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  • 1
    Electronic Resource
    Electronic Resource
    Developing innervation of the chick heart: A histofluorescence and light microscopic study of sympathetic innervation (1980)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 196 (1980), S. 333-340 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The available descriptions of the development of sympathetic innervation of the chick heart conflict with the known sympathetic innervation of the adult chicken heart. The adult heart is innervated by bilateral sympathetic cardiac nerves originating from the first thoracic sympathetic ganglia. These nerves travel lateral and anterior to the lung and join the vagi just before entering the pericardium along the great vessels. Using catecholamine histofluorescence techniques and silver preparations, we have observed the development of the sympathetic cardiac nerves. The sympathetic cardiac nerves arise from the first thoracic sympathetic ganglia on the 7th day of incubation. They grow lateral and then ventral to the developing lungs to join the vagi, and are found in the bulbar region of the heart and atrium on the 10th day of incubation. Fluorescent cells without processes mark the course of the sympathetic cardiac nerves and are present in the bulbar region on the 10th day and thereafter. Sympathetic ganglion cells lose their fluorescence between day 8 and day 16 of incubation. This is presumably due to dilution of the transmitter in the rapidly increasing volume of cytoplasm in the sprouting neurons. Small intensely fluorescent (SIF) and adrenal medullary cells do not undergo a diminution of fluorescence during this period. SIF cells appear well differentiated at 16 days.
    Additional Material: 12 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091960309
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  • 2
    Electronic Resource
    Electronic Resource
    Norepinephrine-induced cardiac hypertrophy of the cat heart (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 229 (1991), S. 505-510 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Norepinephrine administration causes progressive hypertrophy of the mammalian heart as measured by myocardial mass. The purpose of this study was to determine the growth response of the myocardial tissue components as well as the myocardial cell itself to norepinephrine. Young, adult cats were given low doses of norepinephrine in dextrose or dextrose alone twice daily for 15 days. On day 16, there were no changes in the animals body weight, right ventricular systolic pressure, right ventricular end-diastolic pressure, heart rate, cardiac index, or blood pressure. However, the right ventricle/body weight, the left ventricle/body weight and the total heart weight/body weight were increased significantly in the norepinephrine treated animals. The increase was on the order of 40%. The cardiac muscle cell was also significantly increased in size and both the right and left ventricular cardiac muscle cells exhibited a dramatic increase in size as measured by cross sectional area. Upon stereological examination it was found that the amount of hypertrophy as seen in the cardiac muscle cells was paralleled by the hypertrophy seen in the other tissue components of the myocardium. The volume density of the muscle cells, the interstitial components, as well as the blood vessel compartment were identical in the control and in the norepinephrine-treated groups. In conclusion, this study demonstrates that the response of the myocardium to norepinephrine is similar to that seen in response to a volume overload rather than that seen in response to pressure overload.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092290411
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  • 3
    Electronic Resource
    Electronic Resource
    Colloidal gold localization of type IV collagen in the extracellular matrix of rat gastric mucosa: Influence of alcohol and prostaglandin (1991)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 230 (1991), S. 235-242 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The effect of acute alcohol exposure on the gastric mucosal basal lamina, and its major structural protein type IV collagen, was assessed by transmission electron microscopy (TEM) and immunogold (IG) labeling of this collagenous material. Fasted rats orally received either 50% or 100% ethanol. Five or 60 minutes later animals were sacrificed and mucosal samples were obtained from the glandular epithelium for TEM or IG localization of type IV collagen. For IG studies, the number of gold particles/area lamina densa was quantified in interfoveolar, pit, and gland regions as an index of the molecular integrity of type IV collagen. Both ethanol concentrations induced epithelial exfoliation with pleating of the denuded lamina densa. Absolute ethanol, and to a lesser extent 50% ethanol, caused frequent rupture of a thickened, precipitated lamina densa. Immunolabeling of type IV collagen varied with the experimental protocol. In control tissues exposed to oral saline, binding was greatest in the interfoveolar zone. Low binding occurred with 100% ethanol in all regions when compared with controls, but 50% ethanol evoked significantly higher binding in interfoveolar regions, in a similar fashion to controls. In additional studies in which 16,16 dimethyl prostaglandin E2 (PGE2) (10 μg/kg) was injected subcutaneously prior to oral ethanol exposure, PGE2 pretreatment prevented the large decrease in IG binding induced by absolute ethanol, but the level still remained significantly less than with corresponding controls. In contrast, pretreatment with PGE2 prior to 50% ethanol exposure restored type IV collagen immunolabeling to control levels. These results indicate that ethanol induces a concentration-dependent lowering of IG binding to type IV collagen which also effects its reversibility by PGE2.
