Junior Recital: Emily Nunemaker, Clarinet

Kemp Recital Hall Sunday Afternoon November 19, 1995 3:00p.m

A Quality Improvement Initiative to Increase Statin Therapy Adherence Among Patients With Diabetes Aged 65 Years and Older

The purpose of this project was to improve statin therapy adherence among diabetic patients aged 65 and older treated at a small family practice clinic in western San Antonio. Additionally, the project aimed to decrease LDL cholesterol (LDL-C) levels in this patient population as recommended to 70 mg/dl or less. Diabetic patients are more likely to die from a cardiac event than patients without diabetes. Statin therapy is an important factor in lowering cholesterol, which reduces the patient’s risk for atherosclerosis. Educating patients aged 65 and older about the role of statin therapy in preventing cardiovascular events, stroke, and vascular compromise may increase medication adherence in this population, resulting in appropriate LDL-C levels for prevention of these serious comorbidities. One hundred thirty-five chart reviews took place, from which thirty-three patients were identified for the education intervention. The patients were screened for medication adherence using the MMAS-8 survey before and after the intervention period to measure adherence to statin therapy. Education about cholesterol and statin therapy was provided during the patient appointment, and a handout was provided for reinforcement of education. LDL-C levels were drawn by the clinic laboratory before and after the intervention period to measure improvement. Results showed significant medication adherence increase and LDL-C level decrease among project participants after the 10-week implementation, though the target LDL-C level of 70 mg/dl or less was not met

Senior Recital:Emily Nunemaker, Clarinet

Kemp Recital Hall Saturday Evening March 21 , 1998 8:00 p.m

Student Recital: Deanna Bush, Clarinet Christine Hoover, Clarinet Emily Nunemaker, Clarinet

Kemp Recital Hall Thursday Evening April 28, 1994 9:00p.m

Nurses\u27 Alumnae Association Bulletin - Volume 2 Number 3

The Jefferson Nurse Letter from the President Delegates to Biennial Convention Attention Blood Transfusion - Plasma Unit Life in the Army Nurse Corps Secretary\u27s Report Elected to New Office 1892-1942 Progress or Alumnae Association 1892-1942 Report of the School of Nursing Staff News Please Change My Address Air Cooled Red Cross Report Fingerprinting Graduates in the U.S. Army and Navy Degrees Received Promotions Jubilee Report Engagements Marriages Births New Positions - 1941-1942 New Positions on the Nursing Staff of the Hospita

Investigating the Expression and Function of the Glucose Transporter GLUT6 in Obesity

Obesity-related insulin resistance is a highly prevalent and growing health concern, which places stress on the pancreatic islets of Langerhans by increasing insulin secretion to lower blood glucose levels. The glucose transporters GLUT1 and GLUT3 play a key role in glucose-stimulated insulin secretion in human islets, while GLUT2 is the key isoform in rodent islets. However, it is unclear whether other glucose transporters also contribute to insulin secretion by pancreatic islets. Herein, we show that SLC2A6 (GLUT6) is markedly upregulated in pancreatic islets from genetically obese leptin-mutant (ob/ob) and leptin receptor-mutant (db/db) mice, compared to lean controls. Furthermore, we observe that islet SLC2A6 expression positively correlates with body mass index in human patients with type 2 diabetes. To investigate whether GLUT6 plays a functional role in islets, we crossed GLUT6 knockout mice with C57BL/6 ob/ob mice. Pancreatic islets isolated from ob/ob mice lacking GLUT6 secreted more insulin in response to high-dose glucose, compared to ob/ob mice that were wild type for GLUT6. The loss of GLUT6 in ob/ob mice had no adverse impact on body mass, body composition, or glucose tolerance at a whole-body level. This study demonstrates that GLUT6 plays a role in pancreatic islet insulin secretion in vitro but is not a dominant glucose transporter that alters whole-body metabolic physiology in ob/ob mice

Two Types of Burst Firing in Gonadotrophin‐Releasing Hormone Neurones

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/92106/1/j.1365-2826.2012.02313.x.pd

Metformin Inhibits Mouse Islet Insulin Secretion and Alters Intracellular Calcium in a Concentration-Dependent and Duration-Dependent Manner near the Circulating Range

