Biomedical subjects
Publications and source records attributed to M Brogan.
This article reviews the literature relating to healthcare provision for lesbians. The author discusses the attitudes of healthcare providers to this client group and the experiences of these women in a prejudiced healthcare system.
The subject of sexuality and elderly people has until recently, largely been ignored by nurses. This article stresses the importance of acknowledging that sexual activity and interest changes with ageing and that to deny that it exists is detrimental to the holistic care nurses should aim to provide.
Through the illustration of a clinical vignette and excerpts from interviews with trainees, this paper suggests that communication and communication disorders are essential issues in child psychiatry training. The vignette shows how communication issues pervade a multidisciplinary psychoeducational day treatment program. The importance of communication in the clinical experience and its impact on the professional preparation of psychiatry residents and mental health trainees are examined, and conclusions and recommendations for the goals of a training program in child psychiatry are presented which expand upon those findings.
Post-traumatic atypical facial pain syndromes are refractory to medical therapy and thus challenging to treat. Some of these patients have a facial causalgia syndrome that may include autonomic as well as trigeminal fibers as the anatomic mediators. A procedure that may be of both diagnostic and therapeutic benefit is a nerve block in the region of the foramen rotundum. This allows access to both the maxillary nerve and the sphenopalatine ganglion. A simple technique developed to perform this procedure is described, and the results in a series of six patients are presented.
Many of the structural brain abnormalities found in schizophrenia (SC) and bipolar disorder (BD) over the past decade are believed to represent impaired neurodevelopmental processes. The authors hypothesized that incidental developmental anomalies would be more frequently present in the brains of subjects with SC and BD compared with healthy control subjects. The authors systematically assessed the MRI scans of 167 subjects (SC = 67, BD/schizoaffective = 63, healthy control subjects = 37) for the presence of 23 developmental anomalies involving cortical and subcortical structures. No excess neurodevelopmental anomalies were found in the schizophrenic or bipolar/schizoaffective groups. These findings do not support the hypothesis that SC and BD are associated with an excess of gross neurodevelopmental brain anomalies.
Previous studies of the frequency of high-signal lesions in human immunodeficiency virus (HIV) infection have had methodological weaknesses regarding lack of control groups, differing machine strengths, and biased subject selection. To obtain a more accurate estimate of prevalence, MRI scans were performed on 243 HIV-positive and HIV-negative homosexual or bisexual men with no history of intravenous drug use. Axial T2-weighted (long TR/TE, spin-echo) MRI scans were rated blindly for presence of focal white matter high-signal lesions. Incidence of hyperintensities was low in all groups, although slightly higher in patients with AIDS, and was not associated with neuropsychological performance. The lower incidence of hyperintensities appears to relate to elimination of methodological problems in previous studies.
Human skin fibroblasts in suspension are able to degrade [1-14C]-labeled alpha- and gamma-methyl branched chain fatty acids such as pristanic and homophytanic acid. Pristanic acid was converted to propionyl-CoA, whereas homophytanic acid was beta-oxidized to acetyl-CoA. Incubation of skin fibroblasts with [1-14C]-labeled fatty acids for longer periods produced radiolabeled carbon dioxide, presumably by further degradation of acetyl-CoA or propionyl-CoA generated by beta-oxidation. Under the same conditions similar products were produced from very long chain fatty acids, such as lignoceric acid. Inclusion of digitonin (> 10 micrograms/ml) in the incubations strongly inhibited carbon dioxide production but stimulated acetyl-CoA or propionyl-CoA production from fatty acids. ATP, Mg2+, coenzyme A, NAD+ and L-carnitine stimulated acetyl-CoA or propionyl-CoA production from [1-14C]-labeled fatty acids in skin fibroblast suspensions. Branched chain fatty acid beta-oxidation was reduced in peroxisome-deficient cells (Zellweger syndrome and infantile Refsum's disease) but they were beta-oxidized normally in cells from patients with X-linked adrenoleukodystrophy (ALD). Under the same conditions, lignoceric acid beta-oxidation was impaired in the above three peroxisomal disease states. These results provide evidence that branched chain fatty acid, as well as very long chain fatty acid, beta-oxidation occurs only in peroxisomes. As the defect in X-linked ALD is in a peroxisomal fatty acyl-CoA synthetase, which is believed to be specific for very long chain fatty acids, we postulate that different synthetases are involved in the activation of branched chain and very long chain fatty acids in peroxisomes.
