under the curve (AUC) was 0.712 (95% CI: 0.650-0.774, P < 0.05). There was no significant difference between the group with a score of one and the occurrence of MACCEs (P > 0.05). Conclusions: Low response to clopidogrel in CHD patients is correlated with CYP2C19 gene polymorphism. CYP2C19 genotyping combined with platelet reactivity is an independent predictor of 12-months MACCEs in patients with clopidogrel treatment after PCI, which is better than either test alone.

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Improvements are required in the quality of life (QoL) of patients with ischemia and non-obstructive coronary artery disease (INOCA). Several patients with INOCA experience vascular endothelial dysfunction. However, the relationship between endothelial function and QoL remains unelucidated. This study aimed to initially investigate the relationship between endothelial function and QoL in patients with INOCA. This prospective observational study included 121 patients with INOCA (aged 31-85 years). Vascular endothelial function was assessed by flow-mediated dilatation (FMD) of the peripheral brachial artery. QoL was evaluated using the 36-Item Short-Form Health Survey (SF-36). Patients with INOCA were divided into two groups according to the median FMD change during the 1-year follow-up (group A, ≥ median FMD change cut-off; group B, < median FMD change cut-off). The median change in FMD was 0.92%. The mean baseline SF-36 scores were comparable between the two groups (53.95 ± 6.46 vs. 53.92 ± 4.29, p = 0.98). The QoL at follow-up was better in group A than in group B (56.61 ± 5.50 vs. 53.32 ± 5.58, p = 0.002). The change in FMD (r = 0.34, p < 0.01), rather than FMD at baseline (r = - 0.01, p = 0.89) or follow-up (r = 0.13, p = 0.15), was related to the follow-up SF-36 scores. FMD improvement was an independent predictor of increased QoL (odds ratio, 3.90; 95% confidence interval: 1.59-9.53, p = 0.003). Endothelial function change is associated with QoL, and patients with improved endothelial function have a better QoL than those without.

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BACKGROUND: Although the relationship of either hemoglobin or red blood cell distribution width (RDW) with contrast-induced nephropathy (CIN) has been reported individually. To date, no studies have evaluated the predictive value of hemoglobin-to-red blood cell distribution width ratio (HRR) for CIN. METHODS: A total of 1658 elderly patients with ST-segment elevation myocardial infarction (STEMI) undergoing emergency percutaneous coronary intervention (PCI) were retrospectively screened. Preoperative complete blood count was collected and the HRR was calculated as the ratio of hemoglobin to RDW. CIN was defined as an absolute ≥0.5 mg/dL (44.2 µmol/L) or a relative ≥25% increase in creatinine level at 72 h after contrast administration. Univariate and multivariate regression analysis were conducted to determine the effective predictors for CIN. The ROC curve analysis was plotted to determine the optimal cutoff value for HRR in predicting CIN. RESULTS: The overall incidence of CIN was 8.38%. The HRR was significantly lower in the CIN group compared with the non-CIN group (0.87 ± 0.15 vs 1.24 ± 0.23, p < 0.001). After multivariate regression analysis was performed, HRR was noted to be an effective predictor for the development of CIN (OR 1.617, 95% CI 1.439-2.706, p = 0.014), along with age, creatinine, eGFR, hs-CRP and contrast volume. An optimal cutoff value of 0.94 or lower for HRR was identified with 82.4% sensitivity and 63.5% specificity to predict CIN. CONCLUSION: Lower HRR on admission was an effective predictor for CIN in elderly patients with STEMI undergoing emergency PCI. HRR may be a convenient, economical and reliable biomarker for risk stratification.

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PURPOSE: Contrast-induced nephropathy (CIN) remains a dreaded complication in the cardiac diagnostic and interventional area. We investigated the relationship between red blood cell distribution width-to-albumin ratio (RAR) and CIN in elderly patients with ST-segment elevation myocardial infarction (STEMI) undergoing emergency percutaneous coronary intervention (PCI). METHODS: A total of 1532 elderly patients were enrolled and divided into the CIN group and the non-CIN group. The risk factors of CIN were evaluated by univariate and multivariate regression analysis. Receiver-operating characteristic (ROC) curve analysis was used to identify the best predictive value. RESULTS: CIN occurred in 129 (8.42%) patients. Patients in the CIN group had significantly higher RAR than those in the non-CIN group (4.69 ± 0.73 vs. 3.18 ± 0.64, P < 0.001). In multivariate regression analysis, RAR was an independent risk factor for the development of CIN (OR: 1.506, 95% CI: 1.227-2.083, P = 0.025), along with age, creatinine, eGFR, hs-CRP and contrast agent dose. The AUC of RAR was 0.755 (95% CI 0.703-0.807), and an optimal cutoff value of 3.64 or higher predicted CIN with a sensitivity of 76.2% and specificity of 65.7%. CONCLUSION: As a combined inflammatory-related index, RAR was an independent risk factor for the development of CIN in elderly patients with STEMI undergoing emergency PCI. The RAR could be a simple but relatively reliable parameter for identifying high-risk patients.

