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Biomedical subjects

G W Moore

Publications and source records attributed to G W Moore.

At least 145 records · Page 8Linked to original sources
PubMed1981

The estimated age of staged human embryos and early fetuses.

The appearance of anatomic features during embryogenesis relative to menstrual history is not well established. The 621 staged human embryos and fetuses in the Carnegie Embryological Collection were examined, and morphologic features were recorded in 494 specimens in good condition, from 382 intrauterine, 49 ectopic, and 55 pregnancies of other or unknown source. There were menstrual data on 276 specimens, and for 10 the date of a single coitus was known. The embryo develops to 1 mm at the twenty-eighth menstrual day, after which its crown-rump length increases by 0.7 mm per day. Coital ages and postovulatory ages estimated from menstrual data correlated significantly (p less than 0.001) with crown-rump length and Carnegie stage, but estimated postovulatory age was highly variable (standard deviation, 10.5 days). Morphologic features appeared within a narrow interval (standard deviation, 0.0 to 1.5 Carnegie stages). Normal human embryogenesis is a stereotyped sequence with little statistical variation, but menstrual data in individual cases may be unreliable in dating this sequence.

Coitus↗
PubMed1981

Development of the outflow tract and closure of the interventricular septum in the normal human heart.

The majority of congenital heart malformations in humans involve defects in the atrioventricular valves, the crest of the interventricular septum, and/or the outflow tract, but the position and timing of these structures during cardiac development is controversial. We examined all 622 staged, serially sectioned normal human embryos and fetuses in the Carnegie Embryological Collection, and obtained a statistical tabulation of the appearance of the endocardial cushion components and surrounding structures for 382 embryos in good condition between stages 9 and 23 inclusive, when the heart normally develops. Accurately scaled drawings of ventral and lateral views of the hearts of seven embryos from stage 13 through 22 were prepared from graphic reconstructions in order to visualize the relationships of the structures under consideration. We found that development of the outflow tract septum follows the apparent functional separation of both the left and right ventricles and the blood streams leaving them. Elevations of the endocardial cushion material are continuous throughout the outflow tract and develop as a consequence of the elliptical configuration imposed on the circular cross section of the outflow tract. The membranous interventricular septum is formed of cushion material in the space bounded by the outflow tract septum, interventricular septum, and the fused AV cushion and right outflow tract cushion. The results of this study are consistent with the assertion that functional separation of the aortic and pulmonary outflow tracts precedes anatomic septation, and that anatomic septation is brought about by mechanical modeling of developing myocardium and endocardial cushion material.

Gestational Age↗
PubMed1981

A proposed mechanism for the early development of the human tracheobronchial tree.

The development of the lung in 25 human embryos and early fetuses up to 140 mm crown-rump length was studied by examination of serial histologic sections, morphometry, and selected reconstructions. The proportion of pulmonary tissue consisting of tracheobronchial tree increases during this period. Bronchial cross-sectional diameter, length of the most distal bronchial branches, and thickness of the distal mesenchyme decline during development. The results are consistent with the concept that the dichotomous branching of the growing tracheobronchial tree occurs because of resistance to forward growth f the bronchial branch by compresses mesenchyme, pleura, or adjacent structures. Division and further growth of the bronchus takes place in areas of lower resistance. This process produces a "filling in" of space available for lung development and brings the epithelial and mesenchymal elements into their definitive relationships.

Bronchi↗
PubMed1981

Postnatal endocardial fibroelastosis of the valve of the foramen ovale.

The valve of the foramen ovale of the heart changes at birth from a prenatal shunting device for the transseptal flow of systemic venous return to a postnatal active barrier to backflow of left atrial blood at higher pressure. To investigate the morphologic response to this functional change in the valve of the foramen ovale, we examined 200 hearts from embryos, fetuses and autopsy patients spanning over a millionfold range of heart weights (0.001 to 1,230 g). The relation of valve thickness to log heart weight was studied by a stepwise linear regression procedure that fitted the data to two linear regressions, one including observations made before birth and the other including observations made after birth. Analysis of variance tables demonstrated that the data are significantly better explained (p < 0.001) by two linear regressions that abruptly separate from one another at the time of birth than by a single linear regression. Histologic study showed that the prenatal valve consists of a thin myocardial layer with delicate endocardium. The postnatal thickening of the valve tissue occurs mainly by fibroelastotic thickening of the endocardium. The endocardial fibroelastosis of the valve develops after it closes and becomes a component of the left atrial wall. The observations support the concept that fibroelastosis is a nonspecific response of the lining of the cardiovascular system to increased mural tension.

Adolescent↗
PubMed1981

The lung in systemic lupus erythematosus. Analysis of the pathologic changes in 120 patients.

