Modified FMCW system for non-contact sensing of human respiration

Abstract

Small displacement detection capability becomes an important key for developing non-contact sensor for human respiration based on radar system. Frequency modulated continuous wave (FMCW) radar has been widely studied and applied for many applications. With respect to the conventional perspective, large bandwidth is needed for detecting the small displacement related to the human respiration. Meanwhile, extracting the respiration pattern from Doppler response has a drawback in identifying the small displacement location. In this paper, the modification on FMCW system was proposed for obtaining the capability in detecting the human respiration and its distance from the radar. Detecting the phase value of the low pass filter (LPF), output from conventional FMCW was investigated and applied as a modification concept. The pattern, rate and amplitude of respiration are extracted from phase detector output. Beat frequency detection is still elaborated for synthesising the reference signal for phase detection. The result shows that the modified FMCW system proposed the capability of detecting the rate and amplitude respiration and location of the target.     

Insulin and Metformin Regulate Circulating and Adipose Tissue Chemerin

OBJECTIVE

To assess chemerin levels and regulation in sera and adipose tissue from women with polycystic ovary syndrome (PCOS) and matched control subjects.

RESEARCH DESIGN AND METHODS

Real-time RT-PCR and Western blotting were used to assess mRNA and protein expression of chemerin. Serum chemerin was measured by enzyme-linked immunosorbent assay. We investigated the in vivo effects of insulin on serum chemerin levels via a prolonged insulin-glucose infusion. Ex vivo effects of insulin, metformin, and steroid hormones on adipose tissue chemerin protein production and secretion into conditioned media were assessed by Western blotting and enzyme-linked immunosorbent assay, respectively.

RESULTS

Serum chemerin, subcutaneous, and omental adipose tissue chemerin were significantly higher in women with PCOS (n = 14; P < 0.05, P < 0.01). Hyperinsulinemic induction in human subjects significantly increased serum chemerin levels (n = 6; P < 0.05, P < 0.01). In adipose tissue explants, insulin significantly increased (n = 6; P < 0.05, P < 0.01) whereas metformin significantly decreased (n = 6; P < 0.05, P < 0.01) chemerin protein production and secretion into conditioned media, respectively. After 6 months of metformin treatment, there was a significant decrease in serum chemerin (n = 21; P < 0.01). Importantly, changes in homeostasis model assessment–insulin resistance were predictive of changes in serum chemerin (P = 0.046).

CONCLUSIONS

Serum and adipose tissue chemerin levels are increased in women with PCOS and are upregulated by insulin. Metformin treatment decreases serum chemerin in these women.Polycystic ovary syndrome (PCOS), a common endocrinopathy affecting 5–10% of women in the reproductive age, is characterized by menstrual dysfunction and hyperandrogenism and is associated with insulin resistance and pancreatic β-cell dysfunction, impaired glucose tolerance (IGT), type 2 diabetes, dyslipidemia, and visceral obesity (1,2). The consequent hyperinsulinemia is more prevalent in lean and obese women with PCOS when compared with age- and weight-matched normal women (3).The metabolic syndrome is associated with excessive accumulation of central body fat. As well as its role in energy storage, adipose tissue produces several hormones and cytokines termed ‘adipokines’ that have widespread effects on carbohydrate and lipid metabolism. They appear to play an important role in the pathogenesis of insulin resistance, diabetes, and atherosclerosis (4). Furthermore, it is apparent that accumulation of visceral adipose tissue poses a greater cardiometabolic risk than subcutaneous adipose tissue (5) as removal of visceral rather than subcutaneous adipose tissue has been shown to improve insulin sensitivity (6). Moreover, differences in gene expression of adipocyte-secreted molecules (adipokines) suggest that there are inherent adipose tissue depot–specific differences in the endocrine function of adipose tissue. In relation to this, we have published data on the increased levels of vaspin in women with PCOS (7); vaspin is a recently described adipokine mainly formed in human visceral adipose tissue that has insulin-sensitizing effects (8).Recently, Bozaoglu et al. (9) reported chemerin as a novel adipokine, circulating levels of which significantly correlated with BMI, circulating triglycerides, and blood pressure, features of the metabolic syndrome. In addition, chemerin or chemerin receptor knockdown impaired differentiation of 3T3-L1 cells and attenuated the expression of adipocyte genes involved in glucose and lipid homeostasis (10).With the aforementioned in mind and the fact that there is no literature with regards to chemerin in human adipose tissue and its regulation, in study 1, we assessed circulating chemerin as well as mRNA expression and protein levels of chemerin in subcutaneous and omental adipose tissue depots in women with PCOS against age, BMI, and waist-to-hip ratio (WHR) in matched control subjects. Furthermore, we studied the in vivo (study 2) and ex vivo effects of insulin on circulating chemerin levels via a prolonged insulin-glucose infusion in humans and primary adipose tissue explant cultures, respectively. In study 3 we studied the effects of metformin therapy, widely used in the treatment of PCOS in women, on circulating chemerin levels in tandem with associated changes to clinical, hormonal, and metabolic parameters in the same cohort of PCOS in women. Additionally, we studied the ex vivo effects of metformin and steroid hormones in human primary adipose tissue explants.     

