Denitrificimonas halotolerans sp. nov., a novel species isolated from UASB sludge treating landfill leachate.

A Gram-stain-negative, facultative anaerobe, rod-shaped strain JX-1T was isolated from UASB sludge treating landfill leachate in Wuhan, China. The isolate is capable of growing under conditions of pH 6.0-11.0 (optimum, pH 7.0-8.0), temperature 4-42 â„ƒ (optimum, 20-30 â„ƒ), 0-8.0% (w/v) NaCl (optimum, 5.0%), and ammonia nitrogen concentration of 200-5000 mg/L (optimum, 500 mg/L) on LB plates. The microorganism can utilize malic acid, D-galactose, L-rhamnose, inosine, and L-glutamic acid as carbon sources, but does not reduce nitrates and nitrites. The major fatty acids are C18:1ω7c/C18:1ω6c, iso-C15:0, and anteiso-C15:0. The respiratory quinones are Q9 (91.92%) and Q8 (8.08%). Polar lipids include aminolipid, aminophospholipid, diphosphatidylglycerol, glycolipid, phosphatidylethanolamine, phosphatidylglycerol, and phospholipid. Compared with other strains, strain JX-1T and Denitrificimonas caeni HY-14T have the highest values in terms of 16S rRNA gene sequence similarity (96.79%), average nucleotide identity (ANI; 76.06%), and average amino acid identity (AAI; 78.89%). Its digital DNA-DNA hybridization (dDDH) result is 20.3%. The genome of strain JX-1T, with a size of 2.78 Mb and 46.12 mol% G + C content, lacks genes for denitrification and dissimilatory nitrate reduction to ammonium (DNRA), but contains genes for ectoine synthesis as a secondary metabolite. The results of this polyphasic study allow genotypic and phenotypic differentiation of the analysed strain from the closest related species and confirm that the strain represents a novel species within the genus Denitrificimonas, for which the name Denitrificimonas halotolerans sp. nov. is proposed with JX-1T (= MCCC 1K08958T = KCTC 8395T) as the type strain.

Risk factors and predicting nomogram for the clinical deterioration of non-severe community-acquired pneumonia.

BACKGROUND: Currently, there remains insufficient focus on non-severe community-acquired pneumonia (CAP) patients who are at risk of clinical deterioration, and there is also a dearth of research on the related risk factors. Early recognition of hospitalized patients at risk of clinical deterioration will be beneficial for their clinical management. METHOD: A retrospective study was conducted in The First Affiliated Hospital of Wenzhou Medical University, China, spanning from January 1, 2018 to April 30, 2022, and involving a total of 1,632 non-severe CAP patients. Based on whether their condition worsened within 72 h of admission, patients were divided into a clinical deterioration group and a non-clinical deterioration group. Additionally, all patients were randomly assigned to a training set containing 75% of patients and a validation set containing 25% of patients. In the training set, risk factors for clinical deterioration in patients with non-severe CAP were identified by using LASSO regression analysis and multivariate logistic regression analysis. A nomogram was developed based on identified risk factors. The effectiveness of the nomogram in both the training and validation sets was assessed using Receiver Operating Characteristic (ROC) curves, calibration curves, and decision curve analysis (DCA). RESULTS: Age, body mass index (BMI), body temperature, cardiovascular comorbidity, respiratory rate, LDH level, lymphocyte count and D-dimer level were identified as risk factors associated with the clinical deterioration of non-severe CAP within 72 h of admission. The area under curve (AUC) value of the nomogram was 0.78 (95% CI: 0.74-0.82) in the training set and 0.75 (95% CI: 0.67-0.83) in the validation set. Furthermore, the calibration curves for both the training and validation sets indicated that the predicted probability of clinical deterioration aligned with the actual probability. Additionally, DCA revealed clinical utility for the nomogram at a specific threshold probability. CONCLUSION: The study successfully identified the risk factors linked to the clinical deterioration of non-severe CAP and constructed a nomogram for predicting the probability of deterioration. The nomogram demonstrated favorable predictive performance and has the potential to aid in the early identification and management of non-severe CAP patients at elevated risk of deterioration.

