Breaking the Curve

Imagine you are up to bat in a major league baseball game. Would you rather face a pitch with smaller curvature or smaller break? Would you know the difference? In this paper we will derive a model for the path of a pitch based on actual data from MLB.com\u27s GameDay™ feature. Then, employing our model, we shall analyze the curvature and break of the pitch

Breaking the Curve

Imagine you are up to bat in a major league baseball game. Would you rather face a pitch with smaller curvature or smaller break? Would you know the difference? In this paper we will derive a model for the path of a pitch based on actual data from MLB.com\u27s GameDay™ feature. Then, employing our model, we shall analyze the curvature and break of the pitch

Open Educational Resources and their Implementation at Miami University

A white paper submitted on 9/8/2015 by the members of the 2014 –2015 Faculty Learning Community Exploring Open Educational Resources at Miami University. Covers OER definition, best practices, benefits and evidence, OER as a strategy to meet 2020 goals, implementing an OER culture at Miami University, and a preliminary plan.Center for Teaching Excellence (CTE) at Miami University Miami University Librarie

Role of Receptor-Interacting Protein 140 in human fat cells

<p>Abstract</p> <p>Background</p> <p>Mice lacking <it>Receptor-interacting protein 140 (RIP140) </it>have reduced body fat which at least partly is mediated through increased lipid and glucose metabolism in adipose tissue. In humans, <it>RIP140 </it>is lower expressed in visceral white adipose tissue (WAT) of obese versus lean subjects. We investigated the role of <it>RIP140 </it>in human subcutaneous WAT, which is the major fat depot of the body.</p> <p>Methods</p> <p>Messenger RNA levels of <it>RIP140 </it>were measured in samples of subcutaneous WAT from women with a wide variation in BMI and in different human WAT preparations. <it>RIP140 </it>mRNA was knocked down with siRNA in <it>in vitro </it>differentiated adipocytes and the impact on glucose transport and mRNA levels of target genes determined.</p> <p>Results</p> <p><it>RIP140 </it>mRNA levels in subcutaneous WAT were decreased among obese compared to lean women and increased by weight-loss, but did not associate with mitochondrial DNA copy number. <it>RIP140 </it>expression increased during adipocyte differentiation <it>in vitro </it>and was higher in isolated adipocytes compared to corresponding pieces of WAT. Knock down of <it>RIP140 </it>increased basal glucose transport and mRNA levels of <it>glucose transporter 4 </it>and <it>uncoupling protein-1</it>.</p> <p>Conclusions</p> <p>Human <it>RIP140 </it>inhibits glucose uptake and the expression of genes promoting energy expenditure in the same fashion as the murine orthologue. Increased levels of human <it>RIP140 </it>in subcutaneous WAT of lean subjects may contribute to economize on energy stores. By contrast, the function and expression pattern does not support that <it>RIP140 </it>regulate human obesity.</p

A possible inflammatory role of twist1 in human white adipocytes.

International audienceOBJECTIVE: Twist1 is a transcription factor that is highly expressed in murine brown and white adipose tissue (WAT) and negatively regulates fatty acid oxidation in mice. The role of twist1 in WAT is not known and was therefore examined. RESEARCH DESIGN AND METHODS: The expression of twist1 was determined by quantitative real-time PCR in different tissues and in different cell types within adipose tissue. The effect of twist1 small interfering RNA on fatty acid oxidation, lipolysis, adipokine secretion, and mRNA expression was determined in human adipocytes. The interaction between twist1 and specific promoters in human adipocytes was investigated by chromatin immunoprecipitation (ChIP) and reporter assays. RESULTS: Twist1 was highly expressed in human WAT compared with a set of other tissues and found predominantly in adipocytes. Twist1 levels increased during in vitro differentiation of human preadipocytes. Gene silencing of twist1 in human white adipocytes had no effect on lipolysis or glucose transport. Unexpectedly, and in contrast with results in mice, twist1 RNA interference reduced fatty acid oxidation. Furthermore, the expression and secretion of the inflammatory factors tumor necrosis factor-alpha, interleukin-6, and monocyte chemoattractant protein-1 were downregulated by twist1 silencing. ChIP and reporter assays confirmed twist1 interaction with the promoters of these genes. CONCLUSIONS: Twist1 may play a role in inflammation of human WAT because it can regulate the expression and secretion of inflammatory adipokines via direct transcriptional effects in white adipocytes. Furthermore, twist1 may, in contrast to findings in mice, be a positive regulator of fatty acid oxidation in human white adipocytes

ERβ overexpression did not influence the expression of PUFA elongases and desaturases in MCF7 cells.

<p>A) MCF7 cells were transfected with different concentrations (50ng or 500ng) of <i>ERβ</i> or empty plasmid (V) as indicated for 24 hours followed by incubation with 10 nM E2 or vehicle (c) for 6 hours. (A) <i>ERα</i>, (B) <i>ERβ</i>, (C) <i>Elovl2</i>, (D) <i>Elovl5</i>, (E) <i>Fads1</i> and (F) <i>Fads2</i> mRNA expression were determined by quantitative RT-PCR normalized to the reference gene 36B4. Results shown are means ± SE of two individual experiments in triplicate. Statistical significances are indicated as *P<0.05, **P<0.01 and ***P<0.001, n.d = not detectable.</p

Binding of ERα to ChIP analysis of the <i>Elovl2</i> enhancer in MCF7 cells.

<p>(A) Schematic representation of two putative estrogen response elements, ERE1 and ERE2, within the <i>Elovl2</i> enhancer with the primer pairs used for ChIP assays illustrated as black arrows denoted a, b and c with the “a” primer pair positioned 5’ adjacent to the ERE1, the “b” primer pair covering the ERE1, the “c” primer pair 3’ of the ERE1 and the “d” primer pair covering the ERE2 site. (B) Fold difference for ERα and IgG (control) binding for E2 and vehicle treated MCF7 cells using primer pair a, primer pair b, primer pair c and primer pair d. Statistical significances are indicated as *P<0.05, **P<0.01 and ***P<0.001.</p

E2 time-response of PUFA synthesizing enzyme expression in MCF7 cells.

<p>MCF7 cells were treated with 10 nM E2 or vehicle (c) for 0, 6, 12 or 24 hours and <i>Elovl2</i>, <i>Elovl5</i>, <i>Fads1</i> and <i>Fads2</i> mRNA levels (A, B, C and D) were determined by quantitative RT-PCR and normalized to the reference gene 36B4. Results shown are means ± SE of two individual experiments in triplicate. Statistical significances are indicated as *P<0.05 and **P<0.01.</p