Integrative analysis from multi-center studies identifies a weighted gene co-expression network analysis-based Tregs signature in ovarian cancer.

Ovarian cancer (OC) is a malignancy associated with poor prognosis and has been linked to regulatory T cells (Tregs) in the immune microenvironment. Nevertheless, the association between Tregs-related genes (TRGs) and OC prognosis remains incompletely understood. The xCell algorithm was used to analyze Tregs scores across multiple cohorts. Weighted gene co-expression network analysis (WGCNA) was utilized to identify potential TRGs and molecular subtypes. Furthermore, we used nine machine learning algorithms to create risk models with prognostic indicators for patients. Reverse transcription-quantitative polymerase chain reaction and immunofluorescence staining were used to demonstrate the immunosuppressive ability of Tregs and the expression of key TRGs in clinical samples. Our study found that higher Tregs scores were significantly correlated with poorer overall survival. Recurrent patients exhibited increased Tregs infiltration and reduced CD8+ T cell. Moreover, molecular subtyping using seven key TRGs revealed that subtype B exhibited higher enrichment of multiple oncogenic pathways and had a worse prognosis. Notably, subtype B exhibited high Tregs levels, suggesting immune suppression. In addition, we validated machine learning-derived prognostic models across multiple platform cohorts to better distinguish patient survival and predict immunotherapy efficacy. Finally, the differential expression of key TRGs was validated using clinical samples. Our study provides novel insights into the role of Tregs in the immune microenvironment of OC. We identified potential therapeutic targets derived from Tregs (CD24, FHL2, GPM6A, HOXD8, NAP1L5, REN, and TOX3) for personalized treatment and created a machining learning-based prognostic model for OC patients, which could be useful in clinical practice.

Elevated serum neuropeptide Y levels are associated with carotid plaque formation in Chinese adults: a cross-sectional study.

BACKGROUND: Carotid plaque (CP) formation is an important consequence of atherosclerosis and leads to significant complications. Levels of neuropeptide Y (NPY), which is a sympathetic neurotransmitter, are elevated in cardiovascular diseases. It also has important roles in inflammatory conditions. This study aimed to explore the relationship between serum NPY and CP and to study further the influence of NPY and inflammatory factors on CP. METHODS: This cross-sectional study was conducted among 300 adults who underwent a health examination at the Second Affiliated Hospital of Fujian Medical University in Fujian Province, of whom 177 were finally enrolled. The participants were divided into the CP (n = 120) and non-CP (NCP) or control (n = 57) groups according to the results of carotid artery color Doppler ultrasound. The CP group was further classified into stable plaque (SP, n = 80) and vulnerable plaque (VP, n = 40) groups based on plaque characteristics. Serum NPY and pro-inflammatory cytokine tumor necrosis factor-α (TNF-α) levels were examined. Univariate and correlation analyses were used to evaluate the correlation between serum NPY levels, pro-inflammatory cytokines, and the CP phenotype. RESULTS: The serum NPY and TNF-α levels of patients in the CP group were significantly higher than those in individuals from the NCP group [ (177.30 ± 43.29) pg.mL- 1 vs. (121.53 ± 40.16)pg.mL- 1, P < 0.001; (41.94 ± 14.19) pg.mL- 1 vs.(33.54 ± 13.37)pg.mL- 1, P = 0.003]. The serum NPY levels of the patients in the VP group were significantly higher than those in patients from the SP group [(191.67 ± 39.87)ng.L- 1 vs.(170.12 ± 43.37)ng.L- 1, P = 0.01, P < 0.05]. Serum TNF-α and NPY levels were positively correlated among patients from the CP group (r = 0.184, P = 0.044). The binary logistic regression analysis showed that serum NPY and TNF-α were independent influencing factors of CP [(OR = 1.029, P < 0.001);(OR = 1.030, P = 0.023)]. The area under the ROC curve of NPY predicting the CP showed statistical significance at a value of 0.819. CONCLUSION: Together, elevated serum NPY levels seem to be associated with the occurrence of coronary atherosclerosis in Chinese adults.