Dauricine alleviates cognitive impairment in Alzheimer's disease mice induced by D-galactose and AlCl3 via the Ca2+/CaM pathway.

Alzheimer's disease (AD) is a common neurodegenerative disease in the elderly. Dysregulation of intracellular Ca2+ homeostasis plays a critical role in the pathological development of AD. Dauricine (DAU) is a bisbenzylisoquinoline alkaloid isolated from Menispermum dauricum DC., which can prevent the influx of extracellular Ca2+ and inhibit the release of Ca2+ from the endoplasmic reticulum. DAU has a potential for anti-AD. However, it is unclear whether DAU can exert its anti-AD effect in vivo by regulating the Ca2+ related signaling pathways. Here, we investigated the effect and mechanism of DAU on D-galactose and AlCl3 combined-induced AD mice based on the Ca2+/CaM pathway. The results showed that DAU (1 mg/kg and 10 mg/kg for 30 days) treatment attenuated learning and memory deficits and improved the nesting ability of AD mice. The HE staining assay showed that DAU could inhibit the histopathological alterations and attenuate neuronal damage in the hippocampus and cortex of AD mice. Studies on the mechanism indicated that DAU decreased the phosphorylation of CaMKII and Tau and reduced the formation of NFTs in the hippocampus and cortex. DAU treatment also reduced the abnormally high expression of APP, BACE1, and Aß1-42, which inhibited the deposition of Aß plaques. Moreover, DAU could decrease Ca2+ levels and inhibit elevated CaM protein expression in the hippocampus and cortex of AD mice. The molecular docking results showed that DAU may have a high affinity with CaM or BACE1. DAU has a beneficial impact on pathological changes in AD mice induced by D-galactose and AlCl3 and may act by negative regulation of the Ca2+/CaM pathway and its downstream molecules such as CaMKII and BACE1.

Total alkaloids from the seed embryo of Nelumbo nucifera Gaertn. improve cognitive impairment in APP/PS1 mice and protect Aß-damaged PC12 cells.

The seed embryo of Nelumbo nucifera Gaertn. is a famous traditional Chinese medicine and food which is considered conducive to the prevention of Alzheimer's disease (AD). In this study, the effect and mechanism of TASENN (total alkaloids from the seed embryo of Nelumbo nucifera Gaertn.) on AD mice and amyloid-ß (Aß) injured PC12 cells were evaluated. HPLC-UV analysis showed that the extracted TASENN (purity = 95.6%) mainly contains Liensinine, Isoliensinine, and Neferine (purity was 23.01, 28.02, and 44.57%, respectively). In vivo, oral treatment with TASENN (50 mg/kg/day for 28 days) improved the learning and memory functions of APP/PS1 transgenic mice, ameliorated the histopathological changes of cortical and hippocampal neurons, and inhibited neuronal apoptosis. We found that TASENN reduced the phosphorylation of Tau and the formation of neurofibrillary tangles (NFTs) in APP/PS1 mouse brain. Moreover, TASENN down-regulated the expression of APP and BACE1, ameliorated Aß deposition, and inhibited microglial proliferation and aggregation. The elevated protein expression of CaM and p-CaMKII in APP/PS1 mouse brain was also reduced by TASENN. In vitro, TASENN inhibited the apoptosis of PC12 cells injured by Aß25-35 and increased the cell viability. Aß25-35-induced increase of cytosolic free Ca2+ level and high expression of CaM, p-CaMKII, and p-Tau were decreased by TASENN. Our findings indicate that TASENN has a potential therapeutic effect on AD mice and a protective effect on PC12 cells. The anti-AD activity of TASENN may be closely related to its negative regulation of the CaM pathway.

Optimal pathways for upgrading China's wastewater treatment plants for achieving water quality standards at least economic and environmental cost.

