This study aimed to determine whether cyclo-oxygenase-1 (COX-1) mediates dilatation of mouse arteries via synthesis of prostacyclin (PGI 2 ) and, if so, how PGI 2 (IP) receptors contribute and whether thromboxane prostanoid (TP) receptors are implicated in the process. Mesenteric arteries were isolated from wild-type mice or mice with COX-1 deficiency (COX-1 −/− ). The vasomotor reaction to the COX substrate arachidonic acid (AA) was determined with isometric force measurement, while the in vitro production or the plasma level of the PGI 2 metabolite 6-keto-PGF 1α was analysed with high-performance liquid chromatography-mass spectroscopy or enzyme immunoassay, respectively. Results showed that AA, which evoked endotheliumdependent 6-keto-PGF 1α production, elicited relaxation that was inhibited or enhanced by antagonizing IP or TP receptors, respectively. Also, IP receptor blockade resulted in contraction in response to AA (following NO synthase inhibition), which was prevented by a concomitant TP receptor antagonism. Meanwhile, COX-1 −/− or COX-1 inhibition abolished the in vitro 6-keto-PGF 1α production and reduced the relaxation or contraction observed with AA. Real-time PCR showed that whereas TP receptor mRNAs were detected at similar levels, IP receptor mRNAs were present at higher levels in the branches than in the main stem of the mesenteric artery. In addition, antagonizing the IP receptors enhanced the contraction evoked by PGI 2 in the carotid artery. Also, we noted that COX-1 −/− mice had a reduced basal plasma 6-keto-PGF 1α level. These results demonstrate an explicit vasodilator role for COX-1-mediated endothelial PGI 2 synthesis and suggest that the functionally opposing IP and TP receptors concomitantly mediate the vasomotor reaction to PGI 2 , with the dilator activity of IP receptors being compromised by the vasoconstrictor effect of TP receptors and vice versa.
BackgroundAtherosclerosis is a systemic, lipid-driven immune-inflammatory disease.MethodsWe retrospectively reviewed institutional electronic medical records to seek chest pain patients who were suspicious of acute coronary syndrome (ACS) between January 2011 and December 2013. All the patients were identified by undergoing coronary angiography. On admission white blood cell and its subtypes were measured as part of the automated complete blood count and fasting venous blood samples were obtained and analyzed for lipids profiles used automated analysis.ResultsA total of 376 consecutive patients with ACS were investigated. In the same period, 378 patients admitted with chest pain suspicious of ACS were also included in this study for control. Blood glucose, serum creatinine, white blood cell, neutrophil and monocyte were insignificantly higher in the ACS group. ACS group had higher total cholesterol and lower high density lipid-cholesterol. However, triglyceride and low density lipid-cholesterol were similar between ACS and control groups. Atherogenic index of plasma (AIP) was significantly higher in ACS group compared to control group (p = 0.029). Similarly, ACS group had higher neutrophil–lymphocyte ratio (NLR) than those in control group. In the subgroups, the NLR were significantly higher in the STEMI group (p < 0.001). However, AIP were similar between the three subgroups (p = 0.748).ConclusionsOur data firstly investigated the lipid-driven inflammatory state in acute coronary syndrome through two easily feasible parameters. There suggest that there are higher AIP and NLR in the ACS patients. Moreover, ACS subgroups are all lipid-driven states, but inflammation levels are different in the entity ACS subgroups.
ObjectiveThe objectives of this study were to forecast epidemic peaks of typhoid and paratyphoid fever in China using the grey disaster model, to evaluate its feasibility of predicting the epidemic tendency of notifiable diseases.MethodsAccording to epidemiological features, the GM(1,1) model and DGM model were used to build the grey disaster model based on the incidence data of typhoid and paratyphoid fever collected from the China Health Statistical Yearbook. Model fitting accuracy test was used to evaluate the performance of these two models. Then, the next catastrophe date was predicted by the better model.ResultsThe simulation results showed that DGM model was better than GM(1,1) model in our data set. Using the DGM model, we predicted the next epidemic peak time will occur between 2023 to 2025.ConclusionThe grey disaster model can predict the typhoid and paratyphoid fever epidemic time precisely, which may provide valuable information for disease prevention and control.
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