Learning curve of robotic distal and total gastrectomy.

BACKGROUND: This study aims to assess the learning curve of robotic distal gastrectomy (RDG) and robotic total gastrectomy (RTG) for gastric cancer. METHODS: Data on consecutive patients who underwent robotic gastrectomy for gastric cancer by five surgeons between March 2010 and August 2019 at two high-volume institutions were collected. The learning curve was determined based on the analyses of operation time and postoperative complications within 30 days. Cumulative sum analysis (CUSUM) and risk-adjusted-CUSUM (RA-CUSUM) were applied to identify the turning points (TPs). RESULTS: A total of 899 consecutive patients were included. The mean number of patients needed to overcome the learning curve for operation time of RDG and RTG were 22 and 20, respectively. The number of patients needed to overcome the learning curve for postoperative complications after RDG and RTG were 23 and 18, respectively. The surgical outcomes in the post-TP group were better than in the pre-TP group and improved as surgeons' experience increased. Also, increased case numbers in RDG promoted the RTG learning process. CONCLUSION: The present study demonstrated a substantial influence of surgical cumulative volume on improved surgical outcomes in robotic gastrectomy. Increased experience in RDG may help surgeons to achieve proficiency faster in RTG.

Morbidity and short-term surgical outcomes of robotic versus laparoscopic distal gastrectomy for gastric cancer: a large cohort study.

BACKGROUND: Robotic distal gastrectomy (RDG) has been increasingly used for the treatment of gastric cancer in recent year. However, whether RDG could reduce the morbidity when compared to laparoscopic distal gastrectomy (LDG) remains controversial. This study aimed to compare the morbidity and short-term surgical outcomes of RDG and LDG for gastric cancer and identify the related risk factors. METHODS: Between March 2010 and August 2019, consecutive patients undergoing RDG or LDG (519 and 957 patients, respectively) at our institution were included in this study. Postoperative complications were stratified according to the Clavien-Dindo (C-D) classification. We performed one-to-one propensity score matching (PSM) analysis, and evaluated postoperative morbidity and short-term surgical outcomes in PSM 1032 patients undergoing RDG or LDG. RESULTS: After PSM, the two groups were well-balanced. The mean blood loss of the RDG group was about 27 mL less than that of the LDG group (112.1 vs 139.0 mL, P < 0.001). The RDG group had more retrieved lymph nodes than that in the LDG group (32.7 v 30.2, P < 0.001). The RDG group showed a similar overall (9.9% vs 10.7%, P = 0.682), severe (2.7% vs 3.7%, P = 0.376), local (5.6% vs 5.2%, P = 0.783), and systemic complication rates (5.4% vs 6.0%, P = 0.688). There were no significant differences in mortality between the two groups (RDG 0% vs LDG 0.2%, P = 1.000). Subgroup analyses showed no significant differences in most stratified parameters. Age > 65 years and ASA III were identified as two major risk factors for complications. CONCLUSION: RDG could be a safe and feasible in treating gastric cancer compared to LDG. However, we did not observe significant reduction in postoperative complications of RDG compared with LDG, although the use of robotic system is assumed to provide a technically superior operative environment.

A new species of Metaurus Stål, 1866 (Hemiptera, Fulgoromorpha, Dictyopharidae), supplemented with mitogenome data from China.

A new planthopper species, Metaurusmohanensis Zheng & Chen, sp. nov., is described and illustrated from Yunnan, China. A key to differentiate species within the genus Metaurus is provided. The geographical distribution of Metaurus species and mitochondrial genome data of the newly described species are also included.

A novel radiomics-based technique for identifying vulnerable coronary plaques: a follow-up study.

