Long-term release of carbon dioxide from Arctic tundra ecosystems in Alaska

Author Posting. © The Author(s), 2016. This is the author's version of the work. It is posted here by permission of Springer for personal use, not for redistribution. The definitive version was published in Ecosystems 20 (2017): 960–974, doi:10.1007/s10021-016-0085-9.Releases of the greenhouse gases carbon dioxide (CO2) and methane (CH4) from thawing permafrost are expected to be among the largest feedbacks to climate from arctic ecosystems. However, the current net carbon (C) balance of terrestrial arctic ecosystems is unknown. Recent studies suggest that these ecosystems are sources, sinks, or approximately in balance at present. This uncertainty arises because there are few long-term continuous measurements of arctic tundra CO2 fluxes over the full annual cycle. Here, we describe a pattern of CO2 loss based on the longest continuous record of direct measurements of CO2 fluxes in the Alaskan Arctic, from two representative tundra ecosystems, wet sedge and heath tundra. We also report on a shorter time series of continuous measurements from a third ecosystem, tussock tundra. The amount of CO2 loss from both heath and wet sedge ecosystems was related to the timing of freeze-up of the soil active layer in the fall. Wet sedge tundra lost the most CO2 during the anomalously warm autumn periods of September – December 2013 - 2015, with CH4 emissions contributing little to the overall C budget. Losses of C translated to approximately 4.1% and 1.4% of the total soil C stocks in active layer of the wet sedge and heath tundra, respectively, from 2008 – 2015. Increases in air temperature and soil temperatures at all depths may trigger a new trajectory of CO2 release, which will be a significant feedback to further warming if it is representative of larger areas of the Arctic.This work was funded by the National Science Foundation Division of Polar Programs Arctic Observatory Network grant numbers 856864, 1304271, 0632264, and 1107892. This study was also partially funded by the NSF Alaska Experimental Program to Stimulate Competitive Research award number OIA-1208927.2017-11-2

Animal Models of Bone Loss in Inflammatory Arthritis: from Cytokines in the Bench to Novel Treatments for Bone Loss in the Bedside—a Comprehensive Review

Throughout life, bone is continuously remodelled. Bone is formed by osteoblasts, from mesenchymal origin, while osteoclasts induce bone resorption. This process is tightly regulated. During inflammation, several growth factors and cytokines are increased inducing osteoclast differentiation and activation, and chronic inflammation is a condition that initiates systemic bone loss. Rheumatoid arthritis (RA) is a chronic inflammatory auto-immune disease that is characterised by active synovitis and is associated with early peri-articular bone loss. Peri-articular bone loss precedes focal bone erosions, which may progress to bone destruction and disability. The incidence of generalised osteoporosis is associated with the severity of arthritis in RA and increased osteoporotic vertebral and hip fracture risk. In this review, we will give an overview of different animal models of inflammatory arthritis related to RA with focus on bone erosion and involvement of pro-inflammatory cytokines. In addition, a humanised endochondral ossification model will be discussed, which can be used in a translational approach to answer osteoimmunological questions

Serum vitamin D levels are associated with structural and functional properties of the carotid artery in older men and women

Background and aims: This cross-sectional study aimed to assess the relationship between serum vitamin D levels and carotid and brachial artery distensibility in patients older than 55 years, referred to the outpatient clinic of the department of internal medicine and geriatric medicine of the Erasmus Medical Center, in Rotterdam. Methods and results: From April to July 2006 we consecutively enrolled 49 elder patients (21 men and 28 women, mean age 78 ± 8 years) without a cardiovascular event within 6 weeks before the visit. Carotid and brachial artery distensibility coefficients and serum 25(OH)D levels (mean 50 ± 28.8 nmol/L) were assessed. Multivariate analysis (with linear regression model) was performed to investigate the relation between these parameters: carotid artery distensibility coefficient was associated with serum 25(OH)D levels (β = 0.112; 95% CI 0.053 0.172; p = 0.001). Moreover, a negative association was also observed between carotid artery distensibility coefficient and mean arterial pressure (β = −0.279; 95% CI, −0.339 −0.159; p = 0.0001). On the contrary, brachial artery distensibility has shown no association with 25(OH)D levels, being negatively linked to LDL-cholesterol levels and heart rate. An association was also observed between serum 25(OH)D level and carotid artery intima–media thickness. Conclusion: Our results revealed that serum 25(OH)D levels of older men and women were associated with both structural and functional properties of the carotid artery. No association was found with the brachial artery distensibility

