[This corrects the article DOI 10.1155/2020/8243473.].The outbreak of novel coronavirus disease 2019 (COVID-19) first occurred in Wuhan, Hubei Province, China, and spread across the country and worldwide quickly. It has been defined as a major global health emergency by the World Health Organization (WHO). Human cathelicidin concentration As this is a novel virus, its diagnosis is crucial to clinical treatment and management. To date, real-time reverse transcription-polymerase chain reaction (RT-PCR) has been recognized as the diagnostic criterion for COVID-19. However, the results of RT-PCR can be complemented by the features obtained in chest computed tomography (CT). In this review, we aim to discuss the diagnosis and main CT features of patients with COVID-19 based on the results of the published literature, in order to enhance the understanding of COVID-19 and provide more detailed information regarding treatment.
The current study explored the radio-protective property of γ-linolenic acid (GLA) in C57BL/6J mice against low linear energy transfer ionizing radiation (IR; X-rays) and its modulatory effect on the production of lipid mediators such as prostaglandin E
(PGE2), leukotriene E
and lipoxin A
(LXA4) in mice plasma.
The effect of GLA pre-treatment on radiation induced inflammation was assessed by estimating plasma levels of high mobility group box 1 protein (HMGB1), TMOP/NO and various anti-oxidant enzymes.
γ-linolenic acid pre-treated mice exposed to lethal IR dose (7.5 Gy) showed a decrease in plasma levels of HMGB1, PGE2 and LXA4 and a fall in TMOP/NO ratio and improvement in anti-oxidant enzymes catalase, glutathione transferase and glutathione peroxidase compared to IR mice, suggesting that GLA suppresses IR-induced inflammation and restores the pro- vs. anti-oxidant ratio to near normal, which could explain its radioprotective action.
GLA showed radioprotective action.
GLA showed radioprotective action.
Changes in circulating CD34+CD45low stem cells (SC) and CD34+CD45low+KDR+ endothelial progenitor cells (EPC) may reflect pathological endothelial activation. Non-pulsatile/continuous-flow left ventricular assist devices (CF-LVAD) can enhance this process. The aim of this study was to analyse the impact of 12-month CF-LVAD treatment on SC and EPC.
We analysed changes in SC and EPC from the pre-implantation period up until 12 months after implantation over 3-month intervals in 14 patients. Data from 12 patients with heart failure (HF) and from 13 healthy volunteers were used as controls.
Baseline EPC were significantly higher in CF-LVAD and HF patients than in healthy controls, substantially decreasing 3 months after CF-LVAD implantation and then returning to high baseline values at 12 months.
Changes in circulating SC and EPC may reflect pathological endothelial activation after CF-LVAD implantation.
Changes in circulating SC and EPC may reflect pathological endothelial activation after CF-LVAD implantation.
Statins are known to lower CRP, and this reduction has been suggested to contribute to the established efficacy of these drugs in reducing cardiovascular events and outcomes. However, the exact mechanism underlying the CRP-lowering effect of statins remains elusive.
In order to test the possibility of direct interaction, we performed an
study by testing the orientation of the respective ligands (statins) and phosphorylcholine (the standard ligand of CRP) in the CRP active site using Molecular Operating Environment (MOE) software.
Docking experiments showed that all statins could directly interact with CRP. Among statins, rosuvastatin had the strongest interaction with CRP (pKi = 16.14), followed by fluvastatin (pKi = 15.58), pitavastatin (pKi = 15.26), atorvastatin (pKi = 14.68), pravastatin (pKi = 13.95), simvastatin (pKi = 7.98) and lovastatin (pKi = 7.10). According to the above-mentioned results, rosuvastatin, fluvastatin, pitavastatin and atorvastatin were found to have stronger binding to CRP compared with the standard ligand phosphocholine (pKi = 14.55).
This finding suggests a new mechanism of interaction between statins and CRP that could be independent of the putative cholesterol-lowering activity of statins.
This finding suggests a new mechanism of interaction between statins and CRP that could be independent of the putative cholesterol-lowering activity of statins.
In senile osteoporosis countering the age-mediated bone loss, promotion of osteoblastogenesis and identification of responsible micro-RNA (miR) would be a successful strategy.
miR microarray screening was carried out to identify the suppressed miRs after real time polymerase chain reaction (RT-PCR) analysis in mesenchymal stem cells (MSCs) derived from adult bone marrow during the proliferation to the mineralization stage. The primary calvarial pre-osteoblasts (human) were harvested and received transfection of miR-22's antagomir or agomir
. Bioinformatics study suggested YWHAZ as the favorable target gene. Next, YWHAZ knockdown was studied for its effect on differentiation of osteoblasts. For
studies, ovariectomized or sham mice were injected with miR-22's antagomir for a period of 6 weeks. The stromal cells were isolated in the 6
week for
experiments.
miR-22 was found to be down-regulated in bone marrow derived mesenchymal stem cells. miR-22's antagomir converted the pre-osteoblasts to a more differentiated and mineralized phenotype showing upregulated protein expression of COL1A1, ALP and CBFA1. The miR-22's antagomir suppressed YWHAZ, enhanced stability of CBFA1 and promoted the differentiation of osteoblasts.
, miR-22's antagomir promoted mineralization and osteoblastogenesis, elevated bone strength and reversed the ovariectomy mediated bone loss in sham mice.
Inhibition of miR-22 may be a potential target for treating osteoporosis clinically. The findings hence suggest that inhibition of miR-22 may be an effective anabolic therapeutic approach in treating osteoporosis clinically.
Inhibition of miR-22 may be a potential target for treating osteoporosis clinically. The findings hence suggest that inhibition of miR-22 may be an effective anabolic therapeutic approach in treating osteoporosis clinically.Human cathelicidin concentration
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