386 research outputs found

    Sclerostin does not play a major role in the pathogenesis of skeletal complications in type 2 diabetes mellitus

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    In contrast to previously reported elevations in serum sclerostin levels in diabetic patients, the present study shows that the impaired bone microarchitecture and cellular turnover associated with type 2 diabetes mellitus (T2DM)-like conditions in ZDF rats are not correlated with changes in serum and bone sclerostin expression. INTRODUCTION: T2DM is associated with impaired skeletal structure and a higher prevalence of bone fractures. Sclerostin, a negative regulator of bone formation, is elevated in serum of diabetic patients. We aimed to relate changes in bone architecture and cellular activities to sclerostin production in the Zucker diabetic fatty (ZDF) rat. METHODS: Bone density and architecture were measured by micro-CT and bone remodelling by histomorphometry in tibiae and femurs of 14-week-old male ZDF rats and lean Zucker controls (n = 6/group). RESULTS: ZDF rats showed lower trabecular bone mineral density and bone mass compared to controls, due to decreases in bone volume and thickness, along with impaired bone connectivity and cortical bone geometry. Bone remodelling was impaired in diabetic rats, demonstrated by decreased bone formation rate and increased percentage of tartrate-resistant acid phosphatase-positive osteoclastic surfaces. Serum sclerostin levels (ELISA) were higher in ZDF compared to lean rats at 9 weeks (+40 %, p < 0.01), but this difference disappeared as their glucose control deteriorated and by week 14, ZDF rats had lower sclerostin levels than control rats (-44 %, p < 0.0001). Bone sclerostin mRNA (qPCR) and protein (immunohistochemistry) were similar in ZDF, and lean rats at 14 weeks and genotype did not affect the number of empty osteocytic lacunae in cortical and trabecular bone. CONCLUSION: T2DM results in impaired skeletal architecture through altered remodelling pathways, but despite altered serum levels, it does not appear that sclerostin contributes to the deleterious effect of T2DM in rat bone

    Transforming growth factor beta in human milk and allergic outcomes in children: A systematic review

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    BACKGROUND: Human milk (HM) transforming growth factor beta (TGF-β) is critical for inflammation regulation and oral tolerance promotion. Previous reports suggested that variations in HM TGF-β levels are associated with allergic outcomes. OBJECTIVE: We undertook a systematic review (PROSPERO 2017 CRD42017069920) to reassess the evidence on the relationships between HM TGF-β and allergic outcomes in children. METHODS: Electronic bibliographic databases (MEDLINE, EMBASE, Cochrane Library) were systematically searched. Two independent reviewers screened reference lists, extracted the data and assessed risk of bias using the National Institute for Clinical Excellence methodological checklist. RESULTS: A total of 21 studies were identified. Sixteen studies assessed relationships between HM TGF-β and risk of eczema; 14, allergic sensitisation; 9, wheezing/asthma; 6, food allergy; 3, allergic rhinitis/conjunctivitis. Five cohorts (5/18, 28%) reported a protective effect of TGF-β1, while 3 (3/10, 30%) suggested increased risk of allergic outcomes development and 1 (1/10, 10%), a protective effect of TGF-β2 on eczema. Meta-analysis was not possible due to significant heterogeneity in methodology, age of outcome assessment and differing statistical approaches. 71% (15/21) of studies carried a high risk of bias. CONCLUSION AND CLINICAL RELEVANCE: In contrast with previous findings we did not find strong evidence of associations between HM TGF-β and allergic outcomes. Differences in studies' methodology and outcomes do not allow unconditional rejection or acceptance of the hypothesis that HM TGF-β influences the risk of allergy development. Future studies on diverse populations employing standardised methods, accurate phenotyping of outcomes and evaluation of the effect of TGF-β in combination with other HM immune markers, microbiome and oligosaccharides are required

    Loss of Potential Aquatic-Terrestrial Subsidies Along the Missouri River Floodplain

