| 1. |
- Wang, Fang, et al.
(författare)
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Emerging contaminants: A One Health perspective
- 2024
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Ingår i: Innovation. - 2666-6758. ; 5
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Forskningsöversikt (refereegranskat)abstract
- Environmental pollution is escalating due to rapid global development that often prioritizes human needs over planetary health. Despite global efforts to mitigate legacy pollutants, the continuous introduction of new substances remains a major threat to both people and the planet. In response, global initiatives are focusing on risk assessment and regulation of emerging contaminants, as demonstrated by the ongoing efforts to establish the UN's Intergovernmental Science-Policy Panel on Chemicals, Waste, and Pollution Prevention. This review identifies the sources and impacts of emerging contaminants on planetary health, emphasizing the importance of adopting a One Health approach. Strategies for monitoring and addressing these pollutants are discussed, underscoring the need for robust and socially equitable environmental policies at both regional and international levels. Urgent actions are needed to transition toward sustainable pollution management practices to safeguard our planet for future generations.
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| 2. |
- Chen, Chengshui, et al.
(författare)
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Preventive and Therapeutic Effects of Phosphoinositide 3-Kinase Inhibitors on Acute Lung Injury
- 2011
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Ingår i: Chest. - : Elsevier BV. - 1931-3543 .- 0012-3692. ; 140:2, s. 391-400
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Tidskriftsartikel (refereegranskat)abstract
- Background: Phosphoinositide 3-kinases (PI3Ks) are involved in a number of biologic responses. Recent preclinical studies demonstrated that the PI3K-dominant signal pathway could play an important role in the development of acute lung injury, although the mechanism remains unclear. Methods: CD-1 mice were administered different PI3K inhibitors either intranasally or intragastrically once a day for 3 days before intratracheal instillation of lipopolysaccharide at 4 h and 24 h. Effects of SHBM1009 on lipopolysaccharide-induced capillary permeability, leukocyte distribution and activation, and epithelial cell function were measured. Therapeutic effects of SHBM1009 on pancreatic elastase-induced lung injury were evaluated in rats. Results: The data demonstrated that the local delivery of PI3K inhibitors played more effective roles in the prevention of endotoxin-induced lung injury than the systemic delivery. The preventive effects of PI3K inhibitors varied most likely because of chemical properties, targeting sites, and pharmacokinetics. The local PI3K inhibitors prevented both endotoxin- and elastase-induced lung injury in mice and rats, possibly through directly inhibiting or inactivating the function of airway epithelial cells, which could not produce chemoattractant factors to activate neutrophils and macrophages. Conclusions: PI3K may be a therapeutic target for lung injury, and local delivery of PI3K inhibitors may be one of the optimal approaches for the therapy. CHEST 2011; 140(2):391-400
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| 3. |
- Du, Yaoyao, et al.
(författare)
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Cartilage Oligomeric Matrix Protein Inhibits Vascular Smooth Muscle Calcification by Interacting With Bone Morphogenetic Protein-2.
- 2011
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Ingår i: Circulation Research. - 1524-4571. ; 108, s. 79-917
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Tidskriftsartikel (refereegranskat)abstract
- Rationale: Vascular calcification is a significant contributor to cardiovascular morbidity and mortality. We recently reported that cartilage oligomeric matrix protein (COMP) is pivotal for maintaining the homeostasis of vascular smooth muscle cells (VSMCs). Whether COMP affects the process of vascular calcification is unknown. Objective: We aimed to test whether COMP modulates vascular calcification. Methods and Results: VSMC calcification in vitro was induced by calcifying media containing high inorganic phosphate or calcium. In vivo medial vessel calcification was induced in rats by 5/6 nephrectomy with a high-phosphate diet or by periadventitial application of CaCl(2) to the abdominal aorta. COMP protein level was markedly reduced in both calcified VSMCs and arteries. COMP deficiency remarkably exacerbated VSMC calcification, whereas ectopic expression of COMP greatly reduced calcification. Furthermore, COMP knockdown facilitated osteogenic markers expression by VSMCs even in the absence of calcifying media. By contrast, COMP overexpression significantly inhibited high phosphate- or high calcium-induced VSMC osteochondrogenic transition. Induction of osteogenic marker expression by COMP silencing was reversed by a soluble form of bone morphogenetic protein (BMP)-2 receptor IA, which suggests a BMP-2-dependent mechanism. Our data revealed that COMP bound directly to BMP-2 through the C terminus, inhibited BMP-2 receptor binding, and blocked BMP-2 osteogenic signaling, indicating COMP inhibits osteochondrogenic transition of VSMCs at least partially through inhibiting BMP-2. Conclusions: Our data strongly suggest that COMP is a novel inhibitor of vascular calcification. The imbalance between the effects of COMP and BMP-2 may provide new insights into the pathophysiology of vascular calcification.