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BACKGROUND: Early spontaneous reperfusion (ESR) is not an uncommon phenomenon in clinical settings. AIMS: The aim of this study was to detect potential mechanisms of ESR in patients with STEMI. METHODS: This prospective study enrolled a total of 241 consecutive patients with STEMI undergoing optical coherence tomography (OCT) from July 2016 to August 2019. Forty-five patients (18.7%) met angiographic ESR criteria (TIMI 3 flow on the initial angiogram). Among those without ESR (TIMI 0 flow on initial angiogram), 45 patients were assigned to the control group according to propensity score matching with the ESR group. RESULTS: Although the baseline characteristics of the groups were comparable, non-ruptured plaque (62.2% vs 35.6%) predominated and plaque rupture (37.8% vs 64.4%) was less common in the ESR group (p=0.011). Red thrombus (44.4% vs 77.8%) was also less common in the ESR group (p=0.001). Lastly, compared to the control group, the ESR group underwent fewer emergent stent placements (68.9% vs 91.1%, p=0.008). CONCLUSIONS: Relief of coronary occlusion induced by a non-ruptured plaque may contribute to ESR in patients with STEMI.

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BACKGROUND: Endothelial dysfunction may play a key role in non-obstructive coronary artery atherosclerosis. Our study aimed to evaluate the vascular endothelial function and its influencing factors in patients with non-obstructive coronary artery atherosclerosis. METHODS: A total of 131 consecutive patients with non-obstructive coronary artery atherosclerosis were enrolled. Flow-mediated dilatation (FMD) was measured at baseline and 1-year follow-up. Endothelial progenitor cells (EPCs) were counted by staining the fasting venous blood with antibodies against CD34 and vascular endothelial growth factor receptor 2. RESULTS: Systolic blood pressure, pulse pressure and the levels of HbA1c in participants with baseline FMD < 6% (n = 65) were significantly higher than those with baseline FMD ≥ 6% (n = 66). Baseline FMD was negatively associated with EPC counts (r = - 0.199, P < 0.05) and systolic blood pressure (r = - 0.315, P < 0.01). The 1-year FMD was significantly increased compared to the baseline FMD [(9.31 ± 5.62) % vs (7.31 ± 5.26) %, P < 0.001]. Independent predictors of FMD improvement included elevated EPC counts (OR = 1.104, 95% CI: 1.047-1.165, P < 0.001) and decreased levels of serum creatinine (OR = 0.915, 95% CI: 0.843-0.993, P = 0.034). CONCLUSIONS: Family history of premature cardiovascular diseases, hypertension, elevated systolic pressure, and HbA1c > 6.5% are independent risk factors for endothelial dysfunction in non-obstructive atherosclerotic patients. Elevated peripheral blood EPC counts and decreased levels of serum creatinine are independent predictors of endothelial function improvement.

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BACKGROUND: Elevated serum phosphorus levels may be associated with adverse outcomes in cardiovascular disease. This study aimed to investigate the relation between serum phosphorus levels and risk of all-cause mortality in Chinese patients with ST-segment elevation myocardial infarction (STEMI) who had preserved renal function at baseline. METHODS: We enrolled patients with STEMI who had preserved renal function at baseline in Xuanwu Hospital from January 2011 to December 2016. Those patients were divided into four groups based on serum phosphorus levels. All-cause mortality rates were compared between groups. Mean duration of follow up was 54.6 months. We used Cox proportional-hazards models to examine the relation between serum phosphorus levels and all-cause mortality after adjustment for potential confounders. RESULTS: 1989 patients were involved and 211 patients (10.6%) died during follow-up. Based on serum phosphorus levels, patients were categorized into the following groups: < 2.50 mg/dL (n = 89), 2.51-3.50 mg/dL (n = 1066), 3.51-4.50 mg/dL (n = 672) and > 4.50 mg/dL (n = 162), respectively. The lowest mortality occurred in patients with serum phosphorus levels between 2.51-3.50 mg/dL, with a multivariable-adjusted hazard ratio of 1.19 (95% CI: 0.64-1.54), 1.37 (95% CI: 1.22-1.74), and 1.46 (95% CI: 1.35-1.83) in patients with serum phosphorus levels of < 2.50 mg/dL, 3.51-4.50 mg/dL and > 4.50 mg/dL, respectively. CONCLUSIONS: Elevated serum phosphorus levels were associated with all-cause mortality in Chinese patients with STEMI who had preserved renal function at baseline.