The nature and frequency of pulmonary involvement in systemic lupus erythematosus (SLE) is controversial. We reviewed the clinical and pathologic features of 120 patients with SLE described in autopsy records at The Johns Hopkins Hospital to determine the pulmonary parenchymal changes that could be attributed directly to SLE. Each case was reviewed to determine the extent of extrapulmonic SLE and possible alternative explanations for the observed lung pathology. Moderate or severe pulmonary parenchymal alterations that were attributed to SLE were found in 22 patients (18 percent). Five patients with interstitial fibrosis, two with pulmonary vasculitis, and one with pulmonary hematoxylin bodies were attributable only to SLE, as were 11 of 15 (73 percent) patients with interstitial pneumonitis. Alternative explanations for findings previously attributed to SLE included congestive heart failure, renal failure, infection, aspiration, oxygen toxicity and increased intracranial pressure. Alveolar hemorrhage, thought to be a feature of acute lupus pneumonitis, was unexplained in only two of 29 (7 percent) patients, alveolar wall necrosis was unexplained in one of seven (14 percent) and edema was unexplained in three of 70 (4 percent). Hyaline membranes, present in four patients, were always explained. Pleuritis and pleural effusions were attributed to SLE in 22 of 36 (61 percent) and three of 28 (11 percent) patients, respectively. The findings suggest that many nonspecific pulmonary lesions previously attributed to SLE, such as alveolar hemorrhage, alveolar wall necrosis, edema and hyaline membranes, are probably secondary to intercurrent infection, congestive heart failure, renal failure or oxygen toxicity.

Adolescent↗
PubMed1981

Ara-C lung: noncardiogenic pulmonary edema complicating cytosine arabinoside therapy of leukemia.

Unexplained fatal pulmonary edema observed at autopsy in leukemic patients treated with cytosine arabinoside (Ara-C) suggested a possible role of the drug in causing increased alveolar capillary permeability. We reviewed clinical and pathologic features of the 181 patients with leukemia who were examined at autopsy at The Johns Hopkins Hospital in the past 12 years, 93 (51 percent) of whom had received intravenous Ara-C in doses of 7.5 to 30 mg/kg/day (average dose, 16 mg/kg/day). Fifty-one patients had received their last treatment within 30 days, and 42 patients between 31 and 894 days, prior to death. Among the 181 patients examined at autopsy 43 (24 percent) had massive edema, 59 (33 percent) had moderate edema, and 79 (44 percent) had either slight edema or no pulmonary edema. The 51 patients who had received Ara-C within 30 days of their death, compared to the other 130, had a highly significant increase in the frequency of pulmonary edema (p less than 0.001), which was massive in 24 and moderate in 18. In these 42 patients, causative or contributing factors that explained the edema were present in 14 (33 percent) of them, but in 28 (67 percent) there was no apparent explanation. In contrast, 60 of the 130 patients who had no or remote Ara-C therapy had massive (19 patients) or moderate (41 patients) pulmonary edema, which was explained in 55 (92 percent) and unexplained in only five (8 percent) (p less than 0.001). The unexplained pulmonary edema, a highly proteinaceous interstitial and intra-alveolar infiltrate, correlated with gastrointestinal lesions typical of Ara-C toxicity (p less than 0.001). Multivariate regression analysis showed that unexplained pulmonary edema was predicted by the recent administration of Ara-C, but by no other chemotherapeutic agent, including daunomycin, a potential cardiotoxin frequently given in conjunction with Ara-C. The study suggests that increased alveolar capillary permeability may result from the intravenous administration of cytosine arabinoside and that this complication should be considered when pulmonary edema develops in leukemic patients treated with Ara-C.

Adolescent↗
PubMed1981

The cardiac malformations. Double inlet left ventricle and corrected transposition explained as deviations in the normal development of the interventricular septum.

To examine the hypothesis that malpositions of cardiac ventricles could be explained by altered development of the interventricular septum, we studied hearts from the Johns Hopkins Hospital autopsy files with double inlet left ventricle (16 cases) or corrected transposition (nine cases). In double inlet left ventricle (16 cases) or corrected transposition (nine cases). In double inlet ventricle both atrioventricular valves connect normally developed and positioned right and left atria to a posterior morphologic left ventricle. In hearts with corrected transposition the atria are normally positioned and the morphologic right ventricle is on the left and is continuous with the anteriorly positioned aorta. The morphologic left ventricle is on the right, connected to the posteriorly positioned pulmonary trunk. Normal ventricular septation may be understood as arising from the mechanics of a spiral fold in the primary heart tube produced by the left interventricular sulcus. The ventral limb of the spiral induces the muscular interventricular septum while the dorsal limb becomes a component of the crista supraventricularis. We propose that double inlet left ventricle and corrected transposition are the result of minor deviations in the position of the interventricular sulcus on the primary heart tube. Double inlet left ventricle may develop from the formation of a closed unspiraled ring around the interventricular canal. Corrected transposition may result from a left interventricular sulcus whose ventral limb gives rise to a left sided crista supraventricularis, which determines in part the right ventricular morphology of the left sided ventricle. The dorsal limb spirals toward th atrioventricular canal, gives rise to a malpositioned interventricular septum, and displaces the embryonic trabeculated right ventricle to the left. The concept presented accounts for the morphologic findings characteristic of double inlet left ventricle and corrected transposition.

