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Biomedical subjects

R Liddell

Publications and source records attributed to R Liddell.

6 recordsLinked to original sources

Structure and localization of mouse Pmscl1 and Pmscl2 genes.

Sera from some patients with polymyositis-scleoderma overlap syndrome (PM-SCL) recognize two antigenically unrelated proteins, PMSCL1 and PMSCL2. Complete mouse Pmscl1 and Pmscl2 cDNA sequences, chromosomal localizations, exon/intron structure, and promoter region sequences of the mouse Pmscl2 gene are presented. The PMSCL1 gene was found to overlap significantly with cyclin A2 in both human and mouse. As such, it may be deduced that PMSCL1 sequences map to human chromosome 4q27 and the proximal portion of mouse chromosome (Chr) 3 where human and mouse cyclin A2 genes reside. Analysis of human and mouse PMSCL1 cDNA sequences provides evidence that the PMSCL1 protein is 68 amino acids longer than previously thought. A BAC containing mouse Pmscl2 was localized to distal mouse Chr 4 by FISH. This BAC contains the microsatellite D4Mit310. D4Mit310 colocalizes with a number of genes that map to human 1p36. In fact, a STS (G25404) located 54.6 cR from the top of human chromosome 1 was found to contain PMSCL2 sequence upon BLAST search.

5' Untranslated Regions↗

Comparative analysis of smooth muscle isoactin gene expression in normal and neoplastic tissues.

Monoclonal antibodies derived from the actin multigene family are routinely used as an adjunct to morphologic diagnoses of smooth muscle tumors. Northern blot analysis was performed on 60 surgical resections utilizing isoactin-specific cDNAs. A comparison of this analysis to immunohistochemical studies demonstrated that actin-specific monoclonal antibodies represent reliable markers of the smooth muscle lineage. Smooth muscle neoplasms showed a unique pattern of gamma-smooth muscle isoactin gene expression, providing a potentially valuable molecular adjunct to the morphologic diagnosis of uterine smooth muscle tumors.

Actins↗

Intravascular stenting of acute experimental type B dissections.

To evaluate the efficacy of intravascular stenting for acute aortic dissection, 12 dogs underwent surgical creation of an acute type B dissection. Intravascular ultrasound evaluated luminal diameter, distal propagation, and branch involvement. Three animals underwent no further treatment (control). In 9 dogs, balloon-expandable intravascular stents (15-20 mm) were placed proximally to compress the intimal flap. One dog with a small dissection had complete obliteration of the false lumen after initial stent placement. Six dogs with extension below the diaphragm were initially stented proximally to restore flow; 3 were left with a residual distal false lumen, while 3 had additional stents placed to obliterate their entire false lumen. In the final 2 dogs, proximal stenting resulted only in partial compression of the false lumen. Two animals died within 24 hr due to prolonged hemodynamic instability and aortic rupture at the intimal flap, respectively. Six weeks later, radiologic and histologic evaluation was performed on the 10 surviving animals. All stented true lumens were patent without thrombus formation, and stents were covered by neointima. In dogs with stenting of the entire dissection, the aortic wall had healed and no false lumen was present. However, in all dogs with only proximal obliteration, 1/2 with partial compression, and 2/3 controls, a patent false channel was present indicative of a chronic dissection. Thus, we found that intravascular stents can restore true lumen flow and obliterate the false lumen in experimental dissections; however, stenting limited to the proximal dissection does not prevent formation of a chronic residual patent false lumen.

Acute Disease↗

The management of suspected myocardial infarction by Scottish general practitioners with access to community hospital beds.

General practitioners working in 20 community hospitals in Scotland participated in a survey of the management of myocardial infarction. During one year they suspected acute myocardial infarction in 451 patients. Of these patients, 278 (62%) were admitted to a community hospital, 125 (28%) to a district general hospital and 48 (11%) were kept at home. The main reasons given for admission to a community hospital were for monitoring and investigation, while the main reasons for admission to a district hospital rather than a community hospital were the relative youth of the patient and the severity of the illness. Acute myocardial infarction was confirmed in 323 (72%) cases, but in 26 (6%) cases the final diagnosis was other than ischaemic heart disease. Patients with acute myocardial infarction who entered a community hospital did so a median of two hours 25 minutes after the onset of symptoms. Among 18 patients admitted to a community hospital in whom resuscitation was attempted after cardiac arrest four (22%) were subsequently discharged from hospital. The mortality rate from acute myocardial infarction in the community studied was 171/418 (41%), of whom 95 died suddenly before coming under medical care. It is concluded that in rural areas of Scotland an acceptable standard of care for patients with acute myocardial infarction, including the administration of thrombolytic therapy, could be provided rapidly by general practitioners working in community hospitals.

Adult↗

Temporal analysis of a dose-response relationship: leukemia mortality in atomic bomb survivors.

A data analysis that incorporates time dependencies is demonstrated for the dose response of leukemia mortality in the atomic bomb survivors. The time dependencies are initially left unspecified and the data on leukemia mortality--up to the end of 1978--are used to infer them. Several findings based on T65 revised doses (T65DR) are obtained. First, it is shown that the fits to the data of time-dependent L (linear in gamma dose)-Q (quadratic in gamma dose)-L (linear in neutron dose), L-L, and Q-L dose-response models are significantly improved (P less than 0.001) by using the corresponding time-dependent dose-response models. Second, it is shown that the increased risk of leukemia mortality due to gamma irradiation decreases in time while the increased risk due to neutron exposure decreases more slowly, if at all, in time. Consequently, relative biological effectiveness (RBE) of neutrons is shown to increase in time (P = 0.002) and the current definition of RBE as a time-independent quantity is therefore challenged. It is demonstrated with time-dependent models that the L-L model has a poor fit (P = 0.01) to the data for the first 7 years of study, but has an adequate fit for the remaining 21 years. In contrast the Q-L model has an adequate fit for the entire follow-up period (P greater than 0.30).

Adult↗