OBJECTIVETo investigate the effect of smoking on the microRNAs (miRNAs) expression in pneumoconiosis patients.

METHODSReal-time qPCR was used to measure the expression levels of miR-21, miR-200c, miR-16, miR-204, miR-206, miR-155, let-7g, miR-30b, and miR-192 in 36 non-smoking patients with pneumoconiosis and 38 smoking patients with pneumoconiosis, and the differences in expression levels between the two groups were evaluated by two-independent samples t-test.

RESULTSThe expression of miR-192 in serum showed a significant difference between non-smoking and smoking pneumoconiosis patients (P < 0.05), and it decreased gradually in smoking patients with stage I and II pneumoconiosis. In the serum of all pneumoconiosis patients, the expression level of miR-16 was the highest, while the expression level of miR-204 was the lowest.

CONCLUSIONPneumoconiosis patients have differential expression of miRNAs in serum, and smoking has an effect on the miRNAs expression in pneumoconiosis patients.

Humans ; MicroRNAs ; biosynthesis ; Pneumoconiosis ; metabolism ; physiopathology ; Polymerase Chain Reaction ; Smoking ; adverse effects

FIZZ/RELM is a new gene family named "found in inflammatory zone" (FIZZ) or "resistin-like molecule" (RELM). FIZZ1/RELMα is specifically expressed in lung tissue and associated with pulmonary inflammation. Chronic cigarette smoking up-regulates FIZZ1/RELMα expression in rat lung tissues, the mechanism of which is related to cigarette smoking-induced airway hyperresponsiveness. To investigate the effect of exercise training on chronic cigarette smoking-induced airway hyperresponsiveness and up-regulation of FIZZ1/RELMα, rat chronic cigarette smoking model was established. The rats were treated with regular exercise training and their airway responsiveness was measured. Hematoxylin and eosin (HE) staining, immunohistochemistry and in situ hybridization of lung tissues were performed to detect the expression of FIZZ1/RELMα. Results revealed that proper exercise training decreased airway hyperresponsiveness and pulmonary inflammation in rat chronic cigarette smoking model. Cigarette smoking increased the mRNA and protein levels of FIZZ1/RELMα, which were reversed by the proper exercise. It is concluded that proper exercise training prevents up-regulation of FIZZ1/RELMα induced by cigarette smoking, which may be involved in the mechanism of proper exercise training modulating airway hyperresponsiveness.
Animals ; Lung ; physiopathology ; Male ; Nerve Growth Factor ; metabolism ; Physical Conditioning, Animal ; methods ; Rats ; Rats, Sprague-Dawley ; Respiratory Hypersensitivity ; physiopathology ; Smoking ; physiopathology ; Up-Regulation

OBJECTIVESTo explore the effect of acute smoking on vascular endothelial function, arterial stiffness and the possible underlying mechanisms.

METHODSWe measured the endothelial function and arterial stiffness in 50 healthy chronic smokers before and after acute smoking with EndoPAT2000. The test was carried out on two separate finger tips. The endothelial function was evaluated by PAT ratio of the finger tip and systemic arterial stiffness was evaluated by augmentation index (AI). Plasma soluble intercellular adhesion molecule-1 (sICAM-1) and tissue plasminogen activator (tPA) before and 20 min after acute smoking were measured with enzyme linked immuno sorbent assay.

RESULTSThe PAT ratio was decreased (1.87 ± 0.40 vs. 1.73 ± 0.28, P = 0.004) while AI was significantly increased after acute smoking (2.94% ± 21.77% vs. 7.11% ± 20.65%, P = 0.01). There was no significant changes in sICAM [(306.5 ± 76.1) µg/L vs. (315.7 ± 90.9) µg/L, P = 0.402], but tPA [7.87 (5.41 - 10.08) µg/L vs. 5.77 (3.77 - 9.68) µg/L, P < 0.01] was significantly decreased after smoking.

CONCLUSIONSSmoking could acutely affect endothelia function, arterial stiffness and deteriorate the activity of fibrinolytic system which could lead to coronary thrombosis in smokers.

Adult ; Arteries ; physiopathology ; Elasticity ; Endothelium ; metabolism ; Endothelium, Vascular ; metabolism ; physiopathology ; Humans ; Intercellular Adhesion Molecule-1 ; blood ; Male ; Middle Aged ; Smoking ; adverse effects ; Tissue Plasminogen Activator ; blood ; Vascular Resistance