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| 4. |
- Alm, Ann-Sophie, et al.
(författare)
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Variation of lipopolysaccharide-induced acute lung injury in eight strains of mice.
- 2010
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Ingår i: Respiratory Physiology & Neurobiology. - : Elsevier BV. - 1878-1519 .- 1569-9048. ; 171, s. 157-164
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Tidskriftsartikel (refereegranskat)abstract
- Clinical and experimental evidence suggests that genetic variations may play an important role in the development of acute lung injury (ALI). Lipopolysaccharide (LPS)-induced ALI models has been widely applied for pathophysiological and pharmacological research. In order to understand the variation of acute pulmonary reactions between mouse strains and find the optimal strain for target-oriented study, the present study investigated the alterations of acute lung hyperinflation, inflammation and injury in C57BL/6J, Balb/cJ, DBA/1J, CD-1, NMRI, DBA/2J, A/J and C3H/HeN mice after the intra-tracheal challenge with LPS. We found that LPS-induced ALI varied between measured variables, durations and strains. General score of LPS-induced acute lung hyperinflation, inflammation and edema followed the order CD-1, A/J, Balb/c, DBA/2J, C57BL/6J, DBA/1J, NMRI, C3H/HeN mice at 4h, and CD-1, C57BL/6J, Balb/c, C3H/HeN, NMRI, A/J, DBA/2J, DBA/1 mice at 24h. Thus, these data provide useful information to select sensitive or resistant strain mouse for understanding genetic variation of pathogenesis and screening of target-oriented drugs.
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| 5. |
- Cohen, Judah, et al.
(författare)
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ARCTIC CHANGE AND POSSIBLE INFLUENCE ON MID-LATITUDE CLIMATE AND WEATHER - A US CLIVAR White Paper
- 2018
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Rapport (övrigt vetenskapligt/konstnärligt)abstract
- The Arctic has warmed more than twice as fast as the global average since the mid 20th century, a phenomenon known as Arctic amplification (AA). These profound changes to the Arctic system have coincided with a period of ostensibly more frequent events of extreme weather across the Northern Hemisphere (NH) mid-latitudes, including extreme heat and rainfall events and recent severe winters. Though winter temperatures have generally warmed since 1960 over mid-to-high latitudes, the acceleration in the rate of warming at high-latitudes, relative to the rest of the NH, started approximately in 1990. Trends since 1990 show cooling over the NH continents, especially in Northern Eurasia. The possible link between Arctic change and mid-latitude climate and weather has spurred a rush of new observational and modeling studies. A number of workshops held during 2013-2014 have helped frame the problem and have called for continuing and enhancing efforts for improving our understanding of Arctic-mid-latitude linkages and its attribution to the occurrence of extreme climate and weather events. Although these workshops have outlined some of the major challenges and provided broad recommendations, further efforts are needed to synthesize the diversified research results to identify where community consensus and gaps exist. Building upon findings and recommendations of the previous workshops, the US CLIVAR Working Group on Arctic Change and Possible Influence on Mid-latitude Climate and Weather convened an international workshop at Georgetown University in Washington, DC, on February 1-3, 2017. Experts in the fields of atmosphere, ocean, and cryosphere sciences assembled to assess the rapidly evolving state of understanding, identify consensus on knowledge and gaps in research, and develop specific actions to accelerate progress within the research community. With more than 100 participants, the workshop was the largest and most comprehensive gathering of climate scientists to address the topic to date. In this white paper, we synthesize and discuss outcomes from this workshop and activities involving many of the working group members.
