Health Status ; Hearing Loss, Noise-Induced/epidemiology* ; Humans ; Manufacturing Industry ; Noise, Occupational/adverse effects* ; Occupational Diseases ; Occupational Exposure

BACKGROUND/AIMS: There are increasing evidences for gastrointestinal motility disorder (GIMD) and gastric stress ulcer induced by noise stress. The present study was to investigate the reversed effect of melatonin on GIMD and gastric stress ulcer induced by noise stress and potential mechanism. METHODS: Noise stress was induced on rats, and melatonin (15 mg/kg) was administered to rats by intraperitoneal injection. Differences were assessed in gastric residual rate (GRR), small intestine propulsion rate (SPR), Guth injury score, cortisol, gastrointestinal hormones (calcitonin-gene-related peptide and motilin) and oxidative stress markers (superoxide dismutase and malondialde hyde) in blood plasma as well as gastric mucosa homogenate with or without melatonin. The pathological examination of gastric mucosa was also performed. RESULTS: The GRR and SPR were improved by noise stress compared with control (P < 0.05). The pathological examination and Guth injury score revealed gastric stress ulcer. Moreover, the levels of cortisol, motilin and malondialdehyde in blood plasma and malondialdehyde in gastric mucosa homogenate were increased by noise stress (P < 0.05). CGRP and superoxide dismutase activity in both of blood plasma and gastric mucosa homogenate were significantly decreased (P< 0.05). Furthermore, melatonin reversed changes in GRR, SPR, pathological examination, Guth injury score, cortisol, motilin, CGRP, superoxide dismutase activity and malondialdehyde (P < 0.05). CONCLUSIONS: Melatonin is effective in reversing the GIMD and gastric stress ulcer induced by noise stress. The underlying mechanism may be involved in oxidative stress and gastrointestinal hormones.
Animals ; Gastric Mucosa ; Gastrointestinal Hormones* ; Gastrointestinal Motility* ; Hydrocortisone ; Injections, Intraperitoneal ; Intestine, Small ; Malondialdehyde ; Melatonin* ; Motilin ; Noise* ; Oxidative Stress* ; Plasma ; Rats* ; Superoxide Dismutase ; Ulcer*

[摘 要] 目的：探讨精氨酸-甘氨酸-天冬氨酸（RGD）修饰对肿瘤抑素19肽（T-19）抗肝癌活性的影响，比较分析T-19及RGD修饰的T-19（RGD-T-19）对肝癌SK-Hep-1细胞增殖、侵袭和迁移能力的影响。方法：用Fmoc固相法合成T-19及RGD-T-19，用高效液相色谱仪和质谱进行分离、鉴定。常规培养SK-Hep-1细胞，用0、50、100、150、200、250 mg/mL的T-19及RGD-T-19分别处理细胞，分为0 mg/mL（对照）组、50 mg/mL组、100 mg/mL组、150 mg/mL组、200 mg/mL组、250 mg/mL组。CCK-8法、克隆形成实验、划痕愈合实验和Tanswell小室实验、WB法和qPCR法分别检测SK-Hep-1细胞的增殖、迁移、侵袭能力，以及环氧合酶-2（COX-2）、基质金属蛋白酶-2（MMP-2）、MMP-9、组织基质金属蛋白酶抑制剂-1（TIMP-1）、TIMP-2蛋白和MMP-1、MMP-2 mRNA的表达。结果：经质谱鉴定，用Fmoc固相法合成的T-19及RGD-T-19纯度高。T-19和RGD-T-19均能显著抑制SK-Hep-1细胞的增殖、迁移、侵袭能力，抑制COX-2蛋白、MMP-2和MMP-9蛋白及mRNA的表达、促进TIMP-1、TIMP-2蛋白的表达（P < 0.05, P < 0.01, P < 0.001），RGD-T-19的抑制或促进效应均明显强于T-19（均P < 0.05）。结论：利用Fmoc固相法合成了纯度高、活性好的T-19及RGD-T-19，两种肽均能抑制SK-Hep-1细胞增殖、侵袭和迁移能力，RGD-T-19作用明显强于T-19。

Objective: To investigate the relationship between body mass index (BMI) and all-cause mortality in hypertensive population. Methods: All participants were selected from a prospective cohort study based on a rural population from Henan province, China. Cox proportional hazards regression models were used to estimate the associations of different levels of BMI stratification with all-cause mortality. Restricted cubic spline models were used to detect the dose-response relation. Results: Among the 5 461 hypertensive patients, a total of 31 048.38 person-years follow-up was conducted. The median of follow-up time was 6 years, and 589 deaths occurred during the follow-up period. Compared to normal weight group (18.5 kg/m(2)%CI: 0.37-1.87), 0.81 (95%CI: 0.67-0.97), and 0.72 (95%CI: 0.56-0.91), respectively. The dose-response analysis showed a nonlinear, reverse "S" shaped relationship (non-linearity P<0.001). Conclusion: Overweight or obese might have a protective effect on all-cause mortality in hypertensive population, which supports the "obesity paradox" phenomenon.
Adult ; Asian People/statistics & numerical data* ; Blood Pressure/physiology* ; Body Mass Index ; Cause of Death ; China/epidemiology* ; Humans ; Hypertension/mortality* ; Middle Aged ; Mortality ; Obesity/mortality* ; Overweight ; Prospective Studies ; Risk Factors ; Young Adult

