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Smoking in people with diabetes markedly elevates their risk of developing complications and increases the likelihood of cardiovascular mortality. This review is the first to specifically provide evidence-based analysis about the influence of quitting smoking on diabetes-related complications in people with type 2 diabetes. The present review was carried out according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) Extension for Scoping Reviews. All human clinical studies assessing the effects of stopping smoking cessation on diabetes-related complications were included. PubMed and Embase were screened until January 2024. References of primary studies and principal peer-reviewed scientific journals in the field were manually screened. We identified a total of 1023 studies. Only 26 met the criteria for eligibility. In general quitting smoking is associated with decreased risks of myocardial infarction and ischemic stroke. Regarding microvascular complications, the strongest evidence for the beneficial effects of smoking cessation is observed in diabetic nephropathy. However, the relationship between smoking cessation and retinopathy, neuropathy, diabetic foot complications and diabetic-related erectile dysfunction, is poorly investigated. Quitting smoking offers significant advantages in managing diabetes-related complications, significantly lowering the risks of myocardial infarction, ischemic stroke, and diabetic nephropathy. This underscores the importance of cessation. Providing evidence-based information on the benefits of stopping smoking for people with type 2 diabetes who smoke, can bolster smoking cessation efforts in the context of diabetes management. • The problem of smoking among people with type 2 diabetes is both critical and urgent. • Quitting smoking significantly lowers the risks of macrovascular complications and nephropathy in people with diabetes. • Smoking cessation efforts should be bolstered to reduce the risk of diabetes complications. [ABSTRACT FROM AUTHOR]

We propose a variation, based on very low energy and extremely intense photon sources, on the well established technique of Light-Shining-through-Wall (LSW) experiments for axion-like particle searches. With radiation sources at 30 GHz, we compute that present laboratory exclusion limits on axion-like particles might be improved by at least four orders of magnitude, for masses m a ≲ 0.01 meV. This could motivate research and development programs on dedicated single-photon sub-THz detectors. [ABSTRACT FROM AUTHOR]

A new solution to the problem of dark matter directional detection might come from the use of large arrays of aligned carbon nanotubes. We calculate the expected rate of carbon ions channeled in single-wall nanotubes once extracted by the scattering with a massive dark matter particle. Depending on its initial kinematic conditions, the ejected carbon ion may be channeled in the nanotube array or stop in the bulk. The orientation of the array with respect to the direction of motion of the Sun has an appreciable effect on the channeling probability. This provides the required anisotropic response for a directional detector. [ABSTRACT FROM AUTHOR]

Abstract: DREF [DRE (DNA replication-related element)-binding factor] controls the transcription of numerous genes in Drosophila, many involved in nuclear DNA (nDNA) replication and cell proliferation, three in mitochondrial DNA (mtDNA) replication and two in mtDNA transcription termination. In this work, we have analysed the involvement of DREF in the expression of the known remaining genes engaged in the minimal mtDNA replication (d-mtDNA helicase) and transcription (the activator d-mtTFB2) machineries and of a gene involved in mitochondrial mRNA translation (d-mtTFB1). We have identified their transcriptional initiation sites and DRE sequences in their promoter regions. Gel-shift and chromatin immunoprecipitation assays demonstrate that DREF interacts in vitro and in vivo with the d-mtDNA helicase and d-mtTFB2, but not with the d-mtTFB1 promoters. Transient transfection assays in Drosophila S2 cells with mutated DRE motifs and truncated promoter regions show that DREF controls the transcription of d-mtDNA helicase and d-mtTFB2, but not that of d-mtTFB1. RNA interference of DREF in S2 cells reinforces these results showing a decrease in the mRNA levels of d-mtDNA helicase and d-mtTFB2 and no changes in those of the d-mtTFB1. These results link the genetic regulation of nuclear DNA replication with the genetic control of mtDNA replication and transcriptional activation in Drosophila. [Copyright &y& Elsevier]

