Non-smoking Controls Research Articles

Effects of smoking on hemoglobin and erythrocytes sedimentation rate and its association with ABO blood groups

Context: “Smoking causes variation in different parameters of blood like hemoglobin (Hb) and erythrocyte sedimentation rate (ESR).” Continuous exposure to carbon monoxide leads to the formation of carboxyhemoglobin, an inactive form of Hb with no oxygen-carrying capacity; carboxyhemoglobin also leads to shifting in the Hb dissociation curve on the left side, causing a reduction in the ability of Hb to deliver oxygen to the tissue. Aims: The aim of this study was to compare the effect of cigarette smoking on Hb and ESR between smokers and nonsmokers and its association with ABO blood groups. Settings and Design: A total of 100 subjects which included 50 smokers and 50 age-matched nonsmoker controls were included in this study. Material and Methods: 5 ml of venous blood was collected by venipuncture method and Hb was measured by cyanmethhemoglobin method, ESR by Westergren's method, and ABO blood grouping by slide method. Statistical Analysis Used: Statistical software SPSS version 20 (SPSS, Chicago, Illinois) was used. Student's t test was performed for parametric numerical data and Chi-square test was performed for nonparametric categorical data. A value of P

Effect of Cigarette and Shisha smoking on cognitive functions impairment: A cross sectional study.

Objectives:Cigarette and Shisha smoking is becoming a common practice in young generation worldwide. Since, this is a growing threat to public health, our study aims to investigate the cognitive function responses of cigarette and Shisha inhalation in adolescents.Methods:This retrospective cross sectional study comprised three groups, cigarette smoker, Shisha smoker, and nonsmoker control group (each n=25). All the participants were apparently healthy male volunteers aged 21-24 years. Cognitive functions were assessed by employing “Cambridge Neuropsychological Test Automated Battery”. The cognitive functions outcome variables were response time tasks (attention switching task (AST) and the percentage of correct answers pattern recognition memory (PRM) task.Results:Cigarette and Shisha smokers exhibited a considerable decline in cognitive performance parameters, AST mean correct latency (p=0.001), AST mean correct latency (congruent) (p=0.001), AST mean correct latency (incongruent) (p=0.001) and AST mean correct latency (switching) (p=0.001) compared to matched control group.Conclusions:Cigarette and Shisha smokers exhibited significant impairment in their cognitive functions. The present study findings convince that cigarette and Shisha smokers should quit smoking.

Comparative Study of Electrocardiographic Parameters among Tobacco Smokers and Tobacco Chewers

Background and Aim: Nicotine and other components of cigarette can produce profound changes in the heart, which can be assessed by doing electrocardiogram (ECG). The present study compares the vitals and ECG parameters among tobacco non-smokers (controls), tobacco smokers and tobacco chewers. Methods: One hundred and fifty healthy male volunteers, age group of 18-25 years from outpatient department, were included for the study. The subjects were divided into group 1 (control, n=50), group 2 (tobacco smokers, n=50) and group 3 (tobacco chewers, n=50). Subjects were asked to abstain tobacco and beverages consumption 2 hours prior to recording ECG. The subject’s vital: blood pressure and ECG parameters: heart rate, QT interval, QTc (corrected QT interval) were recorded in physiology lab of Nobel Medical College and Teaching Hospital, Nepal. Results: The data analysis was done by independent student “t” test. The data analysis showed significant increase in blood pressure on comparison of group 1 with group 2 (p=0.001) and group 3 (p=0.001) respectively. The data analysis of ECG parameters also showed decrease in QT and QTc (corrected QT) comparing group 1 with group 2 (p=0.001) and group 3 (p=0.001) separately which was highly significant. There was significantly increase in heart rate on comparison of group 1 separately with group 2 and group 3. Conclusion: The study concluded that the consumption of either smoked or chewed form of tobacco adversely affects cardiovascular system.

Translation of adapting quantitative CT data from research to local clinical practice: validation evaluation of fully automated procedures to provide lung volumes and percent emphysema.

