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Biomedical subjects

A M Cooper

Publications and source records attributed to A M Cooper.

At least 55 records · Page 3Linked to original sources
PubMed1994

Expression of complement regulatory molecules and other surface markers on neutrophils from synovial fluid and blood of patients with rheumatoid arthritis.

In an effort to elucidate the activation status of neutrophils (PMN) in inflammatory joint disease the expression of relevant cell surface proteins was examined using immunofluorescence and flow cytometry. Paired samples of SF and peripheral blood were obtained from 18 patients with RA and PMN purified using methods designed to minimize activation in vitro. We then used flow cytometry to measure expression of the four membrane complement regulatory molecules, decay accelerating factor (DAF; CD55), complement receptor 1 (CR1; CD35), membrane cofactor protein (MCP; CD46) and CD59; two adhesion molecules of the integrin family LFA1 (alpha chain, CD11a), complement receptor 3 (CR3; alpha chain, CD11b), and their common beta chain (CD18); the major receptor for immune complexes Fc gamma RIII (CD16), and the leucocyte common antigen tyrosine phosphatase (L-CA; CD45). Expression of these molecules was also measured on peripheral blood PMN from 18 age- and sex-matched normal controls. In RA, SF PMN expressed significantly higher levels of the complement regulators CD55 and CD35, the adhesion molecule CR3 (CD11b/CD18) and of CD45 but significantly lower levels of CD46 and CD11a in comparison with blood PMN from the same patient. Expression of CD59 and CD16 did not differ between the two groups. These changes may increase adhesiveness and complement resistance of PMN in SF compared with blood. PMN from RA expressed significantly less of all the complement C3 convertase regulators (CD55, CD46, CD35), all the adhesion molecules (CD11a, CD11b, CD18) and the phosphatase CD45 than did blood PMN from age and sex-matched control individuals.

Adult↗
PubMed1994

T-cell responses to infected autologous monocytes in patients with cutaneous and mucocutaneous leishmaniasis.

Although there is strong evidence that the control and resolution of human leishmanial infections depend primarily on activation of parasite-infected macrophages mediated by lymphokines derived from T cells, less is known about the nature of the responding cell type(s) which is protective or the antigen(s) (Ag[s]) that elicits these cells to respond. Studies using preparations of whole soluble Ag ("dead Ag") show that patients respond to a wide range of leishmanial Ags. The objective of the present study was to characterize the response of T cells from patients with healing or healed cutaneous or mucosal infections to Ag expressed by or derived from actively infected autologous monocytes ("live Ag"). Unfractionated T cells proliferated and produced gamma interferon in response to both live and dead Ags. Depletion of CD4+ T cells resulted in the loss of proliferative and gamma interferon responses to both live and dead Ags. The effect of CD8 depletion, although variable and not limited to the cells stimulated by infected monocytes, was clear for some patients. Expansion of T cells specific for live Ags by using amastigote-infected cells followed by restimulation with fast-protein liquid chromatography-fractionated soluble Ags revealed that a diversity of Ags are associated with infected monocytes. There may, however, be quantitative differences in the expression of certain Ags since prestimulation with live Ag induced higher responses to restimulation in mucocutaneous leishmaniasis patients than in localized cutaneous leishmaniasis patients. Prestimulation with dead Ag induced similar secondary responses in both patient groups.

Animals↗
PubMed1994

Altered Ca2+ signalling in human neutrophils from inflammatory sites.

OBJECTIVES: To determine whether the intracellular store release of Ca2+ in neutrophils from patients with rheumatoid arthritis, other joint disease and active leg ulceration was different from normal neutrophils. METHODS: The release into the cytosol of Ca2+ from stores within individual neutrophils was determined using ratiometric imaging of fura2. The size of the elevated Ca2+ 'cloud' and its concentration were quantified in neutrophils from the circulation of patients with rheumatoid arthritis, other joint diseases, and leg ulcers and from the joints of those with joint disease. RESULTS: In neutrophils isolated from both the synovial fluid of patients with rheumatoid arthritis and other joint conditions, and also arising from leg ulcers, the amount of the cell cytosol occupied by elevated Ca2+ was significantly increased compared with neutrophils from healthy subjects; for neutrophils from rheumatoid, non-rheumatoid joints and leg ulcers p values were 0.0006, < 0.0001, 0.016 respectively (Student's t test). There was also a significant increase in Ca2+ release from circulating neutrophils from patients with rheumatoid arthritis (p = 0.09), but not in circulating neutrophils from patients with leg ulcers or non-rheumatoid joint conditions. CONCLUSIONS: It is proposed that the increased release of free Ca2+ into the cytosol of neutrophil at inflammatory sites results in increased oxidase activation.