BACKGROUND: Previous reports have suggested that coronary computed tomography angiography (CCTA)-based radiomics analysis is a potentially helpful tool for assessing vulnerable plaques. We aimed to investigate whether coronary radiomic analysis of CCTA images could identify vulnerable plaques in patients with stable angina pectoris. METHODS: This retrospective study included patients initially diagnosed with stable angina pectoris. Patients were randomly divided into either the training or test dataset at an 8 : 2 ratio. Radiomics features were extracted from CCTA images. Radiomics models for predicting vulnerable plaques were developed using the support vector machine (SVM) algorithm. The model performance was assessed using the area under the curve (AUC); the accuracy, sensitivity, and specificity were calculated to compare the diagnostic performance using the two cohorts. RESULTS: A total of 158 patients were included in the analysis. The SVM radiomics model performed well in predicting vulnerable plaques, with AUC values of 0.977 and 0.875 for the training and test cohorts, respectively. With optimal cutoff values, the radiomics model showed accuracies of 0.91 and 0.882 in the training and test cohorts, respectively. CONCLUSION: Although further larger population studies are necessary, this novel CCTA radiomics model may identify vulnerable plaques in patients with stable angina pectoris.

[Role of the IGF-1/PI3K pathway and the molecular mechanism of Fuzhenghuayu therapy in a spontaneous recovery rat model of liver fibrosis].

OBJECTIVE: To determine the role of IGF-1/PI3K pathway and investigate the molecular mechanism of Fuzhenghuayu (FZHY) therapy in a spontaneous recovery rat model of liver fibrosis. METHODS: The liver fibrosis model was induced in male Wistar rats by administering 8 weeks of twice weekly CCL4 intraperitoneal injections without (untreated model) or with once daily FZHY (treated model). Normal, untreated rats served as the control group. At weeks 4, 6 and 8 (fibrosis) and 10, 12 and 14 (spontaneous recovery) after modeling initiation, effects on protein (a-SMA, IGF-1, PI3K) and mRNA (IGF-1, PI3K) expression levels were evaluated by immunohistochemistry and RT-PCR, respectively. Serum markers of liver function (alanine aminotransferase (ALT) and aspartate aminotransferase (AST)) and liver cell damage (alkaline hydrolysis, HYP) were measured. Histology was performed to assess the degree of inflammation and fibrosis (Ishak scoring system). RESULTS: In the untreated model group, progression of liver fibrosis (weeks 4, 6 and 8) was accompanied by gradual increases in inflammation, necrosis, serum ALT and AST, and hepatic expression of a-SMA protein and IGF-1 and PI3K protein and mRNA; however, during the spontaneous recovery period (weeks 10, 12 and 14) the IGF-1 and PI3K protein and mRNA levels rapidly decreased and the HYP level, Ishak score, and a-SMA hepatic expression also decreased. The FZHY-treated model group showed significantly lower fibrosis-related up-regulation of IGF-1 and PI3K protein and mRNA expression, HYP level, Ishak score, and a-SMA hepatic expression at each time point (vs. untreated model group). CONCLUSION: The IGF-1/PI3K pathway may contribute to progression of liver fibrosis. The mechanism by which FZHY prevents liver fibrosis in a rat model may involve blocking of the IGF/PI3K pathway and inhibiting HSC activation.

Research progress on the role of exosomes in obstructive sleep apnea-hypopnea syndrome-related atherosclerosis.

Cardiovascular disease (CVD) is a leading cause of mortality worldwide. Atherosclerosis, a multifactorial disease with complicated pathogenesis, is the main cause of CVD, underlying several major adverse cardiovascular events. Obesity is the main cause of obstructive sleep apnea (OSA) and a significant risk for atherosclerosis. OSA is an independent risk factor for CVD. Recent research has focused on understanding the underlying molecular mechanisms by which OSA influences atherosclerosis pathogenesis. The role of exosomes in this process has attracted considerable attention. Exosomes are a type of extracellular vesicles (EV) that are released from many cells (both healthy and diseased) and mediate cell-to-cell communication by transporting microRNAs (miRNAs), proteins, mRNAs, DNA, or lipids to target cells, thereby modulating the functions of target cells and tissues. Intermittent hypoxia in OSA alters the exosomal carrier in circulation and promotes the permeability and dysfunction of endothelial cells, which have been associated with the pathogenesis of atherosclerosis. This review discusses the potential roles of exosomes and exosome-derived molecules in the development and progression of OSA-related atherosclerosis. Additionally, we explore the possible mechanisms underlying OSA-related atherosclerosis and provide new insights for the development of novel exosome-based therapeutics for OSA-related atherosclerosis and CVD.

