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- Visscher, T, et al.
(författare)
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A break in the obesity epidemic? Explained by biases or misinterpretation of the data?
- 2015
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Ingår i: International Journal of Obesity. - : Springer Science and Business Media LLC. - 0307-0565 .- 1476-5497. ; 39:2, s. 189-198
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Tidskriftsartikel (refereegranskat)abstract
- Recent epidemiologic papers are presenting prevalence data suggesting breaks and decreases in obesity rates. However, before concluding that the obesity epidemic is not increasing anymore, the validity of the presented data should be discussed more thoroughly. We had a closer look into the literature presented in recent reviews to address the major potential biases and distortions, and to develop insights about how to interpret the presented suggestions for a potential break in the obesity epidemic. Decreasing participation rates, the use of reported rather than measured data and small sample sizes, or lack of representativeness, did not seem to explain presented breaks in the obesity epidemic. Further, available evidence does not suggest that stabilization of obesity rates is seen in higher socioeconomic groups only, or that urbanization could explain a potential break in the obesity epidemic. However, follow-ups of short duration may, in part, explain the apparent break or decrease in the obesity epidemic. On the other hand, a single focus on body mass index (BMI) ⩾25 or ⩾30 kg m-2 is likely to mask a real increase in the obesity epidemic. And, in both children and adults, trends in waist circumferences were generally suggesting an increase, and were stronger than those reported for trends in BMI. Studies concluding that there is a recent break in the obesity epidemic need to be interpreted with caution. Reported studies presenting a break were mostly of short duration. Further, focusing on trends in waist circumference rather than BMI leads to a less optimistic conclusion: the public health problem of obesity is still increasing.International Journal of Obesity advance online publication, 22 July 2014; doi:10.1038/ijo.2014.98.
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| 115. |
- Warzok, Ulrike, et al.
(författare)
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Surprising solvent-induced structural rearrangements in large [N center dot center dot center dot I+center dot center dot center dot N] halogen-bonded supramolecular capsules : an ion mobility-mass spectrometry study
- 2018
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Ingår i: Chemical Science. - : ROYAL SOC CHEMISTRY. - 2041-6520 .- 2041-6539. ; 9:44, s. 8343-8351
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Tidskriftsartikel (refereegranskat)abstract
- Coordinative halogen bonds have recently gained interest for the assembly of supramolecular capsules. Ion mobility-mass spectrometry and theoretical calculations now reveal the well-defined gas-phase structures of dimeric and hexameric [NI+N] halogen-bonded capsules with counterions located inside their cavities as guests. The solution reactivity of the large hexameric capsule shows the intriguing solvent-dependent equilibrium between the hexamer and an unprecedented pentameric [NI+N] halogen-bonded capsule, when the solvent is changed from chloroform to dichloromethane. The intrinsic flexibility of the cavitands enables this novel structure to adopt a pseudo-trigonal bipyramidal geometry with nine [NI+N] bonds along the edges and two pyridine binding sites uncomplexed.
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| 116. |
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| 117. |
- Zhang, Fan, et al.
(författare)
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VEGF-B is dispensable for blood vessel growth but critical for their survival, and VEGF-B targeting inhibits pathological angiogenesis
- 2009
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424 .- 1091-6490. ; 106:15, s. 6152-6157
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Tidskriftsartikel (refereegranskat)abstract
- VEGF-B, a homolog of VEGF discovered a long time ago, has not been considered an important target in antiangiogenic therapy. Instead, it has received little attention from the field. In this study, using different animal models and multiple types of vascular cells, we revealed that although VEGF-B is dispensable for blood vessel growth, it is critical for their survival. Importantly, the survival effect of VEGF-B is not only on vascular endothelial cells, but also on pericytes, smooth muscle cells, and vascular stem/progenitor cells. In vivo, VEGF-B targeting inhibited both choroidal and retinal neovascularization. Mechanistically, we found that the vascular survival effect of VEGF-B is achieved by regulating the expression of many vascular prosurvival genes via both NP-1 and VEGFR-1. Our work thus indicates that the function of VEGF-B in the vascular system is to act as a "survival," rather than an "angiogenic" factor and that VEGF-B inhibition may offer new therapeutic opportunities to treat neovascular diseases.
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