Adult↗
PubMed1994

Formulations to the patient: explicit and implicit.

Many of our formulations to the patient are conveyed through the day-to-day unremarkable actions, verbal and nonverbal, occurring between analyst and patient as the analyst attempts to understand his patient within the analytic setting. The analyst's confidence, even intensity, concerning the value of analysis is significant in enabling him to communicate successfully with his patient. Unlike what may have been the case in the past, this analytic fervour is not in the service of a single theory or an attempt to prove an analytic proposition, but is aimed at deepening introspective curiosity and opening avenues of communication. Within our characterologic and procedural limits, we use ourselves in a large variety of ways in an attempt to further the analytic process. This use of ourselves, conveyed to the patient in innumerable interactions, becomes a central analytic fact that fosters the patient's participation in his analysis. Clinical vignettes are provided to illustrate these propositions.

Adult↗
PubMed1993

Disseminated tuberculosis in interferon gamma gene-disrupted mice.

The expression of protective immunity to Mycobacterium tuberculosis in mice is mediated by T lymphocytes that secrete cytokines. These molecules then mediate a variety of roles, including the activation of parasitized host macrophages, and the recruitment of other mononuclear phagocytes to the site of the infection in order to initiate granuloma formation. Among these cytokines, interferon gamma (IFN-gamma) is believed to play a key role is these events. In confirmation of this hypothesis, we show in this study that mice in which the IFN-gamma gene has been disrupted were unable to contain or control a normally sublethal dose of M. tuberculosis, delivered either intravenously or aerogenically. In such mice, a progressive and widespread tissue destruction and necrosis, associated with very high numbers of acid-fast bacilli, was observed. In contrast, despite the lack of protective immunity, some DTH-like reactivity could still be elicited. These data, therefore, indicate that although IFN-gamma may not be needed for DTH expression, it plays a pivotal and essential role in protective cellular immunity to tuberculosis infection.

Animals↗
PubMed1993

A psychodynamic model of panic disorder.

Current psychiatric research on panic disorder and its treatment are heavily influenced by neurobiological and cognitive-behavioral models rather than psychodynamic propositions, and psychodynamic treatment is generally considered to be of little benefit in amelioration of symptoms. However, because neither of the current models fully explains the clinical psychopathology, etiology, or pathogenesis of panic disorder, there is a need for further model building. The authors suggest that a psychodynamic approach may add to the understanding of patients with panic disorder. They base their psychodynamic formulation on pilot interviews with nine patients with panic disorder, published reports of psychological characteristics of patients with panic disorder, and data from infant and animal research on temperament. Interview results included the following: 1) all of the patients described themselves as fearful, nervous, or shy as children, 2) they remembered their parents as angry, frightening, critical, or controlling, 3) they frequently indicated discomfort with aggression, 4) most described chronic feelings of low self-esteem, 5) their spouses were characterized as passive, kind, and nonaggressive, and 6) stressors associated with frustration and resentment preceded the onset of panic. The authors propose a model in which inborn neurophysiological irritability predisposes to early fearfulness. Exposure to parental behaviors that augment fearfulness results in disturbances in object relations and persistence of conflicts between dependence and independence, which predispose to fears of feeling trapped, suffocated, and unable to escape and/or feeling alone and unable to get help. Catastrophic fears of helplessness in the face of suffocation or abandonment are easily accessible.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Paranoia: a part of most analyses.

Paranoid defenses appear during most analyses, sometimes with great intensity, but often subtly, and require specific analytic attention. Preoedipal conflicts, inner fears around passivity, narcissistic injury and rage, and subsequent masochistic and projective defenses lie at the core of these patients' pathology. In addition, specific cognitive, object-relational, and affective distortions reflecting multiple developmental levels emerge during analysis. A case vignette is provided to demonstrate the analysis of a neurotic patient without borderline features who showed prominent paranoid formation.

Adult↗
PubMed1992

Psychic change: development in the theory of psychoanalytic techniques. 37th IPA congress overview.

This paper addresses some of the methodological problems in assessing and understanding change in psychoanalysis, including the twin difficulties of not knowing precisely what transpires in an analytic session and not knowing to which of the many aspects of psychoanalytic process any particular change should be assigned. There are alternate models for understanding change. The most commonly used model is that of psychoanalytic growth with the analyst acting as a fostering maternal figure. An alternate model of change is of psychic repair with the analyst in a more physicianly role. Analysts also work with alternative models of trauma. In one model danger stems from the infant's own overwhelming affective states, while in the other model danger comes from parenting failures. Analysts also differ regarding the importance assigned to interpretation and insight rather than to the new relationships and altered experience. This paper elaborates these models and their implications for psychoanalytic technique and our understanding of psychic change.