Stem cell-derived exosomes in the treatment of acute myocardial infarction in preclinical animal models: a meta-analysis of randomized controlled trials.

BACKGROUND: Exosomes (EXOs) derived from stem cells have become a potential new treatment for acute myocardial infarction (AMI). However, their impact is still not fully understood. Therefore, we performed this meta-analysis to systematically review the efficacy of EXOs on AMI in preclinical animal models. METHODS: We searched PubMed, EMBASE, and the Web of Science from September 1, 1980 to September 1, 2021, to retrieve the studies reporting the therapeutic effects of EXOs on AMI animal models. Secondary endpoints include the fractional shortening (FS), infarct size (IS), fibrosis area (FA), the TNF-α, IL-6 and IL-10 levels, the apoptosis rate and the number of autophagic vesicles. Two authors independently screened the articles based on inclusion and exclusion criteria. All statistical analyses were conducted using Stata14.0. RESULTS: Ten studies satisfied the inclusion criteria. Pooled analyses demonstrated that the levels of LVEF (WMD = 3.67%; 95% CI 2.28-5.07%; P = 0.000), FS (WMD = 3.69%; 95% CI 2.06-5.33%; P = 0.000), IS (WMD = -4.52%, 95% CI - 7.14 to - 1.9%; P = 0.001), and FA (WMD = -7.04%, 95% CI - 8.74 to - 5.34%; P = 0.000), TNF-α (WMD = -3.09, 95% CI - 5.47 to - 0.72; P = 0.011), TL-6 (WMD = -6.34, 95% CI - 11.2 to - 1.49; P < 0.01), TL-10 (WMD = 6.37, 95% CI 1.53-11.21; P = 0.01), the apoptosis rate (WMD = -8.23, 95% CI - 15.29 to - 1.17; P = 0.000), and the number of autophagic vesicles (WMD = -4.52, 95% CI - 7.43 to - 1.62; P = 0.000). Subgroup analysis showed that the EXOs were derived from HMSCs. Subgroup analysis showed that the EXOs derived from HMSCs, and that exosome therapy immediately after myocardial infarction can better improve the LVEF. CONCLUSIONS: EXOs therapy has the potential to improve cardiac function, fibrogenesis, and inflammatory response, as well as reducing cell apoptosis and autophagy in preclinical AMI animal models. This can inform future human clinical trials of EXOs.

Updated Role of Neuropeptide Y in Nicotine-Induced Endothelial Dysfunction and Atherosclerosis.

Cardiovascular disease is the leading cause of death worldwide. Endothelial dysfunction of the arterial vasculature plays a pivotal role in cardiovascular pathogenesis. Nicotine-induced endothelial dysfunction substantially contributes to the development of arteriosclerotic cardiovascular disease. Nicotine promotes oxidative inflammation, thrombosis, pathological angiogenesis, and vasoconstriction, and induces insulin resistance. However, the exact mechanism through which nicotine induces endothelial dysfunction remains unclear. Neuropeptide Y (NPY) is widely distributed in the central nervous system and peripheral tissues, and it participates in the pathogenesis of atherosclerosis by regulating vasoconstriction, energy metabolism, local plaque inflammatory response, activation and aggregation of platelets, and stress and anxiety-related emotion. Nicotine can increase the expression of NPY, suggesting that NPY is involved in nicotine-induced endothelial dysfunction. Herein, we present an updated review of the possible mechanisms of nicotine-induced atherosclerosis, with a focus on endothelial cell dysfunction associated with nicotine and NPY.

Clinical assessment of prophylactic chemotherapy in treating with hydatidiform mole: A protocol for systematic review and meta-analysis.