    Additional Material: 10 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092300211
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  • 4
    Electronic Resource
    Electronic Resource
    Observations on the development of the human atrioventricular node and bundleSupported by N.I.H. Grant HL07047. (1978)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 192 (1978), S. 337-350 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: This light microscopic study of the cardiac junctional tissues was based on 27 human embryos, fetuses and postnatal hearts. Evidence was presented that superficial and deep portions of the postnatal AV node were derived from two cellular primordia in the posterior wall of the common atrium at the 6-mm stage. The small right primordia was associated with the right venous valve and gave rise to the loosely organized superficial AV node that extended posteriorly to the coronary sinus ostium. A larger left primordia formed the more compact deep subdivision of the AV node located against the anulus fibrosus. In most postnatal hearts the two subdivisions are partially or completely fused to form the adult AV node. Failure of the nodal primordia to fuse during cardiogenesis may result in two separate nodal cell aggregates above the anulus. The present observations provide a rational explanation for the two AV nodal masses described in the literature and an additional specimen that is illustrated in this communication.An AV bundle was first identified in a 13-mm embryo and appeared to be derived from large clear cells of the posterior AV canal. At 25 mm the bundle formed a broad band across the top of the IV septum and continued into both ventricles. At this stage multiple cell strands penetrated the endocardial cushion to connect the AV bundle to the two nodal primordia. Failure of normal fusion between the AV node primordia and AV bundle can result in a variety of junctional anomalies including congenital heart block.
    Additional Material: 8 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091920302
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  • 5
    Electronic Resource
    Electronic Resource
    Reversibility of the structural effects of pressure overload hypertrophy of cat right ventricular myocardium (1986)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 214 (1986), S. 141-147 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: The purpose of the present quantitative structural study was to determine whether the histological alterations seen in pressure overloaded myocardium return to normal, as in vitro contractile function does, upon removal of the pressure overload stimulus. Three experimental groups of four cats each were studied: a group with pulmonary artery banding to create a pressure overload, a group that had been subjected to an equivalent duration of pressure overload and then had that pressure overload removed, and a group of sham-operated controls. Seven to 10 weeks after each operative procedure, the right ventricular pressure was elevated only in the pulmonary artery-banded group. The right ventricle/body weight ratio was significantly increased in the pressure overloaded group only. The body weight at sacrifice, the left ventricle/body weight ratio, and the right ventricular end-diastolic pressure did not differ significantly in the three groups. The striking histological changes in the right ventricular myocardium hypertrophying in response to a pressure overload were the decrease in the volume density of cardiocytes and the increase in connective tissue in papillary muscles. These were reversed when the pressure overload was removed. This study demonstrates that when a pressure overload is removed, myocardial structure returns to normal as the function returns to normal. Given the critical importance of the proportion of cardiocytes and connective tissue components to both systolic and diastolic cardiac function, these data support the hypothesis that the abnormal proportions of these structures provide a potential morphological basis for at least some of the functional abnormalities observed in pressure overload hypertrophy of the cat right ventricle.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092140206
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  • 6
    Electronic Resource
    Electronic Resource
    A quantitative morphological analysis of interatrial muscle cells in the ferret heart (1981)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 201 (1981), S. 31-42 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Cells located in the interatrial septum of the ferret heart were examined and mean cell volume, surface area, length, width, as well as cell length/width and surface area/volume ratios were obtained. The muscle cells were from two different regions. One region was the area of the middle internodal tract while the other was from the area where the anterior and middle internodal tracts intermingled. Based on the data obtained, at least two different subpopulations of interatrial muscle cells could be defined. The larger cells had a mean cell length of 109.7 μm, a mean cell width of 13.1 μm, a length/width ratio of 8.61, a mean cell surface area of 5,057.6 μm2, a mean cell volume of 5960.8 μm3, and a surface area/volume ratio of 0.87. The smaller cells had a mean cell length of 58.0 μm, a mean cell width of 12.2 μm, a length/width ratio of 4.85, a mean cell surface area of 2494.1 μm2, a mean cell volume of 2553.6 μm3, and a surface area/volume ratio of 1.00. The large cell population had cells that were myofibril rich and also others that were myofibril poor. These quantitative data indicate that the regions of internodal pathways are not composed of a single specialized cell type, but rather are composed of at least two, if not more, cell types that intermingle with each other.
