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Biomedical subjects

R Watts

Publications and source records attributed to R Watts.

At least 55 records · Page 3Linked to original sources

Attitudes of rural general practitioners towards undergraduate medical student attachments.

OBJECTIVE: Increasing exposure of undergraduate medical students to rural practice is a key component of the national effort in Australia to redress the rural workforce shortage. For this exposure to be successful, willing cooperation of current rural general practitioners is essential. To date there has been no formal assessment of rural general practitioners' attitudes to having undergraduate medical students attached to their practice. METHOD: A descriptive survey, using a mailed questionnaire was sent to all 316 general practitioners currently practising in rural areas of South Australia, as identified from the database maintained by the South Australian Rural Practice Training Unit. RESULTS: A 71.5% response rate (n = 225) was achieved, of which 203 were eligible for inclusion. Of these, 176 doctors had medical student attachments in their practice on at least one occasion; 74.4% of whom (n = 131) perceived the attachments to have a positive experience on their continuing medical education experience, and 81.1% (n = 142) described a positive experience on their professional development. However, 52.6% (n = 92) felt the attachments had a negative effect on their income. Almost all the doctors who were included in the survey (94.6%, n = 192) were willing to have students attached to their practice in the future for between one to two weeks. Of these, 169 wanted quality assurance points, 112 wanted financial reimbursement, and 108 wanted 'academic status' with a university. CONCLUSION: The results suggest that rural general practitioners are willing to have students attached to their practice for periods between one to two weeks, providing they receive quality assurance points, and to a lesser extent, financial reimbursement and academic status.

Attitude of Health Personnel↗

The need for acute hospitals to provide counselling following motor vehicle accidents.

This paper examines the need for a systematic way of detecting individuals likely to encounter moderate to severe psychological sequelae after being injured in a motor vehicle accident. It presents the findings of assessments of consecutive adult admissions during a six-month period to the Accident and Emergency Department of Royal Melbourne Hospital, a major acute hospital in Melbourne, within two days of being injured in a motor vehicle accident. Seventy of the 250 subjects surveyed completed the General Health Questionnaire 12 and the Impact of Event Scale questionnaire, with 77 per cent found likely to have had a psychiatric disorder. Seventy-four per cent had at least moderate levels of intrusion or avoidance phenomena. Forty-four per cent had severe levels of one or the other. Prevalence of these psychological sequelae was greater than that found in several recent studies on the effects of motor vehicle accidents. A small number (11-15 per cent) sought or received professional counselling within the first three months. This group did not differ, according to levels of intrusion, avoidance, or scores on the GHQ 12, to subjects who did not seek or receive such assistance. Results identify the necessity of investigating and implementing methods of detecting and treating the many who apparently sustain significant psychological sequelae following injury in a motor vehicle accident.

Accidents, Traffic↗

Molecular cloning of mouse tissue inhibitor of metalloproteinases-3 and its promoter. Specific lack of expression in neoplastic JB6 cells may reflect altered gene methylation.

Mouse tissue inhibitor of metalloproteinases-3 (mTIMP-3), a gene specifically not expressed in neoplastic JB6 cells, have been isolated recently through the use of the mRNA differential display technique (Sun, Y., Hegamyer, G., and Colburn, N. H. (1994) Cancer Res. 54, 1139-1144). We report here the full-length mTIMP-3 cDNA sequence, the promoter sequence and partial characterization, expression and induction of TIMP-3, and the possible molecular basis for the lack of mTIMP-3 expression in neoplastic JB6 cells. There are three transcripts arising from alternative polyadenylation of mouse TIMP-3 gene, having sizes of 4.6, 2.8, and 2.3 kilobase pairs, respectively. All three TIMP-3 transcripts are expressed in preneoplastic but not neoplastic JB6 cells. Computer analysis of cloned TIMP-3 promoter revealed six AP-1 binding sites, two NF-KB sites, a c-Myc site, and two copies of a p53 binding motif separated by eight base pairs with two mismatches at the second motif, along with many other cis elements. TIMP-3 gene expression was inducible by AP-1 and NF-KB activators, 12-O-tetradecanoylphorbol-13-acetate, and tumor necrosis factor-alpha only in preneoplastic cells with an induction peak at 2 h post-treatment, suggesting classification of mTIMP-3 as a member of the immediate early gene family. Southern blot, mutational analysis, and transient transcriptional activation experiments revealed that the lack of expression of mTIMP-3 in neoplastic JB6 cells was due neither to gross deletion nor to promoter mutation of the gene, nor was there a lack of transcription factors required for transcriptional activation. Instead, the lack of TIMP-3 expression in neoplastic JB6 cells may reflect an abnormal methylation of the gene. Both hyper- and hypomethylation of the mTIMP-3 gene are associated with complete down-regulation of gene expression in neoplastic JB6 cell lines. Treatment of neoplastic cells with the methylase inhibitor 5-azacytidine caused reexpression of the mTIMP-3 gene in a tumor cell line that showed hypermethylation but not in another that showed hypomethylation of the gene, suggesting a complex role for methylation in the silencing of gene expression.