Objective: To investigate the expression of MSI1 and HER2 in mammary Paget's disease, and the correlation between the expression levels of MSI1 and HER2 and the clinicopathologic characteristics and prognosis of the patients. Methods: Clinical data and paraffin-embedded specimens of 34 pairs of mammary Paget's disease and underlying breast cancer were collected at the Department of Pathology, Affiliated Lianyungang Oriental Hospital of Xuzhou Medical University from March 2011 to December 2019. Immunohistochemistry was used to detect the expression of MSI1 and HER2 in mammary Paget's disease and the accompanying breast cancer, and to analyze the correlation between the expression levels of MSI1 and HER2 and their clinicopathologic features, as well as their influence on prognosis. Results: In mammary Paget's disease, the positive rate of MSI1 was 91.2% (31/34) and the positive rate of HER2 was 88.2% (30/34); the expression of MSI1 and HER2 was positively correlated (P=0.001, r=0.530). The expression of MSI1 was positively correlated with menopausal status (r=0.372, P=0.030) and lymph node metastasis (r=0.450, P=0.008). HER2 expression was positively correlated with menopausal status (r=0.436, P=0.010), and negatively correlated with ER expression (r=-0.365, P=0.034). The co-expression of MSI1 and HER2 was positively correlated with age (r=0.347, P=0.044) and menopausal status (r=0.496, P=0.003), and negatively correlated with ER expression (r=-0.461, P=0.006). Conclusions: MSI1 and HER2 are highly expressed in mammary Paget's disease and their expression levels are positively correlated. The correlation analysis between clinicopathological features and prognosis suggests that both of them may be involved in the occurrence and development of mammary Paget's disease and are potential therapeutic targets for mammary Paget's disease.
Humans ; Female ; Paget's Disease, Mammary/pathology* ; Breast Neoplasms/pathology* ; Prognosis ; Lymphatic Metastasis ; Nerve Tissue Proteins/metabolism* ; RNA-Binding Proteins

Humans ; Lung ; Pneumoconiosis/diagnostic imaging* ; Radiography ; Tomography, X-Ray Computed

Objective: To study the modification effect of age on the association between body mass index and the risk of hypertension. Methods: People age ≥18 years old were selected by clusters, from a rural area of Henan province. In total, 20 194 people were recruited at baseline during 2007 and 2008, and the follow-up study was completed from 2013 to 2014. Logistic regression model was used to assess the risk of incident hypertension by baseline BMI and age-specific BMI. Results: During the 6-year follow-up period, 1 950 hypertensive persons were detected, including 784 men and 1 166 women, with cumulative incidence rates as 19.96%, 20.51%, and 19.61%, respectively. Compared with those whose BMI<22 kg/m(2), the RRs of hypertension were 1.09 (0.93-1.27), 1.17 (1.01-1.37), 1.34 (1.14-1.58) and 1.31 (1.09-1.56) for participants with BMI as 22-, 24-, 26- and ≥28 kg/m(2), respectively. In young and middle-aged populations, the risk of hypertension gradually increased with the rise of BMI (trend P<0.05). However, in the elderly, the increasing trend on the risk of hypertension risk was not as significantly obvious (trend P>0.05). Conclusion: The effect of BMI on the incidence of hypertension seemed to depend on age. Our findings suggested that a weight reduction program would be more effective on young or middle-aged populations, to prevent the development of hypertension.
Adolescent ; Age Factors ; Aged ; Asian People/statistics & numerical data* ; Body Mass Index ; Cohort Studies ; Female ; Follow-Up Studies ; Humans ; Hypertension/ethnology* ; Incidence ; Logistic Models ; Male ; Middle Aged ; Risk Factors ; Rural Population