    Additional Material: 11 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092010105
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  • 7
    Electronic Resource
    Electronic Resource
    The use of computer imaging techniques to visualize cardiac muscle cells in three dimensions (1980)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 198 (1980), S. 537-546 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Atrial muscle cells and atrioventricular bundle cells were reconstructed using a computer-assisted three-dimensional reconstruction system. This reconstruction technique permitted these cells to be viewed from any direction. The cell surfaces were approximated using triangular tiles, and this optimization technique for cell reconstruction allowed for the computation of cell surface area and cell volume. A transparent mode is described which enables the investigator to examine internal cellular features such as the shape and location of the nucleus. In addition, more than one cell can be displayed simultaneously, and, therefore, spatial relationships are preserved and intercellular relationships viewed directly. The use of computer imaging techniques allows for a more complete collection of quantitative morphological data and also the visualization of the morphological information gathered.
    Additional Material: 7 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1091980314
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  • 8
    Electronic Resource
    Electronic Resource
    Early morphological alterations of pressure-overloaded cat right ventricular myocardium (1983)
    New York, NY [u.a.] : Wiley-Blackwell
    The @Anatomical Record 207 (1983), S. 417-426 
    Details
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: Pressure overload of the right ventricle results in an increase in ventricular mass. It also results in abnormal in vitro contractile function in advance of the onset of congestive heart failure as determined in papillary muscles removed from these ventricles. To correlate these functional abnormalities with any early underlying morphological changes, a band was placed around the proximal pulmonary artery of cats. This band restricted the lumen to 20% of normal and was left in place for 2 weeks. At that time, hemodynamic variables were measured to insure that right ventricular pressure overload had been produced. The hearts were then perfusion fixed, and papillary muscles from the right ventricle were prepared for light and transmission electron microscopy. Quantitative morphological data were obtained for the volume density both of several tissue components and of several organelles. It was found that there are significant increases in myocyte cross-sectional area and diameter in hypertrophied tissue with a concurrent increase in the volume density of interstitial tissue. There are no alterations in the volume density of organelles in the hypertrophied myocytes. We suggest that the substantial increase in the proportion of connective tissue and the decrease in the surface area to volume ratio that accompany pressure overload cardiac hypertrophy may be early underlying structural changes that relate directly to the abnormal contractile function found in this type of hypertrophy.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/ar.1092070304
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  • 9
    Electronic Resource
    Electronic Resource
    1,25-dihydroxyvitamin D3 stimulates the phosphorylation of two acidic membrane proteins of 42,000 and 48,000 daltons in rat colonocytes: An effect modulated by vitamin D status (1995)
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 162 (1995), S. 172-180 
    Details
