Although most patients with asthma have mild disease, data on how mild asthma is defined, and how frequently exacerbations occur in this patient population are scarce, so we aimed to redress this.
 
  We searched Medline and Medline In-Process (PubMed), and Embase in OVID for English-language publications containing "mild asthma" plus at least one relevant therapy and outcome/keyword, limited to randomised controlled trials (RCTs) and observational studies published between January 1990 and February 2019. Publications were filtered to ensure appropriate data extraction. The main outcomes were the definitions of mild asthma and exacerbations, baseline exacerbation rates and exacerbation data for placebo recipients in prospective studies.  https://www.selleckchem.com/products/Romidepsin-FK228.html  Meta-analysis of exacerbation rates was planned.
 
  Of 4064 articles identified, 64 were included in our review (49 743 subjects); 54 RCTs and 10 observational/other studies. Six main types of definitions of mild asthma were identified. While care was taken to ensure inclusion only of patients with mild asthma, marked heterogeneity was revealed in the definitions of mild asthma and hence the study populations. Reporting of exacerbations also varied widely between studies, precluding meta-analysis. Between 0-22% of patients were hospitalised for asthma or had a severe exacerbation in the previous year, according to baseline data from prospective studies. In RCTs, severe exacerbation rates in placebo recipients taking only short-acting β
  -agonist therapy ranged from 0.20-2.88 per year.
 
  These data provide new evidence of the burden of exacerbations in mild asthma and highlight the need for standardised definitions of mild asthma and of exacerbations to progress further research.
 These data provide new evidence of the burden of exacerbations in mild asthma and highlight the need for standardised definitions of mild asthma and of exacerbations to progress further research.Sarcoidosis and tuberculosis share several similar clinical and pathogenic characteristics that make some researchers consider a common pathogenesis for these diseases. Human leukocyte antigen (HLA) genotypes are studied both in sarcoidosis and tuberculosis patients, but to our knowledge, there are no comparative studies of genetic predisposition for sarcoidosis and tuberculosis development. The aim of this review was to analyse the relationship between HLA genotypes and the development of sarcoidosis and tuberculosis. Original and review articles published in various online databases from 1960 to 2019 were studied. The search results showed opposite effects of the HLA genotypes on predisposition to sarcoidosis or tuberculosis. It was revealed that the genotypes predisposing to the development of sarcoidosis (HLA-DRB1*03/07/15) have protective properties against the development of tuberculosis. Moreover, genotypes causing the development of tuberculosis (HLA-DRB1*04) have a protective effect on the development of sarcoidosis. The results of this narrative review of the literature may allude to the existence of genetic predispositions that lead to the development of an antibacterial or autoimmune response to mycobacteria.In the era of this pandemic, the role of medicinal nicotine in the prevention and treatment of #COVID19 disease should be evaluated in placebo-controlled trials, while smoking cessation should be further promoted as a general public health measure https//bit.ly/3fpsBdq.
  Mucus dehydration and impaired mucus clearance are common features of cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). In CF, inhaled hypertonic saline (HS) improves lung function and produces sustained increases in mucociliary clearance (MCC). We hypothesised that administration of HS (7% NaCl) twice daily for 2 weeks would improve clinical outcomes and produce sustained increases in MCC in COPD subjects with a chronic bronchitis (CB) phenotype.
 
  Twenty-two CB subjects completed a double-blinded, crossover study comparing inhaled HS to a hypotonic control solution (0.12% saline) administered 
  nebuliser twice daily for 2 weeks. Treatment order was randomised. During each treatment period, symptoms and spirometry were measured. MCC was measured at baseline, shortly after initial study agent administration, and approximately 12 h after the final dose.
 
  HS was safe and well tolerated but overall produced no significant improvements in spirometry or patient-reported outcomes. CB subjects had slower baseline MCC than healthy subjects. The MCC rates over 60 min (Ave60Clr) in CB subjects following 2 weeks of HS were not different from 0.12% saline but were slower than baseline (Ave60Clr was 9.1±6.3% at baseline 
  5.3±6.9% after HS; p<0.05). Subgroup analyses determined that subjects with residual baseline central lung clearance (14 subjects) had improved spirometry and symptoms following treatment with HS, but not 0.12% saline, treatment.
 
  Inhaled HS appeared to be safe in a general CB population. A specific phenotypic subgroup may benefit from HS but requires additional study.
 Inhaled HS appeared to be safe in a general CB population. A specific phenotypic subgroup may benefit from HS but requires additional study.Coastal acidification in southeastern U.S. estuaries and coastal waters is influenced by biological activity, run-off from the land, and increasing carbon dioxide in the atmosphere. Acidification can negatively impact coastal resources such as shellfish, finfish, and coral reefs, and the communities that rely on them. Organismal responses for species located in the U.S. Southeast document large negative impacts of acidification, especially in larval stages. For example, the toxicity of pesticides increases under acidified conditions and the combination of acidification and low oxygen has profoundly negative influences on genes regulating oxygen consumption. In corals, the rate of calcification decreases with acidification and processes such as wound recovery, reproduction, and recruitment are negatively impacted. Minimizing the changes in global ocean chemistry will ultimately depend on the reduction of carbon dioxide emissions, but adaptation to these changes and mitigation of the local stressors that exacerbate global acidification can be addressed locally.