Objective To understand the prevalence and metabolic abnormalities of fatty liver disease among adults in Mianyang City,Sichuan Province,and to analyze their influencing factors.Methods Totally 294 603 adults aged 18 years and older were enrolled by using a multi-stage stratified random sampling method in Mianyang City from November 1,2014 to September 30,2015.Fatty liver was diagnosed by abdominal ultrasound.The general demographic characteristics,smoking history,drinking history,and history of chronic disease were collected through questionnaires.Meanwhile,10 217 subjects were randomly selected for biochemical tests[fasting plasma gluose(FPG),triacylglycerol(TG),total cholesterol(TC),and alanine aminotransferase(ALT)].Results Of these 294 603 subjects,17 105(5.81%)had fatty liver.After having been age-adjusted based on the results of the sixth national census in 2010,the standardized prevalence was 5.32%.The prevalence was significantly higher in males(6.76%;standardized prevalence:7.24%)than in females(5.09%;standardized prevalence:4.08%)(=365.814,<0.001)。The prevalence of fatty liver disease was significantly higher in people with current smokers(8.52%)/ex-smokers(8.89%),occasional alcohol users(6.79%)/regular alcohol users(10.51%)/daily alcohol users(10.62%),and patients with hypertension(12.14%)/diabetes(15.19%)/coronary heart disease(10.22%)than those without corresponding characteristics(all <0.001).Abnormal increase in body mass index,diastolic blood pressure,FPG,TG,TC,and ALT were risk factors for fatty liver in Logistic regression model.Conclusions The prevalence of fatty liver in adults is relatively low in Mianyang City.Patients with fatty liver usually have varying degrees of abnormal increase in blood lipids,blood glucose,blood pressure,and ALT.Healthy lifestyles and comprehensively assessment of metabolic status are conducive to the prevention and treatment of fatty liver and extrahepatic complications.
Alcohol Drinking ; Body Mass Index ; China ; Fatty Liver ; metabolism ; physiopathology ; Female ; Humans ; Hypertension ; Male ; Prevalence ; Risk Factors ; Smoking

This study was performed to evaluate the changes of tear film and ocular surface caused by smoking. Symptom scoring, tear film break-up time (BUT), basal tear secretion test, corneal sensitivity test, keratoepitheliopathy scoring, and conjunctival impression cytology were performed in 29 smokers (58 eyes) and 26 non-smokers (52 eyes). Tear film BUT, basal tear secretion, corneal sensitivity, and squamous metaplasia were 7.71 +/- 2.66 sec, 6.29 +/- 2.85 mm, 53.69 +/- 5.69 mm, and 2.45 +/- 1.26 in smokers and 9.62 +/- 3.14 sec, 10.04 +/- 3.87 mm, 56.46 +/- 4.79 mm, and 1.12 +/- 0.83 in non-smokers, respectively (p< 0.05). Symptom score, keratoepitheliopathy score, and goblet cell density were not significantly different between the two groups. Tear film BUT was shorter, basal tear secretion and corneal sensitivity were lower, and squamous metaplasia was higher in heavy smokers than in light smokers. In conclusion, smoking deteriorates the tear film and ocular surface with decreased quantity and quality of tear film, decreased corneal sensitivity, and squamous metaplasia, and this deterioration is related to the amount of smoking.
Adult ; Aged ; Cell Count ; Conjunctiva/*metabolism/pathology ; Cornea/*metabolism/pathology ; Epithelial Cells/pathology ; Goblet Cells/metabolism/pathology ; Humans ; Lacrimal Apparatus/*metabolism/physiopathology ; Male ; Metaplasia ; Middle Aged ; Smoking/*metabolism/physiopathology ; Tears/chemistry/*secretion

BACKGROUNDInflammation within vulnerable coronary plaques may cause unstable angina by promoting rupture and erosion. C-reactive protein (CRP) is the most reliable and accessible test method for clinical use for identifying coronary artery disease event. Matrix metalloproteinase 9 (MMP-9) is highly over-expressed in the vulnerable regions of a plaque. Our aim was to evaluate the plasma levels of MMP-9 and hsCRP in subjects with both unstable angina and coronary plaques, as well as in those with unstable angina without coronary plaques.

METHODSPatients with newly diagnosed unstable angina pectoris from clinical presentation and ECG, who were undergoing coronary angiography from April 2007 to April 2009, were included in this study. A total of 170 subjects were enrolled in the study. Before angiography, the baseline clinical data (mainly including conventional risk factors) was collected. These patients were divided into two groups, a non-plaque group (G1) which included 55 patients with no significant stenosis or less than 20% stenosis in at least one of the major coronary artery branches, and a plaque group (G2) which included 115 patients with at least one of the major coronary artery branches unstable angina pectoris with at least 50% stenosis of one major coronary artery. The patients presenting with calcified nodules of a major coronary artery were excluded from this study. We examined the serum levels of MMP-9 for all cases by multi-effect enzyme-linked immunosorbent assay.

