CONSTITUTIONAL LAW—DAMNED IF YOU DO, DAMNED IF YOU DON’T: A PUBLIC EMPLOYEE’S TRILEMMA REGARDING TRUTHFUL TESTIMONY

In the interest of protecting the judicial truth-seeking process, this Note argues that truthful testimony in general, and particularly compelled truthful testimony, should receive First Amendment safeguards, and its protection should not be predicated on “matters of public concern” or “official duties” tests. Instead, truthful testimony should be immunized from job retaliation similar to the way testimony has been immunized from damage claims. Part I of this Note reviews the Supreme Court’s stance regarding public employees’ speech. Part II discusses the protection that witness testimony enjoys from civil damage claims and will argue that a public employee’s truthful testimony should receive the same immunization. Next, Part III identifies the lower courts’ divergent decisions on the issue of truthful testimony pre-Garcetti and discusses the retaliation that public employees face at work as a result of their truthful testimonies. Part IV discusses the lower courts’ split decisions post-Garcetti. Part V demonstrates the ramifications that legal uncertainty has on this issue—not only on public employees, but on the integrity of our judicial system and the functioning of our government as a whole. Lastly, Part V concludes that truthful testimony should be protected and afforded immunity from job retaliation

Mentes masculinas en cuerpos femeninos. Tres mujeres y su poder a través de monedas y sellos

This article investigates coins and seals as instruments that reflect the desire for self-representation and remembrance of ruling women. An analysis of these small but important objects connected to Queen Urraca of León-Castilla (r. 1109-1126), Empress Matilda of England (r. 1135-1154), and Duchess Bertha of Lorraine (r. 1176-1194/95), will show that they each constructed the visual image of their rule by employing a masculine iconography to craft their identities. Originating directly from the power these lordly women, their coins and seals convey how they represented themselves and consequently how they wished to be recognized and recollected. As such, these objects were part of a wider medieval memorial culture to which the creation of artefacts and architecture was crucial. En este artículo las monedas y los sellos se analizan como herramientas que reflejan el deseo de las mujeres gobernantes de autorepresentarse y de ser así recordadas. Un recorrido por estos objetos pequeños pero muy relevantes conectados con la reina Urraca de León-Castilla (r. 1109-1126), la emperatriz Matilde de Inglaterra (r. 1135-1154) y la duquesa Berta de Lorena (r. 1176-1194/95) mostrará que cada una construyó una imagen visual de su reinado, empleando una iconografía masculina para crear sus identidades. Procedentes directamente del poder de estas mujeres señoriales, su moneda y los sellos expresan cómo ellas se representaban y, en consecuencia, cómo deseaban ser reconocidos y recordados. Por definición, estos objetos formaban parte de una cultura medieval de memoria para la cual era crucial la creación de artefactos y arquitectura

Joan de Valence: The Life and Influence of a Thirteenth-Century Noblewoman

Peer reviewe

Mechanism of nitric oxide induced sympatholysis in rat soleus feed arteries

During exercise, the neurotransmitter norepinephrine (NE) binds to arterial adrenergic receptors to cause vasoconstriction, yet arteries and arterioles constrict less to sympathetic stimulation in contracting compared to resting skeletal muscle (sympatholysis). Previous evidence indicates that nitric oxide (NO) can be sympatholytic, but the mechanism is unknown. We hypothesized that NO causes sympatholysis in rat soleus muscle feed arteries, that NO is released from vascular endothelial cells by increased shear stress, and that NO acts through a guanylyl cyclase intracellular signaling pathway. Soleus feed arteries (n = 12 per group) were isolated from male Sprague-Dawley rats and cannulated on two glass micropipettes for in vitro videomicroscopy. We measured the constriction response to the adrenergic agonist phenylephrine (PE; 10-9 M to 10-4 M, 0.5 log increments) in the presence of varying levels of the nitric oxide donor sodium nitroprusside (SNP; 0 nM, 0.1 nM and 100 nM), shear stress (0 dy/cm2, 25 dy/cm2, and 135 dy/cm2), and SNP + ODQ (0.1 nM), an inhibitor of guanylyl cyclase. SNP reduced constriction to PE in a dose-dependent manner (maximum constriction 77.3 % vs. 70.7 % and 56.7 %), indicating that NO interferes with sympathetic constriction. ODQ restored PE-induced constriction (PE alone 77.5%; with SNP 67.6%; with SNP + ODQ 83.5%), indicating that NO causes sympatholysis through a guanylyl cyclase signaling pathway. However, shear stress did not reduce constriction to PE (67.6 % vs. 68.1 %, and 67.6 %), indicating that increased shear stress during exercise is not the source of the NO causing sympatholysis. We conclude that nitric oxide acting through guanylyl cyclase causes sympatholysis, but the source of the nitric oxide during exercise is not shear stress-induced endothelial cell activation

The Effect of Shear Stress, Potassium, and Adenosine on α-1 Adrenergic Vasoconstriction of Rat Soleus Feed Arteries

