The Heterogeneity of White Adipose Tissue

The increasing prevalence of obesity is a major factor driving the worldwide epidemic of type 2 diabetes and metabolic syndrome. Adipose tissue not only stores energy, but also controls metabolism through secretion of hormones, cytokines, proteins, and microRNAs that affect the function of cells and tissues throughout the body. Accumulation of visceral white adipose tissue (WAT) leads to central obesity and is associated with insulin resistance and increased risk of metabolic disease, whereas accumulation of subcutaneous WAT leads to peripheral obesity and may be protective of metabolic syndrome. While much attention has been paid to identifying differences between white, brown and brite/beige adipocytes, there is growing evidence that there is functional heterogeneity among white adipocytes themselves. This heterogeneity, includes depot-specific differences in development, inflammation, and endocrine properties. In addition to the depot-specific differences, even within a single fat depot, WAT is composed of developmentally and phenotypically distinct subpopulations of adipocytes. The following chapter will introduce this concept of white adipocyte heterogeneity

Improvement of adhesive toughness measurement

The double cantilever beam (DCB) method for adhesive toughness measurement was improved by incorporating a sufficiently sharp crack made by a wedge-tapping method. A known route to producing cracks via loading–unloading cycles was proved unreliable because the cycles produced plastic deformation in the adhesive where new cracks propagated. Abnormally high toughness values with large standard deviations were obtained with cracks made by embedding a non-sticky insert. Only instantly propagated cracks made by tapping were sufficiently sharp to produce reproducible, accurate tough-ness measurements. However, toughened resin was insensit

NtGCM User's Manual: 1.1 (High Pressure High Temperature Laser based) Nanotube Growth Chamber Monitor

This manual describes the installation and use of NtGCM software. NtGCM is software designed for monitoring the growth of nanotubes in a high temperature and high pressure chamber using a laser*. NtGCM software monitors a dozen dierent parameters that are important to understanding the growth of the nanomaterials including the laser input power, the temperature at eight separate locations inside and outside the growth chamber, as well as the pressure and ow rate of the gaseous media that control the environment in the chamber. The measurements are all made in real time. The program features a robust user account management layer and a rich data display manager that allows plotted data, displayed units and other parameters to be changed on the y for the operator's convenience

Wireless, Handheld Diffuse Reflectance Spectroscopy to Quantify Tissue Microvascular Hemodynamics

Diffuse Reflectance Spectroscopy (DRS) is a non-invasive optical method to characterize tissue optical properties for disease diagnosis and health monitoring. Two optical fibers are often used in a DRS system: one to deliver light to the tissue and the other to gather diffuse reflectance spectra, which provide quantitative details about the structure and composition of the tissue. The conventional DRS system, however, is expensive, bulky, and composed of fragile optical fibers and multiple electrical connections. Here we propose to build a wireless, handheld, and fiber-less diffuse optical spectroscopy system. Unfortunately, the diffusion approximation utilized for data analysis of the conventional DRS is no longer valid due to the non-contact configuration of the fiber-less DRS system. To analyze the collected diffuse reflectance spectra using the handheld spectrometer, we have built a reflectance lookup table (LUT) using Monte Carlo simulation. Also, we have conducted some tests using a blood liquid phantom that is made of water, intralipid, and bovine blood, simulating human tissues to evaluate our DRS system with our LUT to extract the phantom\u27s oxygen saturation (SO2). The results show that portable spectrometer estimated SO2 values agree with the traditional DRS system. These results demonstrate that our handheld equipment can accurately estimate tissue oxygenation and hemoglobin levels, thus providing a mean of rapid quantitative tools assessing microvascular hemodynamics

Portable Diffuse Reflectance Spectroscopy for Non-invasive and Quantitative Assessment of the Parathyroid Glands Viability During Surgery

Portable Diffuse Reflectance Spectroscopy for Non-invasive and Quantitative Assessment of the Parathyroid Glands Viability During Surgery Mark Romine, Linh Luong, Alex Moazzen, Katie Cho and Paul Lee The parathyroid glands (PTGs) are responsible for the regulation of calcium levels in the blood by secreting a parathyroid hormone. This parathyroid hormone then regulates the body’s absorption, storage, and secretion of calcium, which can directly affect the way muscles and nerves operate. PTGs are often at risk of damage, or accidental removal during thyroid surgeries, because it is challenging to identify PTGs and to determine their viability. Current methods of visual inspections are often subjective and blood panels have long processing times. Diffuse Reflectance Spectroscopy (DRS) may provide a solution for the noninvasive, rapid, and quantitative assessment of the viability of PTGs. DRS is a non-invasive technique that uses the reflectance properties of tissue to quantify the hemoglobin (Hb) and concentrations and tissue oxygenation. DRS consists of a white LED (wavelength 400nm – 700nm) for a light source, a compact spectrometer that records tissue reflectance and a fiber optic probe. In this project, we have built a portable DRS system and verified the performance of the prototyped DRS system. We have characterized a signal-to-noise ratio (SNR) on tissue simulating optical phantom and the computed SNR is around 40 dB as expected. Also, we have demonstrated that DRS can measure the change in oxygenation values in our blood phantom testing. These bench-top tests show that our protype is ready for human study during a thyroid surgery

Forward Genetic Dissection of Biofilm Development by Fusobacterium nucleatum: Novel Functions of Cell Division Proteins FtsX and EnvC.