BACKGROUND: Hydatidiform mole (HM) is more common as molar pregnancy. It is a disease classified under the category of gestational trophoblastic diseases, which could metastasize after originating in the placenta. A majority of females suffering from molar pregnancies are curable by evacuating retained products of conception and the patient's fertility is preserved. In some cases, the growth perseveres and leads to gestational trophoblastic neoplasia, which is an extremely malicious condition that needs chemo-based treatment. There is a possibility to lessen the risk of gestational trophoblastic disease in females with HM through the administration of prophylactic chemo. Yet, there is controversy regarding prophylactic chemotherapy administered pre-or-post removal of HM to curtail the malignant sequelae. Therefore, we will conduct this research to assess both the efficacy as well as security of using prophylactic chemotherapy to treat HM. METHODS: In the preliminary review, the authors will search for randomized controlled trials involving prophylactic chemotherapy to treat HM. The literature search is carried out in the following electronic databases from their inception to May 2021: Chinese National Knowledge Infrastructure, Chinese BioMedical Literature, and WanFang database are the three Chinese language databases. Web of Science, PubMed, Cochrane Library, and EMBASE are the four English language databases. The authors will also perform a manual search through the bibliographies in related literature to find extra articles and ongoing studies. Two independent authors will assess the literature according to an inclusion criteria, use a specialized data collection table to extract data, and use the Cochrane 'Risk of bias' tool for evaluating any possible bias risk in the selected articles. Data synthesis and statistical operations are completed with the RevMan software (v. 5.3). RESULTS: The present systematic analysis provides a rationalized synthesis of existing evidence related to the use of prophylactic chemotherapy in the treatment of HM. CONCLUSION: Our findings will summarize the current evidences for prophylactic chemotherapy in the treatment of HM. ETHICS AND DISSEMINATION: An ethics approval is nonrequired because pre published results will be used. REGISTRATION NUMBER: DOI 10.17605/OSF.IO/6QV52 (https://osf.io/6qv52/).

Two new species of the genus Saigona Matsumura (Hemiptera, Fulgoromorpha, Dictyopharidae) from China.

Two new species of the genus Saigona Matsumura, 1910, S.baiseensis Zheng & Chen sp. nov. and S.maculata Zheng & Chen sp. nov., from China (Guanxi) are described and illustrated. A revised identification key to the 16 species of Saigona is provided. 15 species of the genus are known from China only.

Neuropeptide Y: An Update on the Mechanism Underlying Chronic Intermittent Hypoxia-Induced Endothelial Dysfunction.

Endothelial dysfunction (ED) is a core pathophysiological process. The abnormal response of vascular endothelial (VE) cells to risk factors can lead to systemic consequences. ED caused by intermittent hypoxia (IH) has also been recognized. Neuropeptide Y (NPY) is an important peripheral neurotransmitter that binds to different receptors on endothelial cells, thereby causing ED. Additionally, hypoxia can induce the release of peripheral NPY; however, the involvement of NPY and its receptor in IH-induced ED has not been determined. This review explains the definition of chronic IH and VE function, including the relationship between ED and chronic IH-related vascular diseases. The results showed that that the effect of IH on VE injury is mediated by the VE-barrier structure and endothelial cell dysfunction. These findings offer new ideas for the prevention and treatment of obstructive sleep apnea syndrome and its complications.

Complete mitochondrial genome of the planthopper Orthopagus splendens (Germar, 1830) (Hemiptera: Fulgoromorpha: Dictyopharidae).

The first complete mitochondrial genome of a dictyopharid planthopper, Orthopagus splendens (Germar, 1830) (Hemiptera: Fulgoroidea: Dictyopharidae) is sequenced. The 15,349 bp long complete mitogenome contains 13 protein-coding genes (PCGs), 22 tRNA genes, two rRNA genes, and 1 A + T-rich region with an arrangement identical to that observed in most insect mitogenomes (GenBankNo. MW441850). All PCGs start with ATN, and end with TAN or single T (nad1, nad5, and atp6). A phylogenetic analysis places O. splendens as sister to Fulgoridae confirming a sister relationship between Dictyopharidae and Fulgoridae.