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Exosome secretion is an important paracrine way of endothelial progenitor cells (EPCs) to modulate resident endothelial cells. The osteocalcin (OCN)-expressing EPCs have been found to be increased in cardiovascular disease patients and are considered to be involved in the process of coronary atherosclerosis. Since OCN has been proven to prevent endothelial dysfunction, this study aimed to evaluate the effect of exosomes derived from OCN-overexpressed EPCs on endothelial cells. Exosomes derived from EPCs (Exos) and OCN-overexpressed EPCs (OCN-Exos) were isolated and incubated with rat aorta endothelial cells (RAOECs) with or without the inhibition of OCN receptor G protein-coupled receptor family C group 6 member A (GPRC6A). The effects of exosomes on the proliferation activity of endothelial cells were evaluated by CCK-8 assay, and the migration of endothelial cells was detected by wound healing assay. A tube formation assay was used to test the influence of exosomes on the angiogenesis performance of endothelial cells. Here, we presented that OCN was packed into Exos and was able to be transferred to the RAOECs via exosome incorporation, which was increased in OCN-Exos groups. Compared with Exos, OCN-Exos had better efficiency in promoting RAOEC proliferation and migration and tube formation. The promoting effects were impeded after the inhibition of GPRC6A expression in RAOECs. These data suggest that exosomes from OCN-overexpressed EPCs have a beneficial regulating effect on endothelial cells, which involved enhanced OCN-GPRC6A signaling.

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OBJECTIVE: To study the effect of pre-arrest and post-arrest mild hypothermia after restoration of spontaneous circulation (ROSC) on myocardial function, ultrastructure, apoptosis of myocardial cells in rabbits with ventricular fibrillation. METHODS: Sixty-two male New Zealand rabbits were randomly allocated into five groups: namely normothermic control group (NTC group, n = 10), hypothermia control group (HTC group, n = 10), normothermic resuscitation group (NTR group, n = 14), hypothermia pre-arrest group (HPRA group, n = 14), and hypothermia post-arrest group (HPOA group, n = 14). The normal temperature was controlled at (39.0 ± 0.5) centigrade, and the hypothermia (33.5±0.5) centigrade. Ventricular fibrillation cardiac arrest (CA) was reproduced in rabbits by transcutaneous epicardium electrical stimulation. The parameters of hemodynamics were monitored dynamically for 4 hours in all the groups, including heart rate (HR), left ventricular end diastolic and systolic pressure (LVEDP/LVESP), maximal rate of increase/decrease in left ventricular pressure (±dp/dt max), and mean arterial pressure (MAP). The body temperature of rabbits in hypothermia groups was maintained by surface cooling for 4 hours followed by rewarming. The survived rabbits were sacrificed at 48 hours after resuscitation, and myocardial apical tissue was harvested for observation of ultrastructure with electronic microscope, and to observe apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. RESULTS: (1) Resuscitation investigation: there was no significant difference in rate of ROSC, time of CPR and energy of defibrillation among HPRA, HPOA, and NTR groups [rate of ROSC: 85.71%, 71.43%, 71.43%; time of CPR (seconds): 45.3 ± 30.2, 61.2 ± 41.3, 82.3 ± 63.8; energy of defibrillation (J): 14.3 ± 8.9, 22.0 ± 15.5, 25.0 ± 15.8, all P > 0.05]. (2) Hemodynamics: compared with normal temperature groups, animals in hypothermia groups exhibited lower levels of HR (all P < 0.05). Compared with NTR group, HPRA group exhibited higher levels of LVESP (mmHg, 1 mmHg = 0.133 kPa) at 0.5, 1, 2 and 3 hours post ROSC (0.5 hour: 103.8 ± 14.3 vs. 91.6 ± 13.3, 1 hour: 107.2 ± 14.1 vs. 82.7 ± 8.5, 2 hours: 109.0 ± 16.9 vs. 88.8 ± 12.9, 3 hours: 109.1 ± 14.6 vs. 89.3 ± 14.3, all P < 0.05). Compared with NTR group and HPOA group, HPRA group exhibited lower levels of LVEDP (mmHg) at 0.5 hour post ROSC (3.70 ± 0.85 vs. 7.61 ± 2.73, 7.02 ± 3.12, both P < 0.05). Compared with NTR group, HPRA group exhibited lower levels of LVEDP at 1 hour post ROSC (4.34 ± 1.44 vs. 6.99±1.96, P < 0.05). In HPRA group, the level of +dp/dt max (mmHg/s) was higher than that of NTR group and HPOA group at 1 hour and 2 hours post ROSC (1 hour: 2 759.5 ± 321.6 vs. 2 123.0 ± 304.5, 2 283.7 ± 234.2, 2 hours: 2 730.6±425.1 vs. 2 221.5 ± 392.9, 2 252.6 ± 476.0, all P < 0.05). There were no significant differences in -dp/dt max and MAP levels among three CPR groups. (3) The survival rate at 48 hours post ROSC of NTR, HPRA and HPOA groups was 60%, 75%, and 100%, respectively. Compared with NTR group, higher survival rate was found in HPOA group at 48 hour post ROSC (P < 0.05). (4) Compared with NTR group, less damage to myocardial ultrastructure was found in HPRA and HPOA groups. Apoptosis index (AI) was lower in HPRA and HPOA groups than that in NTR group [(28.05 ± 9.82) %, (26.39 ± 8.98) % vs. (42.02 ± 13.36) %, both P < 0.05]. CONCLUSIONS: Our study shows that mild hypothermia has no effect on ROSC rate. Pre-arrest hypothermia can ameliorate myocardial systolic function of rabbit in early stage after ROSC, and it has no negative influence on diastolic function. Post-arrest mild hypothermia produces no negative influence on myocardial function of rabbit, but it improves 48 hours survival rate in ROSC rabbits. Both pre-arrest and post-arrest mild hypothermia therapy can attenuate myocardial injury in CA model of rabbits by ameliorating mitochondrial injuries and suppressing apoptosis of myocardial cells.