Objective: To explore the association between fatty liver and type 2 diabetes mellitus (T2DM) in the baseline-population of Jinchang cohort study. Methods: Data from all the participants involved in the baseline-population of Jinchang cohort study was used, to compare the risks of T2DM in fatty liver and non fatty liver groups and to explore the interaction between family history or fatty liver of diabetes and the prevalence of T2DM. Results: Among all the 46 861 participants, 10 574 were diagnosed as having fatty liver (22.56%), with the standardized rate as 20.66%. Another 3 818 participants were diagnosed as having T2DM (8.15%) with standardized rate as 6.90%. The prevalence of T2DM increased in parallel with the increase of age (trend χ(2)=2 833.671, trend P<0.001). The prevalence of T2DM in the fatty liver group was significantly higher than that in the non-fatty liver group, both in men or women and in the overall population. Compared with the group of non-fatty liver, the risks of T2DM in fatty liver group were seen 1.78 times higher in males, 2.33 times in women and 2.10 times in the overall population, after adjustment for factors as age, levels of education, smoking, drinking, physical exercise, BMI, family history of diabetes and some metabolic indicators (pressure, TC, TG, uric acid, ALT, AST, gamma-glutamyl transferase). Date from the interaction model showed that fatty liver and family history of diabetes present a positive additive interaction on T2DM (RERI=1.18, 95%CI: 0.59-1.78; AP=0.24, 95%CI: 0.14-0.34; S=1.43, 95%CI: 1.21-1.69). Conclusions: Fatty liver could significantly increase the risk of T2DM and a positive additive interaction was also observed between fatty liver and family history of diabetes on T2DM. It was important to strengthen the prevention program on T2DM, in order to effectively control the development of fatty liver.
China/epidemiology* ; Cohort Studies ; Diabetes Mellitus, Type 2/ethnology* ; Fatty Liver/ethnology* ; Female ; Humans ; Male ; Non-alcoholic Fatty Liver Disease/epidemiology* ; Prevalence ; Risk Factors

Objective: To analyze the epidemiological characteristics, dynamic trend of development and related influencing factors of hepatitis C in Shandong, China, 2007-2016, also to provide epidemiological evidence for prevention and control of HCV. Methods: National surveillance data of hepatitis C from 2007 to 2016 in Shandong was used, with distribution and clustering map of hepatitis C drawn at the county level. Panel Poisson regression was used to explore the influencing factors of hepatitis C at the city level. Results: The incidence of hepatitis C in Shandong increased from 1.49/100 000 in 2007 to 4.72/100 000 in 2016, with the high incidence mainly clustered in the urban regions in Jinan, Zibo, Weihai et al. and surrounding vicinities. Majority of the cases were young adults, with 53.16% (14 711/27 671) of them being farmers. Results from the Multiple panel Poisson regression analysis indicated that factors as: population density (aIRR=1.07, 95%CI: 1.05-1.10), number of hospital per hundred thousand people shared (aIRR=1.16, 95%CI: 1.08-1.24), expenditure of medical fee in rural (aIRR=1.21, 95%CI: 1.08-1.37) and the proportion of the tertiary industry (aIRR=1.08, 95%CI: 1.07-1.09) were all correlated to the incidence of hepatitis C. Conclusions: The incidence of hepatitis C had been increasing rapidly in recent years, in Shandong. Prevention and control of HCV should focus on high risk population. In addition, rural, especially in areas with lower economics provision should be under more attentions, so as to find more concealed cases for early treatment.
Adult ; China/epidemiology* ; Cities ; Hepacivirus ; Hepatitis C/prevention & control* ; Humans ; Incidence ; Population Surveillance ; Young Adult

Given the opposing effects of Akt and AMP-activated protein kinase (AMPK) on metabolic homeostasis, this study examined the effects of deletion of Akt2 and AMPKα2 on fat diet-induced hepatic steatosis. Akt2–Ampkα2 double knockout (DKO) mice were placed on high fat diet for 5 months. Glucose metabolism, energy homeostasis, cardiac function, lipid accumulation, and hepatic steatosis were examined. DKO mice were lean without anthropometric defects. High fat intake led to adiposity and decreased respiratory exchange ratio (RER) in wild-type (WT) mice, which were ablated in DKO but not Akt2−/− and Ampkα2−/− mice. High fat intake increased blood and hepatic triglycerides and cholesterol, promoted hepatic steatosis and injury in WT mice. These effects were eliminated in DKO but not Akt2−/− and Ampkα2−/− mice. Fat diet promoted fat accumulation, and enlarged adipocyte size, the effect was negated in DKO mice. Fat intake elevated fatty acid synthase (FAS), carbohydrate-responsive element-binding protein (CHREBP), sterol regulatory element-binding protein 1 (SREBP1), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), peroxisome proliferator-activated receptor-α (PPARα), PPARγ, stearoyl-CoA desaturase 1 (SCD-1), phosphoenolpyruvate carboxykinase (PEPCK), glucose 6-phosphatase (G6Pase), and diglyceride O-acyltransferase 1 (DGAT1), the effect was absent in DKO but not Akt2−/− and Ampkα2−/− mice. Fat diet dampened mitophagy, promoted inflammation and phosphorylation of forkhead box protein O1 (FoxO1) and AMPKα1 (Ser485), the effects were eradicated by DKO. Deletion of Parkin effectively nullified DKO-induced metabolic benefits against high fat intake. Liver samples from obese humans displayed lowered microtubule-associated proteins 1A/1B light chain 3B (LC3B), Pink1, Parkin, as well as enhanced phosphorylation of Akt, AMPK (Ser485), and FoxO1, which were consolidated by RNA sequencing (RNAseq) and mass spectrometry analyses from rodent and human livers. These data suggest that concurrent deletion of Akt2 and AMPKα2 offers resilience to fat diet-induced obesity and hepatic steatosis, possibly through preservation of Parkin-mediated mitophagy and lipid metabolism.