Wastewater treatment plants (WWTPs) in China must be upgraded to meet new discharge standards, but this incurs both economic and environmental costs and benefits. To select the optimal upgrade pathway, we developed ten upgrade paths based on two common decision-making scenarios for WWTP upgrade in developing countries. Using model simulation, life-cycle assessment, life-cycle cost, and multiple-attribute decision-making, we incorporated the full costs and benefits associated with the construction and operation into the decision-making process. We used a weighting scheme of attributes for the three regions and ranked the upgrade paths using the technique for order preference by similarity to an ideal solution (TOPSIS). The results showed that constructed wetlands and sand filtration were advantageous in terms of lower economic costs and environmental impacts, while the denitrification filter pathways required less land. Optimal pathways differed by region, highlighting the importance of a detailed and integrated assessment of the costs and benefits of WWTP upgrade options over the full life cycle. Our findings can inform decision-making on upgrading China's WWTPs to meet stringent discharge standards and protect inland water and coastal environments.

Potential Mechanisms of Methylglyoxal-Induced Human Embryonic Kidney Cells Damage: Regulation of Oxidative Stress, DNA Damage, and Apoptosis.

Methylglyoxal (MGO) is a reactive carbonyl species that can cause cellular damage and is closely related to kidney disease, especially diabetic nephropathy. The toxic effect of MGO (0.5, 1, and 2 mM) on human embryonic kidney (HEK293) cells and its underlying mechanisms were explored in this study. Cell viability, apoptosis and the signaling pathways were measured with MTT, fluorescent staining and western blot experiments, the results showed that MGO could induce oxidative stress and cell inflammation, the level of reactive oxygen species (ROS) increased, and p38MAPK, JNK and NF-κB signaling pathways were activated. Meanwhile, MGO also induced DNA damage. The expression of DNA oxidative damage marker 8-hydroxy-2'-deoxyguanosine (8-OHdG) increased, the expression of double-strand break marker γH2AX increased significantly, and ATM/Chk2/p53 DNA damage response signaling pathway was activated. Furthermore, the expression of the receptor for advanced glycation end products (RAGE) also increased. Finally, mitochondrial membrane potential (MMP) decreased, fluorescence intensity of Hoechst33258 increased, and the protein expression ratio of Bax/Bcl-2 increased significantly after the treatment of MGO. These results demonstrated that MGO might induce HEK293 cells damage by regulating oxidative stress, inflammation, DNA damage, and cell apoptosis, which revealed the specific mechanisms of MGO-induced damage to HEK293 cells.

Investigating the molecular mechanisms of glyoxal-induced cytotoxicity in human embryonic kidney cells: Insights from network toxicology and cell biology experiments.

Glyoxal, a reactive carbonyl species, can be generated both endogenously (glucose metabolism) and exogenously (cigarette smoke and food system). Increasing evidence demonstrates that glyoxal exacerbates the development and progression of diabetic nephropathy, but the underlying mechanisms of glyoxal toxicity to human embryonic kidney (HEK293) cells remain unclear. In this work, the molecular mechanisms of glyoxal-induced cytotoxicity in HEK293 cells were explored with network toxicology and cell biology experiments. Network toxicology results showed that oxidative stress and advanced glycation end products (AGEs)/RAGE signaling pathways played a crucial role in glyoxal toxicity. Next, further validation was performed at the cellular level. Glyoxal activated the AGEs-RAGE signaling pathway, caused the increase of cellular ROS, and activated the p38MAPK and JNK signaling pathways, causing cellular oxidative stress. Furthermore, glyoxal caused the activation of the NF-κB signaling pathway and increased the expression of TGF-ß1, indicating that glyoxal caused cellular inflammation. Moreover, glyoxal caused cellular DNA damage accompanied by the activation of DNA damage response pathways. Finally, the mitochondrial apoptosis pathway was activated. The results that obtained in cell biology were consistent with network toxicology, which corroborated each other and together indicated that glyoxal induced HEK293 cells damage via the process of oxidative stress, the AGEs-RAGE pathway, and their associated signaling pathways. This study provides the experimental basis for the cytotoxicity of glyoxal on HEK293 cells.

An Improved Sensing Method of a Robotic Ultrasound System for Real-Time Force and Angle Calibration.