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The southeastern margin of the Tibetan Plateau is characterized by complex topography and a discontinuous landscape, creating a sky island situation. However, the way topography shapes genetic structures and demographic histories of endemic species has not been well studied. We examined the phylogeographic pattern and demographic histories of Sorex bedfordiae, a dispersal-limited small mammal, using three nuclear genes [1977bp] and two mitochondrial genes [1794bp] with comprehensive molecular approaches. We recovered five well-supported clades whose distributions are along mountain ridges and roughly subdivided by large rivers. Demographic expansions in the middle Pleistocene were strongly supported by both nuclear and mitochondrial genes. Our results support the hypothesis that sky island topography and river systems strongly affect the genetic structure of non-aquatic terrestrial species. We further clarify that S. bedfordiae and S. cylindricauda are valid sibling species, whereas S. excelsus is most likely a geographic subspecies of S. bedfordiae.

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Biological nitrate removal using wheat straw and polylactic acid (PLA) as both carbon source and biofilm support was investigated. The results showed that biofilm could develop on the surface of wheat straw within 15 d, the denitrification rate was 0.067 mg-N/(g-wheat straw x h) and nitrate removal efficiency was about 100%. For PLA, the time required for biofilm development was 40 d, the denitrification rate was 0.0026 mg-N/(g-PLA x h) and nitrate removal efficiency could also reach 100%. Temperature had a substantial influence on the denitrification performance of both wheat straw and PLA. The FTIR analysis and SEM observation confirmed that wheat straw and PLA were used for denitrification, and explained some reasons for the differences between the two substrates. The wheat straw was superior to PLA when used as carbon source for nitrate removal, in terms of the denitrification rate.

