Effect of Consecutive Cut and Vegetation Stage on Cncps Protein Fractions in Alfalfa (Medicago Sativa L.)

Crude protein (CP) of forages can be separated into fractions of differentiated abilities to provide available amino acids in the lower gut of ruminants. This knowledge is critical to develop feeding systems and to predict animal responses. The objective of this research was to asses whether CP concentrations and the relative proportion of CP fractions by CNCPS in alfalfa (Medicago sativa L.) cv K-28 were affected by different cuts and vegetation stages. Fraction B2, which represents true protein of intermediate ruminal degradation rate, was the largest single fraction in all cuts except in the third cut. Soluble fraction A was less than 400 g kg-1 CP in all cuts except in the third cut, while the unavailable fraction C ranged from 56 g kg-1 CP in the first cut to 134.8 g kg-1 CP in the fourth cut. The remaining fraction B3 (true protein of very low degradation rate) only represented less than 60 g kg-1 of total CP. Results showed that undegraded dietary protein represented a small proportion of total CP in alfalfa from the first to the fourth cut

Cardiopoietic cell therapy for advanced ischemic heart failure: results at 39 weeks of the prospective, randomized, double blind, sham-controlled CHART-1 clinical trial

Cardiopoietic cells, produced through cardiogenic conditioning of patients' mesenchymal stem cells, have shown preliminary efficacy. The Congestive Heart Failure Cardiopoietic Regenerative Therapy (CHART-1) trial aimed to validate cardiopoiesis-based biotherapy in a larger heart failure cohort

Function of s100 Protein in Coronary Atherosclerosis

Atherosclerosis is a complex disease whose pathogenesis includes endothelial activation, accumulation of lipids in the subendothelium, formation of foam cells, fat bands and formation of atherosclerotic plaque. These complex mechanisms involve different cell populations in the intimate sub-endothelium, and the S-100 protein family plays a role in a number of extracellular and intracellular processes during the development of atherosclerotic lesions. The aim of this study was to determine the phenotypic characteristics of smooth muscle cells and the consequent expression of S100 protein in atherosclerotic altered coronary arteries in advanced stages of atherosclerosis. 19 samples of right atherosclerotic coronary arteries in stages of fibro atheroma (type V lesion) and complicated lesions (type VI lesion) have been analyzed. According to the standard protocol, the following primary antibodies have been used in the immunohistochemical analysis: a-smooth muscle actin (α-SMA), vimentin and S-100 protein. All analyzed samples have been in advanced stages of atherosclerosis, fibro atheroma (stage V lesions) and complicated lesions (type VI lesions). Most of them have had the structure of a complicated lesion with atheroma or fibro atheroma as a basis, subsequently complicated by disruption (subtype VI a), hemorrhage (subtype VI b) or thrombosis (subtype VI c), as well as by the presence of several complications on the same sample. Marked hypocellularity is present in the subendothelium of plaques. Cell population at plaque margins is characterized by immunoreactivity to α-SMA, vimentin, and S100 protein. Some of these cells accumulate lipids and look like foam cells. In the cell population at the margins of the plaques, smooth muscle cells of the synthetic phenotype are present, some of which accumulate lipids and demonstrate S100 immunoreactivity. Summarizing numerous literature data and our results, we could assume that smooth muscle cells, due to their synthetic and proliferative activity in the earlier stages of pathogenesis, as well as the consequent expression of S100 protein, could accumulate lipids in the earlier stages of atherosclerosis which, in advanced stages analyzed in this study, result in immunoreactivity of foam cells of smooth muscle origin to S100 protein

Quality of life of the mechanically ventilated patients with community acquired pneumonia