During exercise, blood flow increases to the working skeletal muscle primarily because of dilation of the arteries and arterioles feeding the muscle. Sympathetic nerve activity also increases during exercise, augmenting the release of the neurotransmitter norepinephrine (NE) at the arterial wall and into the blood. NE acts to constrict blood vessels; however, arteries and arterioles within contracting skeletal muscle dilate despite the increased NE present. This has led to the concept of functional sympatholysis (4), the idea that a chemical released from contracting skeletal muscle interferes with NE signaling. NE acts by binding to adrenergic (alpha and beta) receptors, and it is alpha receptors in the arterial wall that cause vasoconstriction (8). While both α-1 and α-2 receptor subtypes have been found in some vascular beds of some species, there is significant evidence that in rat calf muscles, the response to norepinephrine is mediated solely by α-1 receptors (5, 9). Because α-1 receptors are the sole respondents to sympathetic signaling, we studied three proposed substances that may interfere with sympathetic signaling at the α-1 receptors, thereby mediating sympatholysis. There is evidence to suggest that heat and acidosis may partially mediate sympatholysis of α-1 receptors (1, 2). This study sought to determine whether increased levels of shear stress, potassium, or adenosine also contribute to sympatholysis. If shear stress, potassium, and adenosine are, in fact, sympatholytic agents, they will reduce the vasoconstriction mediated by the α-1 receptors in rat soleus muscle feed arteries. We hypothesized that all three variables would be sympatholytic agents

Flow-induced dilation of skeletal muscle feed arteries: relevance to exercise hyperemia

During exercise, an increase in blood flow to working skeletal muscle is accomplished by dilation of arteries and arterioles supplying the muscle. Arterioles, located within contracting muscle, are exposed to dilatory metabolites released by the muscle; however, the mechanism by which feed arteries, located external to the muscle, dilate is still unknown. One potential mechanism for feed artery dilation is flow-induced dilation, occurring when arteries dilate in response to increased vascular wall shear stress. Shear stress is the frictional force between blood and the arterial wall, which increases when blood flow velocity increases. Data from previous in vitro experiments (8) indicate that flow-induced dilation in rat soleus feed arteries occurs at blood flow levels that are far less than normal resting blood flow in conscious rats. This data led to the conclusion that flow-induced dilation was not a plausible mechanism to explain the increase in blood flow during exercise. Furthermore, the soleus muscle is primarily composed of slow-oxidative fibers and used in maintaining posture; thus, it receives a substantial amount of blood flow at rest. We sought to test whether flow-induced dilation could contribute to exercise hyperemia in rat extensor digitorum longus muscle, primarily composed of fast-glycolytic fibers, and rat gastrocnemius, a muscle of mixed fiber type (4). The differences in fiber type of each muscle may be a factor in how the feed arteries dilate during exercise. The purpose of this study was to determine if flow-induced dilation potentially contributes to exercise hyperemia in rat extensor digitorum longus and gastrocnemius muscle feed arteries, EDLFA and GFA, respectively. In this study, blood flow was induced through the arteries and corresponding flow measurements (µl/min) were collected. The flow values were used to calculate intraluminal wall shear stress in the arteries and then compared to calculated in vivo shear stress values from previously published studies (1,2,3,7,10,11,12,13,14,15). We hypothesized that flow-induced dilation in GFA and EDLFA occurs at shear stress values lower than the shear stress normally present in non-exercising rats. This would preclude flow-induced dilation from causing the dilation of feed arteries to gastrocnemius and EDL muscles in exercise

Effect of Shear Stress Direction on Endothelial Function and eNOS Phosphorylation in Soleus Feed Arteries

Blood flow feeding tissues and organs is closely regulated in order to meet metabolic and functional needs. Control of blood flow is accomplished by regulating the diameter of the arteries and arterioles feeding different organs. Several neural, hormonal, chemical and mechanical mechanisms contribute to the constriction and dilation of arteries. Shear stress, the frictional force created by streaming blood on the endothelial layer of arteries, is one of these mechanical mechanisms (1). Shear stress causes both acute and long term effects on endothelial cells (1,2,5). Blood in arteries typically flows away from the heart towards organs (causing antegrade shear stress) during cardiac contraction and briefly flows back toward the heart (causing retrograde shear stress) during cardiac filling. Retrograde flow occurs more often in some disease situations, and studies have shown that retrograde shear stress decreases endothelial cell function (3,4). The specific mechanisms for endothelial dysfunction are unknown, but altered mechanisms could include impaired cell signaling pathways. The most important endothelial cell dilatory signaling pathway is the production of nitric oxide (NO). Retrograde shear stress causes endothelial cells to secrete NO, and increased rates of shear stress cause increased expression and phosphorylation of nitric oxide synthase (eNOS). Regulatory phosphorylation of eNOS can potentially occur on at least four sites: Ser 1177, Ser 116, Ser 635 and Thr 497 (3). The most well characterized of these is Ser 1177, which is phosphorylated by a by PI3K/AKT shear dependent pathway. Regulating phosphorylation of eNOS is critical to endothelial health and maintaining cardiovascular equilibrium. Using rat soleus muscle feed arteries, we seek to determine the effects of changes in shear stress direction on both endothelial cell function and phosphorylation of eNOS at the Ser 1177 site