An ultrasonic examination is a clinically universal and safe examination method, and with the development of telemedicine and precision medicine, the robotic ultrasound system (RUS) integrated with a robotic arm and ultrasound imaging system receives increasing attention. As the RUS requires precision and reproducibility, it is important to monitor the real-time calibration of the RUS during examination, especially the angle of the probe for image detection and its force on the surface. Additionally, to speed up the integration of the RUS and the current medical ultrasound system (US), the current RUSs mostly use a self-designed fixture to connect the probe to the arm. If the fixture has inconsistencies, it may cause an operating error. In order to improve its resilience, this study proposed an improved sensing method for real-time force and angle calibration. Based on multichannel pressure sensors, an inertial measurement unit (IMU), and a novel sensing structure, the ultrasonic probe and robotic arm could be simply and rapidly combined, which rendered real-time force and angle calibration at a low cost. The experimental results show that the average success rate of the downforce position identification achieved was 88.2%. The phantom experiment indicated that the method could assist the RUS in the real-time calibration of both force and angle during an examination.

Microfluidic-based cardiovascular systems for advanced study of atherosclerosis.

Atherosclerosis (AS) is a significant global health concern due to its high morbidity and mortality rates. Extensive efforts have been made to replicate the cardiovascular system and explore the pathogenesis, diagnosis, and treatment of AS. Microfluidics has emerged as a valuable technology for modeling the cardiovascular system and studying AS. Here a brief review of the advances of microfluidic-based cardiovascular systems for AS research is presented. The critical pathogenetic mechanisms of AS investigated by microfluidic-based cardiovascular systems are categorized and reviewed, with a detailed summary of accurate diagnostic methods for detecting biomarkers using microfluidics represented. Furthermore, the review covers the evaluation and screening of AS drugs assisted by microfluidic systems, along with the fabrication of novel drug delivery carriers. Finally, the challenges and future prospects for advancing microfluidic-based cardiovascular systems in AS research are discussed and proposed, particularly regarding new opportunities in multi-disciplinary fundamental research and therapeutic applications for a broader range of disease treatments.

Photolysis of polycyclic aromatic hydrocarbons on soil surfaces under UV irradiation.

Photolysis of some polycyclic aromatic hydrocarbons (PAHs) on soil surfaces may play an important role in the fate of PAHs in the environment. Photolysis of PAHs on soil surfaces under UV irradiation was investigated. The effects of oxygen, irradiation intensity and soil moisture on the degradation of the three PAHs were observed. The results showed that oxygen, soil moisture and irradiation intensity enhanced the photolysis of the three PAHs on soil surfaces. The degradation of the three PAHs on soil surfaces is related to their absorption spectra and the oxidation-half-wave potential. The photolysis of PAHs on soil surfaces in the presence of oxygen followed pseudo first-order kinetics. The photolysis half-lives ranged from 37.87 days for benzo[a]pyrene to 58.73 days for phenanthrene. The results indicate that photolysis is a successful way to remediate PAHs-contaminated soils.

Status, sources, and human health risk assessment of DDT pesticide residues in river sediments in a highly developed agricultural region in the upper Yangtze River in China.

The concentrations of DDT and its metabolites in 19 sediment samples from a highly developed agricultural region in the upper reaches of the Yangtze River were measured. Non-carcinogenic hazard quotient for different age groups was evaluated using reference doses provided by the USEPA, and the excess lifetime cancer risk due to eating fish was assessed based on the local eating habits. The results showed that this region had a high level of residual DDT (12.84 ± 8.97 ng/g), which mainly came from the historically used technical DDT in agriculture. The non-carcinogenic risk was just acceptable in the region, but 11 of the 19 sites showed an unacceptable carcinogenic risk. Although DDT has been banned for decades, there were still notable health risks, especially for children. Special attention should be given to the potential health risks in historically developed agricultural regions.

Effects of [Cnpy]Br (n=3,5) on the growth and physiology of rape seedlings.

