Urine analysis in equine grass sickness.
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Biomedical subjects
Publications and source records attributed to M Kerr.
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Fourteen cases of meningococcal disease (MD) occurred in August September 1996 in western Sydney, Australia. Seven of the 10 young adults affected had a direct or indirect link with a local nightclub. Ten of 11 systemic meningococcal isolates had the phenotype C:2a:P1.5 and showed close genetic relationship by pulsed-field gel electrophoresis (PFGE). Organisms of this phenotype have not previously caused outbreaks in Australia, but have been associated with outbreaks and hyperendemic serogroup C MD in Europe, Canada, and the United States. This is the largest cluster of serogroup C MD reported in urban Australia, and the first involving a nightclub. The strain differentiation results were available rapidly enough to augment epidemiological investigations on a daily basis. Public health staff could thus establish links between cases quickly, follow the spread of new cases in the community, give accurate information to health officials and the press, and utilize existing knowledge about the characteristics of this phenotype to predict likely developments during the outbreak and afterwards. The strain differentiation data was also very helpful when the role of vaccination was considered, and existing guidelines on the management of outbreaks of MD could be used effectively for the first time in western Sydney.
BACKGROUND: Most individuals with current epilepsy are solely under the care of the primary care team for follow-up care. Government working party recommendations, expert epilepsy panels and patients have also stressed the central role of the GP in follow-up care. Problems in the provision of care in the community have, however, repeatedly been highlighted. The views of GPs about service provision for people with epilepsy may be an important barrier to providing care, but have not yet been studied in a systematic manner. OBJECTIVES: We aimed to ascertain the views of GPs on service provision for people with epilepsy in primary care and on specific initiatives to improve care. METHOD: A specially designed postal questionnaire was sent to all 262 GPs on the list of West Glamorgan FHSA. It ascertained what GPs felt their role should be in providing care to people with epilepsy, identified their views on the importance of particular problems in providing this care, as well as obtaining their opinions on possible future initiatives to improve epilepsy care in the community. RESULTS: The overall response rate was 70%. Although a majority of responding GPs (55%) agreed that the care of people with epilepsy should be based in general practice, 23% disagreed. A lack of confidence about knowledge of epilepsy (34% responders), unfamiliarity with new drugs (65% responders) and a lack of time (41% responders) were identified as important perceived barriers to providing epilepsy care. Nearly all responding GPs would welcome guidelines for epilepsy care (93% felt they would be very helpful) and an epilepsy liaison nurse in the community was the most popular option in terms of preferred overall strategy for improving care. CONCLUSIONS: Despite 40 years of official recommendations regarding the central role of the GP in the follow-up care of people with epilepsy, a number of GPs have difficulty in providing this care. Many feel that they lack knowledge or are too time pressured to improve the situation. Nearly all GPs say that they would find guidelines for epilepsy care very helpful and over half would find epilepsy liaison nurses helpful. There is scope for more innovative ideas for epilepsy care in the community.
PURPOSE: To describe the patterns of inpatient and outpatient hospital care for patients with epilepsy in our health district. METHODS: Routine hospital data for the health district of South Glamorgan (population 408,000) underwent record linkage to identify those records relating to the same patients and to flag those records for patients with epilepsy. This data was analyzed to determine inpatient and outpatient activity by specialty and compared with the nonepileptic population. RESULTS: We identified 2.267 patients representing a prevalence of 0.56%. The average age was 46 years in both male and female patients. This group, which constituted 1.5% of the hospital population, was responsible for 2.8% of all admissions but, because of increased length of stay, utilized 7.3% of all bed days. The total cost of care for this group lies between these two extreme values and is dependent on case severity. The patterns of associated diagnoses differed considerably in three arbitrary age groups (0-18, 19-55, >55 years). CONCLUSIONS: This study quantifies for the first time the level of demand that this subpopulation places on the service as a whole, and begins to illustrate that there may be evidence for cost containment by, for example, a reduction in multiple admissions. The demand for inpatient services is greater than we would have predicted.