Adolescent↗
PubMed1981

Symbolic logic analysis of congenital heart disease.

In identifying the primary, genetic or environmental event in human cardiac malformations, it is desirable to separate out the apparently secondary lesions. We have employed the general principle that multiple cardiac lesions within a single patient may often represent a pathogenetic process in which one primary event gives rise to a sequence of secondary lesions. The mechanical paradigm of cardiogenesis suggests that abnormal primary lesions may give rise to secondary lesions through altered blood flow or pressure relations, if the secondary structure normally appears later and represents a reasonable tissue response to altered mechanics. Symbolic logic is a mathematical method in which descriptive statements are placed in formal relation to one another and their logical consequences are deduced. Using the mechanical paradigm as a technique of hypothesis generation and symbolic logic as a technique of hypothesis testing, we have analyzed the following malformation complexes in large series of autopsied patients: coarctation of the aorta, tetralogy of Fallot, arterious malformation, interrupted aortic arch, and semilunar valve malformations.

Aortic Coarctation↗
PubMed1981

Hepatic morphology in cardiac dysfunction: a clinicopathologic study of 1000 subjects at autopsy.

Chronic passive congestion (CPC) and centrilobular necrosis (CLN) are well recognized pathologic changes, but their exact relationship to different forms of cardiac dysfunction is uncertain. We reviewed clinical data and hepatic, renal, and adrenal morphology related to cardiac dysfunction in 1000 autopsy subjects at The Johns Hopkins Hospital whose hearts had been studied after postmortem arteriography and fixation in distention. Fourteen pathologic variables, including body and organ size, and microscopic changes graded on a semiquantitative scale, and 18 clinical variables including congestive heart failure, shock, and cardiovascular disease, were analyzed statistically. Distinct patterns of cardiac dysfunction emerged for the two spectra of hepatic morphologic change. Among patients with variable CPC, but slight or absent CLN, the amount of CPC was predicted in a multivariate analysis by severity of right-sided congestive heart failure. CPC severity correlated with cardiac weight and chamber enlargement (P less than 0.001). Among patients with variable CLN, but slight or absent CPC, CLN was predicted by profound hypotension and by renal failure. In addition, CLN, but not CPC, was significantly correlated with renal acute tubular necrosis (P less than 0.001) and adrenal cortical medullary junction necrosis (P less than 0.05), two lesions associated with shock. Among all 1000 patients CPC and CLN were highly significantly correlated (P less than 0.001). The results show that hepatic CPC arises from conditions producing elevated systemic venous pressure but that CLN arises from reduced systemic arterial pressure; and the presence of one potentiates the development of the other.

Acute Kidney Injury↗
PubMed1980

Connective tissue arrangement in respiratory airways.

Connective tissue provides dynamic stability to the architecture and mechanical function of the lungs. This study examines the parenchymal connective tissue components of the alveolar ducts, their associated respiratory bronchioles and respective alveoli. Thick sections 100 mu and 200 mu, and serial sections at 8 mu of lungs of different ages were examined histologically after fixation in distention. The varying proportions and spatial architecture of the collagen and elastic fibers and the packing and spatial interrelationships of alveoli were studied using graphic serial reconstruction. Alveolar mouth typically have a polygonal configuration as they arise from the airways. Denser connective tissue passes through the polygonal array and forms a helix encircling the airway. Polygonal packing of alveolar mouths provides a mechanically stable ductular structure with conservation of materials. A helical modification of the polygonal arrangement permits reversible changes in linear and circumferential airway dimensions.

Adult↗
PubMed1980

Metabolic effects and pharmacokinetics of intravenously administered dichloroacetate in humans.

Dichloroacetate decreases plasma glucose, lactate, and alanine concentrations in normal and diabetic subjects, and lowers lactate concentrations and increases survival in animals with experimentally induced lactic acidosis. The relationship between these effects and plasma dichloroacetate concentrations have not been previously studied in man. Dichloroacetate (1-50 mg/kg) was infused over 30 min to 16 healthy subjects and plasma drug concentrations were followed by gas chromatography over the next 8 h. Peak plasma concentrations were linearly related to the dose (r = 0.98, p < 0.001) up to 30 mg/kg, above which 4 of 7 subjects had disproportionately high plasma drug concentrations. Nonlinear disposition was also indicated by the convex decreasing plasma elimination curves; levels declining less rapidly initially than later. At plasma concentrations below 10 micrograms/ml, elimination was monoexponential with a half-life of 32 +/- 11 min (mean +/- SD). Plasma drug clearance also decreased with doses greater than 20 mg/kg. Within 2 h of administration of the maximally effective dichloroacetate dose of 35 mg/kg, plasma lactate concentrations fell 75% below baseline and alanine fell 50% below baseline, while blood glucose was unaffected.

