A Tunable Electromagnetic Band-gap Microstrip Filter

In high frequency design, harmonic suppression is a persistent struggle. Non-linear devices such as switches and amplifiers produce unwanted harmonics which may interfere with other frequency bands. Filtering is a widely accepted solution, however there are various shortcomings involved. Suppressing multiple harmonics, if desired, with traditional lumped element and distributed component band-stop filters requires using multiple filters. These topologies are not easily made tunable either. A new filter topology is investigated called Electromagnetic Band-Gap (EBG) structures. EBG structures have recently gained the interest of microwave designers due to their periodic nature which prohibits the propagation of certain frequency bands. EBG structures exhibit characteristics similar to that of a band-stop filter, but in periodically repeating intervals making it ideal for harmonic suppression. The band-gap frequency of an EBG structure may be varied by altering the periodicity of the structure. However, EBG materials are generally static in structure making tuning a challenge. In this thesis, a novel solution for tuning the band-gap properties of an EBG structure is investigated. Designs aimed to improve upon existing solutions are reached. These designs involve acoustic and mechanical tuning methods. Performance is simulated using Agilent’s Advanced Design System (ADS) and a device is constructed and evaluated. Comparing all measured test cases to simulation, band-gap center frequency error is on average 4.44% and absolute band-gap rejection error is 1.358 dB

Hematopoietic Cell–Restricted Deletion of CD36 Reduces High-Fat Diet–Induced Macrophage Infiltration and Improves Insulin Signaling in Adipose Tissue

OBJECTIVE: The fatty acid translocase and scavenger receptor CD36 is important in the recognition and uptake of lipids. Accordingly, we hypothesized that it plays a role in saturated fatty acid-induced macrophage lipid accumulation and proinflammatory activation. RESEARCH DESIGN AND METHODS: In vitro, the effect of CD36 inhibition and deletion in lipid-induced macrophage inflammation was assessed using the putative CD36 inhibitor, sulfosuccinimidyl oleate (SSO), and bone marrow-derived macrophages from mice with (CD36KO) or without (wild-type) global deletion of CD36. To investigate whether deletion of macrophage CD36 would improve insulin sensitivity in vivo, wild-type mice were transplanted with bone marrow from CD36KO or wild-type mice and then fed a standard or high-fat diet (HFD) for 20 weeks. RESULTS: SSO treatment markedly reduced saturated fatty acid-induced lipid accumulation and inflammation in RAW264.7 macrophages. Mice harboring CD36-specific deletion in hematopoietic-derived cells (HSC CD36KO) fed an HFD displayed improved insulin signaling and reduced macrophage infiltration in adipose tissue compared with wild-type mice, but this did not translate into protection against HFD-induced whole-body insulin resistance. Contrary to our hypothesis and our results using SSO in RAW264.7 macrophages, neither saturated fatty acid-induced lipid accumulation nor inflammation was reduced when comparing CD36KO with wild-type bone marrow-derived macrophages. CONCLUSIONS: Although CD36 does not appear important in saturated fatty acid-induced macrophage lipid accumulation, our study uncovers a novel role for CD36 in the migration of proinflammatory phagocytes to adipose tissue in obesity, with a concomitant improvement in insulin action

Tumor Progression Locus 2 (Tpl2) Deficiency Does Not Protect against Obesity-Induced Metabolic Disease

Obesity is associated with a state of chronic low grade inflammation that plays an important role in the development of insulin resistance. Tumor progression locus 2 (Tpl2) is a serine/threonine mitogen activated protein kinase kinase kinase (MAP3K) involved in regulating responses to specific inflammatory stimuli. Here we have used mice lacking Tpl2 to examine its role in obesity-associated insulin resistance. Wild type (wt) and tpl2−/− mice accumulated comparable amounts of fat and lean mass when fed either a standard chow diet or two different high fat (HF) diets containing either 42% or 59% of energy content derived from fat. No differences in glucose tolerance were observed between wt and tpl2−/− mice on any of these diets. Insulin tolerance was similar on both standard chow and 42% HF diets, but was slightly impaired in tpl2−/− mice fed the 59% HFD. While gene expression markers of macrophage recruitment and inflammation were increased in the white adipose tissue of HF fed mice compared with standard chow fed mice, no differences were observed between wt and tpl2−/− mice. Finally, a HF diet did not increase Tpl2 expression nor did it activate Extracellular Signal-Regulated Kinase 1/2 (ERK1/2), the MAPK downstream of Tpl2. These findings argue that Tpl2 does not play a non-redundant role in obesity-associated metabolic dysfunction

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

<i>wt</i> (n = 7) and <i>tpl2^−/−</i> (n = 8) mice were fed a 42% HF diet for 16 weeks.

<p>(A) Fasting plasma glucose. (B) Fasting plasma insulin. (C) Glucose tolerance test. (D) Insulin tolerance test. In C, the inset graph is the incremental area under the curve. Data presented are mean ± SEM. * denotes statistically significant difference between <i>wt</i> and <i>tpl2^−/−</i>.</p

<i>wt</i> (n = 8) and <i>tpl2^−/−</i> (n = 8) mice were fed a standard chow diet for 16 weeks.

<p>(A) Fasting plasma glucose. (B) Fasting plasma insulin. (C) Glucose tolerance test. (D) Insulin tolerance test. In C, the inset graph is the incremental area under the curve. Data presented are mean ± SEM. * denotes statistically significant difference between <i>wt</i> and <i>tpl2^−/−</i>.</p

<i>wt</i> (n = 10) and <i>tpl2^−/−</i> (n = 9) mice were fed a 59% high fat diet for 16 weeks.

<p>(A) Percentage body fat. (B) Fasting blood glucose. (C) Fasting plasma insulin. (D) Glucose tolerance test. (E) Insulin tolerance test. In D, the inset graph is the incremental area under the curve. Data presented are mean ± SEM. In B and C, * denotes statistically significant difference as determined by Student’s T-test. In D and E, * denotes statistically significant difference between <i>wt</i> and <i>tpl2</i>^−/− at indicated time points as determined by 2-way repeated measures ANOVA. Data presented are mean ± SEM.</p