Omeprazole is a new hydrogen-potassium adenosine triphosphatase antagonist with indications for severe reflux esophagitis and Zollinger-Ellison syndrome. Side effects involving the liver have consisted of minimal elevations of hepatocellular enzymes with higher dosages. We present what we believe is the first reported case of fulminant hepatic failure related to omeprazole.
This investigation evaluates whether gadopentetate dimeglumine enhancement of three-dimensional (3-D) acquisition MR angiography can generate clinically useful images of the normal venous anatomy of the brain. 3-D MR angiography of normal cerebral arterial anatomy has made rapid progress, although demonstration of detailed venous anatomy with similar techniques has been much less revealing. To overcome the limitation of slow venous flow, IV gadopentetate dimeglumine contrast enhancement was used to alter the relaxation times of blood, thus augmenting the venous signal. Several groups of patients were evaluated: we studied eight patients both with and without contrast enhancement, 20 patients and volunteers with multiple techniques to determine optimal technical parameters, and seven patients in whom enhanced MR studies were compared with standard selective biplane cut-film arterial angiograms. Only the large dural sinuses (such as the transverse sinus) could be seen on unenhanced studies owing to the saturation of slowly flowing venous spins. With contrast enhancement, many of the important small and large cerebral venous structures were routinely seen with reasonable scanning times (7 min). The venous anatomy was well seen for approximately one-half hour after injection and correlated well with angiograms. There are several important limitations to this technique, including a limited field of view, variable visibility of specific veins owing to technical and physiologic factors, confusion of enhancing non-flow-related structures, and lack of detailed physiologic information. Single excitation 3-D MR angiograms are insensitive in the evaluation of cerebral venous structures. Enhancement with gadopentetate dimeglumine affords rapid scanning and excellent visualization of the pertinent venous anatomy. The best image quality was obtained with a sequence of 50/7/30 degrees (TR/TE/flip angle).
Monoclonal antibodies to the CD3 component of the T-cell antigen receptor can trigger antigen-specific cytotoxic T cells to elicit nonantigen-specific cytotoxicity, possibly by mimicking or bypassing the requirement for antigen triggering. We have used this technique to investigate the possible presence of in vivo primed cytotoxic T cells, of unknown antigen specificity, in peripheral blood of patients with inflammatory bowel disease. Peripheral blood lymphocytes, which were depleted of background natural killer (NK) activity (CD16-), from patients with Crohn's disease exhibited significantly enhanced levels of anti-CD3-triggered T-cell cytotoxicity compared with lymphocytes from normal subjects. Enhanced lytic activity was also found in some patients with ulcerative colitis and in patients with ulcerative colitis postcolectomy. These results were not influenced by treatment or disease activity. There was no correlation between the anti-CD3-triggered T lytic activity and the NK activity in normal subjects or in patients with inflammatory bowel disease. The surface antigen phenotype of the anti-CD3-triggered T killer cell was CD3+, CD8+, CD16-, and Leu 7+. The results provide indirect evidence for increased activity of a subpopulation of cytotoxic T cells, of unknown antigen specificity, in inflammatory bowel disease. Increased activity in patients with ulcerative colitis postcolectomy suggests that this might reflect a fundamental immunological disturbance.