Current clinical chest CT reporting includes limited qualitative assessment of emphysema with rare mention of lung volumes and limited reporting of emphysema, based upon retrospective review of CT reports. Quantitative CT analysis performed in COPDGene and other research cohorts utilize semiautomated segmentation procedures and well-established research method (Thirona). We compared this reference QCT data with fully automated QCT analysis that can be obtained at the time of CT scan and sent to PACS along with standard chest CT images. 164 COPDGene® cohort study subjects enrolled at Brigham and Women's Hospital had baseline and 5-year follow-up CT scans. Subjects included 17 nonsmoking controls, 92 smokers with normal spirometry, 15 preserved ratio impaired spirometry (PRISm) patients, 12 GOLD 1, 20 GOLD 2, and 8 GOLD 3-4. 97% ( ) of clinical reports did not mention lung volumes, and 14% ( ) made no mention of emphysema. Total lung volumes determined by the fully automated algorithm were consistently 47 milliliters (ml) less than the Thirona reference value for all subjects (95% confidence interval to ). Percent emphysema values were equivalent to the Thirona reference values. Well-established research reference data can be used to evaluate and validate automated QCT software. Validation can be repeated as software is updated.

Salivary Cytokine Biomarker Concentrations in Relation to Obesity and Periodontitis.

Systemic low-grade inflammation is associated with obesity. Our aim was to examine the association between obesity and salivary biomarkers of periodontitis. Salivary interleukin (IL)-1-receptor antagonist (IL-1Ra), IL-6, IL-8, IL-10, and tumor necrosis factor (TNF)-α concentrations were measured from 287 non-diabetic obese (body mass index (BMI) of >35 kg/m2) individuals and 293 normal-weight (BMI of 18.5–25 kg/m2) controls. Periodontal status was defined according to a diagnostic cumulative risk score (CRS) to calculate the risk of having periodontitis (CRS I, low risk; CRS II, medium risk; CRS III, high risk). In the whole population, and especially in smokers, higher IL-8 and lower IL-10 concentrations were detected in the obese group compared to the control group, while in non-smoking participants, the obese and control groups did not differ. IL-1Ra and IL-8 concentrations were higher in those with medium or high risk (CRS II and CRS III, p < 0.001) of periodontitis, whereas IL-10 and TNF-α concentrations were lower when compared to those with low risk (CRS I). In multivariate models adjusted for periodontal status, obesity did not associate with any salivary cytokine concentration. In conclusion, salivary cytokine biomarkers are not independently associated with obesity and concentrations are dependent on periodontal status.

Evaluation of Salivary Antioxidants and Oxidative Stress Markers in Male Smokers.

Cigarette smoke free radicals can cause cellular damage and different diseases. All the body fluids have antioxidants which protect against free radicals. The aim of this study was to evaluate salivary total antioxidant capacity and peroxidase, uric acid and malondialdehyde levels in smokers and a nonsmoking control group. Unstimulated saliva was collected from 510 males. A total of 259 subjects were current smokers and 251 were non-smokers. The levels of salivary total antioxidant capacity, uric acid, peroxidase and malondialdehyde were measured using standard procedures. Data were analyzed with t test and ANOVA. The smokers were younger and dental hygiene index was higher than healthy nonsmoking controls. The mean total antioxidant capacity in smokers and nonsmokers was 0.13±0.07 and 0.21±011, respectively (P=0.001). Smokers had significantly lower peroxidase and uric acid levels than healthy controls. In addition, the mean malondialdehyde levels in the smokers and nonsmokers were 4.55 ±2.61 and 2.79 ±2.21, respectively (P=0.001). Cigarette smoke produces free radical and oxidative stress, causing many side effects. Salivary antioxidant levels decreased and malondialdehyde levels increased in smokers, indicating the high oxidative stress among smokers compared to nonsmokers. Cigarette smoke had deleterious effects on main salivary antioxidants levels.

