bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ultrastructure of the pronephric kidney in upstream migrant sea lamprey, Petromyzon marinus L
Authors: Ellis L. C. , Youson J. H. 
Published: February 2005

AbstractThe pronephric kidneys were examined in upstream migrant sea lampreys,Petromyzon marinus L., by transmission and scanning electron microscopy. Each prolcphios consists of an enlarged renal corpuscle (glomus) and ciliated nephrostomes, but there are no renal tubules. The renal corpuscle contains an extensive mesangium, which consists of a highly fibrous extracellular matrix, numerous mesangial cells, granulocytes, and macrophages. The extracellular matrix contains microfibrils with a morphology similar to amyloid P microfibrils, fibrils with a periodicity similar to fibrin, and abundant collagen. Often these fibrillar components are aggregated in the region of the basement membrane, giving it a thickened appearance. Some podocytes of the visceral epithelium appear swollen, and their cytoplasm contains numerous vacuolar inclusions, and many have only primary major processes with only a few or no foot processes. The morphological features of the pronephric kidney of the lamprey at this time in the life cycle reflect the regression of this organ, but some features also resemble those seen in renal pathologies of higher vertebrates.
Characterization by morphometric model of liver regeneration in the rat
Authors: Vizzotto Laura , Romani Federico , Ferrario Virgilio F. , Degna Carlo Tommasini , Aseni Paolo 
Published: February 2005

AbstractA new stereologlcal approach to the study of liver regeneration in the rat is described. The method employs a morphometric model consisting of number and size, as well as surface and volume fractions of hepatocytes, their nuclei, cytoplasm, and their relation to the sinusoidal bed. With this technique, it was found that 8 hr after partial hepatectomy, the number of nuclei increased as did the nucleus/cytoplasm ratio, suggesting an early hyperplastic phase. These data, which have not been reported in other studies, underline the importance of evaluating the complex phenomenon of liver regeneration using a stereological approach, which is more representative of all morphometric changes occuring inside and outside the hepatocyte.
Histologic, morphometric, and immunocytochemical analysis of myometrial development in rats and mice: II. Effects of DES on development
Authors: Brody Joel R. , Cunha Gerald R. 
Published: February 2005

AbstractThe effects of diethylstilbestrol (DES) treatment on myometrial development from the prenatal to adult period were examined in rats and mice by histologic and immunocytochemical methods using anti‐actin, ‐vimentin, and ‐laminin to assess cytodifferentiation of smooth muscle and fibroblastic cells, and by morphometric procedures to assess quantitatively the effect of DES on the expression of cellular orientation in the emerging inner circular myometrial layer. Neonatal rats and mice were treated with DES from day 0 (day of birth) to day 2 with dosages known to perturb myometrial development. Neonatal treatment with DES increased the degree of circular orientation within the uterine mesenchyme, an effect detectable following as little as 24 hr of DES treatment. This effect on spatial organization of the mesenchyme was followed by an increase in the thickness of the actin‐positive middle layer (prospective circular myometrium) of uterine mesenchyme during days 3–15; from day 15 onward, however, the circular myometrial layer began to fragment into irregular bundles of smooth muscle, and the longitudinal myometrial layer became thinner and more irregularly organized than controls. Vimentin localization in rats treated with DES neonatally was more intense than in controls within the circularly orientated uterine mesenchyme at 5 days. By 60 days the circular and longitudinal myometrial layers of DES‐treated animals showed strands and bundles of vimentin‐positive cells, which were not present in controls. Both rats and mice show comparable effects of DES treatment.
Association of fibronectin with the microfibrils of connective tissue
Authors: Inoue S. , Leblond C. P. , Rico P. , Grant D. 
Published: February 2005