Combined immunohistochemical labelling for neurons containing growth hormone (GH) releasing factor (GRF) or somatostatin and single labelling immunohistochemistry combined with Fluorogold retrograde transport labelling were used to examine whether somatostatin or GRF neurons might be reciprocally innervated. Occasional somatostatin-immunoreactive neurons in the periventricular preoptic area were found to be closely approached by GRF-immunoreactive fibres, providing possible evidence of scant innervation of somatostatin neurons by GRF cells. In contrast, many GRF-immunoreactive neurons in the arcuate nucleus appeared to have somatostatin-immunoreactive fibres closely applied to their perikarya suggesting that GRF neurons might be innervated by somatostatin cells. Combined retrograde tracing and fluorescence immunohistochemistry revealed few somatostatin-immunoreactive neurons doubly labelled following injections of Fluorogold in the basal hypothalamus. Occasional GRF-immunoreactive neurons in the basal hypothalamus were doubly labelled following PO/AHA injections of Fluorogold. Numerous somatostatin-immunoractive perikarya were observed in the periventricular arcuate region in colchicine-pretreated animals. We conclude that GH-regulating neurons do not have strong reciprocal innervation. The innervation of GRF neurons by somatostatin fibres may be derived from local somatostatin neurons.
Possible effects of GRF on somatostatin neurons and of somatostatin on GRF neurons were examined by measuring the effects of localised intracerebral injections of these peptides on growth hormone (GH) secretion. Serial GH concentrations were measured in plasma in unanaesthetized male rats chronically prepared with venous and intracerebral cannulae, before and after treatment with bilateral intracerebral injections of somatostatin or GRF in the preoptic anterior hypothalamic area (PO/AHA) and medial basal hypothalamus. Injections of 0.1 and 1 nmol of GRF in medial basal hypothalamus or 10 nmol somatostatin in the PO/AHA, respectively, had stimulatory or inhibitory effects on GH, which were assumed to be due to diffusion of the peptide from the injection site to the median eminence and pituitary gland. Injection of lower doses of somatostatin around GRF neurons in the medial basal hypothalamus were without significant effect on secretion of GH, but 0.1 nmol somatostatin in the PO/AHA resulted in an increase in GH concentrations from 128 +/- 61 to 524 +/- 103 ng/ml, p less than 0.02. Injections of GRF in lower doses amongst somatostatin neurons in the PO/AH or amongst GRF neurons in the medial basal hypothalamus were both without effect on GH secretion. We conclude that somatostatin may stimulate GH secretion by an effect on or close to somatostatin neurons in the PO/AHA. Somatostatin, though present in terminals on GRF neurons, is without effect at this site in our model. Furthermore, we have been unable to demonstrate any significant intrahypothalamic effect of GRF on GH regulation.
The heart rate and respirations of twenty healthy full-term infants between 30 and 60 h postnatal age were studied during quiet sleep with the objective of defining spectral indices which represent normal neonatal heart rate variability (HRV) characteristics. Total HRV power and the distribution of power across different frequency bands varied considerably among infants. Cluster analysis on the measured variables indicated that the population divided into two groups that represented significantly different patterns of HRV behavior. In one group (11 subjects), infants had lower breathing rates and HRV power in a band about the respiration frequency [respiratory sinus arrhythmia (RSA) band] was more than 20% of the total power (TP). Additionally, the ratio of low frequency band power to RSA band power was less than 4. The other group of neonates (nine subjects) had relatively higher breathing rates, RSA power less than 20% of total power, and low frequency to RSA power ratio greater than 4. Regression analysis of low frequency versus TP and RSA versus TP graphs gave strong support to the hypothesis that there were indeed two distinct patterns of HRV behavior. Separation of apparently normal neonates into two groups may be attributed partially to differences in respiratory rates and breathing patterns. However, it is possible that differences in the balance between sympathetic and parasympathetic nervous system control, perhaps related to autonomic maturation, also contribute to group separation. The indices developed from HRV spectral analysis in this investigation may be of value in the study of cardiorespiratory control in neonates.
