Cardiac disease in guinea pigs.
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Biomedical subjects
Publications and source records attributed to I Cox.
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The complex needs of palliative care patients require an informed, expert, and swift response from out-of-hours general medical services, particularly if hospital admission is to be avoided. Few general practitioners (GPs) reported routinely handing over information on their palliative care patients, particularly to GP co-operatives. District nurses and inner-city GPs were least satisfied with aspects of out-of-hours care. Most responders wanted 24-hour availability of specialist palliative care. This indicates a need to develop and evaluate out-of-hours palliative care procedures and protocols, particularly for GP co-operatives, and to improve inter-agency collaboration.
OBJECTIVES: The aim of the study was investigate the prevalence of abnormal values of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) in patients with chronic renal failure (CRF) and their clinical significance. DESIGN AND METHODS: We investigated the concentrations of cTnT and cTnI in 49 CRF patients without heart disease or diabetes. Cardiac TnT values were measured with a second generation immunoassay and cTnI with two immunoassays with different analytical sensitivity. All CRF patients underwent regular clinical follow-up over a 18-month period. RESULTS: No patients with CRF had elevated values of cTnI when measured with one assay and only 2 patients displayed minimally elevated values with the second assay. In contrast, 23 CRF patients (47%) displayed cTnT concentrations elevated above the upper reference limit. The elevated cTnT values observed were below the values detected in acute myocardial infarction and were not associated with adverse cardiac events during follow-up. CONCLUSIONS: Mildly elevated cTnT concentrations are common in patients with CRF and do not appear to be associated with adverse coronary events.
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The relationship was examined between the self-reported cooperativeness of Australian secondary-school students and their involvement in peer abuse at school, both as bullies and as victims. An 18-item Likert-type measure, the Cooperativeness Scale, was developed, and its reliability and concurrent validity were supported by the results of its application to two samples of Australian students (N = 176 and N = 763, respectively) attending different coeducational secondary schools, the first in a predominantly middle-class area and the second in a lower class socioeconomic area. At both schools, girls scored higher in cooperativeness than boys. Students at the second school also anonymously completed multiple measures of the extent of their involvement during the current year in bullying, victimization, or both. As predicted, correlations and multiple regression analyses supported the hypothesis that relatively low levels of cooperativeness were characteristic, not only of both boys and girls who engaged in bullying, but also, to a lesser extent, of those who were frequently victimized by their peers at school.
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OBJECTIVES: To compare the evolution of stenoses responsible for acute coronary events with those not associated with acute coronary syndromes. METHODS AND RESULTS: We prospectively studied angiographic stenosis progression in 190 stable angina patients, with single vessel disease, who were awaiting non-urgent coronary angioplasty. Sixty four patients had a previous history of unstable angina (Group 1) and 126 patients had no history of unstable angina (Group 2). Culprit stenoses were classified as "complex' or "smooth'. At restudy, 8 +/- 4 months after the first angiogram, 12 of 63 culprit stenoses in Group 1 had progressed and seven of 125 in Group 2 (19% vs 6%, P = 0.0044). Thirteen of 68 complex culprit stenoses had progressed, compared with only 6 of 120 smooth culprit stenoses (19% vs 5%, P = 0.003). Coronary events occurred in 12 Group 1 patients and nine Group 2 patients (P = 0.02). CONCLUSIONS: In patients with stable angina, stenoses associated with previous episodes of unstable angina are more likely to progress than stenoses not associated with previous unstable angina. Unstable coronary atherosclerotic plaques, even those that have been clinically stable for more than 3 months, may retain the potential for rapid progression to total occlusion.
OBJECTIVE: The purpose of this study was to show the MR arthrographic imaging features of a normal anatomic variation of the shoulder: the absence of the anterior superior labrum and the presence of a "cordlike" middle glenohumeral ligament,which together are known as the Buford complex. MATERIALS AND METHODS: We retrospectively analyzed the MR arthrographic examinations of 10 patients with arthroscopically proven Buford complexes. RESULTS: MR arthrographic examinations showed an absent anterior superior labrum and an associated cordlike middle glenohumeral ligament in all patients. No contiguous tear of the superior labrum or anterior inferior labrum was evident. Originally, this variation was mistakenly diagnosed as a labral avulsion in two of the 10 patients. Also, a differential diagnosis of a superior labral tear was mistakenly offered for four patients. CONCLUSION: An absent anterior superior labrum and an associated cordlike middle glenohumeral ligament represent the normal variation that is known as the Buford complex rather than an avulsed labrum. This normal variation may be mistaken for a detached labrum.
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Although previous investigators have attempted to calculate the longitudinal spherical aberration inherent in soft and rigid contact lenses both on and off the eye, the use of inappropriate assumptions on which to base their calculations has left the problem unresolved. In this study, the longitudinal spherical aberration of both soft and rigid contact lenses was calculated surface by surface both in air and on the eye using a two-dimensional, exact ray tracing program. The erroneous assumptions made by previous investigators were avoided by using an elliptical model for the anterior corneal surface and assuming that the posterior surfaces of soft lenses aligned exactly with the anterior corneal surface after flexure onto the eye. The results demonstrated that, with a 6-mm pupil, contact lenses induce significant levels of spherical aberration in the ocular system for soft lenses of back vertex power greater than +3.00 D or -6.00 D and for rigid lenses of powers more positive than -3.00 D. It is suggested that visual disturbance due to induced spherical aberration has not been a major clinical problem in the past because these conditions fall outside those experienced by a large proportion of the contact lens-wearing public.