Diffusion tensor imaging of white matter integrity in relation to smoking index and exacerbations in severe chronic obstructive pulmonary disease

BackgroundDiffusion tensor imaging (DTI) is a non-invasive MR modality that provides an evaluation of brain tissue microstructure and architecture in vivo. We aimed to assess the diagnostic value of DTI parameters in evaluating cerebral white matter integrity in patients of severe chronic obstructive pulmonary disease (COPD) and correlate these parameters with smoking index (SI) and the number of exacerbations in the last year.This prospective study included 30 COPD male past smoker patients and 15 age- and sex-matched nonsmoker controls. Staging of COPD, SI and number of exacerbations in the last year were obtained. Routine brain MRI and DTI were done in all subjects. The selected white matter tracts’ fractional anisotropy (FA), and mean diffusivity (MD) were calculated in the region of interest in axial slices.ResultsThe mean FA and MD values of all selected white matter tracts showed a high significant difference (p < 0.001) between patients and control group. The correlation between FA, SI and exacerbation frequency was not significant in the majority of white matter tracts (p > 0.05). The correlation between MD, SI and exacerbation frequency was significant for the majority of tracts (p < 0.05).ConclusionDTI metrics are valuable non-invasive tools in evaluating the white matter abnormalities in COPD patients. Smoking index and frequency of exacerbations have possible relation to extra-pulmonary cerebral manifestations of COPD.

Altered generation of ciliated cells in chronic obstructive pulmonary disease

In COPD, epithelial changes are prominent features in the airways, such as goblet cell hyperplasia and squamous metaplasia. In contrast, it remains unclear whether ciliated cells are reduced and which pathways dysregulate epithelial differentiation. We hypothesized that bronchial epithelial cell lineage specification is dysregulated in COPD because of an aberrant reprogramming through transforming growth factor (TGF)-β1. Surgical lung tissue from 81 COPD and 61 control (smokers and non-smokers) patients was assessed for bronchial epithelial cell phenotyping by immunohistochemistry, both in situ and in vitro in reconstituted air-liquid interface (ALI) cultures. The role of TGF-β1 was studied in vitro. COPD epithelium in large airways, when compared to controls, showed decreased β-tubulin IV + ciliated cells (4.4%, 2.5–8.8% versus 8.5%, 6.3–11.8% of surface staining, median and IQR, p = 0.0009) and increased MUC5AC + goblet cells (34.8%, 24.4–41.9% versus 10.3%, 5.1–17.6%, p < 0.0001). Both features were recapitulated in the ALI-cultured epithelium from COPD patients. Exogenous TGF-β1 reduced mucociliary differentiation while neutralizing TGF-β1 during ALI increased both specialized cell types. The COPD airway epithelium displays altered differentiation for ciliated cells, which recapitulates in vitro, at least in part through TGF-β1.

Transcriptomic analysis of monocytes from HIV-positive men on antiretroviral therapy reveals effects of tobacco smoking on interferon and stress response systems associated with depressive symptoms