The high image quality provided by current high resolution CT bone algorithms in conjunction with the multiplanar and soft tissue imaging capabilities of MRI, provide exquisite anatomic detail of the temporal bone structures. This allows the radiologist to visually dissect this complex, three-dimensional structure, if a firm understanding of normal anatomy exists. In this way, the pathological processes involving the temporal bone can be better understood and correlated with the clinical setting.
We examined the relationship between magnetic resonance imaging (MRI) cerebral findings and clinical evaluations in 66 patients with clinically definite multiple sclerosis (MS). MRI observations included total number and location of lesions visualized, degree of periventricular involvement, degree of degeneration of the corpus callosum, and extent of generalized parenchymal atrophy. Overall physical disability was evaluated by the Kurtzke Expanded Disability Status Scale (EDSS) and individual symptoms were rated according to the Kurtzke Functional Systems (FS) scale. Our results suggest that MRI brain abnormalities are significantly related to the overall severity of disease, but MRI is not particularly useful to predict the presence or absence of individual symptoms. These findings do suggest that the MRI may provide useful information to monitor clinical progression of patients with MS, but the lesions visualized need not always be symptomatic nor are we sure that all symptomatic lesions, particularly in the spinal cord and optic nerves, will be visualized.
PURPOSE: The Hermansky-Pudlak syndrome is an autosomal recessive disorder consisting of the triad of oculocutaneous albinism, a storage pool platelet defect, and multisystem tissue deposition of ceroid pigment. Although the underlying metabolic defect has not been identified, secondary or associated effects on the immune system are suggested by reports of an association with disorders such as pulmonary fibrosis, granulomatous colitis, lupus, and frequent bacterial infections. We evaluated a large group of patients with the Hermansky-Pudlak syndrome to assess immune competence in this condition. PATIENTS AND METHODS: Fifteen patients with this syndrome were studied. Control subjects included healthy volunteers in the same age range as the patients. Peripheral blood lymphocytes and neutrophils were isolated according to previously described methods. Immunofluorescent staining, flow cytometry, and cytotoxicity assays were performed. Determination of lymphocyte transformation, mixed lymphocyte response, and neutrophil function was made. RESULTS: Immunoglobulin levels, complement, lymphocyte subsets, natural killer and lymphokine-activated cytotoxicity, mixed lymphocyte responses, and lectin-induced transformation were normal in all patients. In addition, there was no evidence for a lymphocyte proliferative response to a preparation of urinary ceroid pigment isolated from these patients. Neutrophil function, including luminol-dependent chemiluminescence, chemotaxis, and aggregation was not significantly different from control values. CONCLUSION: The results suggest that there is no generalized defect of peripheral blood lymphocyte or neutrophil function in the Hermansky-Pudlak syndrome. We propose that future studies should examine the possibility that associated disorders arise from a defect within the monocyte-macrophage system, perhaps secondary to ceroid accumulation.
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Freshly separated human NK cells (NKH-1+) inhibited IgE synthesis from IgE myeloma U266/AF-10 as much as 70% whereas they enhanced IgG and IgA synthesis 200 and 500% from the lymphoblastoid cell lines GM-1500 and GM-1056, respectively. The inhibition of IgE synthesis by NK cells was due to a direct cytolytic effect on AF-10. This could be reversed using K562 cells in a cold target competition assay. NK cells also inhibited spontaneous IgE as well as IgG and IgA synthesis from B cells of highly atopic donors. On the other hand the enhancement of Ig secretion by NKH-1+ cells was shown to be mediated by soluble factors released from NK cells. Furthermore when NK cells were preincubated with immune complexes (IgE-IC) constructed of human IgE and mouse IgG1 monoclonal anti-human IgE, inhibition of IgE synthesis was reversed, and in some cases actual enhancement of IgE synthesis was observed, while enhancement of IgG and IgA synthesis was not affected. In contrast to NK cells, T cells depleted of NK cells (T-NK), when activated by IgE-IC, suppressed IgE synthesis in an isotype specific fashion. Thus, NK and T-cell modulation of ongoing Ig synthesis involve distinct mechanisms.