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    The floodplains of large rivers have been heavily modified due to riparian development and channel modifications, both of which can eliminate shallow off-channel habitats. The importance of these habitats for aquatic organisms like fishes is well studied. However, loss of off-channel habitat also eliminates habitats for the production of emerging aquatic insects, which subsidize riparian consumers in terrestrial food webs. We used field collections of insect emergence, historical mapping, and statistical modeling to estimate the loss of insect emergence due to channel modifications along eight segments of the Missouri River (USA), encompassing 1566 river km, between 1890 and 2012. We estimate annual production of emerging aquatic insects declined by a median of 36,000 kgC (95% CrI: 3000 to 450,000) between 1890 and 2012 (a 34% loss), due to the loss of surface area in backwaters and related off-channel habitats. Under a conservative assumption that riparian birds obtain 24% of their annual energy budget from adult aquatic insects, this amount of insect loss would be enough to subsidize approximately 790,000 riparan woodland birds during the breeding and nesting period (May to August; 95% CrI: 57,000 to 10,000,000). Most of the loss is concentrated in the lower reaches of the Missouri River, which historically had a wide floodplain, a meandering channel, and a high density of off-channel habitats, but which were substantially reduced due to channelization and bank stabilization. Our results indicate that the loss of off-channel habitats in large river floodplains has the potential to substantially affect energy availability for riparian insectivores, further demonstrating the importance of maintaining and restoring these habitats for linked aquatic-terrestrial ecosystems

    Forces Sauces and Eggs for Soldiers: food, nostalgia, and the rehabilitation of the British military

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    This article identifies, and considers the political implications of, the association of the contemporary British military and British soldiers with nostalgia. This aspect of the discursive project of rehabilitating the British military post-Iraq has not hitherto been theorized. The article analyses a set of exemplifying texts, four military charity food brands (Eggs for Soldiers, Forces Sauces, Red Lion Foods, and Rare Tea Company Battle of Britain Tea) to ask how nostalgic rehabilitation of the British military unfolds at the intersections of militarization, commemoration, and post-2008 “conscience capitalism”. I outline how military charity food brands are a form of “conscience capitalism” through which the perpetuation of militarized logics are produced as a notionally apolitical social “cause”, rendered intelligible within the terms of existing commoditized discourses of post-2008 vintage nostalgia. I then ask what understandings of British soldiers and the British military are constituted within the discourse of nostalgic rehabilitation, and secondly what forms of commemoration are entailed. I argue that a nostalgic generalization of soldiers and the military nullifies the potential unruliness of individual soldiers and obscures the specifics of recent, controversial, wars. Secondly nostalgic civil–military engagement entails a commemorative logic in which forms of quasi-military service are brought into the most banal spaces of everyday civilian life

    Trans-Epithelial Immune Cell Transfer during Suckling Modulates Delayed-Type Hypersensitivity in Recipients as a Function of Gender

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    INTRODUCTION: Breast feeding has long term effects on the developing immune system which outlive passive immunization of the neonate. We have investigated the transfer of milk immune cells and examined the result of transfer once the recipients were adult. METHODS: Non-transgenic mouse pups were foster-nursed by green fluorescent protein (GFP) transgenic dams for 3 weeks and the fate of GFP+ cells was followed by FACS analysis, immunohistochemistry and RT-PCR for GFP and appropriate immune cell markers. Pups suckled by non-transgenic dams served as controls. RESULTS: Despite a preponderance of B cells and macrophages in the stomach contents of the pups, most cells undergoing trans-epithelial migration derived from the 3-4% of milk cells positive for T lymphocyte markers. These cells homed to the spleen and thymus, with maximal accumulation at 3-4 weeks. By sensitizing dams with an antigen which elicits a T cell-mediated delayed-type-hypersensitivity (DTH) response, we determined that nursing by a sensitized dam (compared to a non-sensitized dam) amplified a subsequent DTH response in females and yet suppressed one in males. DISCUSSION: These results suggest that clinical evaluation weighing the pros and cons of nursing male versus female children by mothers with genetically-linked hypersensitivity diseases, such as celiac disease and eczema, or those in regions of the world with endemic DTH-eliciting diseases, such as tuberculosis, may be warranted

    Stabilization of Ion Concentration Polarization Using a Heterogeneous Nanoporous Junction

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    We demonstrate a recycled ion-flux through heterogeneous nanoporous junctions, which induce stable ion concentration polarization with an electric field. The nanoporous junctions are based on integration of ionic hydrogels whose surfaces are negatively or positively charged for cationic or anionic selectivity, respectively. Such heterogeneous junctions can be matched up in a way to achieve continuous ion-flux operation for stable concentration gradient or ionic conductance. Furthermore, the combined junctions can be used to accumulate ions on a specific region of the device.Korea Research Foundation (Grant MOEHRD: KRF-2007-331-D00040)Korean Science and Engineering Foundation (Grant MOST: R01-2007-000-20675-0)Korea Research Foundation (Grant MOEHRD: KRF-J03000)National Research Foundation of Korea (Grant NRF-2009- 352-D00034)National Institutes of Health (U.S.) (EB005743)National Science Foundation (U.S.). (CBET-0347348
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