8 research outputs found

    Analysis of the Relationship Between Hemorheologic Parameters, Aluminum, Manganese, and Selenium in Smokers

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    Smoking is a significant risk factor in fatal pathologies including cardio-cerebrovascular and respiratory diseases. Aluminum (Al) is a toxic element without known biological function, but with recognized toxic effects. Manganese (Mn) and selenium (Se) are essential trace elements involved in cellular antioxidant defense mechanisms. Al, Mn, and Se carry out their metabolic activities via blood flow and tissue oxygenation. The structure and number of red blood cells (RBC) play important role in tissue oxygenation throughout blood flow. Increased hematocrit (Hct) as a result of probable hypoxia induces disturbed blood flow, RBC aggregation (RBC Agg), RBC deformability index (Tk), and oxygen delivery index (ODI). Therefore, we aimed to investigate the effects of altered Al, Mn, and Se levels on number, structure, and function of RBCs (Hct, blood and plasma viscosity (BV and PV, respectively), RBC Agg, Tk, ODI) in smokers without diagnosis of chronic obstructive pulmonary disease (COPD) in a study group (n=128) categorized as ex-smokers (ES), smokers (S), and healthy controls (HC). Elements were analyzed in serum using ICP-OES. BV and PV were measured via Brookfield and Harkness viscometers at 37 degrees C, respectively. Smokers had statistically higher serum Al and Mn levels, BV, RBC, Hgb, Hct, PV, fibrinogen, RBC Agg, Tk(45), and pulmonary blood flow rate, but lower serum Se levels and ODI45 values versus HC. In conclusion, increased Al, Mn, and hemorheological parameters and decreased Se and ODI45 might result from inflammatory response in defense mechanism in smokers without diagnosis of COPD. Our results point out that serum Al, Mn, and Se with hemorheological parameters may be beneficial markers of tissue oxygenation and defense mechanism before the clinic onset of COPD in smokers

    Oral Microbiota Signatures in the Pathogenesis of Euthyroid Hashimoto’s Thyroiditis

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    One of the most prevalent autoimmune illnesses in the world is Hashimoto’s thyroiditis, whose pathogenesis is still unknown. The gut–thyroid axis is frequently examined, and although oral health affects thyroid functions, there are limited data on how oral microbiota is linked to Hashimoto’s thyroiditis. The study aims to identify the oral microbiota from saliva samples taken from treated (with levothyroxine) and untreated female euthyroid Hashimoto’s thyroiditis patients as well as healthy controls who were age- and sex-matched to compare the oral microbiota across the groups and to contribute preliminary data to the literature. This study was designed as a single-center cross-sectional observational study. Sixty (60) female patients with euthyroid Hashimoto’s thyroiditis (HT) and eighteen (18) age- and gender-matched healthy controls were included in this study. Unstimulated saliva samples were collected. After DNA isolation, sequencing was performed by targeting the V3-V4 gene regions of the 16S rRNA on the MiSeq instrument. R scripts and SPSS were used for bioinformatic and statistical analysis. No significant differences were found in the diversity indices. However, Patescibacteria phylum showed a significantly higher abundance (3.59 vs. 1.12; p = 0.022) in the oral microbiota of HT patients compared to HC. In the oral microbiota, the euthyroid HT group had approximately 7, 9, and 10-fold higher levels of the Gemella, Enterococcus, and Bacillus genera levels than healthy controls, respectively. In conclusion, the results of our study demonstrated that Hashimoto’s thyroiditis causes changes in the oral microbiota, whereas the medicine used to treat the condition had no such effects. Therefore, revealing the core oral microbiota and long-term follow-up of the HT process by conducting extensive and multicenter studies might provide some important data for understanding the pathogenesis of the disease