Animals↗

Regional differences in cardiovascular risk factor prevalence in Tasmania: are they consistent with the increased cardiovascular mortality?

BACKGROUND: The death rate from cardiovascular disease in Tasmania has been among the highest in Australian States for a number of years. The North-West (NW) and Northern regions of Tasmania account for most of the increased mortality. AIMS: To determine the prevalence of cardiovascular risk factors in the North and NW regions of Tasmania and to ascertain whether any differences are consistent with the regional patterns of mortality for ischaemic heart disease (IHD) within the State. METHODS: The design of the study was almost identical to the previous National Heart Foundation (NHF) Risk Factor Prevalence Survey conducted in 1989. The subjects, aged 20-69 years, were randomly selected from the Electoral Roll with 1146 subjects participating in the North and 1219 in the NW. Subjects answered a detailed questionnaire and then underwent a brief physical examination with venipuncture for blood lipids. Hobart data from the NHF Risk Factor Prevalence Survey in 1989 were used as an estimate of risk factor prevalence in the Southern region. RESULTS: In both males and females, mean systolic blood pressure was significantly higher in the NW than the South which was in turn higher than the North. Mean serum cholesterol levels in males were higher in the NW than the North. Smoking behaviour was similar in males and females in all regions. Males and females in the NW and North were more inactive than those in the South. Similar proportions in all regions were on either 'no specific' or 'fat modified' diets. Body mass index in males and females was higher in the NW and North but waist to hip ratios failed to show a consistent trend. CONCLUSIONS: While the NW has an unfavourable risk factor profile compared with the South, the North does not. The risk factor data are broadly consistent with, but unlikely to be sufficient to explain fully, the regional differences in mortality from IHD.

Adult↗

Recombinant vaccinia viruses expressing hepatitis A virus structural polypeptides: detection of an anti-VP0 response in convalescent-phase sera.

We have generated a number of recombinant vaccinia viruses which expressed the hepatitis A virus (HAV) structural polypeptides VP1, VP2, VP3, and VP4, either alone or in combination. The relevant sequences encoding these polypeptides were amplified from cloned cDNA by PCR and then cloned into the insertion vector pGS62. The presence of the HAV structural polypeptide-encoding sequences in the recombinant viruses was confirmed by Southern blot analysis, whilst their transcription and translation were demonstrated by Northern (RNA) blot analysis and immunodetection, respectively. Immunoprecipitation studies using these constructs have detected the presence of an anti-VP0 response in human convalescent sera following HAV infection. The significance of this finding and the usefulness of these constructs in studying cell-mediated immunity during recovery from HAV infection are discussed.

Antibodies, Viral↗

Posttraumatic stress disorder after a bus accident.

There is insufficient information on the prevalence of posttraumatic stress disorder (PTSD) and other psychological reactions caused by surviving serious road accidents. This paper presents the assessments of 29 people who narrowly escaped death in a coach accident that killed eleven people. Their high vulnerability is clearly established, with 41% having PTSD, and 52% severe intrusion or avoidance phenomena, which included 31% who had both. The occurrence of psychological sequelae was associated with being currently distressed by another event, but not with the survivors' age, gender or acquaintance with people killed in the accident. Seeing bodies or witnessing the death of someone was the predominant cause of distress, both at the time of the accident and in a recurring way. Delayed reactions were evident, with the impact of several factors changing over time.

