Cardiac awareness in infarct patients and normals.
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Biomedical subjects
Publications and source records attributed to K R Jones.
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The influence of diltiazem on chronic cerebral vasospasm was studied following subarachnoid hemorrhage (SAH) in a primate model. The model mimics the human experience including the production of neurological deficits. Six monkeys were pretreated with diltiazem (25 mg/kg twice daily) for 2 days prior to surgical production of an SAH and for 5 days after the hemorrhage. This group was compared with six untreated monkeys that also sustained an SAH. The mean diameter of cerebral arteries measured at six angiographic sites was 60.6% of the pre-SAH diameter for the untreated group and 99.7% for the diltiazem-treated group. These values are significantly different (p less than 0.0005). There was no neurological deficit in the pretreated animals. The mean diameter of the "most constricted vessel" in each experiment was 22% of the prehemorrhage diameter for the untreated and 84% for the treated group (p less than 0.0005). Arterial pressure was unaffected by the dosage regimen. These experiments with this primate model of chronic cerebral vasospasm demonstrate that vascular narrowing and neurological deficit can be markedly attenuated by diltiazem pretreatment.
Teaching hospitals have higher charges than nonteaching hospitals, and teaching patients within a single institution incur higher charges than do private patients. Teaching hospitals claim that these higher charges are due to caring for patients with more complex illnesses. Critics claim that the increased charges are primarily related to the hospitals' medical education function. Hospital charges and stay were compared across three physician groups: private patients with a community attending physician, teaching patients with a community attending physician, and teaching patients with a faculty attending physician. Severity of illness differences were controlled for by selecting patients from four Diagnosis Related Groups; refining these groups by surgical codes and age; identifying prehospital and inhospital severity of illness control variables; and omitting death and transfer cases in a second analysis. Least squares regression with logarithmic transformations of the dependent variables revealed that placement of patients on the teaching service with a faculty attending physician led to significantly higher charges as compared with private, nonteaching patients. The patients on the teaching service with a community attending physician did not incur significantly higher charges. It was also revealed that many severity of illness variables predicted a significant amount of variation in hospital charges, even after controlling for diagnostic group and teaching status of the patient.
In the study reported here, the author compared the hospital charges of three groups of patients in one combined university/community hospital: private patients with a community attending physician; teaching patients with a community attending physician; and teaching patients with a faculty attending physician. Control of case mix differences was accomplished by selecting four surgical diagnosis related groups, modifying these groups through use of the International Classification of Diseases procedure codes, and using patient demographic, health status, and severity of illness control variables. The results of the study indicated that teaching patients with a faculty attending physician had significantly higher hospital charges, while teaching patients with a community attending physician had similar charges as compared with the private, nonteaching patients. The higher charges were attributable to increase ordering of diagnostic tests and differential use of supplies and equipment. The level of resident supervision by attending physicians appeared to be influential in determining total charges incurred by the teaching patients.
A DNA sequence specifying tetracycline resistance (Tcr) has been previously cloned from a clinical isolate of Streptococcus mutans designated U202 (J. A. Tobian and F. L. Macrina, J. Bacteriol. 152:215-222, 1982). We used this sequence as a molecular probe in studying the dissemination of Tcr among oral streptococcal species isolated from patients treated with tetracycline. Eleven strains (including S. sanguis I, S. sanguis II, S. mitis, and S. salivarius) from seven patients were examined by Southern blot analysis. Seven strains showed strong hybridization to the Tcr probe, two showed weak hybridization, and two did not display detectable hybridization. Based on previous characterization of the cloned sequence, our data suggest the dissemination of the tetM class of resistance determinants among these oral streptococci. One of the clinical S. sanguis I isolates studied was able to transfer its Tcr phenotype to other oral streptococci and to enteric streptococci in the absence of plasmid DNA. This transfer appeared to be conjugation-like on the basis of its insensitivity to DNase and its dependence on intimate cell-to-cell contact. Using the cloned Tcr sequence, we were able to study the progeny of the matings. Our data suggest that this resistance transfer element occupies a chromosomal location in streptococcal cells and that it strongly resembles the conjugative transposon Tn916 in its behavior.
