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Human body tissues have a strong effect on the antenna operation in wireless body area networks (WBANs). In this study, the authors present the deep investigations of the effect of body tissue thicknesses on the performance of an ultra wideband (UWB) loop antenna by simulations when the antenna is operated on contact with tissues. The planar UWB loop antenna is designed for the examinations, which is targeted to be used in UWB WBAN applications. The effect of tissue thicknesses on the antenna performance is analysed and characterised in the terms of reflection coefficient S11, gain and total antenna efficiency, group delay, radiation patterns and specific absorption rate by simulations. A parametric layered human body tissue model with the frequency-dependent behaviour is exploited in the investigations. Further, the reflection coefficient of the presented antenna is measured in the different locations of the author's body. The main aim of these investigations is to demonstrate how the thickness of outermost body tissues affects the antenna performance.

Stopping power, range, and time of proton in water, lung, bladder, and intestinal human tissues are calculated using density functional theory and Beth’s relativistic equation in range of proton energy (0.01–1,000 MeV). The experimental data extracted from SRIM-2013 program were used to proton to the same human tissues applied in the MATLAB-2021 program, and the mean ionization potential of water and the studied tissues is calculated using Gaussian 09W program. A good agreement has been found between our calculations for stopping power, range, and time of protons in the studied human body tissues and SRIM-2013 program calculations.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures ( P  < 5 × 10 −8 ). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms. Genome-wide association meta-analyses of waist-to-hip ratio adjusted for body mass index in more than 224,000 individuals identify 49 loci, 33 of which are new and many showing significant sexual dimorphism with a stronger effect in women; pathway analyses implicate adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution. Cardiometabolic traits linked to body fat distribution In the first of a pair of Articles in this issue from the GIANT Consortium, genome-wide association meta-analyses of waist and hip circumference-related traits in more than 200,000 individuals have been used to identify 49 loci — 33 of them new — associated with waist-to-hip ratio adjusted for body mass index and an additional 19 loci associated with related waist and hip circumference measures. A subset of these loci shows significant sexual dimorphism, with many showing a stronger effect in women. Analyses implicate adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms and offer potential targets for interventions in the risks associated with abdominal fat accumulation.

Reactive oxygen species (ROS), important mediators of cell and tissue injury during inflammation, are produced by several types of inflammatory cells. The formation of ROS can be monitored by detection of lipid peroxidation products. The extremely broad spectrum of biological effects of aldehydic lipid peroxidation products has necessitated the development of a technique that enables the sensitive routine quantitation of aldehydes formed in biological materials. Malondialdehyde (MDA) is a by-product of enzymatic eicosanoid formation and an end-product of nonenzymatic peroxidation of polyunsaturated fatty acids with three or more bisallylic double bonds. The determination of the thiobarbituric acid derivative of MDA (TBA-MDA) is a widely used method for estimating overall lipid peroxidation. We describe a rapid, isocratic, simple, and sensitive high-performance liquid chromatographic (HPLC) method with spectrofluorimetric detection for measurement of MDA-TBA in human biological samples such as plasma, urine, wound secretions, amniotic fluid, sputum and tissue samples. By use of this method, picomole quantities of MDA can be readily and specifically detected in different biological materials. Coefficients of variation of repeated MDA-TBA assays were 4.4% within run and 6.9% from run to run. Reference values are given for a variety of human body fluids and for rat tissues.

This chapter discusses the electrical properties of human tissues, as well as numerical and physical modeling of the human body, and corresponding numerical and experimental procedures. Electrical properties of each type of tissue result from the interaction between the incident electromagnetic (EM) radiation and the tissue constituents at the cellular and molecular level and control the propagation, attenuation, reflection, and other behavior of EM fields inside and outside the human body. The computational time is usually very long, and it is generally not easy to simulate realistic conditions and include the effects of the surrounding environment. Finally, in order to ensure human safety, recommendations have been set by professional bodies and government agencies on the maximum allowable specific absorption rate (SAR) levels. However, the health hazards occurring from long-term exposure to these new technologies are far from settled.

Background and objectives: It has been well established that the resting energy expenditure (REE) for the whole body is the sum of the REE for each organ-tissue in young and middle-aged healthy adults. Based on these previous studies, although it is speculated that sleeping energy expenditure (SEE, which has small inter-individual variability) changes with a commensurate gain or reduction in the resting metabolic rate of each organ-tissue, it is unclear whether a change in organ-tissue masses is directly attributed to the fluctuation of SEE at present. This study aimed to assess the relationship between changes in organ-tissue mass and sleeping energy expenditure (SEE) following weight change in college Sumo wrestlers. This included blood analysis, which is related to energy expenditure. Materials and Methods: A total of 16 healthy male college Sumo wrestlers were recruited in this study. All measurements were obtained before and after weight change. Magnetic resonance imaging measurements were used to determine the volume of the skeletal muscle (SM), liver, and kidneys, and an indirect human calorimeter was used to determine SEE before and after weight change. Results: The change in body mass and SEE ranged between −8.7~9.5 kg, and −602~388 kcal/day. Moreover, changes in SM, liver, and kidneys ranged between −3.3~3.6 kg, −0.90~0.77 kg, and −0.12~0.07 kg. The change in SEE was not significantly correlated with the change in SM or liver mass, nor with blood analyses; however, a significant relationship between the change in kidney mass and SEE was observed. Conclusions: Based on our results, there is a possibility that the mass of the kidneys has an effect on the change in SEE following weight change in college Sumo wrestlers.