Female↗
PubMed1991

In vitro and in vivo evaluation of whole and half tablets of sustained-release adinazolam mesylate.

The mechanism of release from sustained-release adinazolam mesylate tablets was assessed by the Higuchi equation and by analysis of drug release profiles through 60% released using the Peppas equation. Computed values of the diffusional exponent, n, ranged from 0.59 to 0.66. Values of n in this range are consistent with a mixed mechanism of release, with diffusion of drug through the hydrated polymer matrix and relaxation of this matrix being the principal processes controlling release. The rate of in vitro drug release was increased for half tablets relative to whole tablets and is attributed to an increase in the surface to volume ratio of half tablets of about 16%. This increase in surface-to-volume ratio of half tablets was reflected by an increase in the constant, k, from the Peppas equation of 20-23% and by an increase in the slope of Higuchi plots of 12-18% for four lots of tablets. In vivo/in vitro relationships from two bioavailability studies were thoroughly evaluated. Using either a linear or a quadratic relationship, an in vivo/in vitro correlation exists for sustained-release adinazolam mesylate tablets.

Adolescent↗
PubMed1991

Fasting and post-prandial splanchnic blood flow is reduced by a somatostatin analogue (octreotide) in man.

1. The effects of the subcutaneous administration of a long-acting somatostatin analogue (octreotide) or of placebo on the splanchnic blood flow response to a mixed solid meal has been examined in eight normal subjects by using a transcutaneous Doppler ultrasound technique. Each subject was studied on two occasions more than 1 week apart. 2. On the control day, feeding had a pronounced effect on both superior mesenteric artery and portal venous blood flows, causing a peak rise of 82% in superior mesenteric artery blood flow at 15 min and of 75% in portal venous blood flow at 30 min post-prandially (P less than 0.001). Blood flows remained elevated 2 h after the meal. Pulse and blood pressure showed no significant changes from baseline. 3. Octreotide reduced fasting superior mesenteric artery blood flow by 59% (P less than 0.05) and portal venous blood flow by 49% (P less than 0.01) and blunted the normal post-prandial rise. Pulse and blood pressure did not change in response to either the injection or the ingestion of the meal. 4. Octreotide suppressed the release of insulin, glucagon and pancreatic polypeptide in response to feeding and resulted in post-prandial hyperglycaemia. 5. The mechanism of action of octreotide on splanchnic blood flow is uncertain. It may be mediated via a direct vascular effect or it may act via suppression of vasoactive intestinal hormones.

Adult↗
PubMed1990

The histochemical reaction of horseradish peroxidase in rodent 'whole-brain' preparations.

Subsequent to eye injections of horseradish peroxidase (HRP) 'whole-brain' preparations with only the cortex removed were reacted for HRP using tetramethylbenzidine (TMB) as the chromogen and ammonium heptamolybdate (AHM) as a stabilizer. Retinal projections could be photographed and visualized globally coursing across the surface of the thalamus and midbrain. The brains were then sectioned, and when necessary re-reacted, enabling a 3-D reconstruction of retinofugal pathways to be made.

Animals↗
PubMed1990

Development and retraction of a crossed retinal projection to the inferior colliculus in neonatal pigmented rats.

A transient aberrant projection from the retina to the contralateral inferior colliculus was demonstrated in pigmented rats in both whole-brains and sections following intra-ocular injection of horseradish peroxidase. The projection was prominent on the day of birth but reached its maximum density and extent after injection on day 1, when it covered at least a third of the inferior colliculus. It was absent or nearly absent by day 5. Its consistency, size, orderliness and systematic retraction suggest that it is not merely a developmental accident.

Animals↗
PubMed1990

Retinal topography of the neonatal crossed aberrant exuberant projection to the inferior colliculus in the pigmented rat.

The retinal topography of the neonatal transient projection to the inferior colliculus was investigated in pigmented rats by injecting the retrograde fluorescent tracer Fast Blue into the colliculi. The results show that the projection arises from a small population of ganglion cells scattered across the entire contralateral retina, and that the transient projection is therefore not merely an overshoot of axons from the peripheral nasal retina whose appropriate target is the caudal pole of the superior colliculus.

Afferent Pathways↗