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OBJECTIVE: To investigate the impact of prior cerebral infarction (PCI) on in-hospital mortality in patients with Acute Myocardial Infarction (AMI). METHODS: A retrospective analysis of documents of a total of 3572 consecutive patients with AMI admitted to Xuanwu Hospital of Capital Medical University from 2002 Jan. 1 to 2009 Dec. 31 were performed. RESULTS: There were 564 patients (15.8%) with PCI. Compared with the group of without PCI, the group with PCI were substantially older [(69.4 ± 9.9) vs (64.2 ± 12.9) years, P = 0.000], and had a higher prevalence of hypertensive disease, diabetes mellitus, prior myocardial infarction (MI) and non-ST-segment elevation myocardial infarction (NSTEMI) (respectively, 71.0% vs 57.3%; 41.0% vs 25.7%, 12.9% vs 9.5%; 14.9% vs 10.7%, P < 0.01), and a higher in-hospital mortality (16.5% vs 10.0%, P = 0.000). Univariate analysis demonstrated that in-hospital mortality associated with age, gender, extensive anterior MI, anterior MI, diabetes mellitus, prior cerebral infarction, prior myocardial infarction, coronary angiography and percutaneous coronary intervention. Logistic regression analysis found that risk factors were age, extensive anterior MI, anterior MI, diabetes mellitus and prior cerebral infarction, and protective factors were coronary angiography and percutaneous coronary intervention. PCI was independently associated with in-hospital mortality, OR 1.368, 95%CI 1.047 - 1.787, P = 0.022. CONCLUSION: In patients with acute myocardial infarction, the presence of PCI increases the risk of worse in-hospital outcome.

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OBJECTIVE: To examine the impact of mild hypothermia on cardiac function, myocardial tissue integrity, and 48 hours mortality in a rabbits model of ventricular fibrillation after restoration of spontaneous circulation (ROSC). METHODS: The rabbits were randomly divided into four groups: normothermic post ROSC (NTPR, n = 10), mild hypothermia post ROSC (HTPR, n = 10), normothermic control (NTC, n = 8) and mild hypothermia control (HTC, n = 8). Ventricular fibrillation was induced by trans-epicardium electric-shook with alternating current in all the animals and ROSC was achieved through administration of adrenaline (i.v.) and artificial ventilation in group NTPR and HTPR. The body temperature of the animals was kept either at (39.0 ± 0.5) centigrade (NTPR and NTC) or (33.5 ± 0.5) centigrade (HTPR and HTC) for 4 hours after surgery for hemodynamic index data collection 0.5, 1, 2, 3 and 4 hours after surgery, 48 hours later, the mortality in the animals was recorded, and myocardial tissue samples were collected from survived animals for morphological examination by light and electric microscopy and analysis of apoptosis by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. The content of ATP, ADP and AMP in the tissue samples was measured by high performance liquid chromatography (HPLC) for the calculation of energy charges (EC). RESULTS: (1)Hemodynamic indexes: as compared to the NTC group, HTC group exhibited significantly lower levels of heart rate (HR) and -dp/dt max in all the time points. No significant difference between the two groups in the levels of +dp/dt max and mean artery pressure (MAP) was found in all the time points but 0.5 hour. There was no significant difference in the levels of left ventricular end-diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVESP), and femoral artery blood pressure between the two groups.(2) In comparison with NTPR group, HTPR group exhibited significantly (all P < 0.05) lower levels of HR (bpm) and -dp/dt max in all time points (ROSC 0.5, 1, 2, 3, 4 hours: HR 216.5 ± 33.3 vs. 292.9 ± 38.4, 218.2 ± 28.0 vs. 294.3 ± 37.0, 227.5 ± 25.4 vs. 291.4 ± 25.3, 232.4 ± 27.4 vs. 278.1 ± 30.8, 230.6 ± 22.0 vs. 285.1 ± 38.2; -dp/dt max 1847.1 ± 241.2 vs. 2383.3 ± 470.9, 1860.7 ± 167.8 vs. 2154.6 ± 319.5, 1822.3 ± 389.7 vs. 2239.7 ± 379.0, 1950.6 ± 412.9 vs. 2229.6 ± 392.4, 1875.7 ± 555.6 vs. 2396.7 ± 420.1). There was no significant difference between the two groups in the levels of LVEDP, +dp/dt max, LVESP, and femoral artery blood pressure. (3)Optical and electron microscopy revealed myocardium injury in samples from animals underwent ROSC. However, in comparison with the NTPR group, samples from HTPR group exhibited less damage to the myocardium structure. (4) Apoptosis index (AI) of myocardium was significantly (P < 0.05) higher in NTPR group (42.02%) than in HTPR group (26.39%). (5) Tests of myocardial energy: ATP level (µmol/g) in HTPR was significantly (P < 0.05) higher than NTPR (0.97 ± 0.26 vs. 0.65 ± 0.16). EC in NTPR was significant lower than it in two control groups [(0.33 ± 0.13)% vs. (0.52 ± 0.12)%, (0.55 ± 0.06)%, both P < 0.05], whereas no such difference was found between HTPR [(0.41 ± 0.12)%] and two control groups. (6) 48 hours survival rate in HTPR group was significantly higher (P = 0.043) as compared to NTPR group (100% vs. 60%). CONCLUSIONS: Myocardial dysfunction and myocardium tissue injury both develop in post-resuscitation rabbits with ventricular fibrillation. In these animals, reducing body temperature to the level of mild hypothermia after ROSC may improve the 48 hours survival rate, probably via mechanisms that suppress myocardial cell apoptosis. In our study, such intervention produced no obvious negative impact neither on the cardiac function nor hemodynamics.