Better knowledge on vitamin D and calcium in older people is associated with a higher serum vitamin D level and a higher daily dietary calcium intake

Abstract: Objective: The objective of the present study was to examine knowledge on vitamin D and calcium in a cohort of older adults and to test the association between health knowledge, vitamin D status and dietary calcium intake. Methods: The participants of this cross-sectional survey consisted of 426 individuals (≥65 years), living in residential homes. Participants were tested for their knowledge on vitamin D and calcium using a standardized questionnaire. Serum 25-hydroxyvitamin D3 (25(OH)D3) levels and dietary calcium intake were measured. Results: The mean serum 25(OH)D3 level was 39.1 (±21.4) nmol/l and the mean daily dietary calcium intake was 826 (±242) mg/day. Of the participants, only 3

Interaction between vitamin D receptor genotype and estrogen receptor alpha genotype influences vertebral fracture risk

In view of the interactions of vitamin D and the estrogen endocrine system, we studied the combined influence of polymorphisms in the estrogen receptor (ER) alpha gene and the vitamin D receptor (VDR) gene on the susceptibility to osteoporotic vertebral fractures in 634 women aged 55 yr and older. Three VDR haplotypes (1, 2, and 3) of the BsmI, ApaI, and TaqI restriction fragment length polymorphisms and three ERalpha haplotypes (1, 2, and 3) of the PvuII and XbaI restriction fragment length polymorphisms were identified. We captured 131 nonvertebral and 85 vertebral fracture cases during a mean follow-up period of 7 yr. ERalpha haplotype 1 was dose-dependently associated with increased vertebral fracture risk (P < 0.001) corresponding to an odds ratio of 1.9 [95% confidence interval (CI), 0.9-4.1] per copy of the risk allele. VDR haplotype 1 was overrepresented in vertebral fracture cases. There was a significant interaction (P = 0.01) between ERalpha haplotype 1 and VDR haplotype 1 in determining vertebral fracture risk. The association of ERalpha haplotype 1 with vertebral fracture risk was only present in homozygous carriers of VDR haplotype 1. The risk of fracture was 2.5 (95% CI, 0.6-9.9) for heterozygous and 10.3 (95% CI, 2.7-40) for homozygous carriers of ERalpha haplotype 1. These associations were independent of bone mineral density. In conclusion, interaction between ERalpha and VDR gene polymorphisms leads to increased risk of osteoporotic vertebral fractures in women, largely independent of bone mineral density

Interaction between vitamin D receptor genotype and estrogen receptor alpha genotype influences vertebral fracture risk

In view of the interactions of vitamin D and the estrogen endocrine system, we studied the combined influence of polymorphisms in the estrogen receptor (ER) alpha gene and the vitamin D receptor (VDR) gene on the susceptibility to osteoporotic vertebral fractures in 634 women aged 55 yr and older. Three VDR haplotypes (1, 2, and 3) of the BsmI, ApaI, and TaqI restriction fragment length polymorphisms and three ERalpha haplotypes (1, 2, and 3) of the PvuII and XbaI restriction fragment length polymorphisms were identified. We captured 131 nonvertebral and 85 vertebral fracture cases during a mean follow-up period of 7 yr. ERalpha haplotype 1 was dose-dependently associated with increased vertebral fracture risk (P < 0.001) corresponding to an odds ratio of 1.9 [95% confidence interval (CI), 0.9-4.1] per copy of the risk allele. VDR haplotype 1 was overrepresented in vertebral fracture cases. There was a significant interaction (P = 0.01) between ERalpha haplotype 1 and VDR haplotype 1 in determining vertebral fracture risk. The association of ERalpha haplotype 1 with vertebral fracture risk was only present in homozygous carriers of VDR haplotype 1. The risk of fracture was 2.5 (95% CI, 0.6-9.9) for heterozygous and 10.3 (95% CI, 2.7-40) for homozygous carriers of ERalpha haplotype 1. These associations were independent of bone mineral density. In conclusion, interaction between ERalpha and VDR gene polymorphisms leads to increased risk of osteoporotic vertebral fractures in women, largely independent of bone mineral density