Summary: Background: Gas6 protein is involved in pulmonary embolism (PE) and acute inflammation in animal models. Methods: We enrolled 82 consecutive patients with acute dyspnea and suspected PE (Geneva score with high (HCP) or low/intermediate clinical probability (LICP)+D-dimer ≥0.5μg/mL) and 29 age-matched healthy volunteers. According to clinical and instrumental evaluations the following diagnoses were obtained: heart failure (HF), pulmonary or systemic infection (I), PE, or no illness (N). Twenty-two patients were excluded due to oral anticoagulation (9), lack of CT angiography or pulmonary scintigraphy (6), plasma creatinine ≥3mg/dL (3), and pulmonary cancer (4). Plasma Gas6 was measured with a validated enzyme-linked immunoassay. Non-parametric tests and accuracy measures were calculated. Results: Out of 60 patients included, 8 were N, 12 HF, 11 I and 29 PE. Gas6 median value in the N group (20.4ng/mL, interquartile range 17.6–21.6) matched that of healthy volunteers, 19.1 (17.2–21.4). Median Gas6 values in HF, 26.4 (21.6–33.3) and I groups, 34.1 (30.0–38.7), were significantly higher than those in PE 18.2 (16.3–23.3) or N (Kruskal–Wallis test p ≤0.05) groups. Gas6 test improved PE diagnosis with an area under the curve of 0.80 and 0.91 (in all and LICP patients). A 24ng/mL threshold excluded PE in 33% of LICP patients without loosing any diagnosis. Conclusions: The data link Gas6 protein to infection/inflammation, but not to PE, in humans. Gas6 assay was useful in PE diagnosis, improving D-dimer accuracy particularly in LICP patients, and limiting false positives. [Copyright &y& Elsevier]

Summary: Despite undoubted efficacy of the combination of inhaled corticosteroids and β2-agonists for most asthmatic patients with moderate-to-severe disease, there remains ∼10% of the asthmatic population with serious unremitting symptoms, resulting in considerable impact on quality of life, disproportionate use of health care resources, and adverse effects from regular systemic steroid use. In an ideal world, optimal treatment of severe refractory asthma should achieve the best possible asthma control and quality of life with the least dose of systemic corticosteroids. The choice and formulation of therapeutic agent are dictated by the severity of disease and may include immunological modifiers and biologic therapies. Unfortunately, current asthma guidelines offer little contribution to the management of the challenging patient with severe refractory asthma and none of them have addressed therapeutic alternatives to oral corticosteroids. This article reviews the current evidence for immunomodulating and biologic approaches in severe refractory asthma. [Copyright &y& Elsevier]

Summary: Although smoking cessation is clearly beneficial, many smokers respond poorly to smoking cessation efforts with rather disappointing overall success rate of long-term abstinence. The perceived lack of effectiveness of smoking cessation may well influence how physicians set their priorities with regard to an effective use of their consultation time. Negative beliefs and attitudes can be resolved by advancing the general understanding of the natural history of quitting, by making sensible use of smoking cessation services, and by being aware of the correct use of drugs for nicotine dependence when prescribed. In particular, a better understanding of predictors of success in smoking cessation can help physicians in id entifying smokers who stand a fair chance of quitting. The purpose of the present article is to review those predictors of smoking cessation that can be of help in routine clinical consultation. [Copyright &y& Elsevier]

Background: Asthma and rhinitis are often comorbid conditions, and several studies have suggested that rhinitis often precedes asthma. Sensitization to allergen has been shown to be one of the strongest determinants of incident asthma, but little is known about the effects of cigarette smoking among individuals with allergic rhinitis. Objective: We sought to evaluate the importance of cigarette smoking as an additional risk factor for incident asthma in a cohort of hospital-referred nonasthmatic adult subjects with allergic rhinitis. Methods: The study population selected at baseline was invited for a follow-up visit 10 years later to check for possible asthma features. Categories of smokers, exsmokers, and never smokers were used in the analyses together with pack-years to calculate the level of cumulative exposure. Results: Complete data were available from 325 patients. Smoking was significantly related to the risk of incident asthma, with the odds ratio (OR) being 2.67 (95% CI, 1.70-4.19) for univariate and 2.98 (95% CI, 1.81-4.92) for multivariate analyses. A clear dose-response association for exposure to tobacco and risk of new-onset asthma was observed in the multivariate analyses: those with 1 to 10 pack-years had an OR of 2.05 (95% CI, 0.99-4.27), those with 11 to 20 pack years had an OR of 3.71 (95% CI, 1.77-7.78), and those with 21 or more pack-years had an OR of 5.05 (95% CI, 1.93-13.20) compared with never smokers. Conclusions: The current findings support the hypothesis that cigarette smoking is an important independent risk factor for the development of new asthma cases in adults with allergic rhinitis. [Copyright &y& Elsevier]