Tissue morphogenesis, development, and maintenance of function are mediated by signals generated through the composition of the extracellular matrix. The regulation of the composition of matrix is determined by enzymes specific for their degradation, the matrix metalloproteinases. Chronic injections of the beta-adrenergic receptor agonist, isoproterenol, result in a non-neoplastic hypertrophy and hyperplasia of the rat parotid gland. The activity of matrix metalloproteinases, as measured by gelatin zymography and enzymatic digestion of Azocoll substrates by gland lysates, decreased significantly (P < 0.05) following 24 hrs of agonist treatment, and slowly recovered to control values by 6 days of treatment. Daily administration of the broad-spectrum matrix metalloproteinase inhibitor Galardin for 3 days in combination with isoproterenol resulted in enhanced gland hypertrophy compared with that produced by isoproterenol alone. Given alone, Galardin also caused hypertrophy. The relative abundance of mRNA for the extracellular matrix molecules, collagens I and III and fibronectin, declined rapidly following the initiation of beta-agonist treatment in vivo, while laminin B1 and B2 mRNA levels increased initially before declining below control levels. These changes in patterns of mRNA levels also were observed in the concentrations of glandular protein when Western dot blot analysis of collagens I and III and laminin, respectively, was used. The importance of laminin, in vivo, was demonstrated by coinjection of anti-laminin antibody along with isoproterenol, which resulted in the inhibition of beta-agonist-induced parotid gland hypertrophy and hyperplasia. These data suggest that modulation of the ECM is associated with isoproterenol-induced salivary gland hypertrophy and hyperplasia. It is likely that this modulation of the ECM takes place through transcriptional regulation of some ECM genes and regulation of matrix-degrading enzyme activity.
The purpose of this study was to examine prospectively the impact of family transition on deviant development in a sample of 427 French-Canadian boys participating in a longitudinal study from kindergarten onwards. During the course of the study some boys experienced family transition. We grouped the boys by developmental period and number of marital transitions they experienced: divorced between ages 6 and 11; divorced between ages 12 to 15; remarried between ages 6 and 11; and remarried between ages 12 and 15. From ages 11 to 15 we assessed boys' delinquency and their family processes (parental supervision, punishment, and communication) annually. The results suggest that boys who experienced remarriage between ages 12 and 15 are at greater risk for delinquency. In particular, they showed evidence of comparatively more theft and fighting at earlier ages than their peers from families that had remained intact. At similar points in development, they perceived less expressive parent-child relationships. Finally, these boys also perceived less monitoring by their parents, both overall and at different points in adolescence.
OBJECTIVE: Matrix metalloproteinases (MMP) and their substrates, components of the extracellular matrix, regulate environmental signals for cellular differentiation and tissue function. Changes in the levels of these enzymes may influence cell survival as well as pathology involving ectopic apoptosis. Using the non-obese diabetic (NOD) mouse model for Sjögren's syndrome, we evaluated the synthesis and expression of MMP in the exocrine target tissues of autoimmunity. METHODS: NOD, immunodeficient NOD-scid, and nondiabetic NOD.B10.H2b mice were evaluated for MMP activity in their saliva and exocrine gland lysates by gelatin zymography and reverse transcriptase-polymerase chain reaction (RT-PCR). In addition, changes in protein content of saliva and gland lysates were determined by specific Western blot and by enzymatic activity of amylase and cysteine proteases. Mice continuously treated with the MMP inhibitor GM6001 were evaluated from 7 to 20 weeks of age for the contribution of MMP activity to development of these hallmark biochemical markers of Sjogren's syndrome-like disease of NOD mice. RESULTS: Gelatin zymography of whole saliva and gland lysates indicated the presence of increased proteolytic activity, corresponding to proteins with a molecular mass ranging from 50 to 95 kDa, in the saliva of older (> 20 weeks of age) NOD mice as well as NOD.B10.H2b and NOD-scid mice compared to BALB/c controls. Elevated steady state levels of mRNA transcripts for the gelatinases MMP-2 and MMP-9 were detected in total RNA extracted from parotid and submandibular glands by RT-PCR. Despite prophylactic injection of the broad spectrum MMP inhibitor GM6001 into mice beginning at 7 weeks of age and continuing to 20 weeks, development of the autoimmune exocrinopathy was neither stopped nor retarded. CONCLUSION: These observations suggest that excessive MMP activity is associated with autoimmune Sjögren's syndrome-like disease in NOD mice. However, a possible contribution by increased MMP activity in initiation and progression of this autoimmune disease is yet to be elucidated.