BackgroundTobacco smoking induces immunomodulatory and pro-inflammatory effects associated with transcriptome changes in monocytes and other immune cell types. While smoking is prevalent in HIV-infected (HIV+) individuals, few studies have investigated its effects on gene expression in this population. Here, we report whole-transcriptome analyses of 125 peripheral blood monocyte samples from ART-treated HIV+ and uninfected (HIV−) men enrolled in the Multicenter AIDS Cohort Study (MACS) (n = 25 HIV+ smokers, n = 60 HIV+ non-smokers, n = 40 HIV− non-smoking controls). Gene expression profiling was performed using Illumina HumanHT-12 Expression BeadChip microarrays. Differential expression analysis was performed with weighted linear regression models using the R limma package, followed by functional enrichment and Ingenuity Pathway analyses.ResultsA total of 286 genes were differentially expressed in monocytes from HIV+ smokers compared with HIV− non-smokers; upregulated genes (n = 180) were enriched for immune and interferon response, chemical/stress response, mitochondria, and extracellular vesicle gene ontology (GO) terms. Expression of genes related to immune/interferon responses (AIM2, FCGR1A-B, IFI16, SP100), stress/chemical responses (APAF1, HSPD1, KLF4), and mitochondrial function (CISD1, MTHFD2, SQOR) was upregulated in HIV+ non-smokers and further increased in HIV+ smokers. Gene expression changes associated with smoking in previous studies of human monocytes were also observed (SASH1, STAB1, PID1, MMP25). Depressive symptoms (CES-D scores ≥ 16) were more prevalent in HIV+ tobacco smokers compared with HIV+ and HIV− non-smokers (50% vs. 26% and 13%, respectively; p = 0.007), and upregulation of immune/interferon response genes, including IFI35, IFNAR1, OAS1-2, STAT1, and SP100, was associated with depressive symptoms in logistic regression models adjusted for HIV status and smoking (p < 0.05). Network models linked the Stat1-mediated interferon pathway to transcriptional regulator Klf4 and smoking-associated toll-like receptor scaffolding protein Sash1, suggesting inter-relationships between smoking-associated genes, control of monocyte differentiation, and interferon-mediated inflammatory responses.ConclusionsThis study characterizes immune, interferon, stress response, and mitochondrial-associated gene expression changes in monocytes from HIV+ tobacco smokers, and identifies augmented interferon and stress responses associated with depressive symptoms. These findings help to explain complex interrelationships between pro-inflammatory effects of HIV and smoking, and their combined impact on comorbidities prevalent in HIV+ individuals.

Cerebellar Morphometry and Cognition in the Context of Chronic Alcohol Consumption and Cigarette Smoking.

Cerebellar atrophy (especially involving the superior-anterior cerebellar vermis) is among the most salient and clinically significant effects of chronic hazardous alcohol consumption on brain structure. Smaller cerebellar volumes are also associated with chronic cigarette smoking. The present study investigated effects of both chronic alcohol consumption and cigarette smoking on cerebellar structure and its relation to performance on select cognitive/behavioral tasks. Using T1-weighted Magnetic Resonance Images (MRIs), the Cerebellar Analysis Tool Kit segmented the cerebellum into bilateral hemispheres and 3 vermis parcels from 4 participant groups: smoking (s) and nonsmoking (ns) abstinent alcohol-dependent treatment seekers (ALC) and controls (CON) (i.e., sALC, nsALC, sCON, and nsCON). Cognitive and behavioral data were also obtained. We found detrimental effects of chronic drinking on all cerebellar structural measures in ALC participants, with largest reductions seen in vermis areas. Furthermore, both smoking groups had smaller volumes of cerebellar hemispheres but not vermis areas compared to their nonsmoking counterparts. In exploratory analyses, smaller cerebellar volumes were related to lower measures of intelligence. In sCON, but not sALC, greater smoking severity was related to smaller cerebellar volume and smaller superior-anterior vermis area. In sALC, greater abstinence duration was associated with larger cerebellar and superior-anterior vermis areas, suggesting some recovery with abstinence. Our results show that both smoking and alcohol status are associated with smaller cerebellar structural measurements, with vermal areas more vulnerable to chronic alcohol consumption and less affected by chronic smoking. These morphometric cerebellar deficits were also associated with lower intelligence and related to duration of abstinence in sALC only.

End-product of fibrinogen is elevated in emphysematous chronic obstructive pulmonary disease and is predictive of mortality in the ECLIPSE cohort