1-Alkylpyridinium bromide [Cnpy]Br is a common intermediate in chemical synthesis. With the discharge of industrial wastewater, it enters the environment and is toxic to plants. In this study, the impacts of two pyridine-based ionic liquids (ILs), [C3py]Br and [C5py]Br, on the growth and physiology of rape seedlings were investigated at concentrations of 10, 50, 100, 200, 300, and 400 mg/L. Within the concentration range (10-400 mg/L) of [C3py]Br and [C5py]Br treatment, the root length, plant height, activities of antioxidant enzymes (SOD, POD, and CAT), and the contents of Chla and Chlb showed an increase at low concentrations and a decrease at high concentrations. [C3py]Br and [C5py]Br increased MDA content in rape seedlings leaves in a concentration-dependent manner. It was also found that [C5py]Br was more toxic to rape seedlings than [C3py]Br. The toxicity of pyridine ILs such as [C3py]Br and [C5py]Br to plants should be highly concerned.

Molecular characteristics of biochar-derived organic matter sub-fractions extracted by ultrasonication.

Biochar-derived organic matter is key to carbon dynamics and pollutant transport in soils remediated by biochar. A limited understanding of the molecular composition of biochar-derived organic matter limits the ability to accurately predict the chemical cycle within soil and how biochar-derived organic matter will interact with contaminants. To describe the relatively comprehensive structure information of soybean straw biochar-extractable organic matter (BEOM) at the molecular level, we used solvents of different polarities, namely, petroleum ether (PE), carbon disulfide (CS2), methanol (CH3OH) and acetone (CH3COCH3), to extract organic samples from soybean straw biochar and used Fourier transform ion cyclotron resonance mass spectrometry (FTICR MS) for analysis. We found that a high percentage of unique molecular formulas were extracted by each solvent. This molecular diversity is mainly due to variance in solvent polarity and various intermolecular bonds destroyed by different solvents. The molecular signatures of the sub-fractions reveal that some recalcitrant BEOM sub-fractions will be easily released in the environment and preserved for a long time in the soil environment, while the majority of the labile BEOM sub-fractions tend to be preserved in the biochar itself. In addition, the most readily available organic N and S in biochar will be primarily released. These results reveal that biochar could provide nutrients efficiently and maintain soil organic carbon over the long term, suggesting that biochar is a promising material for soil improvement. By using high-resolution mass spectrometry, we revealed the BEOM signature at the molecular level in various possible environmental processes, which provides a theoretical basis for further research on the interactions between BEOM and organic contaminants.

Protective effects of Liensinine, Isoliensinine, and Neferine on PC12 cells injured by amyloid-ß.

Excessive accumulation of amyloid-ß (Aß) is the leading cause of Alzheimer's disease (AD). Liensinine, Isoliensinine, and Neferine are main alkaloids in lotus seed embryos. In this paper, the protective effects of Liensinine, Isoliensinine, and Neferine on Aß25-35 -injured PC12 cells were studied. It was found that Liensinine, Isoliensinine, and Neferine could improve the viability and reduce the apoptosis of PC12 cell induced by Aß25-35 . These three alkaloids could also reduce the level of intracellular free Ca2+ and CaM expression in Aß25-35 -treated cells, thereby inhibiting the phosphorylation of CaMKII and tau. In addition, these three compounds can inhibit the production of ROS in PC12 cells injured by Aß25-35 . Our results suggest for the first time that Liensinine, Isoliensinine, and Neferine can inhibit hyperphosphorylation of tau protein by inhibiting the Ca2+ -CaM/CaMKII pathway, thereby reducing the apoptosis and death of PC12 cells damaged by Aß25-35 . PRACTICAL APPLICATIONS: This study highlighted the protective effects and mechanisms of three main active ingredients (Liensinine, Isoliensinine, and Neferine) in the lotus embryo on a typical cell model of Alzheimer's disease (AD). The results revealed that three alkaloids in this healthy food might exert therapeutic potential for AD.

Tumor Microenvironment in Hepatocellular Carcinoma: Key Players for Immunotherapy.

