My Life is a Manifesto: From Rich, To Poor, To Teacher

This inquiry travels through stages of my education and life in order to explore the following three questions: How do a teacher’s values and personal experiences translate into teaching lives and teaching acts? How do teachers and students live counterstories inside and outside of the classroom? How do class, gender and place impact teaching and learning? Building on the works of critical theorists, (Apple, 2004; Ayers, 2004; Delpit, 2006; Freire, 2005; hooks, 1994; Kincheloe, 2004; Kincheloe & Pinar, 1991; Kozol, 1992; Watkins, 2001,2004), autobiographical studies (He, 2003, 2010; Miller, 2005; Pinar, 1994; Schubert & Ayers; 1990) and memoirs (Angelou, 1993; Ayers, 2001; Barrington, 2002; Karr, 2015; Lamott, 1994; Lawson, 2015; Sedaris, 2000; Walls, 2005) and others, I use memoir as methodology to recount passages that occurred during three distinct phases of my life: my life as a rich girl, my life as poor trash, and my life as a teacher. I illuminate how my personal experience of moving between socioeconomic classes, geographical places, and roles of womanhood shaped who I was and how I become who I am as a teacher and how class, place and gender impact the process of becoming educated. This memoir engages in a pedagogy of liberation (Shor & Friere, 1986) that celebrates the voice of individuals and interrogates how personal experience affects the process of becoming educated and the development of any individual as a student, a teacher, and a critically engaged member of society (Ayers, 2004b; Freire; 2005; Kincheloe, 1999). My life manifests how class, place, gender and race helps us understand who we are and how we become who we are but cannot define who we are in a constantly changing and contested world. My life manifests how education could be catalyst for greater understanding of ourselves, our world, and our choices in the world. My life manifests that teaching is personal and political. My life curriculum is a manifesto constantly in the making, and I hope that it will speak to my daughter, and son, and other people’s children as they compose their lives in a contested and unjust world. INDEX WORDS: Memoir, Autobiographical Research, Place, Class, Critical Theor

Pulmonary vasoconstrictor action of KCNQ potassium channel blockers

KCNQ channels have been widely studied in the nervous system, heart and inner ear, where they have important physiological functions. Recent reports indicate that KCNQ channels may also be expressed in portal vein where they are suggested to influence spontaneous contractile activity. The biophysical properties of K+ currents mediated by KCNQ channels resemble a current underlying the resting K+ conductance and resting potential of pulmonary artery smooth muscle cells. We therefore investigated a possible role of KCNQ channels in regulating the function of pulmonary arteries by determining the ability of the selective KCNQ channel blockers, linopirdine and XE991, to promote pulmonary vasoconstriction. Linopirdine and XE991 both contracted rat and mouse pulmonary arteries but had little effect on mesenteric arteries. In each case the maximum contraction was almost as large as the response to 50 mM K+. Linopirdine had an EC50 of around 1 μM and XE991 was almost 10-fold more potent. Neither removal of the endothelium nor exposure to phentolamine or α,β-methylene ATP, to block α1-adrenoceptors or P2X receptors, respectively, affected the contraction. Contraction was abolished in Ca2+-free solution and in the presence of 1 μM nifedipine or 10 μM levcromakalim

PHARMACOKINETIC AND PHARMACODYNAMIC STUDIES WITH CARDIOVASCULAR DRUGS (PROPANOLOL, ISOPROTERENOL, DIGITOXIGENIN, DIGOXIN).

Part I. Seven healthy male subjects each received on a weekly basis placebo or 10, 20, 40, 80, or 160 mg oral propranolol (P) doses q.i.d. The effect of P on resting heart rate (HR) and the HR response to the Valsalva's maneuver, tilt, isoproterenol (ISO), and exercise were measured. The results indicate that the resting HR and the Tachycardiac response to Valsalva and tilt cannot be used to estimate beta blockade (BB). Although P serum levels correlated well (r² = 0.80) with the ISO dose ratio minus one, ISO challenges appear clinically inappropriate. Reduction in exercise tachycardia correlated best with P serum levels (r² = 0.89). In patients on P therapy, in which exercise would be contraindicated, there appears to be no reliable and safe method of clinically documenting BB. Part II. The parmacokinetics of intravenous P were studied in calves before and after biochemical induction of thyrotoxicosis. The beta adrenergic response to P was measured in both euthyroid and thyrotoxic (T) animals at steady-state serum levels of P by administration of ISO. No pharmacokinetic differences were detected between animal groups; however, T calves displayed a markedly different pharmacologic response to P. On the average, 2-9 times higher serum levels of P were required to facilitate BB in the T calves. These results suggest that in the calf model, thyrotoxicosis induces a decreased sensitivity to P independent of laterations in P's disposition. Part III. The aim of this study was to find a digitalis glycoside (DG) with a t(½) shorter than that of digitoxin (DT), but similar to that of digoxin, and whose disposition characteristics are not influenced by alterations in renal function, as is the case with digoxin. Consequently, the pharmacokinetics of two metabolites of DT, digitoxigenin-bisdigitoxoside (BIS) and digitoxigenin-monodigitoxoside (MONO), were compared to those of DT in a dog model. In normal dogs, appreciable differences were found between the systemic clearance (CL) of DT and the CL of either of the two other DG's. These differences in CL were primarily responsible for the 2.0 and 3.5 fold decrease seen in the t(½)'s of BIS and MONO, respectively. Renal disfunction did not influence the pharmacokinetic parameters of any of the DG's studied. These findings in the dog model suggest that BIS or MONO may provide a pharmacokinetic advantage over DT