Chronic obstructive pulmonary disease (COPD) is characterized by abnormal epithelial repair process that may result in intra-airway accumulation of fibrin. Given that plasma fibrinogen is the only FDA approved biomarker that predicts mortality and COPD exacerbations, we hypothesized that changes in the processing of fibrinogen may provide additional characterization of disease phenotype and COPD progression. A subpopulation of subjects with COPD, (n = 983) smoker (n = 205) and non-smoker controls (n = 98) were included from The Evaluation of COPD Longitudinally to Identify Predictive Surrogate End-points (ECLIPSE) cohort. Two biomarkers that specifically target the thrombin-mediated conversion of fibrinogen into fibrin (PRO-FIB), and plasmin-mediated degradation of cross-linked fibrin (X-FIB) were measured and compared with fibrinogen measurements. X-FIB had a predictive value for two-year mortality, with an adjusted hazard ratio of 1.48 per SD (n = 980; 95% Cl 1.18-1.84; p < 0.0001), and comparable to the fibrinogen hazard ratio of 1.59 per SD (n = 983; 95% Cl 1.29-1.96; p = 0.0003). X-FIB (p < 0.001), fibrinogen (p < 0.0001) and PRO-FIB (p < 0.05) were significantly elevated in symptomatic COPD (mMRC ≥ 2) as compared to asymptomatic COPD. X-FIB was the only biomarker that was associated with emphysema (p < 0.001), and only plasma fibrinogen (p < 0.05) was associated with exacerbations. There is a need for biomarkers to characterize the heterogeneity of COPD, to continuously improve clinical trial design and to identify disease progressors for efficient health care utilization. Each of three fibrinogen biomarkers studied provide information representing distinct aspects of COPD which may be used to characterize disease endotypes and to assess mortality risk in COPD.

Evaluation of foveal avascular zone and capillary plexus in smokers using optical coherence tomography angiography

PurposeTo evaluate the macular microvasculature in smokers in comparison to healthy subjects using optical coherence tomography angiography (OCTA). MethodsFifty chronic, regular smokers and 50 healthy non-smokers, as a control group, were recruited for the study. Foveal avascular zone (FAZ) area (mm2) and vessel density (VD) (%) in the superficial (SCP) and deep capillary plexus (DCP) were evaluated. ResultsFAZ area was 0.424 ± 0.100 mm2 in the smoker group and 0.333 ± 0.093 mm2 in the non-smoking control group (P = 0.002). The deep foveal VD was 31.76 ± 6.33% in the smoker group and 53.09 ± 5.88% in the non-smoking control group (P = 0.006). Superficial foveal and parafoveal, deep parafoveal VD were not statistically different between the groups (P = 0.120), (P = 0.337), (P = 0.287), respectively. ConclusionIn our study, there was an enlargement of FAZ and reduction of foveal VD at DCP in the eyes of smokers compared with non-smoking adults.

Might smoking assuage the pro‐inflammatory effect of diabetes in periodontal sites?

This study evaluated the effects of type 2 diabetes mellitus (DM), smoking, and these two factors combined on gingival crevicular fluid levels and ratios of pro-/anti-inflammatory cytokines. Associations between cytokines with each other and with key periodontal pathogens in periodontal sites under the challenge of one or both of these risk factors were also assessed. A total of 102 subjects with periodontitis were included in this cross-sectional study and assigned to one of the following groups: non-diabetic non-smokers (control group, n=25), non-smokers with DM (DM group, n=30), non-diabetic smokers (S group, n=26), and smokers with DM (S+DM group, n=21). The levels of 13 pro-inflammatory (IFN-γ, TNF-α, MIP-1α, GM-CSF, IL-1β, IL-2, IL-6, IL-7, IL-8, IL-12, IL-17, IL-21, and IL-23) and 5 anti-inflammatory (IL-4, IL-5, IL-10, IL-13, and TGF-β) cytokines were assessed in healthy and diseased sites, using multiplex immunoassay. Ratios of pro-/anti-inflammatory cytokines were obtained in all possible permutations. The levels of 7 key periodontal pathogens were evaluated by qPCR. Overall, the ratios of pro-/anti-inflammatory cytokines were higher in healthy and diseased sites of the DM group and in healthy sites of the S+DM group, and lower in diseased sites of the S group, compared with the control (p<.05). The proportion of the pro-inflammatory cytokines in relation to the 18 cytokines studied was higher in the DM group and lower in the S group, whereas the proportion of the anti-inflammatory cytokines was lower in both diabetic groups and higher in the S group, compared to the control (p<.05). A cluster of six common cytokines (IL-4, IL-5, IL-12, IL-13, IL-21, and IL-23) was observed in the diseased sites of all groups studied. Eight common cytokines (IL-4, IL-5, IL-12, IL-13, IL-17, IL-21, IL-23, and IFN-γ) grouped closely in the healthy sites of both diabetic groups. Significant associations between pathogens and cytokines occurred mainly in the diseased sites of the S + DM group (p<.05). Diabetes mellitus induced an overall pro-inflammatory state, while smoking mainly stimulated immunosuppression in periodontal sites. When the two risk factors overlapped, smoking seemed to partially assuage the hyperinflammatory effect of DM.