AbstractThe association of fibronectin with the microfibrils of connective tissue was examined in the zonular fibers of the mouse eye by immunohistochemical methods at the light and electron microscopic level. Mouse eyes fixed in formaldehyde were embedded either in paraffin for immunostaining by the peroxidase–antiperoxidase (PAP) method or in Lowicryl for immunolabeling by antirabbit globulin antibodies bound to 5 or 15 nm gold particles. Ultrastructural studies were also carried out after glutaraldehyde perfusion.Both the PAP and immunogold procedures demonstrated the association of fibronectin with microfibrils. After immunolabeling with 5 nm gold particles, examination at high magnification localized fibronectin to fine filaments that appeared to be attached to the surface of microfibrils. The filaments extended outward singly or formed loose aggregates. Their diameter ranged from 1.2 to 3 nm, with a mean of 1.5 nm. Because of their similarity to the fibronectin molecules previously described after rotary shadowing, the filaments were likely to be fibronectin molecules themselves.Since fibronectin is known to have high affinity for the amyloid P component, a model is presented in which fibronectin filaments are bound to the amyloid P component making up the tubular core of microfibrils in mice. Evidence is presented that fibronectin filaments may link microfibrils to one another and thus insure the continuity and strength of zonular fibers. More generally, it is likely that connective‐tissue microfibrils, whether or not inserted into elastic fibers, are bonded through fibronectin to surrounding cells, collagen fibrils, or proteoglycans, and thus insure cohesion among connective tissue elements.
Postnatal growth of pulmonary acini and alveoli in normal and oxygen‐exposed rats studied by serial section reconstructions
Authors: Randell S. H. , Mercer R. R. , Young S. L. 
Published: February 2005

AbstractThree‐dimensional reconstructions from serial sections were used to examine postnatal lung development of rats reared in air (control) or oxygen. From birth to age 21 days, control lung volume increased ninefold, and the average volume of each ventilatory unit (all airspaces distal to a single respiratory bronchiole) increased seven times. There were approximately 5,000 ventilatory units at birth and on day 21, indicating that the lung grew by enlargement and subdivision of ventilatory units and not by their multiplication. Growth in hyperoxia (>97%) for 7 days had no effect on the number of ventilatory units but, compared to controls, total lung volume and ventilatory unit volume were reduced 32% and 16%, respectively. At birth there were 0.6 × 106 alveoli, and at age 7 days in controls alveolar number increased 16‐fold while the average volume of a single alveolus fell to one‐sixth that at birth. Exposure to hyperoxia for 7 days stopped alveolarization; the surface area to volume ratio (Sa/V) of the ventilatory unit was lower, alveolar number was the same as at birth, and the alveoli present were large. At age 21 days, after 14 days of recovery in air, lung volume and ventilatory unit volume were greater than in controls but the Sa/V of the ventilatory unit was still depressed 20%. Alveoli from oxygen‐exposed lungs were larger than in controls, and a greater size distribution coefficient showed them to be more variable. A shape coefficient for alveoli did not change as a function of the animal's age or oxygen treatment; it demonstrated proportional growth of alveolar height and diameter.
An electron microscopic study of mitosis in mouse duodenal crypt cells confirms that the prophasic condensation of chromatin begins during the DNA‐synthesizing (S) stage of the cycle
Authors: El‐Alfy Mohamed , Leblond Charles Philippe 
Published: February 2005

