Determinants of health-service use by low-income people.

Poverty influences health status, life expectancy, health behaviours, and use of health services. This study examined factors influencing the use of health-related services by people living in poverty. In the first phase, 199 impoverished users of health-related services in 2 large Canadian cities were interviewed by their peers. In the second phase, group interviews with people living in poverty (n = 52) were conducted. Data were analyzed using thematic content analysis. Diverse health-related services were used to meet basic and health needs, to maintain human contact, and to cope with life's challenges. Use of services depended on proximity, affordability, convenience, information, and providers' attitudes and behaviours. Use was impeded by inequities based on income status. To promote the health of people living in poverty, nurses and other health professionals can enhance the accessibility and quality of services, improve their interactions with people living in poverty, provide information about available programs, offer coordinated community-based services, collaborate with other sectors, and advocate for more equitable services and policies.     

A role for lasers in the treatment of pigmented skin grafts

The development of aberrant pigmentation represents an unwelcome complication to an otherwise successful split skin graft resulting in a loss of colour match and, so it follows, of cosmesis. We present two cases where lasers have been successful in the treatment of this problem.     

Asthma and hyperthyroidism. A report of 4 cases

For many years it has been known that thyrotoxicosis can worsen asthma, increasing both the frequency and severity of asthma attacks and increasing requirements for medication. Clinical recognition of this association may be difficult. Thyrotoxic asthmatics frequently experience side-effects from medications, particularly beta-receptor agonists and theophyllines. Four case reports of asthmatics in whom thyrotoxicosis was diagnosed are presented. All 4 patients improved on returning to euthyroid status. The mechanism responsible for the harmful interaction is not known.     

Experimental autoimmune encephalomyelitis (EAE) in CCR2(-/-) mice: susceptibility in multiple strains

Chemokines are low molecular weight cytokines which act as chemoattractants for infiltrating cells bearing appropriate receptors (CCR) to sites of inflammation. It has been proposed that CCR2 on monocytes is responsible for their recruitment into the central nervous system (CNS) in experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis, and two previous reports have described resistance of CCR2(-/-) mice to EAE. The present study examined three different mouse strains with CCR2 deletions for susceptibility to EAE. Animals were studied up to 4 months post-sensitization and were examined by neuropathology, RNase protection assay, in situ hybridization, and in vitro assays. All three strains were found to be susceptible to EAE: C57BL/6 x J129 and Balb c strains, 100%; and C57BL/6, 67%. Unusual in CNS lesions of CCR2(-/-) mice was an overabundance of neutrophils versus monocytes in wild-type animals. An attempt of the immune system to develop compensatory mechanisms for the lack of CCR2 was evidenced by a corresponding increase in mRNA for other chemokines and CCR. Inasmuch as neutrophils replaced monocytes and led to demyelination, our findings support the concept that promiscuity of chemokines and CCR was able to surmount the deletion of CCR2, still resulting in full expression of this autoimmune disease.     

Glial bridges and Schwann cell migration during chronic demyelination in the C.N.S.

Summary The formation of fibrotic bridges from subpial astrocytes into the subarachnoid space of the spinal cord and the migration of Schwann cells to the central nervous system (C.N.S.) is appraised in chronically demyelinated C.N.S. lesions. Spinal cord tissue was studied from inbred, Strain 13 guinea pigs with chronic experimental allergic encephalomyelitis (EAE). It has been found that uncommitted Schwann cells are present around remyelinated fibres in nerve root entry zones, between meningeal cells at a distance from the roots and along blood vessels within the spinal cord parenchyma. It is speculated that these cells migrate via the above route to the C.N.S. In the present model, this invasion might be aided by glial fibrosis, a process which leads to surface irregularities in the spinal cord, an extensive extracellular space and possible breaches in the glia limitans through which Schwann cells might penetrate.     