    Biophysical Overview of Covid-19 Infection

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    Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection was declared a global pandemic by WHO on March 11, 2020. Coronavirus disease (COVID-19) is the infectious disease caused by SARS-CoV-2. It is transmitted from person to person through droplets, progresses asymptomatically in 70% of the sufferers, while it may manifest itself in severe clinical conditions, ranging from viral upper respiratory tract infection to pneumonia, sepsis, septic shock, and even acute respiratory distress syndrome (ARDS), in symptomatic patients. Studies on the epidemiological and clinical features of COVID-19 have shown that these patients can develop symptoms of mild or severe acute respiratory infection. In cases with mild symptoms, upper respiratory tract symptoms such as fever, dry cough, and fatigue may develop, and abnormal chest CT findings may also be present. In cases with severe symptoms, dyspnea, diarrhea, severe pneumonia, ARDS or multiple organ failure develop, and mortality rates vary between 4.3% and 15% according to different study reports

    Evaluation of trace elements in essential thrombocytosis and reactive thrombocytosis

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    Background: Trace elements (TE) are vital for cellular mechanisms at biological, chemical and molecular levels. The effects of TE in diagnosis, progression and treatment of essential thrombocytosis (ET), which is one of the chronic myeloproliferative neoplasms is a rare clonal stem cell disease characterized by increased thrombocyte numbers with impaired function, have not been elucidated in detail yet. The aim of the present study was to investigate the effects of TE alterations in an ET model and the efficacy of TE in ET treatment protocol by means of a vast number of TE.Methods: Study groups were categorized as patients with ET diagnosis (ET group, n:30), patients with reactive thrombocytosis secondary to iron deficiency anemia (IDA-RT) (IDA-RT group, n:30) and healthy controls (HC group, n:30). Serum levels of copper (Cu), iron (Fe), cobalt (Co), chromium (Cr), aluminum (Al), silicon (Si), nickel (Ni), zinc (Zn), selenium (Se), manganese (Mn), boron (B) and magnesium (Mg) were analyzed utilizing inductively coupled plasma-optical emission spectrophotometer instrument (ICP-OES). Statistical analysis was evaluated using SPSS 23.0.Results: ET group had statistically higher serum levels of Co and Mg (p < 0.05), Ni and Mn (p < 0.001), and lower Si (p < 0.05) than IDA-RT group. ET group had statistically higher serum levels of Co and Mn (p < 0.05), and Ni (p < 0.001), and lower Al, Si and Se (p < 0.001) than HC group. Serum levels of Fe, Al and Se (p < 0.001), and Mg (p < 0.01), and Zn (p < 0.05) in IDA-RT group were significantly lower than HC group.Conclusion: This novel study pointed out that alterations of many serum TE by means of both increment or decrement might have close relationship with mechanisms and complications of ET onset and follow-up. We consider that further research of TE would elucidate ethiopathogenesis and prognosis of ET. Thus, analysis of serum trace elements in essential thrombocytosis patients may be an important protocol by means of diagnosis, treatment and follow-up intervals

    Effects of cigarette smoking on hemorheologic parameters, plasma osmolality and lung function

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    BACKGROUND: Cigarette smoking deteriorates human health via vascular disorders, cancer and especially respiratory diseases. The aim of this study is to investigate effects of cigarette smoking on hemorheologic parameters, plasma osmolality and lung function in individuals without diagnosis of chronic obstructive pulmonary disease (COPD)

    The evaluation of plasma viscosity and endothelial dysfunction in smoking individuals

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    BACKGROUND: Smoking is considered to be one the of risk factors effecting atherosclerosis which is associated the physical forces, biological and chemical stimuli occuring in vessel wall. The aim of this study is analysis of the biomechanical (plasma viscosity) and biochemical effect (nitric oxide, NOx; asymmetric dimethylarginine, ADMA) of smoking on endothelial function

    Annexin A1 as a potential prognostic biomarker for COVID-19 disease: Case-control study

