Adaptation of Clinical Laboratories to COVID 19 Pandemic: Changes in Test Panels, Overcoming Problems and Preparation Suggestions for Future Pandemics Adaptation of Clinical Laboratories to COVID 19 Pandemic.

BACKGROUND: For Coronavirus Disease 2019 (Covid-19) infection, clinical laboratories provide essential contributions in the diagnosis of infection, stage prognostication, and evaluation of disease severity. We aimed to show laboratory problems including changes of test numbers, changes of test panels, and differences of preanalytical errors during Covid-19 pandemic and, in the current study, we also intended to give solutions for the obstacles to guide other possible pandemics. METHODS: Our study was based on data between January 10, 2020, and May 10, 2020. The first Covid-19 case of the Republic of Turkey was seen March 10, 2020, which was determined as the threshold date for comparisons. This was a single center, data mining, retrospective study. RESULTS: The number of patients admitted to hospital were 34,260 and 15,573, the number of total tests were 66,263 and 42,066 before and after pandemic, respectively, for the two-month interval. Test percentage changes were increased for D-dimer 136%, fibrinogen 3,113%, troponin 6%, and LDH 17%. Test percentage changes were decreased for CBC 37%, sedimentation 45%, aPTT 30%, PT 37%, CRP 28%, ProCT 10%, ferritin 29%, CK-MB 27%, blood gases 47%, ALT 43%, AST 42%, urea 42%, creatinine 42%, triglycerides 45%, sodium 42%, potassium 41%, chloride 21%, urine culture 58%, and blood culture 44%. When preanalytical sources of errors were investigated no differences were found. CONCLUSIONS: Laboratories must take quick action and be prepared for changes in patient services during pandemics. The most reliable ways for this are past experiences, statistical analysis, co-operation with administrations, high quality communication skills, and a risk-based management system.

Asymmetric Dimethylarginine and Its Relation As a Biomarker in Nephrologic Diseases.

It is encouraging to observe that a search for publications on "asymmetric dimethylarginine (ADMA)" in PubMed, as updated on June 2016, yielded >2500 items, 24 years after a splendid paper published by Vallance et al in which the authors proposed that ADMA accumulation could be a cardiovascular risk factor in chronic kidney diseases. ADMA is the endogenous inhibitor of nitric oxide synthase and is related to endothelial dysfunction, which plays an important role in vascular damage elicited by various cardiometabolic risk factors. Although current knowledge suggests that ADMA has critical central roles in renal diseases, there are still unexplained details. The present article aims to provide a review on ADMA and its relation as a biomarker in nephrologic diseases. We aimed to systematize articles in which ADMA levels were assessed in order to clarify its role in many diseases and establish its reference values in different populations.

Increased protein oxidation and loss of protein-bound sialic acid in hepatic tissues of D-galactose induced aged rats.

A redox basis of the increased oxidative protein damage and free radical-mediated desialylation have not been fully elucidated in aging. It is well known that the incidence of several liver diseases increase with age. This original research focuses on protein oxidation mechanisms and protein-bound sialic acid levels in liver tissue of the mimetic aging rats. Injection of D-galactose (60 mg/kg/day) for six weeks to male Sprague-Dawley rats (20-week-old) used to establish mimetic aging model. We investigated the tissue levels of various protein oxidation markers such as protein carbonyl groups, suitable advanced oxidation protein products and protein thiol groups. Our study also covered protein-bound sialic acid in liver tissue of D-galactose-induced aging rats. PCO (Protein Carbonyl Groups), P-OOH (Protein Hydroperoxides) and AOPP (Advanced Oxidation Protein Products) levels in aging rats were significantly higher compared to young control groups. On the other hand, P-SH (Protein Thiol Groups) levels were not found to be different between two groups. SA (Sialic Acid) levels in D-galactose-induced aging rats were significantly lower compared to control groups. Our results demonstrated greater susceptibility to hepatic oxidative protein damage and desialylation of hepatocellular proteins in Dgalactose- induced aging rats. These molecular mechanisms may be operative in the many age-related liver diseases, which are pertinent to increased oxidative stress and altered redox homeostasis.

Protein and DNA oxidation in different anatomic regions of rat brain in a mimetic ageing model.

It has been reported that d-galactose administration causes an increase in oxidative and osmotic stresses in several tissues of rodents. In this study, we established a brain ageing model by using d-galactose and investigated the concentrations of oxidative stress markers on the hippocampus, parietal and frontal lobes of male Sprague-Dawley rats. A mimetic ageing model was established by injecting d-galactose (60 mg/kg/day/i.p.) in the experimental group for 42 days. At the end of this period, we tested spatial memory using the Morris water maze test. To investigate the magnitude of oxidative damage in proteins, lipids and DNA, we studied the concentrations of various oxidative stress parameters in the hippocampus, parietal and frontal lobes of the brain. Glial and neuronal cell oxidative damage was observed in each of the three anatomic regions. It was found that protein carbonyl groups and advanced oxidation product concentrations in the d-galactose applied group were significantly high in each of the three brain lobes compared with the control group. Thiol concentration was found to be decreased in the parietal lobe. A concurrent increase in lipid hydroperoxides was also observed in this lobe. On the other hand, 8-hydroxy-2'-deoxyguanosine concentration was significantly increased in the hippocampal lobe of rats in the experimental group when compared with the controls. The results obtained from the mimetic ageing model rats showed that various anatomical regions of brain have different susceptibility to oxidative damage of proteins, lipids and DNA.