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Biomedical subjects

R E Carr

Publications and source records attributed to R E Carr.

At least 37 records · Page 2Linked to original sources

Catecholamine interference with enzymatic determination of nonesterified fatty acids in two commercially available test kits.

We present evidence that catecholamines, which are commonly used to stimulate lipolysis in adipose tissue in vitro, interfere with the enzymatic determination of non-esterified fatty acid (NEFA) in two commercially available kits. Measurement of a 100 mumol/L standard with the Wako "NEFA C" test kit was 60% inhibited by 100 mumol/L norepinephrine and was completely inhibited by 100 mumol/L isoproterenol or by 1 mmol/L norepinephrine or epinephrine. Measurement with the Boehringer Mannheim "Free Fatty acids, Half-micro test" was completely inhibited by 100 mumol/L norepinephrine and was also affected by concentrations as low as 0.1 mumol/L. We propose that this effect is due to the catecholamines interfering with a step common to the two kits, the generation of hydrogen peroxide and oxidation of a chromagen; furthermore, this interference appears to be stoichiometric. We also give details of an alternative in-house method, which does not depend on the generation of hydrogen peroxide and is not affected by catecholamines.

Acyl-CoA Oxidase↗

Anxiety sensitivity and panic attacks in an asthmatic population.

The purpose of this study was to examine the relationship among anxiety sensitivity, the experience of frequent, spontaneous panic attacks, and pulmonary function in individuals with asthma. Ninety-three asthmatics participated by completing a battery of questionnaires and a spirometric assessment. Twenty-three percent of the asthmatics reported a history of spontaneous panic attacks with 9.7% reporting attacks that were severe and frequent enough to meet the DSM-IIIR criteria for panic disorder (PD). Anxiety sensitivity (ASI) scores, but not pulmonary function, was significantly related to PD. In addition, we compared the asthmatics (with and without PD) to 10 clinically diagnosed PD Ss without asthma and to 32 nonanxious, nonasthmatic controls on the ASI, the Body Sensations Questionnaire, and the Agoraphobic Cognitions Questionnaire. Whereas Ss with PD (asthmatic and nonasthmatic) displayed significant elevations on these measures compared to those without PD, the presence of asthma alone had no effect. The present study concurs with that of Porzelius et al. [Behaviour Research and Therapy, 30, 75-77 (1992)] in extending the validity of the cognitive model of PD to individuals with pulmonary disease.

Adult↗

Reply to Ley's "dyspneic-fear theory explains hyperventilatory panic attacks".

In a critique of the study by Carr, Lehrer and Hochron (1992), Ley (Behaviour Research and Therapy, 32, 109-111, 1994) attributes the lack of confirmation for his dyspneic-fear theory among panic disorder patients to a basic flaw of that study: Ss were selected according to DSM-IIIR criteria. Ley argues that dyspneic-fear theory pertains exclusively to hyperventilatory (characterized by intense dyspnea) panic attacks not to all attacks that come under the classification of DSM-IIIR. We address the premise concerning the selection of Ss and argue that cognitive theory continues to offer a more convincing explanation of our study and of more recent findings by others.

Dyspnea↗

Phenotypic variation including retinitis pigmentosa, pattern dystrophy, and fundus flavimaculatus in a single family with a deletion of codon 153 or 154 of the peripherin/RDS gene.

BACKGROUND AND OBJECTIVES: Mutations of the peripherin/RDS gene have been reported in autosomal dominant retinitis pigmentosa, pattern macular dystrophy, and retinitis punctata albescens. We report herein the occurrence of three separate phenotypes within a single family with a novel 3-base pair deletion of codon 153 or 154 of the peripherin/RDS gene. DESIGN: Case reports with clinical features, fluorescein angiography, kinetic perimetry, electrophysiological studies, and molecular genetics. SETTING: University medical centers. PATIENTS: A 75-year-old woman, her two daughters (aged 44 and 50 years), and her 49-year-old son were screened for peripherin/RDS mutations because of the presence of multiple phenotypes within the same family. RESULTS: The mother presented at age 63 years with a profoundly abnormal electroretinogram (ERG) and adult-onset retinitis pigmentosa that progressed dramatically over 12 years, with marked loss of peripheral visual field. One daughter developed pattern macular dystrophy at age 31 years. At age 44 years, her ERG was moderately abnormal but her clinical disease was limited to the macula. Another daughter presented at age 42 years with macular degeneration and over 10 years developed the clinical picture of fundus flavimaculatus. Her peripheral visual field was preserved but her ERG was moderately abnormal. The son had onset of macular degeneration at age 44 years. Pericentral scotomas were present and the ERG was markedly abnormal. Fluorescein angiography revealed punctate pigment epithelial transmission defects. CONCLUSIONS: A 3-base pair deletion of codon 153 or 154 of the peripherin/RDS gene can produce clinically disparate phenotypes even within the same family.

