Macdonaldsalomonsen7800

We sought to distinguish area at risk from salvage myocardial zone and to predict left ventricle functional recovery in the convalescent stage by Texture Analysis (TA) of T2-Mapping.

One hundred and six patients diagnosed with AMI and treated with percutaneous coronary intervention (PCI) underwent acute cardiac magnetic resonance imaging (CMR) and 45 of whom had a subsequent CMR scan following recovery. Cine imaging, T2-Mapping, T2-weighted STIR imaging, and LGE imaging were performed. In the texture analysis, regions of interest (infarcted, salvageable, and remote) were drawn by two blinded, independent readers.

Seven independent texture features on T2-Mapping were selected Perc.50%, S(2,2)InvDfMom, S(2.-2)AngScMom, S(4,0)Entropy, 45dgrLngREmph, 45dgr_Fraction and 135dr_GLevNonU. Among them, the average value of 135dr_GLevNonU in the infarct zone, AAR zone, and the remote zone was 61.96±26.03, 31.811±18.933 and 99.839±26.231, respectively. Additionally, 135dr_GLevNonU provided the highest area under the curve (AUC) from the receiver operating characteristic curve (ROC curve) for distinguishing AAR from the infarct zone in each subgroup (all patients, patients with MVO and)were 0.845 ± 0.052 0.855 ± 0.083 and 0.845 ± 0.066, respectively, and were more promise than T2-Mapping mean (p<0.001). The AUC for differentiating AAR from the remote zone is 0.942±0.041. Texture features are not associated with convalescent decreased strain, ejection fraction (EF) or left ventricle remodeling (LVR) in analysis (p>0.05).

TA of T2-mapping can distinguish AAR from both the infarct zone and the remote myocardial zone without LGE imaging in reperfused AMI. However, these features are not able to predict patients' functional recovery in the convalescent stage.

TA of T2-mapping can distinguish AAR from both the infarct zone and the remote myocardial zone without LGE imaging in reperfused AMI. However, these features are not able to predict patients' functional recovery in the convalescent stage.

The purpose of this study was to determine whether the epidermal growth factor receptor (EGFR), which is a classical receptor tyrosine kinase, is involved in the protective effect of morphine against ischemia/reperfusion (I/R)-induced myocardial mitochondrial damage.

Isolated rats hearts were subjected to global ischemia followed by reperfusion. Cardiac H9c2 cells were exposed to a simulated ischemia solution followed by Tyrode's solution to induce hypoxia/reoxygenation (H/R) injury. Triphenyltetrazolium chloride (TTC) was used to measure infarct size. The mitochondrial morphological and functional changes were determined using transmission election microscopy (TEM), mitochondrial stress assay, and mitochondrial swelling, respectively. Mitochondrial fluorescence indicator JC-1, DCFH-DA, and Mitosox Red were used to determine mitochondrial membrane potential (△Ψm), intracellular reactive oxygen species (ROS) and mitochondrial superoxide. A TUNUL assay kit was used to detect the level of apoptosis. Western of morphine was inhibited by AG1478, indicating that morphine promotes intracellular ROS generation by activating EGFR. However, morphine did not increase ROS generation when cells were transfected with siRNA against EGFR. In addition, EGFR activity was markedly increased by morphine, but the effect of morphine was reversed by naltrindole. selleck These results suggest that morphine may activate EGFR via δ-opioid receptor activation.

Morphine may prevent I/R-induced myocardial mitochondrial damage by activating EGFR through δ-opioid receptors, in turn increasing RISK and SAFE pathway activity via intracellular ROS. Moreover, morphine may reduce myocardial injury by regulating autophagy but not apoptosis.

Morphine may prevent I/R-induced myocardial mitochondrial damage by activating EGFR through δ-opioid receptors, in turn increasing RISK and SAFE pathway activity via intracellular ROS. Moreover, morphine may reduce myocardial injury by regulating autophagy but not apoptosis.The Veterans RAND 12-Item Health Survey (VR-12) was added to the German Pain Questionnaire (DSF) as a self-report measure of health-related quality of life in 2016, replacing the previously used SF-12, which required a license. Both measures have 12 items and include a physical component summary (PCS) and a mental component summary (MCS). Evaluations with a larger sample on characteristic values and on the test-statistical goodness of the VR-12 in patients with chronic pain are so far missing. Data on the VR-12 and other procedures of the DSF were evaluated from 11,644 patients from 31 centers participating in KEDOQ pain. The patients filled out the DSF before starting a pain therapy treatment. Change sensitivity was determined for 565 patients for whom the VR-12 was available from a follow-up questionnaire of the DSF several months after the initial survey.The reliability (Cronbach's alpha) of the PCS was rtt = 0.78 and for the MCS rtt = 0.84. The MCS had significant relationships with the depression, anxiety and stress scales (r = -0.51 to r = -0.72), and the PCS correlated more highly with areas of pain-related impairment (r = -0.48 to r = -0.52). Patients with higher pain chronicity, those with higher pain severity, and those with evidence of high psychological distress described significantly lower health-related quality of life in PCS and MCS. The effect size (ES) of change in terms of improvement in health-related quality of life was ES = 0.33 in the MCS and ES = 0.51 in the PCS.The results are in agreement with the findings of the SF-36 and SF-12 in patient collectives with chronic pain. In summary, they show that the VR-12 is an adequate substitute for the SF-12 in the German pain questionnaire.

To evaluate the 24-h efficacy and safety of fixed combination carteolol/latanoprost (LCFC) and timolol/latanoprost (LTFC) in patients with primary open-angle glaucoma and ocular hypertension.

Prospective, randomized, crossover study METHODS Twenty-two patients pretreated with a prostaglandin analog at baseline were randomly assigned at a 11 ratio to either LCFC or LTFC treatment. The patients received the assigned study drug in both eyes daily in the evening (2000). Each treatment group crossed over after a 2-month treatment period. The 24-h curves of intraocular pressure (IOP), pulse rate, and blood pressure were evaluated. Safety was also assessed.

The changes in mean daytime IOP from baseline at the end of the 2-month treatment period in the LCFC and LTFC groups were  - 0.93 and  - 1.15mmHg, respectively. The changes in peak IOP in the 2 groups were  - 0.91 and  - 0.68mmHg, respectively. The nighttime pulse rate in the LCFC group increased; that in the LTFC group was lower at all time points. The changes in pulse rate from baseline at 2200, 200, 400, and 600 differed statistically between the 2 groups.