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T K Marshall

Publications and source records attributed to T K Marshall.

8 recordsLinked to original sources
PubMed1990

Drosophila RNA polymerase II elongation factor DmS-II has homology to mouse S-II and sequence similarity to yeast PPR2.

DmSII is a Drosophila RNA polymerase II elongation factor which suppresses pausing by RNA polymerase II at specific sites on double stranded templates. Using antibodies produced against the purified protein, a Drosophila cDNA expression library was screened and a cDNA was isolated which encoded a portion of DmSII. When this cDNA was used to probe Kc cell mRNA the predominant species was found to be 1.4 kb in length. The original cDNA was used to screen a Drosophila Kc cell cDNA library resulting in the isolation of a 1.4 kb cDNA which was then sequenced. The deduced protein sequence for DmSII exhibited high similarity to mouse SII protein sequence. In addition, significant sequence similarity was found with the protein encoded by the yeast gene PPR2, which is involved in regulation of URA4 gene expression. The comparison of amino acid sequences suggests that DmSII is comprised of two domains homologous to mouse SII separated by a flexible, serine rich region of low homology. The shorter yeast protein has sequence similarity only to the carboxy terminal domain.

Amino Acid Sequence↗
PubMed1978

De subitaneis mortibus. XXIX. Randomly distributed focal myocardial lesions causing destruction in the His bundle or a narrow-origin left bundle branch.

Most focally destructive lesions of the heart (e.g., myocarditis) have an essentially random distribution. Any mechanical significance of such diseases depends primarily on there being a very large number of foci. However, single even very small lesions can have profound electrophysiological significance if appropriately located within the cardiac conduction system. Two cases of sudden unexpected death are here reported which had destructive lesions involving the His bundle and a narrow-origin left bundle branch. Not much is known of the electrical or mechanical effects of acute left branch block which is due to complete anatomical transection of that structure in the human heart, and some possible consequences (including sudden unexpected death) are considered. Myocarditis or any other focally destructive disease in the heart may be of little functional importance if it is not widespread, unless some of the lesions happen to damage any of several small but crucially important sites in the cardiac conduction system. Studies to determine the presence or absence of this precise type of damage should be done especially in cases of sudden unexpected death.

Adolescent↗
PubMed1976

De subitaneis mortibus. XVII. Multifocal stenoses due to fibromuscular dysplasia of the sinus node artery.

The sinus node artery was focally narrowed by fibromuscular dysplasia in two examples of sudden unexpected death reported here. Although both cases had additional histological abnormalities in the conduction system of the heart, the more striking feature was the focal fibromuscular dysplasia. These findings are discussed in relationship to a large number of similar examples of focal fibromuscular dysplastic narrowing of the sinus node artery observed in other victims of sudden unexpected death, considering some possible mechanisms for lethal electrical instability of the heart and also the possible pathogenesis of such fibromuscular dysplasia.

Arteries↗
PubMed1976

XVIII. Persistent fetal dispersion of the atrioventricular node and His bundle within the central fibrous body.

In the hearts of two victims of sudden unexpected death (one age 20 years and the other 11 years) there was abnormally delayed persistence of the pattern of fetal dispersion of the A-V (atrioventricular) node and His bundle within the central fibrous body. This pattern is characterized by a splayed or excessively fragmented histological appearance of these structures viewed in cross-section. Some of the fronds of A-V nodal tissue formed loops connecting one portion of the node to another. Other fragments of nodal tissue appeared isolated within the central fibrous body, occasionally connecting directly to the crest of the interventricular septum. A number of the A-V nodal fragments were undergoing resorptive degeneration. Directly adjacent to the A-V node of the 11-year-old subject there was an island of cartilage within the central fibrous body. Since these anatomically separated fragments of A-V nodal tissue were so numerous and varied widely in size and thickness, in length, in histological organization, and in their apparent state of preservation probably extant during life, it is suggested that they form potential routes for abnormal conduction or impulse formation within the A-V junctional region and that some of these electrophysiological disturbances might be quickly lethal.

Adult↗
PubMed1976

De subitaneis mortibus. XX. Cardiac electrical instability in the presence of a left superior vena cava.

Abnormalities of cardiac rhythm have been reported by others in patients with a persistent left superior vena cava. We present the histological findings from postmortem examination of the cardiac conduction system of two such patients. The first patient was a schoolboy who died suddenly and unexpectedly. His sinus node was abnormally small, his A-V node contained numerous venous lacunae and was stretched out beneath the enlarged coronary sinus, both A-V node and His bundle were dispersed in the central fibrous body in a fetal pattern, and isolated fragments of A-V nodal tissue were connected to the myocardium at the crest of the interventricular septum. The second patient complained of palpitations many months prior to surgical correction of an interventricular septal defect; his postoperative course included multiple arrhythmias and he died suddenly on the 16th postoperative day. Although his sinus node was histologically normal, the nutrient artery contained a polypoid fibromuscular mass virtually occluding its lumen; his A-V node and His bundle were also dispersed in the central fibrous body in the fetal pattern, and the A-V node contained numerous venous lacunae as well as being histologically disorganized in its cytological pattern. These anatomical findings may indicate a basis for various forms of cardiac electrical instability, and deserve consideration in the future evaluation of any patient found to have a persistent left superior vene cava, but particularly if there is clinical evidence suggesting an arrhythmia or conduction disturbance.

Adolescent↗
PubMed1975

De subitaneis mortibus. XII. Asymmetrical hypertrophy of the heart.

Subjects with asymmetrical hypertrophy of the heart are prone to sudden death. Neither the pathogenesis of the eccentric hypertrophy nor the mechanism of sudden death is fully understood. In this report we describe certain postmortem findings in the hearts of 22 subjects who died suddenly, silently and unexpectedly, and in whom the only significant abnormality at autopsy was asymmetrical hypertrophy of the heart. Deep clefts were present in the septum in seven hearts, the small coronary arteries were abnormally narrowed in ten, the sinus node was sclerosed by fibrosis in 12, there was variable narrowing of the atrioventricular (A-V) node artery in many and the His bundle was too thin in three. There were multiple cysts or channels in the central fibrous body and of the adjacent A-V node and His bundle in four hearts. Most of the hearts displayed a fetal dispersion of the A-V node and His bundle throughout the central fibrous body, but this was particularly conspicuous in 13 hearts. These abnormalities in all parts of the conduction system suggest a variety of possible mechanisms by which the heart could become electrically unstable but do not indicate that one single mechanism is at fault in all. They offer some explanation for the reported high incidence of atrial fibrillation in such patients, and why they fare so badly with this arrhythmia. While the pathogenesis of asymmetrical hypertrophy may in some part be attributable to narrowed small coronary arteries or to an abnormal sequence or speed of septal and ventricular activation or to mechanical deficiency caused by deep septal clefts, none of these features was universally present in our series. Both asymmetrical hypertrophy of the heart and the sudden death which so frequently accompanies it probably develop by a variety of pathogenetic mechanisms.

Adolescent↗