Hepatocellular carcinoma (HCC) remains a serious medical therapeutic challenge as conventional curative avenues such as surgery and chemotherapy only benefit for few patients with limited tumor burden. Immunotherapy achieves clinical progress in the treatment of this prevalent malignant disease by virtue of the development of tumor immunology; however, most patients have experienced minimal or no clinical benefit in terms of overall survival. The complexity and diversity of tumor microenvironment (TME) built by immune and stromal cell subsets has been considered to be responsible for the insufficiency of immunotherapy. The advance of bioanalytical technology boosts the exploration of the composition and differentiation of these infiltrated cells, which reflect the immune state of the TME and impact the efficacy of the antitumor immune response. Targeting these cells to remodel the TME is one of the important immunotherapeutic approaches to improve HCC treatment. In this review, we focused on the role of these non-cancerous cells in the tumor progression, and elaborated their function on cancer immunotherapy when manipulating them as potential targets.

DNA Damage in Liver Cells of the Tilapia Fish Oreochromis mossambicus Larva Induced by the Insecticide Cyantraniliprole at Sublethal Doses During Chronic Exposure.

Cyantraniliprole can effectively control lepidopteran pests and has been used all over the world. In general, the risk of cyantraniliprole seems low for fish, but the toxicity selectivity among different fish species was not clear. Here, we present the methods for the acute toxicity and chronic effects of cyantraniliprole by using juvenile tilapia (Oreochromis mossambicus). Based on this test, 96 h LC50 of cyantraniliprole to tilapia was 38.0 mg/L. After exposed for 28 days, specific growth rates of the blank control, solution control, and the treatments of 0.037, 0.37 and 3.7 mg/L of cyantraniliprole were 1.14, 0.95, 0.93, 0.82, and 0.70% per day, respectively. The results of micronucleus experiment and single cell gel electrophoresis showed that cyantraniliprole damaged DNA in liver cells of tilapia larvae. Quantitative PCR results showed that cyantraniliprole could induce the upregulation of Rpa 3 that is responsible for the DNA repair. The significant downregulation of Chk 2 gene was related to p53 pathway. It is therefore proposed that cyantraniliprole causes DNA damage in liver cells of tilapia and activates DNA damage and repair pathways.

DNA damage in liver cells of the tilapia fish Oreochromis mossambicus larva induced by the insecticide cyantraniliprole at sublethal doses during chronic exposure.

Cyantraniliprole can effectively control lepidopteran pests and has been used all over the world. In general, the risk of cyantraniliprole seems low for fish, but the toxicity selectivity among different fish species was not clear. Here the acute toxicity and chronic effects of cyantraniliprole to juvenile tilapia (Oreochromis mossambicus) were assessed. The results showed that 96 h LC50 of cyantraniliprole to tilapia was 38.0 mg/L. After exposed for 28 days, specific growth rates of the blank control, solution control, and the treatments of 0.037, 0.37 and 3.7 mg/L of cyantraniliprole were 1.14, 0.95, 0.93, 0.82 and 0.70% per day, respectively. The results of micronucleus experiment and single cell gel electrophoresis showed that cyantraniliprole damaged DNA in liver cells of tilapia larvae. Quantitative PCR results showed that cyantraniliprole could induce the up-regulation of Rpa 3 that is responsible for the DNA repair. The significantly down-regulation of Chk 2 gene was related to p53 pathway. It is therefore proposed that cyantraniliprole causes DNA damage in liver cells of tilapia and activates DNA damage and repair pathways.

[Tongxinluo improves vascular endothelial function in patients with type 2 diabetes].

OBJECTIVE: To investigate the effects of Tongxinluo on vascular endothelial function in patients with type 2 diabetes. METHODS: A total of 80 patients with type 2 diabetes were recruited and divided into two groups: Tongxinluo therapy group (n = 40) and conventional therapy group (n = 40). Plasma levels of NO, ET, 6-keto-PGF1alpha and TXB2 and diastolic functions of humeral arteries (measured by high-resolution ultrasound) were measured at baseline and 4 weeks later. RESULTS: The flow-mediated dilation was significantly increased from (8.19 +/- 0.71)% to (12.47 +/- 0.98)% (P < 0.05) in Tongxinluo therapy group after 4 weeks therapy compare to baseline level. Their plasma NO was significantly increased [(47.65 +/- 4.38) pg/ml to (52.91 +/- 4.83) pg/ml, P < 0.001] and plasma ET significantly reduced [(31.23 +/- 2.46) pg/ml to (24.34 +/- 2.46) pg/ml, P < 0.001] post 4 week Tongxinluo therapy. Parameters remained unchanged in the placebo group (P > 0.05) at baseline and 4 weeks later. Non-flow-mediated dilation was unaffected by Tongxinluo therapy. CONCLUSIONS: Tongxinluo improved the vascular endothelial dependent diastolic function in patients with type 2 diabetes by regulating the balance of plasma NO/ET.

