Anatomical Record最新文献

Morris (J. Anat., 1976;121:47-64) proposed that the subepicardial mesenchyme might represent a continuing source of myocardioblasts during embryonic and fetal development. Recent studies have shown that the epicardium and subepicardial mesenchyme, and the coronary vasculature are all derived from a region of the pericardial wall, called the proepicardial serosa. In avian embryos, the cells from the proepicardial serosa colonize the heart via a secondary tissue bridge formed by attachment of proepicardial villi to the heart. In the present study, Morris's hypothesis was tested by tracing the fate of the proepicardial serosa. This was achieved by constructing quail-chick chimeras. The proepicardial serosa was transplanted from HH16/17 quail embryos to HH16/17 chick embryos (ED3). A new transplantation technique facilitated an orthotopic attachment of the quail proepicardial villi to the chicken heart, and prevented the attachment of the chicken proepicardial villi to the heart. The fate of the grafted quail cells was traced in chimeras from ED4 to ED18 with immunohistochemistry, using quail-specific antibodies (QCPN, QH-1). From ED4 onward, the transplant was connected to the dorsal heart wall via its proepicardial villi. Starting from the point of attachment of the quail proepicardial villi to the heart, the originally naked myocardium became almost completely covered by quail-derived epicardium, and quail mesenchymal cells populated the subepicardial, myocardial, and subendocardial layers including the av-endocardial cushions. Quail cells formed the endothelial and smooth muscles cells of the coronary vessels, and the perivascular and intramyocardial fibroblasts. Quail myocardial cells were never found in the subepicardial, myocardial, and subendocardial layers. This suggests that the subepicardial mesenchyme normally does not contribute a substantial number of myocardioblasts to the developing avian heart. The new transplantation technique presented facilitates the production of chimeric hearts in which the derivatives of the proepicardial serosa are almost completely of donor origin. This technique might be useful for future studies analyzing the role of certain genes in cardiac development by the creation of somatic transgenics.

Early graft dysfunction after lung transplantation is a significant and unpredictable problem. Our study aimed at a detailed investigation of structure-function correlations in a rat isolated heart-lung model ofischemia/ reperfusion injury. Variable degrees of injury were induced by preservation with potassium-modified Euro-Collins solutions, 2 hr of cold ischemia, and 40 min of reperfusion. Pulmonary artery pressure (Ppa), pulmonary vascular resistance (PVR), peak inspiratory pressure (PIP), and perfusate gases (deltaPO2, deltaPCO2) were recorded during reperfusion. Right lungs were used to calculate W/D-weight ratios. Nineteen experimental and six control left lungs were fixed for light and electron microscopy by vascular perfusion. Systematic random samples were analyzed by stereology to determine absolute and relative volumes of lung structures, the amount of interstitial and intraalveolar edema, and the extent of epithelial injury. Lectin- and immunohistochemistry using established epithelial cell markers were performed in three animals per group to reveal sites of severe focal damage. Experimental lungs showed a wide range in severity of ischemia/ reperfusion injury. Intraalveolar edema fluid amounted to 77-909 mm3 with a mean of 448+/-250 mm3 as compared with 22+/-22 mm3 in control lungs (P<0.001). Perfusate oxygenation (deltaPO2) decreased from 30.5+/-15.2 to 21.7+/-15.2 mm Hg (P=0.05) recorded after 5 and 40 minutes of reperfusion. In experimental lungs, a surface fraction of 1% to 58% of total type I pneumocyte surface was damaged. Intraalveolar edema per gas exchange region (Vv ape,P) and deltaPO2 were related according to deltaPO2 = 96 - 60 x log10(Vv ape,P) [mm Hg]. The extent of epithelial injury did not correlate with deltaPO2 nor with intraalveolar edema, but increased significantly with PVR. Lectin- and immunohistochemistry revealed focal severe damage to the alveolar epithelium at the border of perivascular cuffs.

In this study, we present a new computerized reconstruction of the Le Moustier 1 Neanderthal skull and discuss its significance for Neanderthal growth and variability. Because of the precarious state of preservation of the original material, we applied entirely noninvasive methods of fossil reconstruction and morphometry, using a combination of computed tomography, computer graphics, and stereolithography. After electronic restoration, the isolated original pieces were recomposed on the computer screen using external and internal anatomical clues to position the bone fragments and mirror images to complete missing parts. The inferred effects of general compressive deformation that occurred during fossilization were corrected by virtual decompression of the skull. The resulting new reconstruction of the Le Moustier 1 skull shows morphologic features close to the typical Neanderthal adult state. Residual asymmetry of skeletal parts can be traced to in vivo skeletal modification: the left mandibular joint shows signs of a healed condylar fracture, and the anatomy of the occipital region suggests mild plagiocephaly. Using micro-CT analysis, the left incus could be recovered from the matrix filling of the middle ear cavity. Its morphometric dimensions are similar to those of the La Ferrassie III incus. The morphometric characteristics of the inner ear deviate substantially from the condition reported as typical for Neanderthals and fall within the range of modern human variability.

