PubMed · 14295955
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S COBB. 1965. BRAIN SIZE.. https://doi.org/10.1001/archneur.1965.00460300003001
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The presence of left ventricular bands has drawn attention to their possible clinical importance, though there are no concrete data to support their role in serious clinical diseases. We have investigated the incidence, location, microscopic and macroscopic structure of left ventricular bands in the human and animals. We examined 100 hearts: 28 human and 72 animal (dog, goat, sheep). Left ventricular bands were present in 13 of 28 (46%) human hearts and 62 of 72 (86%) animal hearts. The bands usually extended from the interventricular septum to the free walls in human hearts and from the papillary muscles to the interventricular septum in animal hearts. They were composed of muscle tissue in various proportions in human and dog hearts, and of connective and conductive tissue in sheep and goat hearts.
Because of the increasing availability of tools for genetic manipulation, the mouse has become the most popular animal model for studying normal and abnormal cardiac development. However, despite the enormous advances in mouse genetics, which have led to the production of numerous mutants with cardiac abnormalities resembling those seen in human congenital heart disease, relatively little comparative work has been published to demonstrate the similarities and differences in the developmental cardiac anatomy in both species. In this review we discuss some aspects of the comparative anatomy, with emphasis on the atrial anatomy, the valvuloseptal complex, and ventricular myocardial development. From the data presented it can be concluded that, apart from the obvious differences in size, the mouse and human heart are anatomically remarkably similar throughout development. The partitioning of the cardiac chambers (septation) follows the same sequence of events, while also the maturation of the cardiac valves and myocardium is quite similar in both species. The major anatomical differences are seen in the venous pole of the heart. We conclude that, taking note of the few anatomical "variations," the use of the mouse as a model system for the human heart is warranted. Thus the analysis of mouse mutants with impaired septation will provide valuable information on cellular mechanisms involved in valvuloseptal morphogenesis (a process often disrupted in congenital heart disease), while the study of embryonic lethal mouse mutants that present with lack of compaction of ventricular trabeculae will ultimately provide clues on the etiology of this abnormality in humans.
This study investigates whether macaques and humans possess a common pattern of relative growth during the fetal period. The fetal samples consist of 16 male pigtailed macaques (mean age, 20.5 gestational weeks) and 17 humans (9 males and 8 females; mean age, 29.5 gestational weeks). For each individual, three-dimensional coordinates of 18 landmarks on the skull were collected from three-dimensional computed tomographic (CT) reconstructed images and two-dimensional CT axial slices. Early and late groups were created from the human (early mean age, 24 weeks, N = 8; late mean age, 34 weeks, N = 9) and macaque samples (early mean age, 17.7 weeks, N = 7; late mean age, 23 weeks, N = 9). Inter- and intraspecific comparisons were made between the early and late groups. To determine if macaques and humans share a common fetal pattern of relative growth, human change in shape estimated from a comparison of early and late groups was compared to the pattern estimated between early and late macaque groups. Euclidean distance matrix analysis was used in all comparisons. Intraspecific comparisons indicate that the growing fetal skull displays the greatest amount of change along mediolateral dimensions. Changes during human growth are primarily localized to the basicranium and palate, while macaques experience localized change in the midface. Interspecific comparisons indicate that the two primate species do not share a common pattern of relative growth, and the macaque pattern is characterized by increased midfacial growth relative to humans. Our results suggest that morphological differences in the craniofacial skeleton of these species are in part established by differences in fetal growth patterns.