RESULTSThere was a significant difference in the serum levels of MMP-9 between the two groups (P < 0.001). The percentage of patients with hypertension, diabetes and current smokers were significantly different between the two groups (P = 0.034, P = 0.031, and P = 0.044 respectively). The univariate Logistic regression analyses of risk factors showed that smoking was the main risk factor for angina in the non-plaque group with the OR being 1.95 (95%CI 1.02 - 3.75). Hypertension, diabetes mellitus were negatively related with the occurrence of angina in the non-plaque group with the ORs being 0.50, and 0.36, respectively (95%CI 0.26 - 0.96 and 0.14 - 0.94). The MMP-9 level was negatively related to the occurrence of angina in the non-plaque group with an OR of 0.59 (95%CI 0.47 - 0.81).

CONCLUSIONSThere is a significantly difference in MMP-9 levels between the plaque and non-plaque groups. Current smoking has a significant influence on unstable angina patients without documented plaques. The serum MMP-9 level may be a significant biomarker which can help differentiate patients with unstable angina with plaques from those with unstable angina but without plaques.

Aged ; Angina, Unstable ; blood ; metabolism ; physiopathology ; C-Reactive Protein ; metabolism ; Coronary Angiography ; Coronary Artery Disease ; blood ; metabolism ; physiopathology ; Coronary Vessels ; metabolism ; pathology ; Female ; Humans ; Male ; Matrix Metalloproteinase 9 ; blood ; Middle Aged ; Multivariate Analysis ; Risk Factors ; Smoking ; adverse effects

AIMTo show the oxidative stress after cigarette smoke exposure in rat testis and to evaluate the effects of caffeic acid phenethyl ester (CAPE).

METHODSTwenty-one rats were divided into three groups of seven. Animals in Group I were used as control. Rats in Group II were exposed to cigarette smoke only (4 x 30 min/d) and rats in Group III were exposed to cigarette smoke and received daily intraperitoneal injections of CAPE (10 micromol/kg x d). After 60 days all the rats were killed and the levels of nitric oxide (NO) and anti-oxidant enzymes such as superoxide-dismutase, catalase and glutathione peroxidase (GSH-Px) and the level of malondialdehyde were studied in the testicular tissues of rats with spectrophotometric analysis.

RESULTSThere was a significant increase in catalase and superoxide-dismutase activities in Group II when compared to the controls, but the levels of both decreased after CAPE administration in Group III. GSH-Px activity was decreased in Group II but CAPE caused an elevation in GSH-Px activity in Group III. The difference between the levels of GSH-Px in Group I and Group II was significant, but the difference between groups II and III was not significant. Elevation of malondialdehyde after smoke exposure was significant and CAPE caused a decrease to a level which was not statistically different to the control group. A significantly increased level of NO after exposure to smoke was reversed by CAPE administration and the difference between NO levels in groups I and III was statistically insignificant.

CONCLUSIONExposure to cigarette smoke causes changes in the oxidative enzyme levels in rat testis, but CAPE can reverse these harmful effects.

Animals ; Antioxidants ; therapeutic use ; Caffeic Acids ; therapeutic use ; Catalase ; metabolism ; Glutathione Peroxidase ; metabolism ; Male ; Malondialdehyde ; metabolism ; Nitric Oxide ; metabolism ; Oxidative Stress ; physiology ; Phenylethyl Alcohol ; analogs & derivatives ; therapeutic use ; Rats ; Rats, Wistar ; Smoking ; Superoxide Dismutase ; metabolism ; Testis ; drug effects ; physiopathology

OBJECTIVES: This study was conducted to show the intraocular pressure (IOP) distribution and the factors affecting IOP in subjects with type 2 diabetes mellitus (DM) in India. METHODS: We measured the anthropometric and biochemical parameters for confirmed type 2 DM patients. A comprehensive ocular examination was performed for 1377 subjects aged > 40 years and residing in Chennai. RESULTS: A significant difference in IOP (mean +/- standard deviation) was found between men and women (14.6+/-2.9 and 15.0+/-2.8 mmHg, p = 0.005). A significantly elevated IOP was observed among smokers, subjects with systemic hypertension and women with clinically significant macular edema (CSME). After a univariate analysis, factors associated significantly with higher IOP were elevated systolic blood pressure, elevated resting pulse rate and thicker central corneal thickness (CCT). In women, elevated glycosylated hemoglobin was associated with a higher IOP. After adjusting for all variables, the elevated resting pulse rate and CCT were found to be associated with a higher IOP. CONCLUSIONS: Systemic hypertension, smoking, pulse rate and CCT were associated with elevated intraocular pressure in type 2 DM. Women with type 2 DM, especially those with CSME, were more prone to have an elevated IOP.
Adult ; Aged ; Blood Pressure ; Cornea/physiology ; Diabetes Mellitus, Type 2/complications/*physiopathology ; Female ; Heart Rate ; Hemoglobin A, Glycosylated/metabolism ; Humans ; Hypertension/complications ; India ; Intraocular Pressure/*physiology ; Macular Edema/complications ; Male ; Middle Aged ; Risk Factors ; Smoking

BACKGROUNDSmoking is related with insulin resistance and type 2 diabetes mellitus. Retinol-binding protein-4 is a new adipocytokine associated with insulin resistance. We investigated the serum levels of a series of adipocytokines including retinol-binding protein-4 in smokers and non-smokers to explore the possible roles of adipocytokines on smoking induced insulin resistance.