AbstractThe phases of mitosis were examined in the columnar cells at the base of duodenal crypts in adult male mice given an intravenous injection of 3H‐thymidine and sacrificed 20 min later. The duodenum was fixed by immersion into glutaraldehyde‐formaldehyde, and the cells were examined in the electron microscope, with or without processing for radioautography.Interphase nuclei are characterized by the distribution of chromatin; aside from the cortical chromatin spread along nuclear envelope and nucleolus, there are chromatin accumulations that belong mainly in two different classes: (1) numerous chromatin “specks” ranging in size from about 5 to 70 nm and averaging 47 nm; (2) a few roughly circular or elongated chromatin “packets” measuring from 70 to 230 nm. Early prophase nuclei differ mainly by a large increase in the number of chromatin packets to 20–30 or more per nuclear profile; their average diameter is 128 nm. During mid‐prophase, the chromatin packets enlarge gradually to an average 221 nm diameter. Between mid‐ and late prophase, there is a further increase in diameter to 679 nm. At metaphase, the packets take on the appearance of mature chromosomes, and their diameter increases to 767 nm. At anaphase, daughter chromosomes migrate to each pole, where they fuse into a compact chromatin mass. At telophase, nucleo‐plasmic areas progressively enlarge within the chromatin mass and separate strands of chromatin, which gradually become segmented into chromatin clumps.Counts of mitotic cells show a high proportion of prophase and telophase nuclei. Calculation from the counts yields the duration of the phases, that is, 5.6, 0.2, 0.1, and 1.6 hr, respectively, for pro‐, meta‐, ana‐, and telophase.Finally, radioautography 20 min after 3H‐thymidine injection shows labeling in 54% of the interphase nuclei, 85% of early prophase nuclei, and 73% of mid‐prophase nuclei, while there is no label in late prophase, metaphase, anaphase and telophase nuclei. In confirmation of previous light microscopic work, the S stage of the cycle begins when a cell is in interphase and continues through the early prophase and part of mid‐prophase. Moreover, the main sites of DNA synthesis are the chromatin specks during interphase and the cortical chromatin during early and mid‐prophase. The chromosome condensation taking place in the meantime may be separated into two main steps: (1) a slow, moderate condensation of the chromatin packets during early and mid‐prophase and (2) a rapid, pronounced one during late prophase and prometaphase when the packets become chromosomes.
Effects of catecholamines on fetal rat cardiocytes in vitro
Authors: Marino Thomas A. , Walter Ruth Ann , D'Ambra Kimberly , Mercer W. Edward 
Published: February 2005

AbstractNorepinephrine stimulates the growth in size of non‐dividing, neonatal cardiac muscle cells, and it can stimulate the growth in numbers of dividing hepatocytes and endothelial cells in culture. The objective of this study was to test the hypothesis that in dividing fetal cardiocytes, norepinephrine would stimulate growth in cell number rather than in cell size. Fourteen‐day fetal heart cells were placed in serum‐free or serum‐supplemented cultures in the presence or absence of norepinephrine (NE), NE plus propranolol, or isoproterenol for 4 days. Almost 90% of the cardiocytes in serum‐supplemented medium were in the cell cycle as determined by proliferating cell nuclear antigen (PCNA) antibody staining during this period. In addition, between days 2 and 4 of culture, 35% and 40% of these cardiocytes were labeled with 3H‐thymidine. After 4 days the cardiocytes increased in cell number in the serum‐supplemented NE cultures as compared to serum‐free cultures. In contrast, there was no significant change in cardiocyte volume between any of the groups examined. It was concluded that in dividing muscle cell populations the effect of norepinephrine was to enhance cell proliferation rather than to stimulate cell growth in size.
Morphology of the prairie dog gallbladder: Normal characteristics and changes during early lithogenesis
Authors: Haley‐Russell Diane , Husband Kathryn J. , Moody Frank G. 
Published: February 2005

AbstractStudies were undertaken to describe the normal structure of the prairie dog gallbladder and adjacent cystic duct, and then to determine sequential changes that occurred as abnormalities in bile composition developed during high cholesterol feeding. Control animals were fed a diet with trace cholesterol, while experimental animals were fed a diet enriched with 1.2% cholesterol for 1, 2, 3, or 4 weeks. Light microscopy and scanning and transmission electron microscopy were used to characterize morphologic changes at each time interval. Biliary lipid composition was altered in all experimental groups, evidenced by significant decreases in bile‐acid‐to‐cholesterol ratios. Cholesterol crystals appeared in experimental bile at 1 and 2 weeks, while stones formed at 3 and 4 weeks. The cystic duct and neck of the gallbladder occasionally displayed goblet cells. Little mucus was demonstrable in principal cells of the gallbladder, but much more in those lining the cystic duct. After 2 weeks of lithogenic diet, there was an increase in mucus content and secretion from all areas, as well as an influx of polymorphonuclear and mononuclear leukocytes. Accumulation of plasma cells in the lamina propria was an especially prominent feature of experimental tissues. These results suggest that (1) there is regional heterogeneity in the mucus content of the gallbladder and cystic duct of the prairie dog, and (2) both regions respond to lithogenesis with mucus hypersecretion and acute and chronic inflammatory changes prior to the appearance of cholesterol gallstones.
Endocardial surface and atrial morphological changes during development and aging
Authors: Gilloteaux Jacques , Linz David 
Published: February 2005

