Fortinbras and Laertes and the Composition of Hamlet

Paper by Harold Jenkin

Shakespeare's "Twelfth Night"

Lecture delivered at the Rice Institute on March 26, 195

General-purpose sprays for home fruit plantings

Cover title

Endurance or sprint interval exercise, & metformin treatment differently modify insulin-induced vasodilation in skeletal muscle arterioles of obese insulin resistant rats

A key contributor to insulin-mediated glucose uptake is insulin-induced vasodilation of skeletal muscle arterioles, which is impared with obesity and Type 2 diabetes (T2D). Abnormalities in the vascular reactivity to insulin can limit perfusion, and delivery of glucose and insulin to muscle tissue. In human patients with T2D, exercise improves insulin sensitivity and glucose uptake T2D. Furthermore, we have previously shown that daily exercise prevents impairments in insulin-induced vasodilation in OLETF rats. However, the efficacy of exercise interventions which utilize different muscle recruitment patterns (i.e. aerobic vs. sprint training) to ameliorate or reverse impairments in microvascular insulin reactivity has not been elucidated. The current ADA standard of care for T2D is treatment with metformin in combination with a diet and exercise program. Therefore, we studied the effects of endurance exercise and interval sprint training with and without metformin on the vasoreactivity to insulin in skeletal muscle arterioles from red and white muscles

Cardiac myocyte-specific knock-out of calcium-independent phospholipase A2γ (iPLA2γ) decreases oxidized fatty acids during ischemia/reperfusion and reduces infarct size

Calcium-independent phospholipase A(2)γ (iPLA(2)γ) is a mitochondrial enzyme that produces lipid second messengers that facilitate opening of the mitochondrial permeability transition pore (mPTP) and contribute to the production of oxidized fatty acids in myocardium. To specifically identify the roles of iPLA(2)γ in cardiac myocytes, we generated cardiac myocyte-specific iPLA(2)γ knock-out (CMiPLA(2)γKO) mice by removing the exon encoding the active site serine (Ser-477). Hearts of CMiPLA(2)γKO mice exhibited normal hemodynamic function, glycerophospholipid molecular species composition, and normal rates of mitochondrial respiration and ATP production. In contrast, CMiPLA(2)γKO mice demonstrated attenuated Ca(2+)-induced mPTP opening that could be rapidly restored by the addition of palmitate and substantially reduced production of oxidized polyunsaturated fatty acids (PUFAs). Furthermore, myocardial ischemia/reperfusion (I/R) in CMiPLA(2)γKO mice (30 min of ischemia followed by 30 min of reperfusion in vivo) dramatically decreased oxidized fatty acid production in the ischemic border zones. Moreover, CMiPLA(2)γKO mice subjected to 30 min of ischemia followed by 24 h of reperfusion in vivo developed substantially less cardiac necrosis in the area-at-risk in comparison with their WT littermates. Furthermore, we found that membrane depolarization in murine heart mitochondria was sensitized to Ca(2+) by the presence of oxidized PUFAs. Because mitochondrial membrane depolarization and calcium are known to activate iPLA(2)γ, these results are consistent with salvage of myocardium after I/R by iPLA(2)γ loss of function through decreasing mPTP opening, diminishing production of proinflammatory oxidized fatty acids, and attenuating the deleterious effects of abrupt increases in calcium ion on membrane potential during reperfusion

Fluency Assistance Device (FAD): Masker Upgrades

Around seventy million people internationally have a stutter, a form of a fluency disorder. Some fluency assistance devices are available to the public, but most are highly expensive or unreliable. The Fluency Assistive Device (FAD) team seeks to assist a niche community of these individuals who currently rely on a device known originally as the Edinburgh Masker by partnering with Dave Germeyer. Utilizing his expertise in repairing the Edinburgh Masker, FAD is developing two new versions of the masker to increase its portability, functionality, and cost-effectiveness. The first is an update of the original called the Analog Masker (Version 1.1). A prototype of the Analog Masker v1.1 has been developed, tested and is currently being revised based on the results. Revisions include updating the layout of the board and finalizing the power supply circuitry. The second version, known as the Digital Masker (Version 1.0), will use a Bluetooth-enabled microcontroller to achieve masker functionality. Bluetooth audio output for the Digital Masker has been tested, and two algorithms have been created for the masking output. The supporting software for the Digital Masker is nearing completion. The schematic and the layout design have been started for future implementation of the hardware.https://mosaic.messiah.edu/engr2021/1005/thumbnail.jp