Background Obesity is a complex disease marked by excessive, dysfunctional adipose tissue accumulation. Recent research underscores the pivotal role of brown adipose tissue (BAT) in metabolic health and its potential as a therapeutic target for obesity management. Emerging preclinical and clinical evidence suggests that second-generation anti-obesity drugs, especially dual agonists such as tirzepatide, may enhance BAT activity. Additionally, beige adipose tissue, derived from white adipose tissue (WAT), may contribute significantly to whole-body thermogenesis, yet its role remains underexplored. Methods This investigator-initiated, randomized, placebo-controlled clinical trial aims to evaluate the effects of tirzepatide on BAT activity and WAT browning in premenopausal women with obesity. Thirty-four participants will be randomized 1:1 to receive either tirzepatide or a placebo for 24 weeks. Primary outcomes include changes in BAT volume and activity, assessed using 18F-FDG-PET/CT, MRI, and infrared thermography, as well as the induction of WAT browning, evaluated through changes in mRNA expression patterns and histomorphometric alterations in subcutaneous adipose tissue samples. Secondary outcomes will involve the assessment of whole-body composition, resting energy expenditure, and various metabolic health markers, correlated with thermogenic adipose tissue changes. Comparative analysis of BAT assessment methods will refine protocols for research and clinical use. Discussion This study is the first to systematically explore the potential of pharmacological obesity management to enhance BAT activity and induce WAT browning. Results may establish thermogenic adipose tissue augmentation as a novel mechanism of action for second-generation anti-obesity medications. Trial registration ClinicalTrials.gov NCT06893211. Registered on 2025 March 25.

Mammalian adipose tissue is traditionally categorized into white and brown relating to their function and morphology: while white serves as an energy storage, brown adipose tissue acts as the heat generator maintaining the core body temperature. The most recently identified type of fat, beige adipocyte tissue, resembles brown fat by morphology and function but is developmentally more related to white. The synthesis of beige fat, so-called browning of white fat, has developed into a topical issue in diabetes and metabolism research. This is due to its favorable effect on whole-body energy metabolism and the fact that it can be recruited during adult life. Indeed, brown and beige adipose tissues have been demonstrated to play a role in glucose homeostasis, insulin sensitivity, and lipid metabolism—all factors related to pathogenesis of type 2 diabetes. Many agents capable of initiating browning have been identified so far and tested widely in humans and animal models including in vitro and in vivo experiments. Interestingly, several agents demonstrated to have browning activity are in fact secreted as adipokines from brown and beige fat tissue, suggesting a physiological relevance both in beige adipocyte recruitment processes and in maintenance of metabolic homeostasis. The newest findings on agents driving beige fat recruitment, their mechanisms, and implications on type 2 diabetes are discussed in this review.

A large-scale epigenome-wide association study identifies changes in DNA methylation associated with body mass index in blood and adipose tissue, and correlates DNA methylation sites with high risk of incident type 2 diabetes. Body fat and diabetes risk Obesity is a major risk factor for type 2 diabetes and related metabolic disorders. Genetic association studies have identified genomic loci associated with obesity, and recent studies have also suggested associations with DNA methylation. These authors report an epigenome-wide association study for body mass index (BMI), identifying an association with DNA methylation at 187 loci in blood and adipose tissue. They find that these methylation changes are secondary to adiposity and are also associated with an increased risk of developing type 2 diabetes, independent of conventional risk factors. Approximately 1.5 billion people worldwide are overweight or affected by obesity, and are at risk of developing type 2 diabetes, cardiovascular disease and related metabolic and inflammatory disturbances 1 , 2 . Although the mechanisms linking adiposity to associated clinical conditions are poorly understood, recent studies suggest that adiposity may influence DNA methylation 3 , 4 , 5 , 6 , a key regulator of gene expression and molecular phenotype 7 . Here we use epigenome-wide association to show that body mass index (BMI; a key measure of adiposity) is associated with widespread changes in DNA methylation (187 genetic loci with P  < 1 × 10 −7 , range P  = 9.2 × 10 −8 to 6.0 × 10 −46 ; n  = 10,261 samples). Genetic association analyses demonstrate that the alterations in DNA methylation are predominantly the consequence of adiposity, rather than the cause. We find that methylation loci are enriched for functional genomic features in multiple tissues ( P  < 0.05), and show that sentinel methylation markers identify gene expression signatures at 38 loci ( P  < 9.0 × 10 −6 , range P  = 5.5 × 10 −6 to 6.1 × 10 −35 , n  = 1,785 samples). The methylation loci identify genes involved in lipid and lipoprotein metabolism, substrate transport and inflammatory pathways. Finally, we show that the disturbances in DNA methylation predict future development of type 2 diabetes (relative risk per 1 standard deviation increase in methylation risk score: 2.3 (2.07–2.56); P  = 1.1 × 10 −54 ). Our results provide new insights into the biologic pathways influenced by adiposity, and may enable development of new strategies for prediction and prevention of type 2 diabetes and other adverse clinical consequences of obesity.