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    Background Annexin A1 (AnxA1) is an important endogenous glucocoticoid protein that contributes to the suppression of inflammation by limiting the production of neutrophil and pro-inflammatory cytokines. This study aims to determine the clinical predictivity value of blood AnxA1 levels in patients with mild and severe-critical pneumonia induced by COVID-19. Methods This study employed a prospective, case-control study design and was conducted at Ankara Training and Research hospital between 10 February 2021 and 15 March 2021. A total of 74 patients (42 of whom had moderate and 32 of whom had severe/critical cases of COVID-19 disease according to World Health Organization guidelines) and 50 nonsymptomatic healthy volunteers participated in the study. Blood samples were taken from patients at the time of hospital admission, after which serum was isolated. Following the isolation of serum, AnxA1 levels were evaluated using the enzyme-linked immunosorbent assay method. Results The serum AnxA1 levels were measured as 25.5 (18.6-38.6) ng/ml in the control group, 21.2 (14.7-32) ng/ml in the moderate disease group, and 14.8 (9.7-26.8) ng/ml in the severe/critical disease group. Serum AnxA1 levels were significantly lower in the severe/critical disease group compared with the control and moderate disease groups (P = .01 and P = .0001, respectively). Using receiver operating characteristic analysis, a larger area under the curve (AUC) for the serum AnxA1 levels of the control group (AUC = 0.715, 95% CI = 0.626-0.803; P = .0001) was calculated compared with the COVID-19 patient group for the diagnosis of COVID-19 disease. The AnxA1 level was found to be 80% sensitive and 54.1% specific at a cut-off level of 18.5 ng/ml for the diagnosis of COVID-19 disease. Moreover, the AnxA1 level was found to be 69.8% sensitive and 58.1% specific at a cut-off level of 17.2 ng/ml in predicting the need for intensive care unit (ICU) treatment. Conclusion AnxA1 levels may be a beneficial biomarker in the diagnosis of COVID-19 pneumonia and in predicting the need for ICU treatment in patients with COVID-19 pneumonia at the time of admission to the emergency department

    Analysis of the Relationship Between Hemorheologic Parameters, Aluminum, Manganese, and Selenium in Smokers

    No full text
    Smoking is a significant risk factor in fatal pathologies including cardio-cerebrovascular and respiratory diseases. Aluminum (Al) is a toxic element without known biological function, but with recognized toxic effects. Manganese (Mn) and selenium (Se) are essential trace elements involved in cellular antioxidant defense mechanisms. Al, Mn, and Se carry out their metabolic activities via blood flow and tissue oxygenation. The structure and number of red blood cells (RBC) play important role in tissue oxygenation throughout blood flow. Increased hematocrit (Hct) as a result of probable hypoxia induces disturbed blood flow, RBC aggregation (RBC Agg), RBC deformability index (Tk), and oxygen delivery index (ODI). Therefore, we aimed to investigate the effects of altered Al, Mn, and Se levels on number, structure, and function of RBCs (Hct, blood and plasma viscosity (BV and PV, respectively), RBC Agg, Tk, ODI) in smokers without diagnosis of chronic obstructive pulmonary disease (COPD) in a study group (n=128) categorized as ex-smokers (ES), smokers (S), and healthy controls (HC). Elements were analyzed in serum using ICP-OES. BV and PV were measured via Brookfield and Harkness viscometers at 37 degrees C, respectively. Smokers had statistically higher serum Al and Mn levels, BV, RBC, Hgb, Hct, PV, fibrinogen, RBC Agg, Tk(45), and pulmonary blood flow rate, but lower serum Se levels and ODI45 values versus HC. In conclusion, increased Al, Mn, and hemorheological parameters and decreased Se and ODI45 might result from inflammatory response in defense mechanism in smokers without diagnosis of COPD. Our results point out that serum Al, Mn, and Se with hemorheological parameters may be beneficial markers of tissue oxygenation and defense mechanism before the clinic onset of COPD in smokers
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