Metformin Treatment May Increase Omentin-1 Levels in Women With Polycystic Ovary Syndrome

OBJECTIVE

Polycystic ovary syndrome (PCOS) is associated with the metabolic syndrome. Decreased omentin-1 levels are associated with obesity and diabetes. To study the effects of metformin treatment on omentin-1 levels in PCOS subjects and effects of omentin-1 on in vitro migration and angiogenesis.

RESEARCH DESIGN AND METHODS

Serum omentin-1 was measured by ELISA. Angiogenesis was assessed by studying capillary tube formation in human microvascular endothelial cells (HMEC-1) on growth factor reduced Matrigel. Endothelial cell migration assay was performed in a modified Boyden chamber. Nuclear factor-κB (NF-κB) was studied by stably transfecting HMEC-1 cells with a cis-reporter plasmid containing luciferase reporter gene linked to five repeats of NF-κB binding sites. Akt phosphorylation was assessed by Western blotting.

RESULTS

Serum omentin-1 was significantly lower in PCOS women (P < 0.05). After 6 months of metformin treatment, there was a significant increase in serum omentin-1 (P < 0.01). Importantly, changes in hs-CRP were significantly negatively correlated with changes in serum omentin-1 (P = 0.036). In vitro migration and angiogenesis were significantly increased in serum from PCOS women (P < 0.01) compared with matched control subjects; these effects were significantly attenuated by metformin treatment (P < 0.01) plausibly through the regulation of omentin-1 levels via NF-κB and Akt pathways. CRP and VEGF induced in vitro migration, and angiogenesis was significantly decreased by omentin-1.

CONCLUSIONS

Increases in omentin-1 levels may play a role but are not sufficient to explain the decreased inflammatory and angiogenic effects of sera from metformin-treated PCOS women.Polycystic ovary syndrome (PCOS) is a proinflammatory state associated with type 2 diabetes, visceral obesity, and cardiovascular complications, features of the metabolic syndrome (1–5). The metabolic syndrome is associated with accumulation of visceral adipose tissue. Visceral adipose tissue produces cytokines termed “adipokines” implicated in the pathogenesis of diabetes and atherosclerosis (6–9).Omentin-1 has been described as a novel adipokine preferentially produced by visceral adipose tissue. In vitro experiments revealed that treatment with recombinant omentin-1 enhances insulin-stimulated glucose uptake in human adipocytes. Also, omentin-1 was shown to trigger Akt signaling in both the absence and presence of insulin (10,11). Additionally, omentin plasma levels and omentin gene expression in visceral adipose tissue are decreased in obesity (12). Recently, we have reported novel data showing a significant decrease of adipose tissue and circulating omentin-1 levels in overweight PCOS women (13). Thus, given the above functions of omentin-1, increasing omentin-1 levels in PCOS women may alleviate cardiometabolic dysfunction in these women.We studied the effects of metformin treatment on omentin-1 levels in PCOS subjects and effects of omentin-1 and serum on in vitro migration and angiogenesis. Researchers have used serum to perform functional experiments in endothelial, cardiac, and neural cells (14–16). Finally, given the link between inflammation and angiogenesis (17), we explored nuclear factor-kappaB (NF-κB), Erk1/2, and Akt pathways, important regulators of inflammation and angiogenesis (18,19).     