AbstractLight, scanning, and transmission electron microscopic observations related to morphological changes of the right atrium as well as the atrial endocardium during development (15th embryonic day and 1 day old) and aging (560 days old) in the Syrian hamster were described and correlated. From the fetus to the adult, the atrial endocardium differentiates in parallel with, or in response to, the subjacent proliferating myocytes in the atrial wall and the trabeculae. Simultaneously, the atrium compartmentalizes grossly into a main chamber and an appendicular region. There is a progressive differentiation from a rudimentary, open chamber with primitive mural ridges in the fetal atria to a distinct, separate, atrial main chamber and appendage with a dense network of trabeculae in the adult. The fetal and neonatal endocardial, endothelial cells are convex with a central nuclear bulging and attenuated cytoplasmic extensions; the adult endocardium shows a squamous endothelium. Two cell surface specializations were observed in all age groups: microvilli and blebs or cytoplasmic protrusions. The general atrial morphology and surface endocardial changes were correlated with growth and the role of the endocardial endothelium as a barrier which controls metabolic exchanges, including the transport of atrial natriuretic factor, between the myocytes and the blood. This endothelial function appears to be essential in the fetal and neonatal age groups since no blood vessels are detected in these groups.
Errors in bone remodeling: Toward a unified theory of metabolic bone disease
Authors: Burr David B. , Martin R. Bruce 
Published: February 2005

AbstractRecent evidence suggests that skeletal adaptation is organized by a functional unit that includes cells of diverse origin working in coordination. Genetic and metabolic factors control and regulate the processes of modeling and remodeling, only rarely acting on the isolated individual functions of specific cell lines. Errors in the genetic or metabolic regulation of the functional unit affect the entire process of skeletal adaptation rather than specific elements of it. Viewed in this way, some metabolic bone diseases can be understood as relatively simple errors in factors that control the coordinated activities of the entire functional unit. This paper reviews the modeling and remodeling processes and demonstrates how abnormal morphological characteristics of bone tissue can be viewed as products of specific errors in the adaptive process.
Aberrant differentiation of neuroepithelial cells in developing mouse brains subsequent to retinoic acid exposure in utero
Authors: Yasuda Yoshiko , Konishi Hiroyoshi , Matsuo Takuya , Kihara Takahide , Tanimura Takashi 
Published: February 2005

AbstractAll‐trans‐retinoic acid induced 2 types of disorganized neuroepithelium, localized and continuous, in the exencephaly of 9‐day‐old mouse embryos exposed to 60 or 40 mg/kg for 27 to 30 hr in utero. The localized effect appeared as a protuberance in the wall of the telencephalon and thick neural folds in the mesencephalon with the discontinuity of the apical terminal sheet. The continuous disorganization was seen from the olfactory placode to the myelencephalon with rosettes of cells and many dense bodies in the neuroepithelium. Ultrastructurally, cells in the localized disorganizations showed swelling of Golgi complexes, coated vesicles, and rough endoplasmic reticulum resulting in degeneration. The continuous disorganizations consisted of undifferentiated homogeneous cells in which the nuclei exhibited expansion of nucleolar granular portions and coagulated heterochromatin, and cytoplasm showed monosomal dispersion. In both types of disorganized neuroepithelium, junctional complexes were seen focally at the apical side or apical processes of the rosette, with few or no microfilament bundles. A layer of microfilaments at the base of the neuroepithelial cells in controls, just above the basal lamina, was not present in the monosome dispersed cytoplasm. In the neuroepithelium of controls, one phagosome was seen in the perinuclear region in 0.8% of the cells examined, whereas in the experimental neuroepithelium 2 or more phagosomes were seen in a cell, and phagocytosis occurred by pseudopods. These findings suggest that all‐trans‐retinoic acid induces not only cytotoxicity but also dedifferentiation in the neuroepithelial cells leading to more cell death, which activates the phagocytosis. These lesions in the neuroepithelium may be a cause of exencephaly.
Morphology of pulmonary intravascular macrophages (PIMs) in ruminants: Ultrastructural and cytochemical behavior of dense surface coat
Authors: Atwal O. S. , Minhas K. J. , Ferenczy B. G. , Jassal D. S. , Milton D. , Mahadevappa V. G. 
Published: February 2005