Adult↗

Effects of early diabetic retinopathy on rod system sensitivity.

Previous studies have shown that S-cone pathway sensitivity is selectively decreased in the early stages of diabetic retinopathy. In the present study, rod system sensitivity was evaluated in a group of diabetic patients using psychophysical techniques. The course of dark adaptation was first determined, then absolute thresholds were measured in the horizontal and vertical meridians. For all patients, although the recovery of the initial portions of rod dark adaptation were normal, absolute thresholds were increased in both the horizontal and vertical meridians. The findings provide evidence that patients with early diabetic retinopathy show a generalized dysfunction of the rod system.

Adult↗

The effects of acetazolamide on visual function in retinitis pigmentosa.

PURPOSE: To study the effects of acetazolamide on central and peripheral visual function in patients with retinitis pigmentosa (RP) who showed no evidence of macular edema. METHODS: Thirteen patients with retinitis pigmentosa participated in a preliminary study. Measures of central and peripheral visual function were obtained before and after an 8 wk period on acetazolamide. An additional 10 patients participated in a cross-over study. They were placed on a placebo for an 8 wk period, then on acetazolamide for a second 8 wk period. RESULTS: None of the patients in the preliminary study showed significant changes in visual acuity, color vision, foveal cone pathway sensitivities, focal electroretinogram (ERG) amplitudes, or in any ERG parameter. Three patients, however, showed significant changes in visual field area and in dark-adapted thresholds. None of the patients in the cross-over study showed significant increases in visual field area. CONCLUSIONS: Given the results and the reports of side-effects, it is difficult to justify using acetazolamide to improve retinal function in RP patients who show no evidence of cystoid macular edema.

Acetazolamide↗

Panic symptoms in asthma and panic disorder: a preliminary test of the dyspnea-fear theory.

Ley's (Behaviour Research and Therapy, 27, 549-554, 1989) dyspnea-fear theory was tested on three groups of subjects: 10 with panic disorder, 24 with asthma, and 12 who were nonanxious and nonasthmatic, using measures of pulmonary function, muscle tension; and self-report measures of generalized anxiety, dyspnea, and psychopathology. Results are supportive of dyspnea-fear theory for asthmatics but not for individuals with panic disorder. Differences between groups on panic/fear measures were explained by a combination of general anxiety and dyspnea. Within-group regression analyses showed that only generalized anxiety symptoms contributed significantly to scores on the Asthma Symptom Checklist scale of panic/fear within the panic disorder group; while only dyspnea contributed to panic/fear among asthmatics. Additional results show that panic disorder subjects performed normally on pulmonary function tests but reported respiratory symptoms as severe as did asthmatics. Compared with normal subjects, both patient groups displayed lower correlations between self-rated symptoms of bronchoconstriction and objective pulmonary measures. Panic disorder subjects showed a negative relationship between pulmonary function and hyperventilation symptoms, suggesting a heightened sensitivity to, and discomfort with, sensations associated with normal pulmonary function. Asthmatics displayed a significant relationship between degree of airway obstruction and both trapezius surface EMG and ratings of hyperventilation symptoms.

Age Factors↗

Phospholipid-containing toxic malaria antigens induce hypoglycaemia.

Hypoglycaemia is associated with severe malaria and is an important prognostic indicator. Molecules liberated during overnight incubation of erythrocytes infected with Plasmodium yoelii induce marked hypoglycaemia in normal mice, with a delayed time course compared with insulin; some, though weaker, activity could also be obtained by overnight incubation of uninfected erythrocytes. The active component shares many properties with the phospholipid-containing molecules which we have previously shown to be toxic and to induce the release of tumour necrosis factor (TNF) from macrophages. However a MoAb which neutralizes the cytotoxicity of tumour necrosis factor in vitro did not prevent this induction of hypoglycaemia, whereas antiserum against the toxic antigens did, as did immunization of normal (but not the immunoglobulin-deficient SCID) mice with the same material. Furthermore, normal mice injected with the antigens after immunization with phosphatidyl inositol or inositol monophosphate did not develop hypoglycaemia; the latter compound was also inhibitory when mixed with the antigens before injection. These compounds were previously shown to block the induction of TNF by the antigens and to induce the production of inhibitory antibodies. The role of these molecules in the etiology of the hypoglycaemia of malaria is discussed.

