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Sun L.,Harbin Medical University | Gao Y.,Harbin Medical University | Liu H.,Harbin Medical University | Zhang W.,Harbin Medical University | And 5 more authors.
Science of the Total Environment | Year: 2013

In this study, the relationships between high water fluoride exposure and essential hypertension as well as plasma ET-1 levels were investigated. A total of 487 residents aged 40 to 75 were randomly recruited from eight villages in Zhaozhou County from Heilongjiang Province in China and were divided into 4 groups according to the concentrations of fluoride in their water. Consumption levels of drinking water fluoride for normal, mild, moderate, and high exposure groups were 0.84±0.26mg/L, 1.55±0.22mg/L, 2.49±0.30mg/L, and 4.06±1.15mg/L, respectively. The prevalence of hypertension in each group was 20.16%, 24.54%, 32.30%, and 49.23%, respectively. There were significant differences between all the groups; namely, with the increase in water fluoride concentrations, the risk of essential hypertension in adults grows in a concentration-dependent manner. Significant differences were observed in the plasma ET-1 levels between the different groups (P<0.0001). In the multivariable logistic regression model, high water fluoride concentrations (F- 3.01mg/L, OR4/1=2.84), age (OR3/1=2.63), and BMI (OR2/1=2.40, OR3/1=6.03) were closely associated with essential hypertension. In other words, the study not only confirmed the relationship between excess fluoride intake and essential hypertension in adults, but it also demonstrated that high levels of fluoride exposure in drinking water could increase plasma ET-1 levels in subjects living in fluoride endemic areas. © 2012 Elsevier B.V. Source


Ma X.,Harbin Medical University | Han S.,Harbin Medical University | Zhang W.,Harbin Medical University | Zhang W.,Key Laboratory of Etiology and Epidemiology | And 4 more authors.
Molecular Medicine Reports | Year: 2015

Previous studies have suggested that hepatocyte apoptosis may be a fundamental underlying mechanism of liver injury and diseases, such as liver fibrosis. Relaxin3 has been reported to have antifibrotic actions in the heart and to attenuate isoproterenolinduced myocardial injury; however, the beneficial role of relaxin3 on hepatocyte apoptosis remains to be elucidated. The aim of the present study was to explore the role and possible mechanisms of relaxin3 through hydrogen peroxide (H2O2)induced apoptosis in primary human hepatocytes. Cells were treated with relaxin3 and then cell viability, morphological features, the presence of cleaved caspases as well as the levels of endoplasmic reticulum stress (ERS) protein markers and autophagy markers were evaluated. The H2O2 group showed significantly decreased cell viability, increased apoptosis as well as upregulation of caspases (cleaved caspase3, 8 and 9) and ERS protein markers compared with those of the control group. However, cells treated with relaxin3 (10 ng/ml) demonstrated improved cell viability, reduced apoptosis and decreased expression of cleaved caspases and ERS markers. However, the expression of autophagy markers remained unchanged following H2O2induced apoptosis and relaxin3 treatment. In conclusion, relaxin3 was shown to protect hepatocytes from H2O2induced apoptosis via downregulation of cleaved caspase8 and 9, as well as inhibition of the ERS pathway. Source


Zhu D.,Harbin Medical University | Zhang L.,Harbin Medical University | Cheng L.,Harbin Medical University | Ren L.,Harbin Medical University | And 3 more authors.
Kidney and Blood Pressure Research | Year: 2016