BACKGROUND: In some studies, shyness and anxiety have protected at-risk boys from developing delinquency. In others, shyness and withdrawal have increased risk. We argue that this is because behavioral inhibition, which is the protective factor, has been confounded with social withdrawal and other constructs. Our study addresses 3 major questions: (1) is behavioral inhibition, as distinguished from social withdrawal, a protective factor in the development of delinquency; (2) does the protective effect depend on whether disruptiveness is also present; and (3) does inhibition increase the risk of later depressive symptoms even if it protects against delinquency? METHODS: The subjects were boys from low socioeconomic status areas of Montreal, Quebec. Age 10- to 12-year predictors were peer-rated inhibition, withdrawal, and disruptiveness; age 13- to 15-year outcomes were self-rated depressive symptoms and delinquency. Eight age 10- to 12-year behavioral profiles were compared with 4 age 13- to 15-year outcome profiles. RESULTS: Inhibition seemed to protect disruptive and nondisruptive boys against delinquency. Disruptive boys who were noninhibited were more likely than chance to become delinquent; disruptive boys who were inhibited were not. Inhibition did not increase the risk for depression among disruptive boys. Among nondisruptive boys, only nondisruptive-inhibited boys were significantly less likely than chance to become delinquent. However, withdrawal was not protective. Disruptive-withdrawn boys were at the greatest risk for delinquency or delinquency with depressive symptoms. CONCLUSION: Inhibition and social withdrawal, although behaviorally similar, present different risks for later outcomes and, therefore, should be differentiated conceptually and empirically.
People with epilepsy plus learning disabilities pose a challenge in terms of clinical management and research investigation, and, to date, the measurement of outcomes in this population has been limited. There have been uncertainties concerning both the 'what' and the 'how' of assessment. This paper presents a comprehensive review of available outcome measures across nine domains, i.e. relating to seizures, drugs, cognitive function, behaviour, social functioning, carer functioning, attitudes, motivation and 'quality of life'. This last domain reflects more global measures designed to encompass several assessment strands. The uses and limitations of each scale is discussed and, where data are available, psychometric properties are also presented. The paper concludes with suggestions for the further development of outcome measures in this population.
There are many possible means of determining exposure ranging from self-reports of physical exposure to measures of muscle activations and estimated spinal loads. In epidemiologic studies, issues of validity make instrumented measures preferable, however issues of cost and practicability tend to force investigators to less costly but less valid and less reliable measures of exposure, such as self-report questionnaires. This paper presents a method by which estimates of exposure from self-report questionnaires, expert observers, work sampling, video analysis and electromyograms can be reported in a common metric, Newtons of force on a tissue, and show, as an example of its application, estimation of spinal compression on auto workers. A common metric allows a flexible approach to selection of measurement methods in occupational settings: no matter which instrument is used the results can be combined to provide an overall picture of exposure. This approach to exposure assessment for the low back allows for comparability across studies and settings.
The epilepsies are a group of disorders characterised by recurrent seizures caused by episodes of abnormal neuronal hyperexcitability involving the brain. Up to 60 million people are affected worldwide and genetic factors may contribute to the aetiology in up to 40% of patients. The most common human genetic epilepsies display a complex pattern of inheritance. These are categorised as idiopathic in the absence of detectable structural or metabolic abnormalities. Juvenile myoclonic epilepsy (JME) is a distinctive and common variety of familial idiopathic generalised epilepsy (IGE) with a prevalence of 0.5-1.0 per 1000 and a ratio of sibling risk to population prevalence (lambda(s)) of 42. The molecular genetic basis of these familial idiopathic epilepsies is entirely unknown, but a mutation in the gene CHRNA4, encoding the alpha4 subunit of the neuronal nicotinic acetylcholine receptor (nAChR), was recently identified in a rare Mendelian variety of idiopathic epilepsy. Chromosomal regions harbouring genes for nAChR subunits were therefore tested for linkage to the JME trait in 34 pedigrees. Significant evidence for linkage with heterogeneity was found to polymorphic loci encompassing the region in which the gene encoding the alpha7 subunit of nAChR (CHRNA7) maps on chromosome 15q14 (HLOD = 4.4 at alpha = 0.65; Z(all) = 2.94, P = 0.0005). This major locus contributes to genetic susceptibility to JME in a majority of the families studied.
An intellectual disability attitude questionnaire was used to explore the attitudes of general practitioners (GPs) towards primary health care, organizing health promotion and the role of specialist services for people with intellectual disability. The results of this questionnaire from GPs in Gwent (Wales) and GPs in west Gloucestershire (England) were compared. The GPs in both areas responded similarly and tended to agree that they were responsible for the medical care of people with intellectual disability in the community. They also tended to feel that the move from hospitals to the community of people with intellectual disability would greatly increase their workload. The GPs in both areas were generally against a responsibility on their part for health promotion and health screening initiatives for people with intellectual disability. However, GPs in west Gloucestershire felt more strongly against these issues. Further analysis of the data revealed factors which influenced the response of GPs to the questionnaire, including their position regarding health promotion and screening, and their view of the role of specialist health services. The GPs generally felt that community learning disability teams provided useful support, and there is clearly scope for team members to liaise more closely with GP practices and to provide helpful information to GPs about intellectual disability and the specialist health services available. Professionals seeking to work collaboratively with GPs should be sensitive to their workload pressures and to their attitudes towards health promotion initiatives and health screening.