Rearing cats with esotropia is known to cause a number of deficits in visual behavior tested through the deviated eye. These include a loss of orienting response to stimuli presented in the nasal visual field of the deviated eye, a reduction in visual acuity, and a general reduction in contrast sensitivity at all spatial frequencies. To assess the involvement of the lateral geniculate nucleus (LGN) in these deficits, we measured the following: 1) the visual responsiveness of lamina A1 cells with peripheral (more than 10 degrees from area centralis) receptive fields in three esotropic and three normal cats and 2) the spatial resolution and contrast sensitivity of lamina A X-cells with central (within 5 degrees of the area centralis) receptive fields in six esotropic and six normal cats. For comparison, we also measured LGN X-cell spatial resolutions in four exotropic cats and in two cats raised with an esotropia in one eye and the lids of the other eye sutured shut (MD-estropes). Recordings from the lateral portion of lamina A1 in esotropic cats yielded similar numbers of visually responsive cells with far nasal receptive fields as were seen in normal animals. Peak and mean response rates to a flashing spot also were normal. In addition, no differences were found between esotropes and normals in the percentages of X- and Y-cells encountered. These results suggest that the loss of orienting response to stimuli presented in the nasal field (12, 20) is not due to a loss of neural responses in the LGN of esotropic cats. In addition, they suggest that decreases in cell size in lamina A1 of esotropic cats (13, 36; R. E. Kalil, unpublished observations) are not accompanied by marked functional abnormalities of the cells and that cortical abnormalities ipsilateral to the deviated eye (22) are likely to have their origin within striate cortex itself. Recordings from lamina A cells with receptive fields near area centralis revealed that the average X-cell spatial resolution in esotropes (2.1 cycles/deg) was significantly lower than that in normal cats (3.1 cycles/deg). This reduction was seen in all esotropic cats tested and was due both to an increase in the proportion of X-cells with very low spatial resolution and to a loss of X-cells responding to high spatial frequencies (greater than 3.25 cycles/deg). The average spatial resolution of X-cells driven by the deviated eye in MD-esotropes fell midway between those of esotropes and normals. In exotropes, mean X-cell spatial resolution was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
The critical period of susceptibility to effects of monocular deprivation was compared in striate cortex and the lateral suprasylvian (LS) visual area of cortex. Twenty-three cats received monocular lid suture for a period of 4 weeks beginning at 4, 12, 18, 26, or 35 weeks of age or as adults. Immediately following the deprivation, single cell recordings were carried out in both cortical areas of each cat. Recordings also were made from five normally reared control cats. For both striate and LS cortex, early monocular deprivation had marked effects on neuronal ocular dominance, including an increased percentage of cells dominated by the nondeprived eye, a decreased percentage of cells dominated by the deprived eye, and a decreased percentage of binocularly driven cells. In both cortical areas, these effects were maximal in animals deprived at 4 weeks of age. Both areas then showed similar monotonic declines in effects of the deprivation following onsets from 4 to 18 weeks of age. However, in older animals there were clear differences in the effects of monocular deprivation on LS and striate cortex. In LS cortex, the monotonic decline in effects continued until 26 weeks of age, and no significant abnormalities were present in animals deprived at 26 weeks of age or older. In striate cortex, however, the effects of monocular deprivation remained relatively constant following onsets from 18 to 35 weeks of age, and significant abnormalities in all measures of ocular dominance were present when deprivation was begun as late as 35 weeks of age. Within-animal comparisons indicated that the greater effects of monocular deprivation on striate cortex than on LS cortex were present in every cat deprived at 26 or 35 weeks of age. Neither cortical area showed significant abnormalities following monocular deprivation in adult cats. These results indicate that the critical period for effects of the same regime of monocular deprivation is over sooner in LS cortex (between 18 and 26 weeks of age) than in striate cortex (after 35 weeks of age). This observation has important implications for an understanding of the sites and mechanisms of effects of visual deprivation and the mechanisms that control critical periods of development.
Mycoplasma gallisepticum was isolated from 2 wild-type turkeys (Meleagris gallopavo) and 1 domestic turkey living in close contact on a farm in Tehama County, California. Sinusitis was detected in 2 of 14 wild-type turkeys and in 1 of 12 feral broad-breasted bronze turkeys, but in none of several chickens on the premises. The entire mixed flock was captured, sinus aspirates were collected from affected birds, and blood samples were obtained from all birds for serologic testing. Blood samples also were obtained from 10 domestic turkeys on adjacent premises from which breeding stock had been borrowed. The M gallisepticum isolated from sinus aspirates was typed and inoculated into susceptible chickens, resulting in airsacculitis. California wild turkeys with and without histories of exposure to domestic fowl and wild turkeys shipped into California from Texas for release were tested for antibodies to M gallisepticum, using the plate agglutination test. Evidence of M gallisepticum infection was not found in wild turkeys at any location other than the original premises.
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A novel plasmid vector that is able to replicate both in Escherichia coli and in Streptococcus sanguis is described. This 9.2-kb plasmid, designated pVA856, carries Cmr, Tcr, and Emr determinants that are expressed in E. coli. Only the Emr determinant is expressed in S. sanguis. Both the Cmr and the Tcr of pVA856 may be insertionally inactivated. This plasmid affords several different cleavage-ligation strategies for cloning in E. coli followed by subsequent introduction of chimeras into S. sanguis. In addition, we have modified a previously described E. coli-S. sanguis shuttle plasmid [pVA838; Macrina et al., Gene 19 (1982) 345-353], so that it is unable to replicate in S. sanguis. The utility of such a plasmid for cloning and selecting sequences enabling autonomous replication in S. sanguis is demonstrated.
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A plasmid that is able to replicate in both Escherichia coli and Streptococcus sanguis has been constructed by the in vitro joining of the pACYC184 (Cmr Tcr) and pVA749 (Emr) replicons. This plasmid, designated pVA838, is 9.2 kb in size and expresses Emr in both E. coli and S. sanguis. Its Cmr marker is expressed only in E. coli and may be inactivated by addition of DNA inserts at its internal EcoRI or PvuII sites. The pVA838 molecule also contains unique SalI, SphI, BamHI, NruI and XbaI cleavage sites suitable for molecular cloning. pVA838 may be amplified in E. coli but not in S. sanguis. We have used the pVA838 plasmid as a shuttle vector to clone streptococcal plasmid fragments in E. coli. Such chimeras isolated from E. coli were readily introduced into S. sanguis by transformation.
The use of computed tomographic (CT) attenuation measurements to characterise lung pathology is hindered by the wide variations occurring with respiration. A simple strain-gauge has been used as a respiratory monitor with feedback to the patient giving a visual indication of chest expansion during CT. Significant improvement was achieved in reproducibility of mean attenuation values of nominally identical lung sections when the gauge was used as compared with control sections. Respiratory feedback monitoring has wide potential application in thoracic and upper abdominal CT.
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