Associations between livestock ownership and lower odds of anaemia among children 6–59 months old are not mediated by animal‐source food consumption in Ghana

Livestock ownership may mitigate anaemia among young children by providing access to animal‐source foods (ASFs) yet exacerbate anaemia by exposing children to animal‐source pathogens. This study aimed to assess the association between household livestock ownership and child anaemia and examine whether this relationship is mediated by child ASF consumption or by child morbidity and inflammation. We conducted a cross‐sectional study of 470 children aged 6–59 months in Greater Accra, Ghana. Child blood samples were analysed for haemoglobin concentration, iron status biomarkers and inflammatory biomarkers. Caregivers were asked about the child''s frequency of ASF consumption in the past 3 months. Livestock ownership was categorized into five typologies to distinguish households by the number and combinations of species owned. In adjusted logistic regression, children from households in Type 5, owning cattle, small livestock (goats, sheep or pigs) and poultry, had lower odds of anaemia compared with those in Type 1, owning no livestock (OR [95% CI]: 0.32 [0.14, 0.71]). Although children from households that owned poultry were more likely to consume chicken meat, and children from households with cattle were more likely to drink cow''s milk, consumption of these ASFs did not mediate the observed association between livestock ownership and child anaemia. There were no associations between livestock ownership and children''s symptoms of illness or inflammation. Further research is needed to understand how ownership of certain livestock species, or a greater diversity of livestock species, may be associated with the risk of child anaemia, including the role of dietary and income‐based pathways.     

Formation of Iron Sulfides on Carbon Steel in a Specific Cement Grout Designed for Radioactive Waste Repository and Associated Corrosion Mechanisms

Carbon steel coupons were buried in a specific low-pH cement grout designed for radioactive waste disposal and left 6 months in anoxic conditions at 80 °C. The corrosion product layers were analyzed by µ-Raman spectroscopy, XRD, and SEM. They proved to be mainly composed of iron sulfides, with magnetite as a minor phase, mixed with components of the grout. Average corrosion rates were estimated by weight loss measurements between 3 and 6 µm yr⁻¹. Corrosion profiles revealed local degradations with a depth up to 10 µm. It is assumed that the heterogeneity of the corrosion product layer, mainly composed of conductive compounds (FeS, Fe₃S₄, and Fe₃O₄), promotes the persistence of corrosion cells that may lead to locally aggravated degradations of the metal. New cement grouts, characterized by a slightly higher pH and a lower sulfide concentration, should then be designed for the considered application.     

Identification and expression of iron regulators in human synovium: evidence for upregulation in haemophilic arthropathy compared to rheumatoid arthritis,osteoarthritis, and healthy controls

Recurrent joint bleeding is the most common manifestation of severe haemophilia resulting in haemophilic arthropathy (HA). Iron plays a central role in the pathogenesis of the two main features of HA: synovitis and cartilage destruction. The aim of this study was to investigate the synovial presence of the iron regulator proteins ferroportin (FPN), hepcidin, haemoglobin scavenger receptor CD163 (CD163), feline leukaemia virus subgroup C (FLVCR), and heme carrier protein 1 (HCP‐1). A comparison of the expression in HA with rheumatoid arthritis (RA), osteoarthritis (OA), and healthy controls (HC) is made. Synovial expression of iron regulators was investigated by immunohistochemistry in human synovial tissue and in a murine haemophilia model. We demonstrate for the first time the synovial presence of the investigated iron regulator proteins. Expression of the iron regulator proteins FPN, CD163, FLVCR, and HCP‐1 was enhanced in HA in comparison to RA, OA, and HC synovium. In addition, in a murine haemophilia model of acute joint bleeding, synovial expression of FPN, CD163, and HCP‐1 was increased. In both human and murine experiment, synovial expression of hepcidin was not altered. These findings indicate the presence of iron regulator proteins in the synovium, demonstrate an enhanced expression of FPN, CD163, FLVCR, and HCP‐1 in HA, and suggest a synovial adaptation mechanism to maintain synovial iron homeostasis in HA.     

不同浓度超顺磁性氧化铁纳米粒子对小鼠RAW264．7巨噬细胞的影响

目的 评价不同浓度超顺磁性氧化铁纳米粒子（superparamagnetic iron oxides,SPIO）对小鼠RAW264.7巨噬细胞的细胞活性及吞噬功能的影响.方法 常规方法培养小鼠RAW264.7巨噬细胞,应用不同浓度SPIO（0 μg/ml、14μg/ml、28μg/ml、56μg/ml、84μg/ml、140μg/ml、280μg/ml、560μg/ml、840μg/ml）标记小鼠RAW264.7巨噬细胞,采用普鲁士蓝染色检测细胞标记率,台盼蓝染色检测细胞活性,四唑盐（MTT）比色实验检测细胞增殖能力,中性红吞噬实验检测细胞吞噬功能.结果 SPIO含铁浓度84 μg/ml标记24小时,细胞标记率可以达到100%;以后随SPIO浓度的增加,细胞内吞噬的铁颗粒增加,当SPIO含铁浓度为280 μg/ml时,细胞内吞噬铁颗粒达到饱和;当SPIO含铁浓度大于280 μg/ml时,细胞活性下降,吞噬能力降低;当SPIO含铁浓度大于140 μg/ml时,细胞增殖能力下降.结论 SPIO含铁浓度为（84～140）μg/ml标记24h,细胞的标记率为100%并且不影响细胞活性、细胞增殖能力及吞噬能力.     

Diagnosis and treatment of hereditary hemochromatosis: an update

Hereditary hemochromatosis is an inherited iron overload disorder caused by inappropriately low hepcidin secretion leading to increased duodenal absorption of dietary iron, most commonly in C282Y homozygous individuals. This can result in elevated serum ferritin, iron deposition in various organs and ultimately end-organ damage, although there is incomplete biochemical and clinical penetrance and variable phenotypic expression of the HFE mutation in hereditary hemochromatosis. An elevated SF <1000 µg/l is associated with an increased risk of cirrhosis and mortality in C282Y homozygotes. Conversely, a SF <1000 µg/l is associated with a very low likelihood of cirrhosis, making liver biopsy unnecessary among C282Y homozygotes in the absence of concomitant risk factors for liver disease. Phlebotomy remains the mainstay of treatment and new treatments being studied include erythrocytapheresis and ‘mini-hepcidins’. Iron overload is being recognized to play a carcinogenic role in hepatocellular carcinoma and other cancers, possibly supporting iron depletion in these patients.     

Magnetic resonance nanoparticles for cardiovascular molecular imaging and therapy

Molecular vascular imaging represents a novel tool that promises to change the current medical paradigm of ‘see and treat’ to a ‘detect and prevent’ strategy. Nanoparticle agents, such as superparamagnetic nanoparticles and perfluorocarbon nanoparticle emulsions, have been developed for noninvasive imaging, particularly for magnetic resonance imaging. Designed to target specific epitopes in tissues, these agents are beginning to enter clinical trials for cardiovascular applications. The delivery of local therapy with these nanoparticles, using mechanisms such as contact-facilitated drug delivery, is in the advanced stages of preclinical research. Ultimately, combined diagnostic and therapeutic nanoparticle formulations may allow patients to be characterized noninvasively and segmented to receive custom-tailored therapy. This review focuses on recent developments of nanoparticle technologies with an emphasis on cardiovascular applications of magnetic resonance imaging.