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Our laboratory has recently demonstrated that 1,25-dihydroxyvitamin D3(1,25(OH)2D3) rapidly stimulated membrane polyphosphoinositide breakdown and increased intracellular calcium, as well as activated protein kinase C (PKC) in vitamin D-sufficient rat colonocytes. These effects of 1,25(OH)2D3 were, however, lost in vitamin D-insufficient rats and restored by the in vivo repletion of 1,25(OH)2D3. In the present studies we have examined the ability of 1,25(OH)2D3 to stimulate the phosphorylation of colonic membrane proteins in intact D-sufficient cells. In addition, we investigated the effects of vitamin D status on the phosphorylation of these membrane proteins in broken cell preparations. These studies demonstrated that 1,25(OH)2D3 increased the phosphorylation of at least two colonic membrane proteins with apparent molecular weights of 42,000 (pp42) and 48,000 (pp48) in intact cells of vitamin D-sufficient rats. Moreover, in vitamin D-sufficient rats, treatment of colonocytes with 1,25(OH)2D3 or 12-Otertradecanoyl phorbol 13-acetate (TPA), a known activator of PKC, significantly increased the phosphorylation of pp42 and pp48 in broken cell preparations. The kinetics of these phosphorylations in response to 1,25(OH)2D3 were both rapid and transient. In addition, PKC19-36, a specific PKC inhibitor, decreased the phosphorylation of pp42 and pp48, whereas okadaic acid (OA), a type 1 and 2A protein phosphatase inhibitor, further augmented their phosphorylation in response to 1,25(OH)2D3. The isoelectric points of pp42 and pp48 were 5.79 and 5.97, respectively, and both were predominantly phosphorylated on threonine residues. In contrast to our findings in colonocytes from vitamin D-sufficient animals, basal phosphorylation of pp42 and pp48 were increased in membranes prepared from vitamin D-insufficient rats. Moreover, these phosphorylations failed to change in response to 1,25(OH)2D3-treatment of colonocytes from vitamin D-insufficient rats. The basal phosphorylation of each of these proteins was restored to control levels, as was their ability to respond to the direct addition of 1,25(OH)2D3 following the in vivo repletion of vitamin D-insufficient rats with this secosteroid. In summary, we have identified two acidic membrane proteins from rat colonocytes that are phosphorylated in both intact and broken cell preparations in response to 1,25(OH)2D3 treatment, an event modulated by vitamin D status and mediated, at least in part, by PKC. © 1995 Wiley-Liss, Inc.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/jcp.1041620203
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  • 10
    Electronic Resource
    Electronic Resource
    Gene dosage compensation in trisomies of Drosophila melanogaster (1985)
    Chichester [u.a.] : Wiley-Blackwell
    Developmental Genetics 6 (1985), S. 39-58 
    Details
    ISSN: 0192-253X
    Keywords: Drosophila melanogaster ; trisomy 3L ; dosage compensation ; heat shock ; Life and Medical Sciences ; Genetics
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology
    Notes: Production of trisomic-3L Drosophila melanogaster has allowed further investigation of compensated levels of gene expression in autosomal trisomies. We find that four enzyme loci on this arm produce diploid levels of gene product in trisomic-3L larvae. For one of these genes, we show that all three alleles are expressed at similar levels. Two genes on 3L display dose-dependent levels of gene product, and their location, relative to the four compensating loci, indicates that these two classes of genes are not regionally separated. In trisomic-2R larvae, the level of enzyme produced from on 2R-linked gene was dose dependent. In contrast, measurements of five loci on the X chromosome in metafemales (X trisomies) suggest that most genes are compensated in these individuals. Heat-shock gene expression in trisomic-3L salivary glands was qualitatively similar to diploids. The quantities of the small hsps (from the 67B cluster on 3L) suggest that these four genes respond independently to the trisomic condition; two produce compensated levels of protein, whereas the other two produce dose-dependent levels of protein. The amount of hsp 83 produced in trisomies was similar to diploids (compensated). However, quantification of hsp 83 RNA showed that a dose-dependent level of transcript was produced. This implies that hsp 83 compensation is controlled post-transcriptionally.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/dvg.1020060104
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