Exploring a New Adaptive Routing Based on the Dijkstra Algorithm in Optical Networks-on-Chip.

The photoelectric hybrid network has been proposed to achieve the ultrahigh bandwidth, lower delay, and less power consumption for chip multiprocessor (CMP) systems. However, a large number of optical elements used in optical networks-on-chip (ONoCs) generate high transmission loss which will influence network performance severely and increase power consumption. In this paper, the Dijkstra algorithm is adopted to realize adaptive routing with minimum transmission loss of link and reduce the output power of the link transmitter in mesh-based ONoCs. The numerical simulation results demonstrate that the transmission loss of a link in optimized power control based on the Dijkstra algorithm could be maximally reduced compared with traditional power control based on the dimensional routing algorithm. Additionally, it has a greater advantage in saving the average output power of optical transmitter compared to the adaptive power control in previous studies, while the network size expands. With the aid of simulation software OPNET, the network performance simulations in an optimized network revealed that the end-to-end (ETE) latency and throughput are not vastly reduced in regard to a traditional network. Hence, the optimized power control proposed in this paper can greatly reduce the power consumption of s network without having a big impact on network performance.

[Study on the chemical constituents of Cudrania tricuspidata].

OBJECTIVE: To study on the chemical constituents of Cudrania tricuspidata. METHODS: The chemical constituents were separated by means of silica gel and Sephadex LH-20 chromatography, and their structures were identified by spectra of 1H-NMR, 13 C-NMR. RESULTS: Seven compounds were isolated and identified as Quercetin (I),5,7,4'-trihydroxyldihydroisoflavone (II), (13alpha, 14beta, 17alpha, 20R)-Lanosta-7, 24-diene-3beta-ol (III), (13alpha, 14beta,17alpha, 20R)-Lanosta-7,24-diene-3beta-0-acetate (IV), Taxifolin (V), Dihydromorin (VI), Cycloartocarpin(VII). CONCLUSION: Compounds III and IV are isolated from the genus for the first time.

A Novel Algorithm for Routing Paths Selection in Mesh-Based Optical Networks-on-Chips.

Optical networks-on-chips (ONoCs) is an effective and extensible on-chip communication technology, which has the characteristics of high bandwidth, low consumption, and low delay. In the design process of ONoCs, power loss is an important factor for limiting the scalability of ONoCs. Additionally, the optical signal-to-noise ratio (OSNR) is an index to measure the quality of ONoCs. Nowadays, the routing algorithm commonly used in ONoCs is the dimension-order routing algorithm, but the routing paths selected by the algorithm have high power loss and crosstalk noise. In this paper, we propose a 5×5 all-pass optical router model for two-dimensional (2-D) mesh-based ONoCs. Based on the general optical router model and the calculation models of power loss and crosstalk noise, a novel algorithm is proposed in ordder to select the routing paths with the minimum power loss. At the same time, it can ensure that the routing paths have the approximately optimal OSNR. Finally, we employ the Cygnus optical router to verify the proposed routing algorithm. The results show that the algorithm can effectively reduce the power loss and improve the OSNR in the case of network sizes of 5×5 and 6×6. With the increase of the optical network scale, the algorithm can perform better in reducing the power loss and raising the OSNR.

G-5555 synergized miR-485-5p to alleviate cisplatin resistance in ovarian cancer cells via Pi3k/Akt signaling pathway.