The effect of cigarette smoking on bronchoalveolar lavage protein profiles from patients with different interstitial lung diseases.

The proteomic approach applied to the analysis of BAL gives a panorama of the complex network of proteins of different origin and function and their modifications at alveolar level. Cigarette smoking may influence BAL protein composition and it represents the most relevant risk factor for several lung diseases. This review, for the first time, discusses the available literature regarding the effects of cigarette smoking on BAL protein composition of healthy subjects and patients affected by interstitial lung diseases (ILD). The comparison of BAL protein profiles of smokers and non-smoker healthy controls revealed alterations of proteins related to oxidative stress and protease/antiprotease imbalance (such as alpha 1 antitrypsin, alpha-1-antichymotrypsin, apolipoprotein A1, peroxiredoxin 1 and glutathione S transferase P). Smoking exposure leads to a significant dysregulation of a large number of molecular pathways involved in interstitial lung diseases and the proteomic studies applied to the study of BAL of idiopathic pulmonary fibrosis, sarcoidosis and other ILD contributed to clarify the underlying pathogenetic mechanisms facilitating ILD development and biomarker discovery.

Structural alterations and markers of endothelial activation in pulmonary and bronchial arteries in fatal asthma

BackgroundThere is interest in better understanding vessel pathology in asthma, given the findings of loss of peripheral vasculature associated with disease severity by imaging and altered markers of endothelial activation. To date, vascular changes in asthma have been described mainly at the submucosal capillary level of the bronchial microcirculation, with sparse information available on the pathology of bronchial and pulmonary arteries. The aim of this study was to describe structural and endothelial activation markers in bronchial arteries (BAs) and pulmonary arteries (PAs) of asthma patients who died during a fatal asthma attack.MethodsAutopsy lung tissue was obtained from 21 smoking and non-smoking patients who died of an asthma attack and nine non-smoking control patients. Verhoeff–Masson trichrome staining was used to analyse the structure of arteries. Using immuno-histochemistry and image analyses, we quantified extracellular matrix (ECM) components (collagen I, collagen III, versican, tenascin, fibronectin, elastic fibres), adhesion molecules [vascular cell adhesion molecule 1 (VCAM-1) and intercellular adhesion molecule 1 (ICAM-1)] and markers of vascular tone/dysfunction [endothelin-1 (ET-1) and angiotensin II type 2 receptor (AT2)] in PAs and BAs.ResultsThere were no significant differences in ECM components, ICAM-1, ET-1 or AT2 between asthma patients and controls. Smoking asthma patients presented with decreased content of collagen III in both BA (p = 0.046) and PA (p = 0.010) walls compared to non-smoking asthma patients. Asthma patients had increased VCAM-1 content in the BA wall (p = 0.026) but not in the PA wall.ConclusionOur data suggest that the mechanisms linking asthma and arterial functional abnormalities might involve systemic rather than local mediators. Loss of collagen III in the PA was observed in smoking asthma patients, and this was compatible with the degradative environment induced by cigarette smoking. Our data also reinforce the idea that the mechanisms of leukocyte efflux via adhesion molecules differ between bronchial and pulmonary circulation, which might be relevant to understanding and treating the distal lung in asthma.