Future Directions in Employment,Occupational Rehabilitation,and Disability: Introduction to the Special Section

Purpose From an array of disciplinary perspectives, the articles in this special section examine opportunities and challenges in the economic, social, and civic participation of individuals across the spectrum of disabilities. Methods At multiple levels of analysis, the contributors consider employment law and policy frameworks, occupational and vocational rehabilitation strategies, and corporate practices in support of the full and equal inclusion of people with disabilities in society. Results and Conclusions The implications for policymakers, public and private sector stakeholders, and occupational rehabilitation professional are presented to help inform future policies, practices, and strategies to improve employment outcomes for people with disabilities.     

Intravenous dexamethasone pulse therapy in diffuse systemic sclerosis

Thirty-five patients with diffuse systemic sclerosis were studied in a randomized, placebo-controlled, double-blind study. Seventeen patients received intravenous dexamethasone pulse therapy, while 18 patients received placebo. Each pulse consisted of 100 mg dexamethasone in 250 ml 5% dextrose infused intravenously over 1 h. Pulse therapy was repeated every month for 6 months. Assessment of disease status with various parameters was done at entry and at completion of trial, i.e. after 6 months. Significant improvement in skin involvement was seen in the study group, with the total skin score (TSS) decreasing from 28.5±12.2 to 25.8±12.8, while in the control group, TSS increased from 30.6±13.2 to 34.7±10. Similarly, significant improvement was noted in the flexion index. Other parametres that included extension index, maximum oral opening, range of movement of joints, functional disability score, Raynaud's phenomenon (frequency and duration), ESR, proteinuria, chest X-ray, ECG, lung function tests, barium swallow and antinuclear antibody were unchanged. Adverse effects of therapy were limited to an increased incidence of minor chest infections. It is concluded that intravenous pulse dexamethasone may be useful in the treatment of diffuse systemic sclerosis.     

Do Healthy People Worry? Modern Health Worries,Subjective Health Complaints,Perceived Health,and Health Care Utilization

Background  

Modern health worries (MHW) are concerns related to modern or technological features of daily life (e.g., air pollution, x-rays, food additives, etc.), and have been associated with subjective health complaints (SHC) and health care use.     

Ex vivo and in vivo regulation of lipocalin-2, a novel adipokine, by insulin

OBJECTIVE—Lipocalin-2, a novel adipokine, has been shown to be elevated in obese, insulin-resistant, and diabetic subjects. We therefore sought to study the ex vivo and in vivo effects of insulin on lipocalin-2 levels in humans.RESEARCH DESIGN AND METHODS—We investigated the in vivo effects of insulin (hyperinsulinemia) on circulating lipocalin-2 levels by enzyme-linked immunosorbent assay via a prolonged insulin-glucose infusion. The ex vivo effect of insulin on adipose tissue lipocalin-2 protein production and secretion into conditioned media was assessed by Western blotting and enzyme-linked immunosorbent assay, respectively.RESULTS—Hyperinsulinemic induction in human subjects significantly increased circulating lipocalin-2 levels (P < 0.01). Also, in omental adipose tissue explants, insulin caused a significant dose-dependent increase in lipocalin-2 protein production and secretion into conditioned media (P < 0.05, P < 0.01, respectively); these effects were negated by both phosphatidylinositol 3-kinase and mitogen-activated protein kinase kinase inhibitors.CONCLUSIONS—Lipocalin-2 is upregulated by insulin via phosphatidylinositol 3-kinase and mitogen-activated protein kinase signaling pathways.Obesity and the metabolic syndrome are associated with serious cardiometabolic sequelae including insulin resistance, hyperinsulinemia, diabetes, dyslipidemia, and cardiovascular disease (1). The metabolic syndrome is associated with visceral obesity. Adipose tissue produces cytokines termed “adipokines” that are implicated in the pathogenesis of the metabolic syndrome (2).Recently, Yan et al. (3) established lipocalin-2 as a novel adipokine, highly expressed by adipose tissue in murine models of obesity. Also, they demonstrated that lipocalin-2 levels are increased by dexamethasone and tumor necrosis factor-α and are reduced by rosiglitazone in murine adipocytes (3). More recently, Wang et al. (4) reported elevated levels of lipocalin-2 in obesity and diabetes.We therefore studied the effects of acute and chronic hyperinsulinemia on circulating lipocalin-2 levels via a prolonged insulin-glucose infusion in humans. We also assessed the effects of insulin on lipocalin-2 protein production and secretion into conditioned media from human visceral adipose tissue explants.