Fusobacterium nucleatum is a key member of the human oral biofilm. It is also implicated in preterm birth and colorectal cancer. To facilitate basic studies of fusobacterial virulence, we describe here a versatile transposon mutagenesis procedure and a pilot screen for mutants defective in biofilm formation. Out of 10 independent biofilm-defective mutants isolated, the affected genes included the homologs of the Escherichia coli cell division proteins FtsX and EnvC, the electron transport protein RnfA, and four proteins with unknown functions. Next, a facile new gene deletion method demonstrated that nonpolar, in-frame deletion of ftsX or envC produces viable bacteria that are highly filamentous due to defective cell division. Transmission electron and cryo-electron microscopy revealed that the ΔftsX and ΔenvC mutant cells remain joined with apparent constriction, and scanning electron microscopy (EM) uncovered a smooth cell surface without the microfolds present in wild-type cells. FtsX and EnvC proteins interact with each other as well as a common set of interacting partners, many with unknown function. Last, biofilm development is altered when cell division is blocked by MinC overproduction; however, unlike the phenotypes of ΔftsX and ΔenvC mutants, a weakly adherent biofilm is formed, and the wild-type rugged cell surface is maintained. Therefore, FtsX and EnvC may perform novel functions in Fusobacterium cell biology. This is the first report of an unbiased approach to uncover genetic determinants of fusobacterial biofilm development. It points to an intriguing link among cytokinesis, cell surface dynamics, and biofilm formation, whose molecular underpinnings remain to be elucidated.IMPORTANCE Little is known about the virulence mechanisms and associated factors in F. nucleatum, due mainly to the lack of convenient genetic tools for this organism. We employed two efficient genetic strategies to identify F. nucleatum biofilm-defective mutants, revealing FtsX and EnvC among seven biofilm-associated factors. Electron microscopy established cell division defects of the ΔftsX and ΔenvC mutants, accompanied with a smooth cell surface, unlike the microfold, rugged appearance of wild-type bacteria. Proteomic studies demonstrated that FtsX and EnvC interact with each other as well as a set of common and unique interacting proteins, many with unknown functions. Importantly, blocking cell division by MinC overproduction led to formation of a weakly adherent biofilm, without alteration of the wild-type cell surface. Thus, this work links cell division and surface dynamics to biofilm development and lays a foundation for future genetic and biochemical investigations of basic cellular processes in this clinically significant pathogen

Korean Red Ginseng inhibits apoptosis in neuroblastoma cells via estrogen receptor β-mediated phosphatidylinositol-3 kinase/Akt signaling

AbstractBackgroundGinseng has been shown to exert antistress effects both in vitro and in vivo. However, the effects of ginseng on stress in brain cells are not well understood. This study investigated how Korean Red Ginseng (KRG) controls hydrogen peroxide-induced apoptosis via regulation of phosphatidylinositol-3 kinase (PI3K)/Akt and estrogen receptor (ER)-β signaling.MethodsHuman neuroblastoma SK-N-SH cells were pretreated with KRG and subsequently exposed to H2O2. The ability of KRG to inhibit oxidative stress-induced apoptosis was assessed in MTT cytotoxicity assays. Apoptotic protein expression was examined by Western blot analysis. The roles of ER-β, PI3K, and p-Akt signaling in KRG regulation of apoptosis were studied using small interfering RNAs and/or target antagonists.ResultsPretreating SK-N-SH cells with KRG decreased expression of the proapoptotic proteins p-p53 and caspase-3, but increased expression of the antiapoptotic protein BCL2. KRG pretreatment was also associated with increased ER-β, PI3K, and p-Akt expression. Conversely, ER-β inhibition with small interfering RNA or inhibitor treatment increased p-p53 and caspase-3 levels, but decreased BCL2, PI3K, and p-Akt expression. Moreover, inhibition of PI3K/Akt signaling diminished p-p53 and caspase-3 levels, but increased BCL2 expression.ConclusionCollectively, the data indicate that KRG represses oxidative stress-induced apoptosis by enhancing PI3K/Akt signaling via upregulation of ER-β expression