Mitochondrial dysfunction in human primary alveolar type II cells in emphysema

BackgroundCigarette smoke is the main risk factor of pulmonary emphysema development, which is characterized by alveolar wall destruction. Mitochondria are important for alveolar type II (ATII) cell metabolism due to ATP generation. MethodsWe isolated ATII cells from control non-smoker and smoker organ donors, and after lung transplant of patients with emphysema to determine mitochondrial function, dynamics and mitochondrial (mt) DNA damage. FindingsWe found high mitochondrial superoxide generation and mtDNA damage in ATII cells in emphysema. This correlated with decreased mtDNA amount. We also detected high TOP1-cc and low TDP1 levels in mitochondria in ATII cells in emphysema. This contributed to the decreased resolution of TOP1-cc leading to accumulation of mtDNA damage and mitochondrial dysfunction. Moreover, we used lung tissue obtained from areas with mild and severe emphysema from the same patients. We found a correlation between the impaired fusion and fission as indicated by low MFN1, OPA1, FIS1, and p-DRP1 levels and this disease severity. We detected lower TDP1 expression in severe compared to mild emphysema. InterpretationWe found high DNA damage and impairment of DNA damage repair in mitochondria in ATII cells isolated from emphysema patients, which contribute to abnormal mitochondrial dynamics. Our findings provide molecular mechanisms of mitochondrial dysfunction in this disease. FundThis work was supported by National Institutes of Health (NIH) grant R01 HL118171 (B.K.) and the Catalyst Award from the American Lung Association (K.B.).

Region-Specific Changes of Insular Cortical Thickness in Heavy Smokers.

Insula plays an essential role in maintaining the addiction to cigarette smoking and smoking-related alterations on the insular volume and density have been reported in smokers. However, less is known about the effects of chronic cigarette smoking on the insular cortical thickness. In this study, we explored the region-specific changes of insular cortical thickness in heavy smokers and their relations with smoking-related variables. 37 heavy smokers (29 males, mean age 47.19 ± 7.22 years) and 37 non-smoking healthy controls (29 males, mean age 46.95 ± 8.45 years) participated in the study. Subregional insular cortical thickness was evaluated and compared between the two groups. Correlation analysis was performed to investigate relationships between the insular cortical thickness and clinical characteristics in heavy smokers. There was no statistical difference on the cortical thickness in the left insula (p = 0.536) between the two groups while heavy smokers had a slightly thinner cortical thickness in the right insula (p = 0.048). In addition, heavy smokers showed a greater cortical thinning in the anterior (p = 0.0084) and superior (p = 0.0054) segment of the circular sulcus of the right insula as well as the inferior (p = 0.012) segment of the circular sulcus of the left insula. Moreover, the cortical thickness of the superior segment of the circular sulcus of the left insula was correlated negatively with nicotine severity (r = −0.423; p = 0.009) and the longer cigarette exposure was associated with the cortical thinning in the long insular gyrus and central sulcus of the right insula (r = −0.475; p = 0.003). Our findings indicate that chronic cigarette use is associated with region-specific insular thinning, which has the potential to improve our understanding of the specific roles of insular subregions in nicotine addiction.

Study of the immunological changes associated with Aspergillus infection among ceramic workers

Ceramic workers are exposed to high levels of respirable dust that contains high microbial levels such as Aspergillus. It is recommended to consider fungal exposure in ceramic industry as a hazardous problem. This work aimed to study the impact of occupational exposure to high environmental concentrations of Aspergillus on the immune parameters related to the respiratory system in ceramic workers. Serum levels of total IgE, intercellular adhesion molecule-1 (ICAM-1), alpha 1-antitrypsin (α1AT), and tumor necrosis factor alpha (TNF-α) were assessed in 40 ceramic workers and 56 matched controls. Statistical analysis revealed that the levels of total IgE and ICAM-1 were higher in both non-smoker and smoker ceramic workers compared to their controls. While TNF-α was significantly lower in non-smoker ceramic workers compared to non-smoker controls. In addition, ceramic workers with sputum negative PCR for Aspergillus had lower TNF-α than those with positive PCR. α1AT levels did not differ significantly among the examined groups. These changes were not correlated to the duration of exposure. In conclusion, occupational exposure to Aspergillus may cause different effects on immunological parameters related to respiratory problems in ceramic workers.

Defective bacterial phagocytosis is associated with dysfunctional mitochondria in COPD macrophages.