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Inflammatory responses are an important element in the atherosclerotic process. Therefore, inflammatory markers can potentially serve as predictors of cardiovascular risk. However, the existing data are limited and controversial. We conducted a prospective cohort study with 263 patients with first acute ST-segment elevation myocardial infarction (STEMI) who were admitted to our Hospital within 6 h after the symptoms onset. Clinical data were recorded and serum admission levels of interleukin-6 (IL-6), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble P-selectin (sP-selectin) were determined. The patients were then followed up for 3 years to document cardiovascular mortality. During the follow-up, 34 patients died from cardiovascular causes. The admission levels of IL-6 were significantly higher in these patients, whereas sICAM-1, sVCAM-1, and sP-selectin were comparable between these and the survived patients. The Kaplan-Meier plots revealed a significant increase in cardiovascular mortality with increasing levels of IL-6 (P = 0.0002, χ(2) test). The logistic regression analysis indicated that IL-6 was an independent predictor for cardiovascular mortality. To conclude, our findings indicate that elevated admission levels of IL-6, but not soluble adhesion molecules, provide valuable information for risk assessment of long-term cardiovascular mortality in patients with STEMI.

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Polylactic acid (PLA) was used as solid carbon source and biofilm support simultaneously, to investigate the applicability of PLA in the denitrification process. The effect of temperature on denitrification performance was also studied. The IR analysis and SEM observation were performed to investigate the PLA surface structure and biofim morphology. The results showed that when the initial concentration of nitrate nitrogen was 50 mg/L and the temperature was 30 degrees C, the average denitrification rate was 2.6 x 10(-1) mg/(g x h) and nitrate could be completely removed within 13h. Temperature had a significant influence on the denitrification rate. The IR analysis and SEM observation of PLA surface structure confirmed the feasibility of PLA as solid carbon source. The SEM observation of biofim showed that the biofilm was thin and mainly consisted of cocci.

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Accumulating evidence suggests that inflammation plays an essential role in the pathogenesis of atherosclerosis. This recognition has stimulated the evaluation of different inflammatory markers as potential predictors of cardiovascular risk. However, the existing data are limited and controversial. This study was designed to simultaneously measure serum levels of interleukin-6 (IL-6), soluble CD40 ligand (sCD40L), metalloproteinase-9 (MMP-9), and tissue inhibitor of metalloproteinase-1 (TIMP-1) in patients with acute ST segment elevation myocardial infarction (STEMI) and to evaluate their ability to predict prognosis. A prospective cohort study was conducted with 263 patients with first STEMI who were admitted to our institute within 6 h of symptoms onset. Clinical data were recorded and serum admission levels of IL-6, sCD40L, MMP-9, and TIMP-1 were measured by sandwich enzyme-linked immunosorbent assay. The patients were then followed prospectively for the occurrence of cardiovascular mortality for 3 years. Follow-up information was available for 228 patients (86.7%) from the 263 STEMI patients; 34 patients died from cardiovascular causes during the 3-year follow-up period. Kaplan-Meier plots demonstrated a significant increase in cardiovascular mortality with increasing IL-6 levels (chi(2) = 14.13, P = 0.0002, by log-rank test). Logistic regression analysis revealed that IL-6 was an independent predictor for cardiovascular mortality. The present study indicates that elevated admission level of IL-6 could provide valuable information for long-term risk stratification in patients with STEMI.

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Wheat straw after radiation pretreatment was used as solid carbon source and biofilm support for denitrifying microorganisms. Denitrification performance of radiation-pretreated wheat straw was compared to that of wheat straw without radiation pretreatment. The results showed that the denitrification rate of radiation-pretreated wheat straw was about 20% higher than that of wheat straw without radiation pretreatment. When the initial nitrate concentration was 65.3 mg/L, the denitrification rate using wheat straw after 300 kGy radiation with gamma-ray could reach 0.087 mg/(g x h) and the nitrate removal efficiency was above 90%. Parts of these results were confirmed by the IR analysis and SEM observation of wheat straw surface structure.

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