Mitochondria of steroid-producing cells are integrally involved with steroidogenesis. For decades, the mitochondrial morphology of Leydig cells, as with other steroid-producing cells, has been known to differ from typical mitochondria in that the cristae are predominately "tubular." In a few species, humans being one example, the cristae have often been further categorized as "tubular and/or lamellar," without further elaboration. In the present study, mitochondria of human Leydig cells were examined with the purpose of providing a more detailed description of "cristae" morphology in these steroid-producing cells. The cristae are found to be rather diverse in morphology, consisting of elements of anastomosing tubules in continuity with small cisternal regions as well as with stacked arrays of lamellae, referred to as "lamellar associations." The tubular elements are found to branch in a tripartite fashion and sometimes to expand into small cisternal elements at these junctures. The lamellar associations are a distinctive feature of cristae in human Leydig cells and consist of two to eight closely apposed lamellae with a consistent gap of approximately 4 nm between the membranes of apposing lamellae. Such a close association of cellular membranes is highly suggestive of an integral transmembrane linkage. Although the lamellar associations often appear isolated, evidence is present of a continuity of this compartment of the cristae with the tubular elements. The connections (termed "initial segments") of the various forms of the cristae to the inner mitochondrial membrane are typically via tubules. Mitochondria exhibiting a central region of matrix delineated by one or more cup-shaped lamellae are also present. The pleomorphic structure of mitochondrial cristae in human Leydig cells reemphasizes our present lack of knowledge of how subcellular structure relates to steroidogenesis.

The development of the testes was studied in rats following prepubertal obstruction of the epididymis. Male rats received bilateral ligation of the corpus epididymidis or a sham operation at 10 days of age, and temporal changes in testicular morphology and weights of reproductive organs were determined at intervals spanning sexual maturation. Development of the testes was normal through 35 days of age. The initial histological changes in the testes of ligated animals, observed at 56 days, included an increased diameter of the seminiferous tubule lumen, depletion of spermatids, and the presence of multinucleate spermatids. Subsequently, germ cells were greatly depleted in the testes of 91- and 128-day-old rats with ligated epididymides. After puberty, testicular weight and volume declined relative to corresponding sham-operated animals. On the other hand, the weights of the epididymides in ligated animals prior to puberty significantly exceeded those of sham-operated rats but weighed significantly less than those of rats in the sham group after sexual maturation. Testicular alterations occurred after increases in the weights of the epididymides. Testicular changes may have contributed to rather than resulted from an autoimmune response to spermatozoa because testicular alterations preceded increases in antisperm autoantibodies.

Programmed cell death (PCD) is an essential event for development. The purpose of this work was to ascertain how PCD, in vivo designated apoptosis, is involved in the development of the external auditory canal. We performed a time sequence study of the distribution of apoptosis during the development of external auditory canal (EAC) of the mouse. ICR mice ranging in age from embryonic day 11.5 (E11.5) to 12 days after birth (DAB) were used in the present study. A part of each head including both ears was removed and was processed according to its purpose. Light and electron microscopy for morphological studies and TUNEL method (Gavrieli et al. [1992] J Cell Biol., 119:493-501) for histochemical studies were used. On E11.5, distinct TUNEL-positive staining occurred in the branchial arch. Between E15.5 and 1DAB, TUNEL-positive cells were observed throughout the EAC and the number of these cells decreased with age. On E15.5 and E16.5, numerous TUNEL-positive cells were observed in a cavity remained in the epithelial plate. Transmission electron microscopy revealed that these cells had the features of apoptosis. From 3-12 DAB, no apoptosis was observed in the EAC except for the terminal differentiation of the skin of the EAC. Apoptosis was not observed during recanalization of the EAC, but occurred during the formation of the epithelial plate. The investigation established that PCD is involved in the formation of the epithelial plate, whereas only cornification of the epithelium of the EAC is associated with recanalization.

An ultrastructural cytochemical study of acid phosphatase activity in the antimesometrial decidua on days 9-11 of pregnancy was performed in fed and acutely fasted mice. Specimens were fixed in a buffered mixture of paraformaldehyde and glutaraldehyde and were incubated in a buffered medium containing sodium beta-glycerophosphate and cerium chloride for ultrastructural localization of acid phosphatase activity. Fed and fasted animals showed extracellular acid phosphatase reaction product in the decidual-trophoblast interface, in the region of loosely and tightly packed, mature decidual cells, and in the region of predecidual cells. Reaction product was absent in the region of nondecidualized stromal cells. Extracellular acid phosphatase activity was more conspicuous in the region of mature decidual cells in fasted mice than in fed mice, and it was apparently similar in the region of predecidual cells in both fed and fasted mice. Acid phosphatase reaction product was also observed in lysosomes in all cells studied. Because acid phosphatase activity reflects the presence of lysosomal hydrolases in general, our results suggest that there is matrix degradation by lysosomal enzymes in both fed and fasted mice. These events may be part of the process of tissue remodeling in regions of predecidual cells and mature decidual cells. However, it is also possible that, in the region of mature decidual cells, breakdown of matrix constituents is a mechanism to provide nutrients for the growing fetus. This mechanism is probably enhanced in fasted mice.