Accidents, Traffic↗

Fulminant hepatitis associated with hepatitis B virus e antigen-negative infection: importance of host factors.

The precore stop-codon variant of hepatitis B virus (HBV) has been implicated in fulminant hepatitis. The precore/core regions of such variants from two sets of patients with interpartner transmission resulting in fulminant hepatitis in the contact, were sequenced to establish whether further sequence variations in the core region are specifically associated with the fulminant disease. In both sets of patients, there was sequence diversity of the precore/core region from the wild type, leading to numerous amino acid substitutions in the core region. Between the infecting source and the contact, there was only one amino acid change in one set of patients and none in the other. In addition, in the second set of patients, serum samples from four different time points were investigated. Sequence data showed no variation in each patient at the nucleotide level in the core region, even in the case of the source, who was followed for 3 years. In this same pair of subjects, the remainder of the genome was sequenced and was identical at the nucleotide level. Therefore, it appears that, at least in some cases of fulminant hepatitis caused by infection with the precore variant, the nucleotide sequence of the patient with fulminant hepatitis is identical to that observed in the asymptomatic source of infection. These data indicate that the severity and outcome of infection in such cases are unrelated to any additional variation in the entire HBV genome, and that the changed clinical picture is dependent on host factors, possibly the HLA environment.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Identification and characterization of a new human DNA reactive monoclonal antibody and a common idiotype, WRI 176 Id beta.

We describe a human monoclonal antibody designated WRI 176 beta and a common idiotype that it carries. This antibody was derived from the spleen of a patient with SLE. WRI 176 is an IgM kappa monoclonal reacting with ssDNA, dsDNA, poly(dT) and it is likely that mAb WRI 176 beta is a representative of the so-called natural autoantibodies. The common Id designated WRI 176 Id beta is located on the heavy chain of the mAb WRI 176 beta molecule and appears to be located outside the binding site. Sequence analysis of the WRI 176 beta heavy chain showed it to be highly homologous (97.3%) with a germline gene 56PI derived from a human fetus. In a retrospective analysis, although 44% of SLE patients had raised levels of the WRI 176 beta no correlation was found with the activity of the disease. The idiotype was also expressed frequently in a range of autoimmune rheumatic and infectious diseases and in some healthy first-degree relatives of SLE patients.

Amino Acid Sequence↗

Carotid chemoreceptors and respiratory adaptations to dead space loading during incremental exercise.

Dead space (VD) loading has been shown to cause an increase in tidal volume and a decrease in respiratory frequency at moderate to high levels of ventilation (VI) during exercise (J. Appl. Physiol. 70: 55-62, 1991). This study examined the role of carotid chemoreceptors (CC) in the breathing pattern response to added VD during maximal incremental exercise; we used hyperoxia to silence the CC. Nine healthy subjects exercised on a bicycle ergometer on 4 different days while inspiring air with VD (AVD) and without VD [air control (AC)] and while inspiring 100% O2 with VD (O2VD) and without VD (O2C). Equipment resistance for VD and control studies was identical, and the exercise tests were done in a randomized order. At a matched level of VI equivalent to 75% VI at the end of the AC experiments (102 l/min), the breathing pattern in the AVD and O2VD tests was significantly deeper and slower (P < 0.05) than that in the AC and O2C tests. The difference in tidal volume between AVD and AC tests (delta = 0.26 +/- 0.16 liter) was not significantly different from that between O2VD and O2C tests (delta = 0.23 +/- 0.23 liter). The breathing pattern was the same in the AC and O2C tests. It is concluded that the altered breathing pattern with VD loading is not mediated by the CC.

Adaptation, Physiological↗

The immunopathogenesis and immunotherapy of autoimmune disease.

A conference entitled 'The Immunopathogenesis and Immunotherapy of Autoimmune Disease' was held at the Royal College of Physicians on 20 May 1992. Its aim was to consider advances in pathogenesis and their translation into therapeutic targets.

Autoimmune Diseases↗