METHODSA total of 136 healthy male subjects (92 smokers and 44 non-smokers) with normal glucose tolerance were enrolled in the study. Adipocytokines including retinol-binding protein-4, visfatin, leptin, resistin, adiponectin were measured for the comparison between the two groups. Serum lipid profile, glucose, true insulin and proinsulin levels were measured as well in both groups. Food intake spectrum was also investigated.

RESULTSBoth groups had similar profile of food consumption; visfatin, leptin, resistin and adiponectin, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, alanine aminotransferase, aspartate aminotransferase, as well as blood pressure and body mass index, were similar in both groups. Triglycerides, retinol-binding protein-4 and homeostatic model assessment index for insulin resistance were higher in smoker group ((2.58 ± 2.53) vs. (1.60 ± 0.94) mmol/L, (26.05 ± 8.50) vs. (21.83 ± 8.40) µg/ml, and 2.25 ± 2.08 vs. 1.58 ± 1.15, respectively).

CONCLUSIONSmoking may have effect on insulin sensitivity, which is correlated with retinol-binding protein-4.

Adiponectin ; blood ; Adult ; Alanine Transaminase ; blood ; Aspartate Aminotransferases ; blood ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Humans ; Leptin ; blood ; Male ; Middle Aged ; Nicotinamide Phosphoribosyltransferase ; blood ; Resistin ; blood ; Retinol-Binding Proteins ; metabolism ; Smoking ; blood ; physiopathology ; Triglycerides ; blood

OBJECTIVE: To observe the role of aminophylline and simvastatin in preventing and curing chronic obstructive pulmonary disease (COPD), and to explore the underlying mechanisms based on airway inflammation and mucus hypersecretion.
 METHODS: The rat model of COPD was established by combination of cigarette smoking with intratracheal lipopolysaccharide (LPS) injection. Male SD rats were randomly divided into 4 groups (n=10 per group): a control group, a COPD group, an aminophylline group and a simvastatin group. The rats in the control group and the COPD group were treated with normal saline once a day via intragastric administration, while the rats in the aminophylline group and the simvastatin group were treated with aminophylline (5 g/L) and simvastatin (0.5 g/L) 1 mL/100 g once a day via intragastric administration, respectively. Pulmonary function and pathological changes in bronchus and lung were observed. The levels of IL-8, IL-17, and TNF-α in bronchoalveolar lavage fluid (BALF) were measured by enzyme-linked immunosorbent assay (ELISA). The mRNA and protein expressions of TLR4 and mucin 5AC (MUC5AC) in bronchi and lung tissues were detected by real-time PCR and Western blot, respectively.
 RESULTS: Pulmonary function and the pathophysiologic changes in bronchi and lung tissues in the COPD rats were consistent with typical phenotype of COPD. Compared with the control group, lung function indexes were significantly attenuated in the COPD group, while the levels of IL-8, IL-17, and TNF-α in BALF as well as the mRNA and protein levels of MUC5AC and TLR4 were significantly increased. Compared with the COPD group, lung function indexes were significantly increased in the aminophylline group and simvastatin group (P<0.01), while pulmonary pathological damages, the levels of IL-8, IL-17, and TNF-α in BALF as well as the mRNA and protein levels of MUC5AC and TLR4 were significantly decreased (P<0.01). Compared with the aminophylline group, the peak expiratory flow as well as the levels of IL-8, IL-17, and TNF-α in the simvastatin group were elevated (P<0.05). There are no significant difference in the mRNA and protein levels of MUC5AC and TLR4 between the 2 groups (P﹥0.05).
 CONCLUSION Aminophylline and simvastatin can decrease IL-8, IL-17, and TNF-α levels in BALF and inhibit the expression of MUC5AC and TLR4 in airway and lung tissues in COPD rats, suggesting that they may have a preventive and therapeutic effect on COPD through reducing the airway inflammation and mucus hypersecretion.
Aminophylline ; pharmacology ; Animals ; Bronchi ; metabolism ; Bronchoalveolar Lavage Fluid ; chemistry ; Cytokines ; chemistry ; Inflammation ; drug therapy ; Lipopolysaccharides ; Lung ; metabolism ; physiopathology ; Male ; Mucin 5AC ; metabolism ; Mucus ; metabolism ; Pulmonary Disease, Chronic Obstructive ; drug therapy ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Simvastatin ; pharmacology ; Smoke ; adverse effects ; Smoking ; adverse effects ; Toll-Like Receptor 4 ; metabolism