Acetates↗
PubMed1980

The concept of homology in quantitative organelle pathology. Application of symbolic logic to glycogenosis type I in the liver.

The process of quantification has led pathology into an objective and abstract direction to which it is unaccustomed. The introduction of the concept of homology in pathology by Doerr has proven to be very fruitful, since it has helped to clarify otherwise poorly understood relationships. As shown in the foregoing paper, the success of the homology concept applies also to quantitative organelle pathology. Homologies have demonstrated relationships within the ergastoplasmic - mitochondrial - peroxisomal system which are apparent only with the help of symbolic logic. These homologies permit inferences, shown here with the example of glycogenosis type I, regarding the adaptive potential of the cell and the degree of cellular damage. In addition, these homologies, which are described in terms of formal logic, may serve as a model for human pathologic anatomy.

Glycogen Storage Disease Type I↗
PubMed1980

Phospholipase B activity in congenitally athymic (nude) mice infected with Trichinella spiralis.

The effects of an infection with 200 Trichinella spiralis larvae on the intestinal phospholipase B activity and bone marrow eosinophilia of congenitally athymic (nude) mice (BALB/c; NU/NU) were studied. Nude mice were used since it had been shown that they do not undergo a typical worm expulsion and also they lack a thymus. The results showed that nude mice do not develop either an increased bone marrow eosinophilia or an elevation in intestinal phospholipase B activity. The findings thus support the hypothesis that phospholipase B is involved in the expulsion of parasitic worms and that elevated enzyme levels and expulsion are thymus cell dependent.

Animals↗
PubMed1980

Constituents of the human ventricular myocardium: connective tissue hyperplasia accompanying muscular hypertrophy.

Left-sided congestive heart failure may be secondary to decreased left ventricular myocardial compliance in some patients. To investigate the anatomic basis for altered wall stiffness, morphometric determinations of muscle cell nuclear density and percent of myocardium consisting of muscle cells were made for right and left ventricular free wall and septum in 127 hearts with normal coronary arteries. The hearts were normal (33 patients), had left ventricular hypertrophy (28 patients), right ventricular hypertrophy (25 patients), or chronic dilatation (41 patients). With cardiac enlargement, the average percent of myocardium consisting of muscle did not change from the approximately 75% value characteristic of normal hearts. In contrast, muscle cell nuclear density decreased proportionate to cardiac enlargement, demonstrating that muscle cell hypertrophy, not hyperplasia, is the basis for weight increase. Some hearts with marked longstanding dilatation also had perivascular and interstitital "striae" of connective tissue differing from replacement fibrosis. An increase in epicardial coronary artery caliber commensurate with increased heart weight suggests that ischemia is not the basis of connective tissue increase. The results show that cardiac muscle cell hypertrophy is accompanied by commensurate increase in interstitial connective tissues. This pattern of myocardial growth with cardiac enlargement may produce increased myocardial stiffness simply as a result of increased wall thickness, and may lead to left-sided congestive heart failure.

Adolescent↗
PubMed1980

Absence of correlation between coronary arterial atherosclerosis and severity or duration of diabetes mellitus of adult onset.

The relation between the severity and duration of diabetes mellitus and the severity of ischemic heart disease is uncertain. The clinical findings and the findings at autopsy were studied in 185 patients with diabetes mellitus of adult onset who ranged in age from 37 to 91 years and had a clinical diagnosis of diabetes established for a few days to 50 years before death. No statistically significant association was demonstrated either by simple correlation or by multivariate regression analysis between the clinically diagnosed severity or duration of diabetes and either the overall coronary disease, the number of diseased vessels or the number of myocardial infarctions. The presence of other expected correlations in the multivariate analysis suggested that the results of this study were not spurious. However, comparison with 185 age- and sex-matched control patients revealed that on the average, diabetic patients have more overall coronary disease (p < 0.002), more diffuseness of coronary disease (p < 0.005), more coronary collateralization (p < 0.001), more vessels involved by atherosclerosis (p < 0.001) and more myocardial infarcts (p < 0.001). The results suggest that although diabetes mellitus of adult onset is a condition in which the larger coronary arteries are subject to more atherosclerosis than are those in nondiabetic subjects, the progression of the atherosclerotic disease is unrelated to the duration or severity of the diabetes mellitus.

Adult↗