Metabolic control and bone health in adolescents with type 1 diabetes

<p>Abstract</p> <p>Background</p> <p>Adults with type 1 diabetes (T1D) have decreased bone mineral density (BMD) and increased fracture risk, yet the etiologies remain elusive. Early detection of derangements in bone biomarkers during adolescence could lead to timely recognition. In adolescents with T1D, we evaluated the relationships between metabolic control, BMD, and bone anabolic and turnover markers.</p> <p>Methods</p> <p>Cross-sectional study of 57 adolescent subjects with T1D who had HbA1c consistently ≥ 9% (Poor Control, PC n = 27) or < 9% (Favorable Control, FC n = 30) for two years prior to enrollment. Subjects had T1DM for at least three years and were without diabetes complications, known celiac disease, or other chronic diseases.</p> <p>Results</p> <p>There were no differences between HbA1c groups in BMD, components of the IGF system, or 25-hydroxyvitamin D status. The prevalence of 25-hydroxyvitamin D abnormalities was similar to that seen in the general adolescent population. Few patients met the recommended dietary allowance (RDA) for vitamin D or calcium.</p> <p>Conclusions</p> <p>These data provide no evidence of association between degree of metabolic control and BMD in adolescents with T1D. Adolescents with T1D have a high prevalence of serum 25-hydroxyvitamin D abnormalities. Longitudinal studies are needed to evaluate the predictive value of vitamin D abnormalities on fracture risk.</p

Pediatric DXA: clinical applications

Normal bone mineral accrual requires adequate dietary intake of calcium, vitamin D and other nutrients; hepatic and renal activation of vitamin D; normal hormone levels (thyroid, parathyroid, reproductive and growth hormones); and neuromuscular functioning with sufficient stress upon the skeleton to induce bone deposition. The presence of genetic or acquired diseases and the therapies that are used to treat them can also impact bone health. Since the introduction of clinical DXA in pediatrics in the early 1990s, there has been considerable investigation into the causes of low bone mineral density (BMD) in children. Pediatricians have also become aware of the role adequate bone mass accrual in childhood has in preventing osteoporotic fractures in late adulthood. Additionally, the availability of medications to improve BMD has increased with the development of bisphosphonates. These factors have led to the increased utilization of DXA in pediatrics. This review summarizes much of the previous research regarding BMD in children and is meant to assist radiologists and clinicians with DXA utilization and interpretation

Surface Treatments for Inkjet Printing onto a PTFE-Based Substrate for High Frequency Applications

This document is the Accepted Manuscript version of a Published Work that appeared in final form in the journal Industrial and Engineering Chemistry Research [copyright © American Chemical Society] after peer review and technical editing by the publisher. To access the final edited and published work see: http://pubs.acs.org/doi/abs/10.1021/ie4006639Inkjet printing onto laminates for use in high frequency applications (high frequency laminates) is challenging, due to the substrate surface roughness present after etching away the copper layer(s). This has a detrimental effect on interconnect losses as the frequency increases. In this paper, different surface treatments to reduce the surface roughness of a typical high frequency laminate (RO3006) are investigated. In particular, the importance of matching the substrate surface energy to the ink to achieve a smooth coated layer for the case of a UV cured insulator is demonstrated. This is achievable within the parameters of heating the platen, which is a more flexible approach compared to modifying the ink to improve the ink-substrate interaction. In printing onto the surface modified substrates, the substrate roughness was observed to affect the printed line width significantly. A surface roughness factor was introduced to take into account the phenomenon by modifying the original formula of Smith et al. Lastly, the authors show that the printed line widths are also influenced by the surface tension arising from charges present on the surface modified substrates

Analytical and Experimental Study on Actuation Time of Displacement Amplified Electromagnetic Actuator

This paper describes an analytical study undertaken on an electromagnetic actuator design with a displacement amplification mechanism by explaining the physical modeling and formulizing the actuation time of the actuator in terms of physical model variables. This is followed by an experimental investigation on the actuation time of the electromagnetic actuator. Increasing the gap between the electromagnet and armatures to increase the stroke of the electromagnetic actuator resulted in a drastic loss of the thrust force. The displacement amplification mechanisms were used to increase the stroke of the actuator without incurring high levels of loss in the thrust force. For the same load and final stroke of the actuator, the actuation time was observed to model the effect of amplification ratio on the actuator. Using the physical and mathematical modeling of the displacement amplified electromagnetic actuator and by formulating the actuation time, simulations were implemented that revealed the relationship between the actuation time and amplification ratio. The design of the experimental setup and methodology of the experimentation are explained to verify the simulation results and calculated relationship between the amplification ratio and actuation time in practice. The results of simulations and experimentations showed that there is an optimum point until which the amplification ratio can be increased while advancing from actuation time for the same load and final stroke of the actuator. The similarity between the simulation and experimental results proved that the value of this optimum point could be formulized and expressed in terms of other variables used to simulate the actuator

GJB2 mutations in Turkish patients with ARNSHL: prevalence and two novel mutations.

Contains fulltext : 47829.pdf (publisher's version ) (Closed access)Mutations in the connexin 26 gene (GJB2) cause a significant proportion of prelingual non-syndromic autosomal recessive deafness in all populations studied so far. To determine the percentage of hearing loss attributed to GJB2 in northeast Turkey, 93 unrelated patients with autosomal recessive non-syndromic hearing loss (ARNSHL) were screened. Seven different mutations were found in 29 of the patients with severe to profound hearing loss. The 35delG mutation was the most common mutation, accounting for 76% of all mutant GJB2 alleles. Four already described mutations, W24X, 310del14, delE120 and R184P and two novel mutations, Q80K and P173S, were identified. The allelic Delta(GJB6-D13S1830), which can cause hearing loss in combination with GJB2 mutations, was not present in our patients. Our results are comparable to those reported in other regions in Turkey and indicate that GJB2 mutations account for about 30% of Turkish patients with ARNSHL. Besides 35delG, W24X and delE120 occur more than once in the Turkish ARNSHL population with a frequency of about 5%

The Influence of Dietary Fatty Acids on Immune Responses

Diet-derived fatty acids (FAs) are essential sources of energy and fundamental structural components of cells. They also play important roles in the modulation of immune responses in health and disease. Saturated and unsaturated FAs influence the effector and regulatory functions of innate and adaptive immune cells by changing membrane composition and fluidity and by acting through specific receptors. Impaired balance of saturated/unsaturated FAs, as well as n-6/n-3 polyunsaturated FAs has significant consequences on immune system homeostasis, contributing to the development of many allergic, autoimmune, and metabolic diseases. In this paper, we discuss up-to-date knowledge and the clinical relevance of the influence of dietary FAs on the biology, homeostasis, and functions of epithelial cells, macrophages, dendritic cells, neutrophils, innate lymphoid cells, T cells and B cells. Additionally, we review the effects of dietary FAs on the pathogenesis of many diseases, including asthma, allergic rhinitis, food allergy, atopic dermatitis, rheumatoid arthritis, multiple sclerosis as well as type 1 and 2 diabetes