Summary: Background: Given the observed association between smoking, inflammation and airway hyperresponsiveness (AHR) one may predict that smoking cessation may improve AHR. However, only a few studies have investigated the effect of smoking on AHR and their results appear to be conflicting depending on the stimulus used in their bronchoprovocation protocol. The aim of the current study was to compare changes in AHR between direct (methacholine (Mch)) and indirect (adenosine 5′monophosphate (AMP)) stimuli before and at different time points after smoking cessation in smokers with allergic rhinitis (±asthma). Methods: We have prospectively studied changes in AHR to inhaled Mch and AMP in smokers with allergic rhinitis (±asthma), before and at 6 and 12 months after smoking cessation. Results: It was found that 28% (16/57) of the participants had quit smoking by the end of the study. No significant change in AHR was observed in smoking cessation failures. A significant improvement in AHR to AMP but not Mch was observed 6 months after smoking cessation in quitters; a 1.2 doubling concentrations change in PC20 AMP was measured whereas only a 0.4 doubling concentrations change was observed for PC20 Mch. However, after 12 months smoking cessation the improvement in AHR became significant for both AMP and Mch, their dose–response curves being displaced to the right to a similar extent (1.4 and 1.1 doubling concentrations for AMP and Mch, respectively). Conclusion: Smoking cessation can improve AHR in smokers who quit with a 6 months improvement being reported for the airways response to AMP but not Mch. AMP challenge may detect earlier changes in AHR in smokers during smoking cessation. [Copyright &y& Elsevier]

TNF-α is a multifunctional proinflammatory cytokine whose effects are regulated both by local concentrations and cell surface receptor dynamics. The importance of TNF-α in asthma and severe refractory asthma in particular has been consolidated in recent times. Here, we review the evidence for TNF-α axis upregulation in refractory asthma and the benefit of suppressing TNF-α activity using humanised monoclonal antibodies or recombinant soluble TNF-α receptors in asthma. [Copyright &y& Elsevier]

Summary: Background: Inhaled corticosteroids (ICS) are the most effective anti-inflammatory agents available for the treatment of asthma but they produce only modest effects on airway inflammation and non-specific bronchial hyperresponsiveness (BHR). However, little is known about the possibility that treatment with ICS might cause additional protection on BHR to inhaled tachykinins such as neurokinin A (NKA). Objective: Therefore, we compared the effects of beclomethasone dipropionate (BDP) on the degree of BHR to inhaled histamine and NKA in a double-blind, controlled, cross-over study of asthmatic patients. Methods: Patients attended the laboratory before and after each 6 weeks treatment period to undertake concentration–response studies with histamine and NKA. Bronchial responsiveness to both funs was expressed as the provocative concentration producing a 20% decrease in FEV1 from baseline (PC20). Results: BDP therapy attenuated the constrictor response to both agonists to a similar degree, their geometric mean (range) PC20 values increasing from 0.47 (0.21–1.41)mg/ml to 2.43 (0.51–4.50)mg/ml (P<0.01, post-salb vs. post-BDP treatment) and from 101.7 (27.3–356.1)μg/ml to 666.7 (151.5–1000)μg/ml (P<0.01, post-salb vs. post-BDP treatment) for histamine and NKA, respectively. Conclusion: Airway responsiveness to histamine and NKA is reduced by BDP to the same extent. As a result of these findings, provocation with NKA is unlikely to provide additional useful information in the assessment of airway inflammation in asthma. [Copyright &y& Elsevier]