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| 6. |
- Liu, Xiangdong, et al.
(författare)
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Cancer risk in patients with hepatitis C virus infection : A population-based study in Sweden
- 2017
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Ingår i: Cancer Medicine. - : Wiley. - 2045-7634. ; 6:5, s. 1135-1140
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Tidskriftsartikel (refereegranskat)abstract
- Increased risks of certain cancers have been observed in patients with hepatitis C virus (HCV) infection. However, data on other cancer sites/types are lacking. We analyzed systematically the risk of developing 35 common cancers in patients with HCV infection using a nationwide Swedish database. Patients with HCV infection were identified from the Swedish Hospital Inpatient and Outpatient Register and Primary Health Care Database, and followed until the diagnosis of cancer. Standardized incidence ratios (SIRs) were calculated for subsequent 35 common cancer sites/types between 1990 and 2010 in patients with HCV infection in Sweden. Increased risks were recorded for six cancers. The highest SIR was seen for liver cancer (36.67; 95% CI: 33.20-40.40). The decreased risk was for prostate cancer (0.73; 95% CI: 0.59-0.90) and melanoma (0.50; 95% CI: 0.30-0.79). A significant sex-difference for cancer was observed only for liver cancer (40.72; 95% CI: 36.36-45.45 for men and 27.21; 95% CI: 21.90-33.41 for women). Also, increased SIRs were noted only for liver cancer during the entire period of follow-up. HCV infection was associated with an increased incidence of liver cancer and additionally five other types of cancer. Active surveillance of other cancers may be needed in order to be diagnosed at an earlier stage.
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| 7. |
- Wang, Xinping, et al.
(författare)
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Nature of three episodes of Paleoproterozoic magmatism (2180 Ma, 2115 Ma and 1890 Ma) in the Liaoji belt, North China with implications for tectonic evolution
- 2017
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Ingår i: Precambrian Research. - : Elsevier BV. - 0301-9268. ; 298, s. 252-267
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Tidskriftsartikel (refereegranskat)abstract
- Three episodes of Paleoproterozoic magmatism with distinctively different nature in the Liaoji belt of the Eastern North China Craton are discussed here: the 2200–2140 Ma Liaoji A-type granites, the 2160–2110 Ma Haicheng mafic sills and the ∼1890 Ma Qingchengzi I-type granites. The Mafeng monzogranitic pluton, representative of the Liaoji A-type granites, gives a SIMS U-Pb zircon age of 2181 ± 6 Ma (n = 20, MSWD = 4.3). The Qingchengzi plagiogranitic pluton, representative of the Qingchengzi I-type granites, gives a SIMS U-Pb zircon age of 1891 ± 10 Ma (n = 8, MSWD = 1.8). The Mafeng monzogranites are high in Fe, Ti, K but low in Mg, Al and Ca. They have high abundance of total REEs (ΣREE = 213–346 ppm). They are relatively depleted in feldspar-compatible elements (e.g., Eu and Sr) and HFSEs (e.g., Nb, Ta, P and Ti). They have high 10000 × Ga/Al ratios of 3.19–3.61 and Zr + Nb + Ce + Y concentrations of 472–656 ppm, which are typical for A-type granite. The Qingchengzi plagiogranites have relatively high Al, Ca, Na but low Fe, Ti and K contents. They have low abundance of total REEs (ΣREE = 17.6–21.6 ppm). They are enriched in LILEs (e.g., Ba, K and Sr) but depleted in HFSEs (e.g., Nb, Ta, P, Ti and Y). These features, combined with extremely high Sr/Y ratios (327–413), are comparable with those of typical modern adakites. The Liaoji A-type granites show a source same to that of the Haicheng mafic sills and they originated from the Archean subcontinental lithospheric mantle plus with contamination from the Archean granites. However, the Qingchengzi I-type granites are interpreted to originate from subducted oceanic crust with significant contributions from sediments. The Liaoji A-type granites and the coeval bimodal volcanism in the Liaohe Group as well as the Haicheng mafic sills may represent episodic magmatism which was related to a protracted intra-continental rifting caused by lithospheric extension. The ca. 1890 Ma Qingchengzi I-type granites and coexisting S-type granites as well as the coeval regional metamorphism are favored to represent an active continental magmatism linked to Paleoproterozoic subduction.