AbstractRecent studies have indicated that pulmonary intravascular macrophages (PIMs) are a resident cell population which in structure and function resemble mature macrophages of the mononuclear phagocyte system (MPS) in various domestic species, particularly the ruminants. The ultrastructural features of PIMs of the goat and calf lungs were studied by using vascular perfusion and direct airway instillation of fixatives. Staining with tannic acid as a component of paraformaldehyde‐glutaraldehyde‐based fixative revealed the presence of an electron‐dense coat on the surface of the cell membrane of the PIMs. The surface coat disappeared after heparin infusion and after enzymatic digestion with lipolytic lipase, suggesting that the surface coat was predominantly lipoprotein in nature. The lipoprotein coat was organized in the form of a linear chain of spherical globules with a consistent periodicity created by the intervening translucent space between individual globules. The surface coat was separated from the outer‐leaflet of the cell membrane by an empty space measuring 35–39 nm in width. PIMs possessed a significant number of coated pits and coated vesicles, the cell organelles of receptor‐mediated endocytosis of lipoproteins. In concurrence with the coated pits and vesicles, microtubules, multivesicular bodies, and lipoprotein‐positive vesicles were also observed. It is conceivable that PIMs are involved in lipid metabolism and are the major source of vasoactive substances, which significantly influence both the dynamics of pulmonary circulation and the surfactant turnover of the ruminant lung.
Ultrastructural morphometric analysis of cultured neonatal and adult rat ventricular cardiac muscle cells
Authors: Delcarpio Joseph B. , Claycomb William C. , Moses R. L. 
Published: February 2005

AbstractNeonatal and adult rat ventricular cardiac muscle cells cultured on laininin differed from similar myocytes grown on plastic in the amount and distribution of their mitochondria and transverse tubules. Point‐count morphometry was used at the electron microscopic level to quantify these differences. Adult myocytes grown on laminin contained more mitochondria per unit volume than adult myocytes grown on plastic. No significant differences were observed in the volume percent of myofibrils in either adult or neonatal ventricular myocytes when grown on laminin and compared to those grown on plastic. The transverse tubule system in neonatal and adult myocytes was reduced significantly when both groups were cultured on laminin. Furthermore, neonatal and adult myocytes cultured on laminin were flatter than those cultured on plastic. This may indicate a relationship between the surface/volume ratio and transverse tubule development in cultured myocytes. These studies establish that point‐count morphometry can be used to quantify changes in the organelle volume densities of cultured cardiac muscle cells.
Condensation of hypertrophic chondrocytes at the chondro‐osseous junction of growth plate cartilage in Yucatan swine: Relationship to long bone growth
Authors: Farnum Cornelia E. , Wilsman Norman J. 
Published: February 2005

AbstractChondrocytes of the cartilaginous growth plate are found in a spatial gradient of cellular differentiation beginning with cellular proliferation and ending with cellular hypertrophy. Although it is recognized that both proliferation and hypertrophy contribute significantly to overall bone growth, mechanisms acting on the chondrocyte to control the timing, the rate, and the extent of hypertrophy are poorly understood. Similarly, mechanisms acting on the terminal chondrocyte to cause its death at the chondro‐osseous junction have not been investigated. In this study we examine the condensation of terminal hypertrophic chondrocytes in proximal and distal radial growth plates of Yucatan swine at 4 weeks of age. The animals were raised in a controlled environment where activity and feeding patterns were synchronized to a given time in the light/dark cycle. We analyzed cellular condensation both as a function of circadian rhythms in a 24‐hr time period, and as a function of overall rate of growth. The data suggest that the magnitude of circadian influences on long bone growth is significantly damped at the level of the hypertrophic chondrocyte compared to that seen by previous investigators studying circadian influences on chondrocytic proliferation. Secondly, the condensation of hypertrophic chondrocytes at the chodro‐osseous junction varies inversely with rate of growth in length of the bone. At any time period, a higher percentage of terminal chondrocytes in the condensed form was found in the slower‐growing of the two growth plates. We relate these findings to current hypotheses concerning controls of chondrocytic hypertrophy and possible controls over the timing of hypertrophic cell death.