Highlights HCWs face a high risk of SARS-CoV-2 transmission during serving health care. Transmission may also occur in nonmedical areas while speaking or eating. Proper use of PPE and basic infection control precautions are essential.

Coronavirus disease 2019 (COVID‐19) is an infectious disease, and the reason behind the currently ongoing pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). Angiotensin‐converting enzyme (ACE2) has been recognized as the specific receptor of the SARS‐CoV‐2 virus. Although the possible effect of ACE2 gene polymorphism remains unknown, human ACE2 receptor expression influences SARS‐CoV‐2 susceptibility and COVID‐19 disease outcome. In this study, we aimed to investigate the relationship between ACE gene I/D polymorphism, ACE2 receptor gene polymorphism, and COVID‐19 severity. ACE gene insertion/deletion (I/D) polymorphism and ACE2 receptor gene rs2106809 and rs2285666 polymorphisms were determined using polymerase chain reaction (PCR) and PCR‐based restriction fragment length polymorphism methods, respectively, in 155 COVID‐19 patients who were divided into three groups (mild, moderate, and severe) according to clinical symptoms. However, the distribution of genotype and allele frequencies of ACE gene I/D, ACE2 receptor gene rs2106809, and rs2285666 polymorphisms were not statistically significant in all groups. In conclusion, in the study population, ACE gene I/D, ACE2 receptor gene rs2106809, and rs2285666 polymorphisms were not associated with the severity of COVID‐19 infection. Although ACE2 receptor gene expression may affect the susceptibility to COVID‐19, there is no existing evidence that the ACE or ACE2 gene polymorphisms are directly associated with COVID‐19 severity. Interindividual differences in COVID‐19 severity might be related to epigenetic mechanisms of ACE2 receptor gene expression or variations in other genes suggested to play a critical role in COVID‐19 pathogenesis such as pro‐inflammatory cytokines and coagulation indicators.

PCT was better than CRP and the N/L ratio for predicting a bacterial infection in hospitalized patients with AECOPD. However, we find PCT not so reliable in predicting bacterial infection in AECOPD due to sensitivity and specificity of less than 80 % and a low AUC value.

PurposeSyncope is an atypical presentation for acute pulmonary embolism (APE). There are conflicting data concerning syncope and prognosis of APE.Patients and methodsOne hundred and seventy-nine consecutive patients aged 22–96 years (median, 68 years) with APE were retrospectively enrolled in the study.ResultsPrevalence of syncope was 13% (n=23) at the time of presentation. Compared to patients without syncope, those with syncope had a higher rate of central embolism (83% vs 43%, respectively, P=0.002), right ventricular dysfunction (91% vs 68%, P=0.021), and troponin positivity (80% vs 39%, P=0.001) but not 30-day mortality (13% vs 10%, P=0.716). Multivariate analysis showed that central localization (odds ratio: 9.08) and cardiac troponin positivity (odds ratio: 4.67) were the independent correlates of the presence of syncope in the patients with APE. Frequency of cardiopulmonary disease was lower, and duration from symptom onset to hospital admission was shorter in patients with syncope (P=0.138 and 0.118, respectively), although not significant.ConclusionSyncope most likely represents an intermediate condition between massive APE and hypotension. In APE patients with syncope, the prognosis seems to depend on the underlying pathology, the patient’s age, comorbidities and duration from symptom onset to hospital admission, and the use of thrombolytic therapy.

Objectives: Coronavirus disease 2019 (COVID-19) is an infectious disease, that’s the reason for the currently ongoing pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Angiotensin-converting enzyme (ACE2) has been recognized as the specific receptor of the SARS-CoV-2 virus. Although the possible effect of ACE2 gene polymorphism remains unknown, human ACE2 receptor expression influences SARS-CoV-2 susceptibility and COVID-19 disease outcome. In this study, we aimed to investigate the relationship between ACE gene I/D polymorphism, ACE2 receptor gene polymorphism, and Covid-19 severity. Methods: ACE gene I/D polymorphism and ACE2 receptor gene rs2106809 and rs2285666 polymorphisms were determined using PCR and PCR-RFLP methods, respectively in 155 Covid19 patients who were divided into 3 groups (mild, moderate, and severe) according to clinical symptoms. Results: However, the distribution of genotype and allele frequencies of ACE gene I/D, ACE2 receptor gene rs2106809, and rs2285666 polymorphisms was not statistically significant in all groups. Conclusions: In conclusion, in the study population, ACE gene I/D, ACE2 receptor gene rs2106809, and rs2285666 polymorphisms were not associated with the severity of Covid-19 infection. Although, ACE2 receptor gene expression may affect the susceptibility to Covid-19, there is no existing evidence that the ACE or ACE2 gene polymorphisms are directly associated with Covid-19 severity. Interindividual differences in covid-19 severity might be related to epigenetic mechanisms of ACE2 receptor gene expression or variations in other genes suggested to have critical role in COVID-19 pathogenesis such as proinflammatory cytokines, coagulation indicators. Keywords: COVID-19 , ACE , ACE2, rs2106809, rs2285666

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BackgroundAccumulating evidence shows that functional impairment in subjects with coal workers’ pneumoconiosis (CWP) is principally due to emphysema and airflow obstruction, rather than underlying restrictive mechanisms. However, cigarette smoking has remained a major confounder. The aim of this study was to assess whether coal dust exposure was associated with emphysema and/or airflow obstruction in the absence of smoking history.Material/MethodThe subjects evaluated for possible pneumoconiosis between 2013 and 2015 were retrospectively enrolled into this study. After excluding those with history of smoking, tuberculosis, or lung cancer, the study population was a total of 57 subjects. The emphysema severity and airflow obstruction were quantified by computed tomographic densitometry analysis and spirometry, respectively. For comparability regarding emphysema, 9 age- and sex-matched nonsmoker (n=9) control subjects without known lung disease were randomly selected from a radiology database.ResultsEmphysema severity was significantly higher in the CWP group compared with the control group (15% vs. 4%, p<0.001). The median percent emphysema and percentage of those with FEV1/FVC <0.7 was 13% and 37% in subjects with simple CWP and 18% and 67% in subjects with complicated CWP, respectively. Percent emphysema and Perc15 (15th percentile of the attenuation curve) was correlated with FEV1/FVC (r=−0.45, r=−0.47) and FEF25–75 (r=−0.36, r=−0.56), respectively, but not with perfusion score. A linear regression analysis showed that factors associated with emphysema were FEV1/FVC (β=−0.24, p=0.009) and large opacity (β=−3.97, p=0.079), and factors associated with FEV1/FVC were percent emphysema (β=−0.51, p=0.018) and tenure (β=−0.63, p=0.044).ConclusionsOur results support the observation that coal dust exposure is associated with emphysema and airflow obstruction, independent of smoking status.