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| 8. |
- Wang, Xiangdong, et al.
(författare)
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Potential effects of peroxisome proliferator-activated receptor activator on LPS-induced lung injury in rats
- 2009
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Ingår i: Pulmonary Pharmacology & Therapeutics. - : Elsevier BV. - 1522-9629 .- 1094-5539. ; 22:4, s. 318-325
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Tidskriftsartikel (refereegranskat)abstract
- Multiple factors contribute to the pathogenesis and prognosis of chronic obstructive pulmonary disease (COPD), still requiring new therapeutic strategies and medications for the disease. The aim of the present study is to investigate the model of lipopolysaccharide (LPS)-induced chronic lung injury and hyperinflation and test therapeutic effects of peroxisome proliferator-activated receptor (PPAR)-gamma agonist. Wister rats were challenged with intra-tracheal instillation of LPS at concentrations of 0.006, 0.060, 0.600, and 6.000 mg/ml per kg, twice a week, for 1, 2, 4 and 6 weeks. PPAR activator, 15-deoxy-Delta(12,14)-prostaglandin J2 (15D-PGJ2), or vehicle (PBS) was administered orally and daily at the dose of 1 and 10 mg/ml per kg in animals challenged with LPS or PBS at the dose of 0.060 mg/ml per kg body weight twice a week for 4 weeks. We found that intra-tracheal exposure of LPS resulted in a dose-dependent pattern of chronic lung hyperinflation and hypertrophy, increased alveolar enlargement, reduced vascular endothelial growth factor (VEGF) and elevated tissue inhibitor of metalloproteinases (TIMP)-1 levels in bronchoalveolar lavage (BAL) fluid, and early changes of leukocyte influx and interferon (IFN)-gamma levels in bronchoalveolar lavage (BAL) fluid. PPAR-gamma agonist ameliorated these changes related with the dose used. LPS-induced lung disease model shows some similarities with human disease, and PPAR-gamma agonist may be an alternative for COPD therapy. (C) 2009 Elsevier Ltd. All rights reserved.
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| 9. |
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| 10. |
- Ai, Sizhi, et al.
(författare)
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Causal associations of short and long sleep durations with 12 cardiovascular diseases : linear and nonlinear Mendelian randomization analyses in UK Biobank
- 2021
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Ingår i: European Heart Journal. - : Oxford University Press. - 0195-668X .- 1522-9645. ; 42:34, s. 3349-3357
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Tidskriftsartikel (refereegranskat)abstract
- Aims Observational studies have suggested strong associations between sleep duration and many cardiovascular diseases (CVDs), but causal inferences have not been confirmed. We aimed to determine the causal associations between genetically predicted sleep duration and 12 CVDs using both linear and nonlinear Mendelian randomization (MR) designs. Methods and results Genetic variants associated with continuous, short (<= 6 h) and long (>= 9 h) sleep durations were used to examine the causal associations with 12 CVDs among 404 044 UK Biobank participants of White British ancestry. Linear MR analyses showed that genetically predicted sleep duration was negatively associated with arterial hypertension, atrial fibrillation, pulmonary embolism, and chronic ischaemic heart disease after correcting for multiple tests (P <0.001). Nonlinear MR analyses demonstrated nonlinearity (L-shaped associations) between genetically predicted sleep duration and four CVDs, including arterial hypertension, chronic ischaemic heart disease, coronary artery disease, and myocardial infarction. Complementary analyses provided confirmative evidence of the adverse effects of genetically predicted short sleep duration on the risks of 5 out of the 12 CVDs, including arterial hypertension, pulmonary embolism, coronary artery disease, myocardial infarction, and chronic ischaemic heart disease (P< 0.001), and suggestive evidence for atrial fibrillation (P < 0.05). However, genetically predicted long sleep duration was not associated with any CVD. Conclusion This study suggests that genetically predicted short sleep duration is a potential causal risk factor of several CVDs, while genetically predicted long steep duration is unlikely to be a causal risk factor for most CVDs. [GRAPHICS] .
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