Metformin is considered the first-line treatment for type 2 diabetes. While metformin primarily increases insulin sensitivity, evidence also suggests that metformin affects the activity of insulin-secreting pancreatic islets. This study was designed to systematically examine the direct effects of metformin by measuring insulin secretion and the kinetics of the calcium response to glucose stimulation in isolated mouse islets using varying concentrations (20 μM, 200 μM, and 1 mM) and durations (~1, 2, and 3 days) of metformin exposure. We observed both concentration- and duration-dependent inhibitory effects of metformin. Concentrations as little as 20 μM (nearing circulating therapeutic levels) were sufficient to reduce insulin secretion following 3-day treatment. Concentrations of 200 μM and 1 mM produced more pronounced effects more rapidly. With 1 mM metformin, islets showed severe impairments in calcium handling, inhibition of insulin secretion, and increased cell death. No stimulatory effects of metformin were observed for any experimental endpoint. We conclude that the direct effects of metformin on islets are inhibitory at near-physiological concentrations. Beneficial effects of metformin observed on islets under various stressors may occur by “resting” fatigued cellular processes. However, metformin may have unintended consequences on normally functioning islets within the circulating range that require further evaluation

Glucose Metabolism, Islet Architecture, and Genetic Homogeneity in Imprinting of [Ca2+]i and Insulin Rhythms in Mouse Islets

We reported previously that islets isolated from individual, outbred Swiss-Webster mice displayed oscillations in intracellular calcium ([Ca2+]i) that varied little between islets of a single mouse but considerably between mice, a phenomenon we termed “islet imprinting.” We have now confirmed and extended these findings in several respects. First, imprinting occurs in both inbred (C57BL/6J) as well as outbred mouse strains (Swiss-Webster; CD1). Second, imprinting was observed in NAD(P)H oscillations, indicating a metabolic component. Further, short-term exposure to a glucose-free solution, which transiently silenced [Ca2+]i oscillations, reset the oscillatory patterns to a higher frequency. This suggests a key role for glucose metabolism in maintaining imprinting, as transiently suppressing the oscillations with diazoxide, a KATP-channel opener that blocks [Ca2+]i influx downstream of glucose metabolism, did not change the imprinted patterns. Third, imprinting was not as readily observed at the level of single beta cells, as the [Ca2+]i oscillations of single cells isolated from imprinted islets exhibited highly variable, and typically slower [Ca2+]i oscillations. Lastly, to test whether the imprinted [Ca2+]i patterns were of functional significance, a novel microchip platform was used to monitor insulin release from multiple islets in real time. Insulin release patterns correlated closely with [Ca2+]i oscillations and showed significant mouse-to-mouse differences, indicating imprinting. These results indicate that islet imprinting is a general feature of islets and is likely to be of physiological significance. While islet imprinting did not depend on the genetic background of the mice, glucose metabolism and intact islet architecture may be important for the imprinting phenomenon

STEAP4 expression in human islets is associated with differences in body mass index, sex, HbA1c, and inflammation

Objective STEAP4 (six-transmembrane epithelial antigen of the prostate 4) is a metalloreductase that has been shown previously to protect cells from inflammatory damage. Genetic variants in STEAP4 have been associated with numerous metabolic disorders related to obesity, including putative defects in the acute insulin response to glucose in type 2 diabetes. Purpose We examined whether obesity and/or type 2 diabetes altered STEAP4 expression in human pancreatic islets. Methods Human islets were isolated from deceased donors at two medical centers and processed for quantitative polymerase chain reaction. Organ donors were selected by status as non-diabetic or having type 2 diabetes. Site 1 (Edmonton): N = 13 type 2 diabetes donors (7M, 6F), N = 20 non-diabetic donors (7M, 13F). Site 2 (Virginia): N = 6 type 2 diabetes donors (6F), N = 6 non-diabetic donors (3M, 3F). Results STEAP4 showed reduced islet expression with increasing body mass index among all donors (P < 0.10) and non-diabetic donors (P < 0.05) from Site 1; STEAP4 showed reduced islet expression among type 2 diabetes donors with increasing hemoglobin A1c. Islet STEAP4 expression was also marginally higher in female donors (P < 0.10). Among type 2 diabetes donors from Site 2, islet insulin expression was reduced, STEAP4 expression was increased, and white blood cell counts were increased compared to non-diabetic donors. Islets from non-diabetic donors that were exposed overnight to 5 ng/ml IL-1β displayed increased STEAP4 expression, consistent with STEAP4 upregulation by inflammatory signaling. Conclusions These findings suggest that increased STEAP4 mRNA expression is associated with inflammatory stimuli, whereas lower STEAP4 expression is associated with obesity in human islets. Given its putative protective role, downregulation of STEAP4 by chronic obesity suggests a mechanism for reduced islet protection against cellular damage