Animals↗

Autosomal dominant congenital stationary night blindness and normal fundus with an electronegative electroretinogram.

We studied three members of three successive generations of a family with autosomal dominant congenital stationary night blindness and normal fundi. Psychophysical studies on two members showed normal final cone thresholds and mildly increased rod thresholds. Full-field electroretinograms on all three members showed normal photopic b-wave amplitudes and implicit times. Under scotopic conditions, the rod response was absent, and with a bright flash stimulus, there was a normal a-wave with no b-wave. This electronegative dark-adapted electroretinogram resembled the Schubert-Bornschein type seen in congenital stationary blindness, which has been seen only in autosomal and X-linked recessive pedigrees.

Adult↗

Clofazamine-induced generalized retinal degeneration.

Clofazamine is an iminophenazine dye with antimycobacterial activity which has recently been used to treat mycobacterium avium complex infections in patients with acquired immunodeficiency syndrome. The authors present the second report of a presumed clofazamine-induced bull's-eye maculopathy and generalized retinal degeneration in a patient with AIDS. The importance of closely following patients on clofazamine, especially those with AIDS who may be particularly susceptible to developing this toxicity, is stressed.

Acquired Immunodeficiency Syndrome↗

The clinical utility of visual-evoked potential acuity testing.

We assessed the clinical utility of objectively measured acuity using visual-evoked potentials. The technique was first standardized in normal emmetropic subjects and then applied to uncorrected myopic subjects. We found that visual-evoked potential acuity could accurately indicate Snellen acuity in emmetropia and corrected myopia; however, the two measures were highly correlated only in those uncorrected myopic subjects with visual acuities of 20/100 or better. In subjects with poorer than 20/200 uncorrected visual acuity caused by myopia, estimates of visual-evoked potential acuity could not be obtained. The correlation between these two measures of visual acuity was also lower in patients with decreased Snellen acuity attributable to retinal or ocular disease. We found that patients with unexplainable claims of decreased visual acuity could be diagnosed as having functional visual loss based on objective visual-evoked potential acuities.

Adolescent↗

The golden tapetal sheen reflex in retinal disease.

A mother and son with dominant cone dystrophy manifested the retinal reflexes seen in Oguchi's disease (mother) and the carrier female of X-linked retinitis pigmentosa (son). Another patient with cone dystrophy (simplex) showed localized areas of a golden reflex in each eye. A patient with juvenile macular dystrophy exhibited a diffuse golden-orange reflex throughout the posterior pole. The latter two patients did not have the Mizuo phenomenon.

Adult↗

S (blue) cone pathway vulnerability in retinitis pigmentosa, diabetes and glaucoma.

A variety of retinal disease lead to a decrease in the sensitivity of the S (blue) cone pathways. To determine the possible sites and mechanisms of this loss we compared the sensitivities of an S (blue/pi-1) and an M (green/pi-4) cone pathway in patients with retinal diseases that differ as to their primary locus of sensitivity loss. The sensitivities of an S and an M cone pathway were assessed in patients with retinitis pigmentosa, insulin-dependent diabetes mellitus and open-angle glaucoma using Stiles two-color increment threshold technique. A greater loss in sensitivity of an S than an M cone pathway was found for all three disease groups; however, the diabetic patients showed a more selective loss. The results suggest that multiple sites are involved and that the combined effects of metabolic abnormalities and hypoxia contribute to the selective loss.

Adaptation, Ocular↗

Progressive peripheral cone dysfunction.

A 22-year-old man had a three-year history of progressive day blindness, most notably peripherally, and denied difficulty with central vision or color vision. Visual function studies demonstrated a diffuse dysfunction of the photopic system and normal scotopic function. The central cone function, however, was essentially normal. Visual acuity was 20/20 in each eye, results on AO-HRR and Ishihara color plate testing were normal, color naming visual fields demonstrated color discrimination in the central 10 degrees, and foveal adaptation was normal.

Adult↗

Visual system toxicity following intra-arterial chemotherapy.

We studied the effects of intra-arterial chemotherapy on the visual system of 29 consecutive patients with gliomas. As expected, infra-ophthalmic carotid infusion of cisplatin or carmustine (BCNU) was associated with clinically apparent anterior visual pathway lesions. Electroretinography revealed retinal dysfunction in patients without clinical abnormalities. Supra-ophthalmic carotid infusion of cisplatin or BCNU caused no retinal or optic nerve lesions. Electroretinography was abnormal in only one of these patients. Our results indicated that BCNU and cisplatin cause ischemic damage and are toxic to both retinal and neural tissue in patients with gliomas.

Brain Neoplasms↗