Background/Aims: We aimed to evaluate whether pancreatic kininogenase (PKase) can relieve renal fibrosis and investigate its mechanisms in diabetic nephropathy (DN) rats Methods: We established streptozotocin (STZ) induced-DN rats. After treatment with PKase for 4 weeks, urinary weight, urinary protein content and blood glucose concentration were detected, and then renal histopathological changes were examined using Hematoxylin and Eosin (H&E) and Masson's thrchrome staining. In addition, the expressions of miR-433, transforming growth factor-β1 (TGF-β1) and antizyme inhibitor 1 (Azin1) were detected by qRT-PCR and/or western blotting. Results: PKase reduced urinary weight, urinary protein contents and blood glucose concentrations. PKase treated DN rats exhibited less renal fibrosis than untreated DN rats (P < 0.05). Furthermore, the expression levels of TGF-β and miR-433 were reduced (P < 0.05), while Azin1 expression was increased in renal tissues of PKase treated DN rats compared with untreated DN rats (P < 0.05). Conclusions: PKase might not only inhibit the development of DN by reducing urinary weight, urinary protein content and blood glucose concentration in DN rats, but also relieve renal fibrosis in DN rats through inhibiting the expression of TGF-β1, and miR-433 and Azin1 might involve in this process. © 2016 The Author(s). Source


Yu J.,Harbin Medical University | Liu P.,Harbin Medical University | Liu Y.,Harbin Medical University | Liu S.J.,Harbin Medical University | And 2 more authors.
BMJ Open | Year: 2014

Objective: To contribute evidence relevant to the policy of supplying iodised salt (IS), non-iodised salt (NIS) or both in Chinese cities. Design: Subnational telephone interview survey. Setting: China. Participants: Totally, 24 557 telephone numbers were dialled and 4833 citizens accepted the telephone interview. The telephone numbers were randomly selected by random digit dialling and a Mitofsky-Waksberg two-stage sampling method in 17 capital cities and 6 coastal cities from 17 iodine deficiency disorder (IDD)-eliminated provinces (municipalities). Results: The 4833 citizens finished the telephone interview. Among them, 3738 (77.3%) citizens chose IS, 481 (10%) citizens chose NIS, and the others chose both IS and NIS. The citizens' awareness rates of IDD and IDD preventive measures were 68.7% and 62.5%, respectively. Conclusions: It is not a suitable time to supply IS and NIS simultaneously in the developed cities of China, but a pilot project may be conducted in the cities where IDD has been sustainably eliminated, there is strong awareness of IDD and the population can make informed decisions regarding IS. IDD health education should be further strengthened, especially regarding the potential for IQ damage. Source


Yu J.,Harbin Medical University | Yu J.,Key Laboratory of Etiology and Epidemiology | Gao Y.,Harbin Medical University | Gao Y.,Key Laboratory of Etiology and Epidemiology | And 2 more authors.
Biological Trace Element Research | Year: 2013

The ratio of osteoprotegerin ligand (OPGL) to osteoprotegerin (OPG) determines the delicate balance between bone resorption and synthesis. The main objective of the present study is to investigate the possible role of OPGL and OPG in the bone metabolism of rats exposed to fluoride and the protective or aggravating effect of calcium (Ca). In a 6-month study, 270 weanling male Sprague-Dawley rats weighing between 70 and 90 g were divided randomly into six groups of 45 rats in each group. Three groups (groups I, III, and V)served as controls and drank deionized water and were fed purified rodent diets containing either 1,000 mg Ca/kg (low Ca), 5,000 mg Ca/kg (normal Ca), or 20,000 mg Ca/kg (high Ca). The three experimental groups (groups II, IV, and VI) were given the same diets but they drank water containing 100 mg F ion/L (from NaF). Every 2 months 15 rats were randomly selected from each group and sacrificed for the study. The ratio of OPGL mRNA to OPG mRNA was significantly increased by the sixth month in the distal femur joints of the F-exposed rats. Serum tartrate-resistant acid phosphatase activity and serum calcitonin activity in the F-exposed groups was increased, although changes were not apparent in the serum alkaline phosphatase or Gla-containing proteins, especially in the low calcium and high calcium diet F-exposed groups. The results indicated that OPG and OPGL may play important roles in skeletal fluorosis, and that fluoride may enhance osteoclast formation and induce osteoclastic bone destruction. A high Ca diet did not play a protective role, but rather may aggravate the damage of fluoride. © 2013 Springer Science+Business Media New York. Source

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