Some investigators have suggested that the poor quality of vision which some spherical, single vision, soft lens-wearing patients report may be a result of spherical aberration induced in the ocular system when a soft lens is placed on the eye. In this study, the longitudinal spherical aberration of spherical soft lenses, both on and off the eye, was calculated using an aspheric corneal model and two-dimensional ray tracing program. Specifically designed front-surface aspheric, soft lenses were produced which demonstrated levels of in-air power variation similar to that calculated for similar-parameter spherically surface lenses. The effect of these lenses on the visual performance of nine subjects was assessed by measuring changes in contrast sensitivity and high contrast visual acuity through 3- and 6-mm artificial pupils. Significant losses of contrast sensitivity were recorded for the spherically aberrated lenses with the 6-mm pupil but not with the 3-mm pupil. High contrast acuity was not affected by any of the aberrated lenses with either the 3- or 6-mm pupils. Theoretical calculations and the contrast sensitivity results indicate that negatively powered lenses produce significantly less spherical aberration in situ than positively powered lenses. Because the majority of the prepresbyopic soft lens-wearing population have low to moderate amounts of myopia, it would appear that soft lens-induced spherical aberration is unlikely to be responsible for the reduction in visual performance which some patients report when corrected with single vision soft lenses.
The maternal inheritance in Leber optic atrophy suggests that it may be caused by a cytoplasmic or mitochondrial defect. However, the strong male bias and the strict tissue specificity can not be readily explained by a single mitochondrial gene defect alone. Wallace suggested a hypothesis that the disease could be the result of an interaction between an X-linked gene and a mitochondrial DNA defect. Linkage relationships between Leber optic atrophy and 15 X-chromosome markers were analyzed in three large Tasmanian families. The results of two-point linkage analysis showed no close linkage between Leber optic atrophy and any of the 15 markers. The results of multipoint linkage analysis suggested the exclusion of the assumed X-linked gene from almost the whole X chromosome in these families.
In this study, 23 subjects wore a rigid extended wear (EW) lens overnight with a light pressure patch covering the eye while 19 subjects wore the same type of lens without patching. Corneal thickness measurements taken immediately upon awakening showed no significant difference in corneal swelling between the two groups. This result indicates that light pressure patching does not significantly affect the overnight corneal swelling found with rigid EW lenses, and it suggests that lagophthalmos during contact lens wear does not contribute significantly to the oxygen reaching the cornea during the closed-eye phase of overnight swelling studies.
Several oncogenes have been reported to be expressed in normal and malignant hematopoietic cells. Since these studies have almost exclusively been done by Northern and dot blot hybridization techniques using mixed populations of cells, any conclusions concerning quantitative changes in gene expression are difficult to document. We have developed a rapid and sensitive RNA-in situ hybridization technique permitting detection of as few as five copies of mRNA per cell. Using this technique we have studied the expression of two genes, c-myc and c-sis, in acute leukemia patients as well as hematologically normal individuals. We have found that expression levels of myc and often sis are higher (greater than 5-fold) in hematopoietic cells obtained from leukemia patients than in normal hematopoietic cells. In regenerating marrow, there is a dramatic increase in the frequency of cells expressing myc at the level of five to 10 copies without the presence of any cells expressing myc at the high levels found in acute leukemia. This is completely different from leukemic remission marrow in which we find a subpopulation of cells which express myc at very high levels. At this time, the leukemic origin of this abnormal cell population is likely because of the close correlation we find between gene overexpression and leukemic phenotype as identified by double-labeling experiments. It appears that gene overexpression may be a more sensitive or an earlier marker for leukemic cells and that such an assay could be used in the detection of residual disease.
Choriocarcinoma of the uterus developed in an Rh0(D)-negative woman six weeks after delivery of a normal Rh0(D)-positive child. Although the patient's medical history did not show any previous sensitization, a strong anti-Rh0(D) antibody was detected during evaluation preceding surgical removal of the tumor. The tumor was considered the most probable cause of the Rh0(D) sensitization, since large Rh0(D)-positive areas of tumor were demonstrated by the immunoperoxidase method. This finding indicates that the Rh0(D) antigen is not restricted to erythrocytes, as commonly assumed, but can also be expressed on other tissue, such as tumor tissue.
In order best to study the karyotypic abnormalities of nine patients with chronic lymphocytic leukemia of B cell origin, we used a combination of T and/or B cell mitogens so as to achieve an optimal proliferative response. As assessed by DNA synthesis, and subsequent cytogenetic study, pokeweed mitogen (PWM) and protein A Sepharose (PROT A) appeared to hold promise as potent stimulators of neoplastic B lymphocytes. Lipopolysaccharide from E. coli (LPS) proved to be an ineffective mitogen. Phytohemagglutinin (PHA), while producing the highest stimulation indices by DNA assay, appeared to induce predominantly diploid metaphases. Pseudodiploid clonal abnormalities were noted in three out of nine patients, while another four patients showed random structural abnormalities, including translocations, which were indicative of damage. Presence of the A33 antigen, as determined by HLA typing, was noted in five out of nine patients. The increased frequency of this antigen in patients with chronic B cell leukemia is discussed.
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