A case study of narcissistic pathology : an object relations perspective

The case-study method of psychological research was applied to the brief psychodynamic therapy of a narcissistically disordered female patient. The aim of this research was to explore, clarify and explain certain diagnostic and psychodynamic anomalies to emerge in the course of treatment, using a conceptual framework derived from select psychoanalytic object relations theorists in the area of narcissistic pathology. The author, discovering that there was no diagnostic or explanatory object relations model adequate to the therapeutic data, formulated his own diagnostic category narcissistic neurosis and an eclectic object relations model in order to explain the anomolous research findings. Narcissistic neurosis was defined as a form of psychopathology in which a primarily neurotic character structure presents with a distinctly narcissistic profile. The narcissistic false self-structure serves the functional purpose of protecting the psyche from a repressed negative self-representation derived from a destructive bipolar self-object introject. The primary etiological factor to emerge was that of a narcissistic mother conditional affection and self-object target child necessitated adaptive whose insensitivity, relationship with the premature self-sufficiency and the defensive emergence of a narcissistic surface self-representation. It was proposed that narcissistic neurosis and narcissistic personality disorder are two discrete forms of pathology differing in terms of severity, psychodynamics, defensive structure, mode of object relating, therapeutic accessibility and prognosis. Assessment criteria were proposed in order to differentiate the two areas of narcissistic pathology and assess suitability for psychotherapeutic treatment. Positive treatment results in this case-study suggest that narcissistic neuroses may receive long-term benefit from short-term psychodynamic therapy

Mobility Disability in Older Adults: At the Intersection of People and Places

Mobility disability is associated with poor lower body function among older adults. This study examines whether specific types of neighborhood characteristics moderate that association

Hypersonic Laminar Boundary Layer Velocimetry with Discrete Roughness on a Flat Plate

Laminar boundary layer velocity measurements are made on a 10-degree half-angle wedge in a Mach 10 flow. Two types of discrete boundary layer trips were used to perturb the boundary layer gas. The first was a 2-mm tall, 4-mm diameter cylindrical trip. The second was a scaled version of the Orbiter Boundary Layer Transition (BLT) Detailed Test Objective (DTO) trip. Both 1-mm and 2.5-mm tall BLT DTO trips were tested. Additionally, side-view and plan-view axial boundary layer velocity measurements were made in the absence of these tripping devices. The free-stream unit Reynolds numbers tested for the cylindrical trips were 1.7x10(exp 6)/m and 3.3x10(exp 6)/m. The free-stream unit Reynolds number tested for the BLT DTO trips was 1.7x10(exp 6)/m. The angle of attack was kept at approximately 5-degrees for most of the tests resulting in a Mach number of approximately 8.3. These combinations of unit Reynolds numbers and angle of attack resulted in laminar flowfields. To study the precision of the measurement technique, the angle of attack was varied during one run. Nitric-oxide (NO) molecular tagging velocimetry (MTV) was used to obtain averaged axial velocity values and associated uncertainties. These uncertainties are as low as 20 m/s. An interline, progressive scan CCD camera was used to obtain separate images of the initial reference and shifted NO molecules that had been tagged by the laser. The CCD configuration allowed for sub-microsecond sequential acquisition of both images. The maximum planar spatial resolution achieved for the side-view velocity measurements was 0.07-mm in the wall-normal direction by 1.45-mm in the streamwise direction with a spatial depth of 0.5-mm. For the plan-view measurements, the maximum planar spatial resolution in the spanwise and streamwise directions was 0.69-mm by 1.28-mm, respectively, with a spatial depth of 0.5-mm. Temperature sensitive paint (TSP) measurements are provided to compliment the velocity data and to provide further insight into the behavior of the boundary layers. The experiments were performed at the NASA Langley Research Center 31-Inch Mach 10 Air tunnel

Activation of native TRPC1/C5/C6 channels by endothelin-1 is mediated by both PIP3 and PIP2 in rabbit coronary artery myocytes

