Etiology of eating disorders within a learned helplessness model of depression

This thesis is an attempt to parallel characteristics of anorexia (AN) and bulimia nervosa (BN: with those of depressive disorder in order to re-frame the etiology and progression of these eating disorders within a learned helplessness model of depression. In their 1993 publication, Seligman and his colleagues (Peterson, Maier, & Seligman) address the significance of the learned helpless theory in a contemporary society: -- Learned helplessness is an important theory for the present because those of us in the Western world seem to be living in an era in which personal control is an overarching issue. We are also wary of the future. Because this incredible emphasis on personal control has its costs. We argue that the epidemic of depression among young adults represents a disorder of personal control. Generally speaking, the incredible selfishness of the American people can be phrased in terms of personal control (p. 307). -- It is proposed that the anorexic and the bulimic patients' symptomatology is rooted in a loss of a sense of control and of mastery, which can be traced to antecedent events. Consequently, these events or situations result in the eating-disordered patients' feeling helpless, powerless, and not in control of circumstances affecting their lives. These feelings ultimately lead to a persistent negative affective state frequently reported in eating-disordered patients. It is suggested that the depressive state is attributable to learned helplessness depression as initially defined by Seligman (1975). The eating-disordered patient thwarts depressive feelings by focussing on her body, more specifically her weight. The patient seeks control over the only perceivably controllable aspect of her life, her weight. The thesis is presented in two parts: Part 1 is a literature review. It provides background information which examines existing research in order to elicit core themes and commonalities that parallel learned helplessness depression with AN and BN. Included is the proposed learned helplessness model of AN and BN. Part 2 is a proposal for empirical research to explore the relationship among three constructs: depression, hopelessness, and locus of control, in a clinically diagnosed eating-disordered population compared to a non-clinical, gender and age-matched student population

Cyclic Nucleotide-Gated Channels of Rat Olfactory Receptor-Cells - Divalent-Cations Control the Sensitivity to Camp

cAMP-gated channels were studied in inside-out membrane patches excised from the apical cellular pore of isolated olfactory receptor cells of the rat. in the absence of divalent cations the dose-response curve of activation of patch current by cAMP had a K-M Of 4.0 mu M at -50 mV and of 2.5 mu M at +50 mV. However, addition of 0.2 or 0.5 mM Ca2+ shifted the K-M of cAMP reversibly to the higher cAMP concentrations of 33 or 90 mu M, respectively, at -50 mV. Among divalent cations, the relative potency for inducing cAMP affinity shifts was: Ca2+ > Sr2+ > Mn2+ > Ba2+ > Mg2+, of which Mg2+ (up to 3 mM) did not shift the K-M at all. This potency sequence corresponds closely to that required for the activation of calmodulin. However, the Ca2+-sensitivity is lower than expected for a calmodulin-mediated action. Brief(60 s) transient exposure to 3 mM Mg2+, in the absence of other divalent cations, had a protective effect in that following washout of Mg2+, subsequent exposure to 0.2 mM Ca2+ no longer caused affinity shifts. This protection effect did not occur in intact cells and was probably a consequence of patch excision, possibly representing ablation of a regulatory protein from the channel cyclic nucleotide binding site. Thus, the binding of divalent cations, probably via a regulatory protein, controls the sensitivity of the cAMP-gated channels to cAMP. The influx of Ca2+ through these channels during the odorant response may rise to a sufficiently high concentration at the intracellular membrane surface to contribute to the desensitization of the odorant-induced response. The results also indicate that divalent cation effects on cyclic nucleotide-gated channels may depend on the sequence of pre-exposure to other divalent cations

Properties of Cyclic-Nucleotide Gated Channels Mediating Olfactory Transduction - Activation, Selectivity, and Blockage

Cyclic nucleotide-gated channels (cng channels) in the sensory membrane of olfactory receptor cells, activated after the odorant-induced increase of cytosolic cAMP concentration, conduct the receptor current that elicits electrical excitation of the receptor neurons. We investigated properties of cng channels from frog and rat using inside-out and outside-out membrane patches excised from isolated olfactory receptor cells. Channels were activated by cAMP and cGMP with activation constants of 2.5-4.0-mu-M for cAMP and 1.0-1.8 for cGMP. Hill coefficients of dose-response curves were 1.4-1.8, indicating cooperativity of ligand binding. Selectivity for monovalent alkali cations and the Na/Li mole-fraction behavior identified the channel as a nonselective cation channel, having a cation-binding site of high field strength in the pore. Cytosolic pH effects suggest the presence of an additional titratable group which, when protonated, inhibits the cAMP-induced current with an apparent pK of 5.0-5.2. The pH effects were not voltage dependent. Several blockers of Ca2+ channels also blocked olfactory cng channels. Amiloride, D 600, and diltiazem inhibited the cAMP-induced current from the cytosolic side. Inhibition constants were voltage dependent with values of, respectively, 0.1, 0.3, and 1 mM at - 60 mV, and 0.03, 0.02, and 0.2 mM at + 60 mV. Our results suggest functional similarity between frog and rat cng channels, as well as marked differences to cng channels from photoreceptors and other tissues

Wall turbulence control

A variety of wall turbulence control devices which were experimentally investigated are discussed; these include devices for burst control, alteration of outer flow structures, large eddy substitution, increased heat transfer efficiency, and reduction of wall pressure fluctuations. Control of pre-burst flow was demonstrated with a single, traveling surface depression which is phase-locked to elements of the burst production process. Another approach to wall turbulence control is to interfere with the outer layer coherent structures. A device in the outer part of a boundary layer was shown to suppress turbulence and reduce drag by opposing both the mean and unsteady vorticity in the boundary layer. Large eddy substitution is a method in which streamline curvature is introduced into the boundary layer in the form of streamwise vortices. Riblets, which were already shown to reduce turbulent drag, were also shown to exhibit superior heat transfer characteristics. Heat transfer efficiency as measured by the Reynolds Analogy Factor was shown to be as much as 36 percent greater than a smooth flat plate in a turbulent boundary layer. Large Eddy Break-Up (LEBU) which are also known to reduce turbulent drag were shown to reduce turbulent wall pressure fluctuation

Potts-Percolation-Gauss Model of a Solid

We study a statistical mechanics model of a solid. Neighboring atoms are connected by Hookian springs. If the energy is larger than a threshold the "spring" is more likely to fail, while if the energy is lower than the threshold the spring is more likely to be alive. The phase diagram and thermodynamic quantities, such as free energy, numbers of bonds and clusters, and their fluctuations, are determined using renormalization-group and Monte-Carlo techniques.Comment: 10 pages, 12 figure