© 2018, Inst. Sci. inf., Univ. Defence in Belgrade. All rights reserved. Background/Aim. Patients with pneumonia who require mechanical ventilation (MV) are associated with several poor outcomes such as prolonged hospitalization, higher rate of mortality and increased spread of antibioticsresistant pathogens. MV in patients with communityacquired pneumonia (CAP) could cause development of psychological symptoms, often neglected in the Intensive Care Units (ICU) as well as decreased quality of life after the withdrawal of the MV. The aim of the study was to evaluate the quality of life in patients with CAPs treated with MV in ICU. Methods. The study was designed as a cohort study of hospital-treated patients with CAP with prospective data collection. The quality of life was defined as the primary outcome, while the use of MV was assumed as the primary prognostic factor that adversely affected the outcome. The patients were recruited from the population of patients with CAPs who were hospitalized at the ICU, Clinical Center Kragujevac, Serbia, from January 2013 to January 2014. The experimental group consisted of patients who were on MV while the control group included patients who were treated for CPAs in the ICU, but were not subjected to MV. The quality of life was assessed by using patient-rated Euro Quality of Life (EuroQoL) Group-EQ-5D index. The calculation of the total EQ-5D-5L score values was performed by using the predefined, validated mapping key according to response combinations. Statistical analysis was performed by using χ2 test, Student's t-test, univariate and multivariate logistic regression analyses. Results. The patients with MV had worse EQ5D-5L values in comparison to the control group for all 5 domains. Mobility, self-care and usual activities were negatively affected during the whole follow-up period. Pain or discomfort and anxiety or depression differed significantly between the study group and the control group at days 7 and 30. Conclusion. Patients with MV tend to have poorer quality of life, especially in 3 domains. The main reasons are the presence of chronic comorbidities in the population that require MV

IL 33 Correlates With COVID-19 Severity, Radiographic and Clinical Finding

Objective: The increased level of interleukin (IL)-33 is considered as a predictor of severe coronavirus disease 2019 (COVID-19) infection, but its role at different stages of the disease is still unclear. Our goal was to analyze the correlation of IL-33 and other innate immunity cytokines with disease severity. Methods: In this study, 220 patients with COVID-19 were included and divided into two groups, mild/moderate and severe/critical. The value of the cytokines, clinical, biochemical, radiographic data was collected and their correlation with disease severity was analyzed. Results: Most patients in the severe/critical group were male (81.8%) and older (over 64.5 years). We found a statistically significant difference (p < 0.05) in these two groups between clinical features (dyspnea, dry cough, fatigue, and auscultatory findings); laboratory [(neutrophil count, lymphocyte count, monocyte count, hemoglobin, plasma glucose, urea, creatinine, total bilirubin (TBIL), direct bilirubin (DBIL), aspartate aminotransferase (AST), albumin (ALB), lactate dehydrogenase (LDH), creatinine kinase (CK), D-dimer, C-reactive protein (CRP), procalcitonin (PCT), Fe, and Ferritin)], arterial blood gases (oxygen saturation-Sa02, partial pressure of oxygen -p02), and chest X-rays (CXR) lung findings (p = 0.000). We found a significantly higher serum concentration (p < 0.05) of TNF-α, IL-1β, IL-6, IL-12, IL-23, and IL-33 in patients with COVID-19 with severe disease. In the milder stage of COVID-19, a positive correlation was detected between IL-33 and IL-1β, IL-12 and IL-23, while a stronger positive correlation between the serum values of IL-33 and TNF-α, IL-1β, IL-6, and IL-12 and IL-23 was detected in patients with COVID-19 with severe disease. A weak negative correlation (p < 0.05) between pO2 and serum IL-1β, IL-12, and IL-33 and between SaO2 and serum IL-33 was noted. The positive relation (p < 0.05) between the serum values of IL-33 and IL-12, IL-33 and IL-6, and IL-6 and IL-12 is proven. Conclusion: In a more progressive stage of COVID-19, increased IL-33 facilitates lung inflammation by inducing the production of various innate proinflammatory cytokines (IL-1β, IL-6, TNF-α, IL-12, and IL-23) in several target cells leading to the most severe forms of the disease. IL-33 correlates with clinical parameters of COVID-19 and might represent a promising marker as well as a therapeutic target in COVID-19