We investigate activation mechanisms of native TRPC1/C5/C6 channels (termed TRPC1 channels) by stimulation of endothelin-1 (ET-1) receptor subtypes in freshly dispersed rabbit coronary artery myocytes using single channel recording and immunoprecipitation techniques. ET-1 evoked non-selective cation channel currents with a unitary conductance of 2.6 pS which were not inhibited by either ET(A) or ET(B) receptor antagonists, respectively BQ-123 and BQ788, when administered separately. However, in the presence of both antagonists, ET-1-evoked channel activity was abolished indicating that both ET(A) and ET(B) receptor stimulation activate this conductance. Stimulation of both ET(A) and ET(B) receptors evoked channel activity which was inhibited by the protein kinase C (PKC) inhibitor chelerythrine and by anti-TRPC1 antibodies indicating that activation of both receptor subtypes causes TRPC1 channel activation by a PKC-dependent mechanism. ET(A) receptor-mediated TRPC1 channel activity was selectively inhibited by phosphoinositol-3-kinase (PI-3-kinase) inhibitors wortmannin (50 nm) and PI-828 and by antibodies raised against phosphoinositol-3,4,5-trisphosphate (PIP(3)), the product of PI-3-kinase-mediated phosphorylation of phosphatidylinositol 4,5-bisphosphate (PIP(2)). Moreover, exogenous application of diC8-PIP(3) stimulated PKC-dependent TRPC1 channel activity. These results indicate that stimulation of ET(A) receptors evokes PKC-dependent TRPC1 channel activity through activation of PI-3-kinase and generation of PIP(3). In contrast, ET(B) receptor-mediated TRPC1 channel activity was inhibited by the PI-phospholipase C (PI-PLC) inhibitor U73122. 1-Oleoyl-2-acetyl-sn-glycerol (OAG), an analogue of diacylglycerol (DAG), which is a product of PI-PLC, also activated PKC-dependent TRPC1 channel activity. OAG-induced TRPC1 channel activity was inhibited by anti-phosphoinositol-4,5-bisphosphate (PIP(2)) antibodies and high concentrations of wortmannin (20 μm) which depleted tissue PIP(2) levels. In addition exogenous application of diC8-PIP(2) activated PKC-dependent TRPC1 channel activity. These data indicate that stimulation of ET(B) receptors evokes PKC-dependent TRPC1 activity through PI-PLC-mediated generation of DAG and requires a permissive role of PIP(2). In conclusion, we provide the first evidence that stimulation of ET(A) and ET(B) receptors activate native PKC-dependent TRPC1 channels through two distinct phospholipids pathways involving a novel action of PIP(3), in addition to PIP(2), in rabbit coronary artery myocytes

The quality of medication use in older adults: Methods of a longitudinal study

The quality of medication use in older adults is a recurring problem of substantial concern. Efforts to both measure and improve the quality of medication use often define quality too narrowly and fall short of addressing the complexity of an older adult's medication regimen

Population Health Solutions for Assessing Cognitive Impairment in Geriatric Patients.

In December 2017, the National Academy of Neuropsychology convened an interorganizational Summit on Population Health Solutions for Assessing Cognitive Impairment in Geriatric Patients in Denver, Colorado. The Summit brought together representatives of a broad range of stakeholders invested in the care of older adults to focus on the topic of cognitive health and aging. Summit participants specifically examined questions of who should be screened for cognitive impairment and how they should be screened in medical settings. This is important in the context of an acute illness given that the presence of cognitive impairment can have significant implications for care and for the management of concomitant diseases as well as pose a major risk factor for dementia. Participants arrived at general principles to guide future screening approaches in medical populations and identified knowledge gaps to direct future research. Key learning points of the summit included: recognizing the importance of educating patients and healthcare providers about the value of assessing current and baseline cognition;emphasizing that any screening tool must be appropriately normalized and validated in the population in which it is used to obtain accurate information, including considerations of language, cultural factors, and education; andrecognizing the great potential, with appropriate caveats, of electronic health records to augment cognitive screening and tracking of changes in cognitive health over time

Dual Users: Real Lessons from Reality Television

This study attempts to understand the differences in activity among an emergent television/Internet audience. The Internet has provided a new entertainment opportunity for producers of television programming. Those television viewers who have also reached out to their favorite television show websites have resulted in a new audience. Examining the programming genre of reality television, two constructs were developed and a written survey administered to a convenience sample of college freshmen. The construct dual users was created to examine the television audience that also visits television programming websites. Single users (those that only watch the television show) were compared to the self-reported levels of activity and involvement of dual users. Early findings suggest that the dual users are more involved during viewing of the television show and engaged in less secondary activity than the single users

Fungal Adenylyl Cyclase Acts As a Signal Sensor and Integrator and Plays a Central Role in Interaction with Bacteria

10.1371/journal.ppat.1003612PLoS Pathogens910