Increased reactive oxygen species (ROS) have been implicated in the pathophysiology of chronic obstructive pulmonary disease (COPD). This study examined the effect of exogenous and endogenous oxidative stress on macrophage phagocytosis in patients with COPD.Monocyte-derived macrophages (MDMs) were generated from non-smoker, smoker and COPD subjects, differentiated in either granulocyte macrophage-colony stimulating factor (G-Mφ) or macrophage-colony stimulating factor (M-Mφ). Alveolar macrophages were isolated from lung tissue or bronchoalveolar lavage fluid. Macrophages were incubated in ±200 µM H2O2 for 24 h, then exposed to fluorescently labelled Haemophilus influenzae or Streptococcus pneumoniae for 4 h, after which phagocytosis, mitochondrial ROS (mROS) and mitochondrial membrane potential (ΔΨm) were measured.Phagocytosis of bacteria was significantly decreased in both G-Mφ and M-Mφ from COPD patients compared with from non-smoker controls. In non-smokers and smokers, bacterial phagocytosis did not alter mROS or ΔΨm; however, in COPD, phagocytosis increased early mROS and decreased ΔΨm in both G-Mφ and M-Mφ. Exogenous oxidative stress reduced phagocytosis in non-smoker and COPD alveolar macrophages and non-smoker MDMs, associated with reduced mROS production.COPD macrophages show defective phagocytosis, which is associated with altered mitochondrial function and an inability to regulate mROS production. Targeting mitochondrial dysfunction may restore the phagocytic defect in COPD.

Relevance of Carotid Intima-Media Thickness and Plaque Morphology in the Risk Assessment of Patients with Acute Ischemic Cerebral Infarcts: A Case-Control Study of Large Series from a Single Center.

Background:Carotid atherosclerosis is not only a marker of systemic atherosclerosis but also a predictor of ischemic stroke. The purpose of this study is to correlate the relationship between atherosclerotic risk factors, plaque categories, percentage of stenosis, stroke subtypes, and carotid intima-media thickness (CIMT) in patients with acute ischemic stroke.Methods:This case–control study was conducted over 4 years from December 2014 to December 2018. A total of 500 cases diagnosed with acute cerebral infarct using computed tomography or magnetic resonance imaging were included in the study. Two hundred and fifty healthy controls were studied for the presence of atherosclerotic risk factors and carotid artery IMT by B-mode Doppler ultrasonography. The IMT value thus calculated was 0.79 mm and such a value would include >95% of the controls. Carotid plaques were detected from both sides of IMT measurement of the carotid system.Results:A total of 500 cases of acute infarct and 250 healthy controls were included in this case–control study. CIMT was abnormal in 348 cases with 192 males and 156 females with a mean value of 0.912 ± 0.124 against 0.794 ± 0.132; P < 0.001 controls. Mean CIMT (averaged right and left) varied directly according to the increasing plaque stenosis ranging from 0.70 mm to 0.96 mm in males and 0.68 mm to 0.94 mm in females ranging from no plaque to cases with ≥50% stenosis (P < 0.001 across stenosis categories). On multivariate analysis, CIMT (>0.79) remained associated as compared to other variables (PR [Probability] 5.33, 95% confidence interval: 1.398–22.784; P = 0.012). Mean right CIMT of patients with lacunar infarction, cardioembolism, and large artery stroke was 0.886 ± 0.230, 0.919 ± 0.171, and 0.938 ± 0.169 mm, respectively (P = 0.032). Mean left CIMT of patients with lacunar infarction, cardioembolism, and large artery stroke was 0.884 ± 0.195, 0.916 ± 0.144, and 0.930 ± 0.137 mm, respectively (P = 0.034).Conclusion:CIMT measurements are independent markers of acute ischemic cerebral infarcts. In the current study, CIMT was found to be higher among acute ischemic stroke patients who were the elderly, smoker, hypertensive, diabetic, and hypercholesterolemic than that of nonsmoker, normotensive, nondiabetic, and normocholesterolemic controls.