The present study was meant for the discovery of the underlying functions of miR-485-5p in ovarian cancer concerning cisplatin resistance in vitro. RT-qPCR assessed the miR-485-5p expression in ovarian cancer cell lines, normal cells and cisplatin-resistant Cell line OVCA433-CR. After OVCA433-CR treated with 0,3,5umol/L cisplatin, miR-485-5p expressions were determined. MTT observed the cell cytotoxicity in OVCA433-CR after regulation of miR-485-5p. Targets can predicted the putative binding between miR-485-5p and PAK1 and Luciferase Assay verified this. RT-qPCR decided the inhibitory effect in between. MTT tested the cytotoxicity in different combinations of miR-485-5p and PAK1. Western Blot tested the phosphorylation of Pi3k and Akt in response to miR-485-5p and PAK1 interplay. We evaluated the role of Pi3k/Akt signaling in regulation of miR-485-5p and cisplatin resistance with Wortmannin. miR-485-5p was lower expressed in ovarian cancer cells than normal ones and even lower in OVCA433-CR than OVCA433. As the cisplatin concerntration increased, miR-485-5p decreased. miR-485-5p mimics induced lower cisplatin resistance while miR-485-5p inhibitor caused higher resistance. PAK1 targeted miR-485-5p and inhibited miR-485-5p. PAK1 inhibitor helped to lower the resistance to cisplatin caused by miR-485-5p upregulation. miR-485-5p mimics silenced Pi3k/Akt signaling and PAK1 inhibitor aggravated the silencing. Inhibition of Pi3k/Akt signaling increased miR-485-5p, thereby decreasing the cisplatin-resistance in OVCA433-CR. miR-485-5p decreased cisplatin resistance in ovarian cancer cells via Pi3k/Akt signaling, suggesting that miR-485-5p upregulation might alleviate the cisplatin resistance in ovarian patients.

Sensitive determination of norepinephrine, synephrine, and isoproterenol by capillary electrophoresis with indirect electrochemiluminescence detection.

A new and sensitive method for the determination of norepinephrine (NE), synephrine, and isoproterenol was developed by CE separation and indirect electrochemiluminescence detection (ECL) based on their quenching effects on the tris(2,2'-bipyridyl)-ruthenium(II)/tripropylamine (TPA) system. The conditions for CE separation and ECL detection were investigated in detail. Under the optimum conditions, the three analytes were well separated within 9 min. The LODs (S/N = 3) in standard solution are 2.6 x 10(-8) mol/L for NE, 6.6 x 10(-9) mol/L for synephrine and 8.4 x 10(-8) mol/L for isoproterenol, respectively. The precisions of intraday and interday are less than 4.4 and 6.1%, respectively. The LOQs (S/N = 10) in real human urine samples are 2.6 x 10(-7) mol/L for NE, 8.8 x 10(-8 ) mol/L for synephrine, and 8.8 x 10(-7) mol/L for isoproterenol, respectively. The applicability of the proposed method was illustrated in the determination of 20 human urine samples from diabetic patients and healthy persons. The results obtained indicated that the level of NE in patients (mean value 0.41 micromol/L) was higher than that in healthy persons (mean value 0.24 micromol/L).

Sensitive detection of tumor marker CA15-3 in human serum by capillary electrophoretic immunoassay with chemiluminescence detection.

A new and sensitive non-competitive immunoassay (IA) for tumor marker carbohydrate antigen 15-3 (CA15-3) by CE coupling with ECL detection has been developed. This method is based on luminol-H(2)O(2 )reaction catalyzed by horseradish peroxidase (HRP). The optimum CE separation and CL detection conditions were investigated. After the non-competitive immunoreaction, the free HRP-labeled CA15-3 antibody (Ab*) and the bound Ab*-antigen (Ab*-Ag) complex were separated in a separation capillary and then catalyzed the CL reaction of luminol and H(2)O(2 )in a reaction capillary following the separation capillary. The calibration curve based on the peak areas of Ab*-Ag complex plotted against the concentrations of CA15-3 is in the range of 0-250 U/mL with a correlation coefficient of 0.9983 and the detection limit is 0.035 U/mL (S/N = 3). The response for five consecutive injections of 125 U/mL CA15-3 resulted in RSDs of 0.83% and 3.1% for the migration time and the peak area, respectively. The method was successfully used for the quantification of CA15-3 in human sera obtained from healthy persons and from patients with breast cancer.