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Activation of the transcription factor NF-κB and expression of pro-inflammatory mediators have been considered as major events of acute pancreatitis (AP). Karyopherin alpha 2 (KPNA2), a member of the importin α family, reportedly modulates p65 subcellular localization.', 'This study aimed to investigate the expression and possible functions of KPNA2 in the AP cell and animal model, focusing on its association with NF-κB activation.', 'An AP cell model was established with the cerulein-stimulated AR42J and isolated rat pancreatic acinar cells. The AP rat model was induced by the intraperitoneal injection of cerulein. The secretion of TNF-α, IL-6, and LDH was detected by ELISA kits and the production of NO using nitric oxide kit. Expression of KPNA2 was measured by RT-PCR and Western blot. Expression levels of IKKα, phosphorylation of p65, and total p65 were detected by Western blot. Co-localization of KPNA2 with p65 was observed by immunofluorescence assay. To determine the biological functions of KPNA2 in cerulein-induced inflammatory response, RNA interference was employed to knockdown KPNA2 expression in AR42J and isolated pancreatic acini cells.', 'Cerulein stimulated KPNA2 expression and IL-6, TNF-α, NO, and LDH production in rat pancreatic acinar cells. Cerulein triggered the phosphorylation and nuclear translocation of NF-κB p65 subunit, indicating the NF-κB activation. The co-localization and nuclear accumulation of KPNA2 and p65 were detected in cerulein-treated cells. Knocking down KPNA2 hindered cerulein-induced nuclear transportation of p65 and alleviated the subsequent inflammatory response in rat pancreatic acinar cells. Additionally, KPNA2 expression was significantly up-regulated in cerulein-induced AP rat model.
Does karyopherin Alpha 2 promote the Inflammatory Response in Rat Pancreatic Acinar Cells Via Facilitating NF-κB Activation?

A distinct velocity pattern represented by a "notch" is observed during the time interval between the end of the systolic and the onset of the early diastolic velocity wave on longitudinal myocardial velocity curve. The origin of the post-systolic velocity notch (PSN) has not been resolved.', 'The high frame rate color tissue Doppler imaging of the apical longitudinal axis was performed in 32 healthy subjects.', 'The time delays of the PSN onset at the posterior aortic wall (AW), the mid anteroseptal wall (MAS) and the posterior mitral annulus (MA) relatively to the anterior aortic annulus (AA) were found to be significantly longer than zero (5.1 ± 2.2, 6.0 ± 2.3, 6.8 ± 2.8 ms; p < 0.001). The amplitude was the highest at the AA when compared to the AW, the MAS and the MA (4.77 ± 1.28 vs. 2.88 ± 1.11, 2.15 ± 0.73, 2.44 ± 1.17 cm/s; p < 0.001). A second PSN spike was identifiable in 10/32 (31%) of the studied subjects at the AA. Of these, 9 (28%) exhibited a second PSN spike at the AW, 3 (9%) at the MAS and no one at the MA.
Does the tissue Doppler imaging derived post-systolic velocity notch originate at the aortic annulus?

Assessing acute myocardial infarction (MI) with respect to long-term survival is not easy. Authorities in the field suggest that inflammation predicts short-range (up to 17 months) coronary death. It is not known whether long-term survival is associated with the inflammatory response. In this study, we evaluate the relationships between survival for more than 8 years and inflammation, i.e., circulating interleukin-6 (IL-6) and neutrophil counts, in acute MI.', 'Patients with ST-segment elevation MIs (STEMI; n=33) and non-ST-segment MIs (non-STEMI; n=39) in 1996 were included in the study. All STEMI patients received thrombolytic therapy. Acute coronary angiography was not an option. Determination of IL-6 and neutrophils was carried out within 24 h after commencement of pain. The subjects were followed for more than 8 years (until December 31, 2005) using the national death registry. Inflammatory markers at the time of MI were compared with long-term survival (n=35).', 'At the time of acute MI, survivors for more than 8 years proved to have lower IL-6 (p<0.01) and decreased neutrophil counts (p<0.05). The differences remained (p<0.01 for both markers) when excluding deaths (n=11) occurring in 1996 and 1997. Subsequently, the subjects were divided into two equally sized groups, depending on their IL-6 values at the beginning of the study. As expected, a lower IL-6 was associated with a more favorable long-term prognosis (p<0.01).

Are interleukin-6 and neutrophils associated with long-term survival after acute myocardial infarction?