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The appearance of real correlation function for spontaneous emission is explicitly presented. The non-Markovian correction is calculated directly by the integro-differential equation. The results are compared with the previous results obtained by stochastic quantum trajectory analysis. Obvious difference appears for smaller γA/ω0. The present analysis is believed more reliable. [Copyright &y& Elsevier]

Abstract: In this work we aimed to observe (1) the changes in adrenomedullin (AM) and its receptor system – calcitonin receptor-like receptor (CRLR) and receptor activity modifying proteins (RAMPs) – in myocardial ischemic injury and (2) the response of injuried myocardia to AM and the phosphorylation of Akt to illustrate the protective mechanism of AM in ischemic myocardia. Male SD rats were subcutaneously injected with isoproterenol (ISO) to induce myocardial ischemia. The mRNA levels of AM, CRLR, RAMP1, RAMP2 and RAMP3 were determined by RT-PCR. Protein levels of Akt, phosphor-Akt, CRLR, RAMP1, RAMP2 and RAMP3 were assayed by Western blot. Results showed that, compared with that of the controls, ISO-treated rats showed lower cardiac function and myocardial injury. The mRNA relative amount of AM, CRLR, RAMP1, RAMP2 and RAMP3 in the myocardia of ISO-treated rats was increased. The elevated mRNA levels of CRLR, RAMP1, RAMP2 and RAMP3 were positively correlated with AM content in injured myocardia. The protein levels of CRLR, RAMP1, RAMP2 and RAMP3 in injured myocardia were increased compared with that of control myocardia. AM-stimulated cAMP generation in myocardia was elevated in the ISO group, and was antagonized by AM22–52 and CGRP8–37. Western blot analyses revealed that AM significantly enhanced Akt phosphorylation in injured myocardia, which was blocked by pretreatment with AM22–52 or CGRP8–37. Ischemia-injured myocardia hyper-expressed AM and its receptors – CRLR, RAMP1, RAMP2 and RAMP3 – and the response of ischemic myocardia to AM was potentiated, and the level of Akt phosphorylation was also increased, which suggests that changes in cardiac AM/AM receptor might play an important role in the pathogenesis of myocardial ischemic injury. [Copyright &y& Elsevier]

Objectives: Healing of gastric endoscopic submucosal dissection (ESD)-induced ulcer is critical for patient recovery. During ESD treatment, submucosal incisions are made with an electrosurgical knife to accomplish en bloc resections of superficial lesions. Nevertheless, excess electrocoagulation may decrease the blood supply of ESD-induced ulcer and delay the ulcer healing. The aim of this retrospective study was to evaluate the effectiveness of conservative electrocoagulation followed by porcine fibrin sealant (FS) as a wound microvessels-protective hemostatic technique in promoting the healing of ESD-induced ulcer.Methods: A total of 332 patients with early gastric cancer (EGCs), or gastric precancerous lesion and gastric adenoma were retrospectively analyzed. Propensity score matching was used to compensate for the differences in age, gender, tumor location, resected specimen area, and pathology. One-month ulcer healing rates and delayed bleeding were compared between two matched groups (combined hemostats group and electrocautery group).Results: A total of 115 matched pairs were created after propensity score matching. There was no difference in tumor location, specimen surface area, tumor differentiation and invasion depth between groups. The completed healing rate 1 month after ESD was 44.3% in combined hemostats group and 30.4% in electrocautery group (P = 0.004). There was no difference in delayed massive bleeding rate between two groups (P = 0.300). In addition, based on the multivariate regression analysis for ulcer healing rate, the use of FS (OR, 0.348, 95% CI 0.196 - 0.617, P = 0.000) and larger specimen size (OR, 2.640, 95% CI 2.015-3.458, P = 0.000) were associated with nonhealing ulcer 1 month after ESD.Conclusion: Applying conservative electrocoagulation followed by porcine FS as a wound microvessels-protective hemostatic technique can promote ESD-induced ulcer healing without increasing delayed bleeding. [ABSTRACT FROM AUTHOR]

Abstract: Adrenomedullin (ADM) is a multifunctional peptide regulating cardiovascular homeostasis. We studied the role of ADM in the pathogenesis of atherosclerosis by investigating changes in ADM and its receptors – calcitonin receptor-like receptor (CRLR) and receptor activity-modifying proteins (RAMPs) – in aorta of apoE−/− mice and the effect of exogenous ADM administration. ApoE−/− mice were fed an atherogenic diet for 4 weeks, and apoE−/−+ADM mice were additionally given subcutaneous injections of ADM, 300ng/kg/h, for 4 weeks. ApoE−/− mice fed an atherogenic diet showed hyperlipidemia, a large plaque area and increased vessel wall thickness. The mRNA expression and protein level of ADM/ADM receptors were increased in the aorta, compared with C57BL/6J mice. The elevated mRNA level of CRLR and RAMPs correlated positively with ADM mRNA level. Radioimmunoassay revealed a higher plasma and aorta ADM content, by 61.6% and 285% (both P <0.01), respectively, in apoE−/− mice than that in C57BL/6J mice. Exogenous ADM significantly ameliorated dyslipidemia in apoE−/− mice. ADM-treated mice showed fewer aortic plaques, decreased plaque area, by 76% (P <0.01), and reduced ratio of plaque area to luminal area, by 65% (P <0.01), and ultrasonography revealed significantly reduced intima-media thickness of the ascending branch and abdominal aorta. The results suggest that atherosclerotic apoE−/− mice fed an atherogenic diet showed upregulated endogenous ADM and its receptors, and exogenous ADM treatment ameliorated the dyslipidemia and vascular atherosclerotic lesions. ADM/ADM receptors might be an important protective system against atherosclerosis and could become a new target of prevention and therapy for atherosclerosis. [Copyright &y& Elsevier]