This study tested 2 competing models of friends' influence on the development of delinquency in disruptive boys. In so doing, we examined whether highly disruptive, moderately disruptive, moderately conforming, and highly conforming boys' delinquency increased or decreased depending on their friends' characteristics. A sample of 868 boys was classified into the 4 groups according to teacher ratings at ages 11 and 12. Each group was then subdivided by mutual friends' peer-rated aggressiveness-disturbance at the same ages: aggressive-disturbing friends, average friends, nonaggressive-nondisturbing friends, and no friends. Subgroups were next compared on self-reported delinquency at age 13 while controlling for average self-reported delinquency and socioeconomic variables at ages 11 and 12. Results indicate that moderately disruptive boys with aggressive-disturbing friends were more delinquent at age 13 than other subgroups of moderately disruptive boys. Highly disruptive and conforming boys, however, were unaffected by their friends' characteristics. We conclude that the results partially support each theoretical model, suggesting that both individual characteristics and deviant peer association might play causal roles.
While antibiotics are broadly used in dental and medical therapy, little attention has been directed towards the potential toxic side effects of antibiotics on tissue regeneration. Here we examined the effect of a quinolone antibiotic, pefloxacin (Rhone Poulenc) on rat parotid gland responses to chronic isoproterenol treatment. Groups of rats received injections of isoproterenol to induce glandular growth, saline (controls), pefloxacin, or isoproterenol and pefloxacin in combination. Parotid gland weight decreased significantly after pefloxacin treatment for 7 days as well as inhibiting glandular enlargement provoked by isoproterenol. The same trend was observed for the rates of DNA synthesis, with the incorporation of [3H]-thymidine in isoproterenol/pefloxacin-treated rats reduced to 49% of isoproterenol treatment alone levels. Saline-treated animals were 42% of the rate of [3H]-thymidine incorporation into DNA observed in isoproterenol treated rats. While isoproterenol treatment increased steady-state mRNA levels for fos, jun, myc, src, c-erbB-2, ras and topo II, inclusion of pefloxacin with the isoproterenol regimen blocked these increases. Pefloxacin treatment by itself did not alter proto-oncogene mRNA levels in the parotid gland. Glandular amylase activity was decreased in the pefloxacin treated group, while the combination of isoproterenol with pefloxacin did not decrease glandular amylase levels to the extent of that observed with beta-agonist treatment alone. In acute experiments, pefloxacin significantly decreased the volume of saliva secreted by the parotid gland. These results suggest that quinolone-based antibiotics disturb the secretory function of the parotid gland and can inhibit cell proliferation and regeneration.
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Human parotid tumors were evaluated for the activation of the phosphotyrosine signaling pathway by Western blot, enzyme activity assay, and reverse transcriptase-polymerase chain reaction. Warthin's tumor and mucoepidermoid carcinomas had the greatest level of tyrosine phosphorylated proteins identified in plasma membrane fractions. These tumors, along with pleomorphic adenocarcinoma, showed high levels of membrane expression of the tyrosine kinase receptor, c-erbB-2, and phosphatidylinositol-3-kinase. Expression of the epidermal growth factor receptor was confined to normal tissue. The level of mRNA for c-erb was elevated only in mucoepidermoid carcinomas. Messenger RNA levels for ras were unchanged from control levels in all tumors, while the level of src mRNA was higher in the tumor samples than the normal parotid tissue. The activities of several signal transduction kinases, including protein kinase A and C were elevated in tumor tissue (7.7- to 18.9- and 0.4- to 3.7-fold higher, respectively), relative to surrounding normal tissue. While the level of glandular amylase was reduced (22%-0% of normal levels) in the tumor tissue, epidermal growth factor (EGF) and transforming growth factor-alpha (TGFalpha) content was dramatically higher in the neoplastic tissue (10- to 170-fold and 4.6- to 6.0-fold, respectively). These results suggest that with the presence of elevated levels of EGF, TGFalpha, and the oncoprotein receptor c-erbB-2 in the membrane of parotid tumors, cell proliferation and activation of the phosphotyrosine signal transduction pathway may involve autocrine stimulation through the expression of high levels of growth factor and receptor in the same tissue.