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It is known that increased frontal QRS-T angle, which is a new ventricular repolarization marker is associated with adverse cardiac outcomes. It has been observed that the coronary slow-flow (CSF) phenomenon can cause arrhythmias and sudden cardiac death. The aim of our study is to investigate the relationship between CSF in patients and the frontal QRS-T angle.

A total of 200 patients, 97 of who had CSF and 103 with the normal coronary flow (NCF), were included in our study. The CSF group was divided into two groups; single-vessel CSF and multi-vessel CSF. The TIMI-frame count was calculated from the coronary angiography images of each patient. 12-lead electrocardiography (ECG) records were examined. The frontal QRS-T angle was obtained from the automated reports of the ECG device.

The mean age of the study population was 50.7±9.5 and 102 (51%) of patients were female. The frontal QRS-T angle was significantly higher in patients with CSF compared to the NCF group [48(31-64) vs 37(25-46), p=0.001]. A positive correlation was observed between the frontal QRS-T angle and TIMI-frame count in the correlation analysis performed separately for LAD, Cx, RCA patients with CSF (respectively; r=0.340 and p<0.001, r=0.262 and p=0.002, r=0.247 and p=0.003). The frontal QRS-T angle was higher in patients with multi-vessel CSF than in patients with single-vessel CSF [53.5(41.5-76.5) vs 43.0(23.5-60.5), p=0.039].

There is a positive correlation between frontal QRS-T angle and TIMI-frame count. The frontal QRS-T angle is higher in patients with CSF. Also, frontal QRS-T angle was higher in the multi-vessel CSF group.

There is a positive correlation between frontal QRS-T angle and TIMI-frame count. The frontal QRS-T angle is higher in patients with CSF. Also, frontal QRS-T angle was higher in the multi-vessel CSF group.

Right Bundle Branch Block (RBBB) has been reported in 5-11% of the acute myocardial infarctions (AMI), and it could be the only electrocardiographic abnormality in this group of patients. We investigated the mortality in patients with AMI and the presence of RBBB.

A retrospective cohort study was conducted between January 2011 to December 2017 at a university hospital in Bogotá, Colombia. Records were obtained from all patients who presented at the emergency department with AMI; patients with early transfer and incomplete follow-up were excluded.

1015 patients were included, the mean age was 66years, 67% of the patients were men, and 38% had STEMI. RBBB was documented in 8% of patients and LBBB in 4% of patients. In-hospital mortality was higher in the group of patients with RBBB vs. patients without RBBB (8.64% vs. https://www.selleckchem.com/products/oxidopamine-hydrobromide.html 3.74%, p=0.034). The percentage of patients with Killip ≥II classification was higher in patients with new RBBB vs. patients with old or unknown duration RBBB (23% vs. 13%, p=0.216).

In patients with AMI, the presence of RBBB was associated with a statistically significant increase of in-hospital mortality.

In patients with AMI, the presence of RBBB was associated with a statistically significant increase of in-hospital mortality.In brain astrocytes, noradrenaline (NA) has been shown to up-regulate IL-6 production via β-adrenoceptors (ARs). However, the underlying intracellular mechanisms for this regulation are not clear, and it remains unknown whether α-ARs are involved. In this study, we investigated the AR-mediated regulation of IL-6 mRNA levels in the cultured astrocytes from rat spinal cord. NA, the α1-agonist phenylephrine, and the β-agonist isoproterenol increased IL-6 mRNA levels. The phenylephrine-induced IL-6 increase was accompanied by an increase in ERK phosphorylation, and these effects were blocked by inhibitors of PKC and ERK. The isoproterenol-induced IL-6 increase was accompanied by an increase in CREB phosphorylation, and these effects were blocked by a PKA inhibitor. Our results indicate that IL-6 increases by α1- and β-ARs are mediated via the PKC/ERK and cAMP/PKA/CREB pathways, respectively. Moreover, conditioned medium collected from astrocytes treated with the α2-AR agonist dexmedetomidine, increased IL-6 mRNA in other astrocytes. In this study, we elucidate that α1- and α2-ARs, in addition to β-ARs, promote IL-6 transcription through different pathways in spinal cord astrocytes.Advanced breast cancer frequently metastasizes to the skeleton causing major mobility issues and hazards to quality of life. To manage osteolytic bone metastasis, bone-modifying agents and chemotherapy are recommended as the standard of care. Here, we investigated serologic biomarkers that might be associated with prognosis in breast cancer patients treated with zoledronic acid (ZA) and taxane-based chemotherapy. We collected serum samples from breast cancer patients with bone metastasis who received taxane plus ZA as palliative treatment. Fourteen biomarkers of angiogenesis, immunogenicity, and apoptosis were assessed, and the correlation between serum cytokine levels and patient's prognosis was statistically analyzed. Sixty-six patients were enrolled, and samples from 40 patients were analyzed after laboratory quality control. Patients with low baseline PDGF-AA, high IFN-γ, low MCP-2, low TGF-β1, and low TNF-α were significantly associated with longer progression-free survival (PFS). Decreasing VEGF and TNF-α and increasing FGF-2 and PDGF-AA in the early treatment phase indicated longer PFS. In univariate and multivariate analyses, low TGF-β1 and TNF-α and high IFN-γ at baseline were associated with a significantly low hazard ratio for disease progression. Further, we designed a risk score with TGF-β1, TNF-α, and IFN-γ levels, which could prognosticate patients for PFS. In conclusion, serum cytokine level, such as TGF-β1, TNF-α, and IFN-γ, could be a potential prognostic biomarker for breast cancer patients with bone metastasis treated with ZA and taxane-based chemotherapy.

this study determines recovery in physical activity and activities of daily living in the early stages after cardiogenic internal carotid artery infarction.

this retrospective comfort study compares assessment data for 334 patients 150 patients had atherosclerotic infarction (67 internal carotid artery, 87 middle cerebral artery) and 180 had cardiogenic infarction (32 internal carotid artery infarction, 148 middle cerebral artery). We used Brunnstrom recovery score, posture assessment scale for stroke, and functional independence measure.

on initial assessment, median Brunnstrom recovery for the cardiogenic internal carotid artery infarction group was I-II in the upper limb, I in the finger, I-II in the lower limb, and IV or higher in all other groups. The median Postural Assessment Scale for Stroke score for the cardiogenic internal carotid artery infarction group was 0; all other groups scored 14 or higher. The median Functional Independence Measure for the cardiogenic internal carotid artery infarction group was 18 (maximum of 100) and the median score for other infarct groups was 25-50 (maximum 126), with P < .

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