Experimental autoimmune encephalomyelitis in mice lacking glial fibrillary acidic protein is characterized by a more severe clinical course and an infiltrative central nervous system lesion.

Insights into the role of the astrocyte intermediate filament protein, glial fibrillary acidic protein (GFAP), have only recently emerged with reports on subtle abnormalities in GFAP-deficient mice, including the documentation of defective long-term maintenance of central nervous system myelination. Here, we extend these observations by examining the astroglial response in GFAP-/- mice with autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. Clinically, the monophasic disease was more severe in GFAP-/- mice than in wild-type littermates despite increased remyelination in the former. More in keeping with the clinical course was the observation of an infiltrative EAE lesion in GFAP-/- mice. GFAP-/- astrocytes had a reduced cytoarchitectural stability as evidenced by less abundant and irregularly spaced hemidesmosomes. The blunt GFAP-/- astrocyte processes possessed intermediate filaments consisting mainly of vimentin, though to a lesser degree than in the wild-type. In contrast, in wild-type littermates, GFAP was most abundant and nestin occurred at lower levels. Taken together, the present study introduces the novel concepts that GFAP plays an important role in the control of clinical disease associated with formation of a clearly defined edge to the EAE lesion and that GFAP is operative in the regulation of the intermediate filament components in reactive fibrillary astrogliosis.     

Evoked potential models of psychopathy: a critical evaluation

Raine (1989) reviewed all evoked potential studies carried out to date and developed an information-processing model of psychopathy from the findings of these studies. Jutai (1989) and Howard (1989) have outlined conceptual and empirical criticism of this model and a reply is made to these comments. Some are found to be invalid, while acceptance of others was not found to necessitate a rejection of the model. However, caveats made in the original paper are reiterated here. The cortical immaturity model outlined by Jutai (1989) as a counter-explanation to that proposed by Raine (1989) is evaluated, and criticisms of this alternative are outlined. It is argued that further progress to a more complete understanding of of psychopathy will be achieved by empirically testing these and other models.     

Tonic heart rate level, social class and antisocial behaviour in adolescents

On the basis of previous empirical research it was hypothesised that (a) antisocial behaviour in adolescence would be characterised by lower tonic heart rate levels and (b) any such relationship would be particularly borne out in the higher social classes where the 'social push' towards antisociality may be relatively weaker. These predictions were tested by relating tonic heart rate levels in a sample of 15 year old male schoolchildren to self-report and teacher ratings of antisocial behaviour/undersocialization. An 'antisocial' group was found to have significantly lower heart rate levels than a 'prosocial' group. Several analyses on high and low class groups resulted in a significant low heart rate/antisociality relationship in the high classes only. It was speculated that the heart rate/antisociality relationship may be mediated by somatotype, or alternatively that low levels in high class antisocials may reflect a vagal passive adaptation to mildly aversive events.     

Neuroanatomical Correlates of Skin Conductance Orienting in Normal Humans: A Magnetic Resonance Imaging Study

Although little is known about the neuroanatomical basis of skin conductance orienting in intact normal humans, the limited literature on animals and humans with neurological and clinical disorders implicate prefrontal, temporal/amygdala, and pons brain areas in mediating skin conductance orienting. This study relates area of these structures using magnetic resonance imaging techniques to skin conductance orienting responses in 17 normal humans in order to test hypotheses that larger area of these excitatory structures will be associated with more orienting responses. Left and right hand skin conductance orienting was significantly associated with left and right prefrontal area (r = .44-.60), area of the pons (r = .43-.54), and left but not right temporal/amygdala area (r = .47-.53). No relationships were observed with areas thought to be unrelated to skin conductance activity (cerebellum, nonfrontal cortical area), medial prefrontal cortex, or the third ventricle. This appears to be the first study relating brain structure to skin conductance orienting in intact normal humans. Although preliminary at the present time, these results implicate prefrontal, pons, and temporal/amygdala areas in the mediation of skin conductance orienting in normal humans.