[The impact of elevated serum creatinine on the prognosis of acute myocardial infarction].

OBJECTIVE: To evaluate the clinical features and outcomes in patients suffering from acute myocardial infarction combined with elevated serum creatinine. METHODS: We enrolled 340 consecutive patients suffering from acute myocardial infarction admitted into our hospital from 2003.2.1 - 2004.8.31. The patients were divided into the following 2 groups, 269 patients in a group with normal serum creatinine and 71 patients in a group with elevated serum creatinine, according to the normal limit of serum creatinine in our hospital. Outcomes during hospitalization were available in all the patients and one year follow-up data were also available in all the patients. The influence of baseline demographic and clinical variables on mortality at day 30 and one year during the follow-up period was evaluated by Cox proportional hazard regression to determine the independent predictors of late adverse events. RESULTS: Elevated creatinine at baseline was present in 71 of the 340 patients. Compared with patients with normal creatinine, patients with elevated creatinine were older and more likely to have old myocardial infarction and to present with cardiac shock, heart failure, ventricular fibrillation and complete AVB. Mortality was markedly increased in patients with baseline elevated creatinine as compared with these without at day 30 (32.39% versus 4.83%, P = 0.000), during hospitalization (35.21% versus 5.20%, P = 0.000) and at 1 year (43.66% versus 11.15%, P = 0.000). By Cox regression analysis, elevated creatinine was a powerful independent hazard predictor of 30-day survival (odds ratio 4.591, 95% confidence interval 2.149 to 9.808, P = 0.000) and remained to be associated with reduced survival at 1 year (odds ratio 3.936, 95% confidence interval 2.264 to 6.845, P = 0.000). CONCLUSIONS: Baseline elevated creatinine is associated with a markedly increased risk of 30-day death, death during hospitalization and mortality at one year in patients suffering from acute myocardial infarction and may be an independent risk factor of prognosis of acute myocardial infarction.

Efficacy of recombinant tissue-type plasminogen activator thrombolysis and primary coronary stenting after acute myocardial infarction.

OBJECTIVE: To compare the efficacy of low dose recombinant tissue-type plasminogen activator (rt-PA) thrombolysis with primary coronary stenting after acute myocardial infarction. METHODS: Of 261 patients with first acute myocardial infarction, 131 were given low dose rt-PA intravenous thrombolysis, and 130 primary coronary stenting. RESULTS: The age, time from onset of chest pain to hospital presentation and infarct location between these two groups were comparable. The patency rate of the infarct-related artery (IRA) in patients in the thrombolysis group was significantly lower than that of patients in the primary stenting group (P < 0.001). Recurrent myocardial infarction, and selective coronary stenting of patients with thrombolytic therapy were higher than that of patients in the primary stenting group (7.6% vs 1.5%, P < 0.05; 20.6% vs 0, P < 0.001, respectively). Left ventricular ejection fraction (LVEF) in patients in the thrombolysis group was lower than that of the stent group (55.6% +/- 13.4% vs 65.8% +/- 9.2%, P < 0.001). Total hospitalization time of the thrombolysis group was longer than that of the stent group (16 +/- 7 d vs 11 +/- 4 d, P < 0.001). Mortality in the thrombolysis group was higher than that of the stent group, but this difference was not significant (6.1% vs 3.1%, P > 0.05). CONCLUSION: Comparing with low dose rt-PA thrombolytic therapy after acute myocardial infarction, primary coronary stenting has a higher patency rate of the IRA, better cardiac function and shorter hospitalization time.