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Biomedical subjects

U Welsch

Publications and source records attributed to U Welsch.

At least 37 records · Page 2Linked to original sources

Cutaneous glands of male and female impalas (Aepyceros melampus): seasonal activity changes and secretory mechanisms.

The cutaneous glands of the forehead and the metatarsus were studied by histological and histochemical methods and electron microscopy in adult male and female impalas in various seasons of the year. All glandular areas consist of apocrine and holocrine glands, which, however, occur in different proportions. Our findings in the apocrine gland cells suggest (1) the synthesis and exocytosis of a glycoproteinaceous secretory product stored in secretory granules, (2) typical apocrine secretion of the transformed apical cytoplasm, and (3) transepithelial fluid transport. The Golgi apparatus and apical membrane have binding sites for several lectins (PNA, HPA, RCA I, WGA). Cytokeratins 7, 14 and 19 are expressed at various intracellular localizations, suggesting an active role in the secretory mechanisms. The glands of the male forehead show marked seasonal changes in activity that are correlated with the main phases of the reproductive cycle, with the highest cellular activity occurring during the rut in April/May. The female forehead glands are only moderately developed and do not undergo seasonal changes. The metatarsal glands are of equal size in males and females and show no seasonal changes in activity. This study supports the hypothesis that (1) forehead glands in the male have a signaling role in the rut and (2) the metatarsal glands have a more general, probably social role maintaining and restoring contact between herd members.

Alcian Blue↗

Secretory cell types and cell proliferation of human bronchial epithelial cells in an organ-culture system.

To study the secretory products and the proliferation of cells of the human respiratory surface epithelium, we established a miniorgan-culture system of bronchial tissue. Biopsies of large airways were grown on agar-coated dishes immersed in a serum-enriched medium. As determined by light and transmission electron microscopy, between 1 and 3 weeks, the organ cultures were covered by a differentiated epithelium consisting of secretory, ciliated, and basal cells. Immunohistochemistry, using antibodies to mucin and lysozyme, and lectin histochemistry revealed both mucous and serous secretory cells in the epithelium. Cell proliferation was studied in situ using antibodies to proliferating cell nuclear antigen (PCNA) and Ki-67. Whereas at the time of explantation the proliferation was low (2.5+/-1.7% of the epithelial cells were PCNA-positive, 1.7+/-0.6 were Ki-67-positive), at 24 h of cultivation, 30.4+/-5.1% or 25.2+/-4.9% of the epithelial cells were labeled with antibodies to PCNA or Ki-67. After 7 days, the number of dividing cells was low again. The results show that the organ-culture system of human respiratory surface epithelium produces a differentiated epithelium that is useful in the study of secretory processes, differentiation, and proliferation.

Bronchi↗

Histo- and cytophysiology of the lactating mammary gland of the African elephant (Loxodonta africana).

The lactating mammary gland of the African elephant (Loxodonta africana) has been studied with a panel of morphological techniques focusing on (1) the functional changes during the secretory process, (2) proliferative process [by application of proliferating cell nuclear antigen (PCNA) immunohistochemistry] and apoptotic phenomena [by use of the TUNEL technique] in the individual lobules, and (3) components of milk and milk-fat-globule membrane. In the lactating gland, the lobules are variably differentiated; within a lobule, however, the alveoli are usually similarly differentiated. The morphology of their alveoli suggests a classification of the lobules into types 1-3. Lobules of type 1 are composed of immature tubular alveoli with mitotic figures and numerous PCNA-positive nuclei; advanced type 1 alveoli contain abundant glycogen and specific secretory granules. Lobules of type 2 are further subdivided. In type 2a lobules, the epithelial cells of the alveoli form tall apical protrusions, which in part are occupied by small lipid droplets and which are pinched off in an apocrine fashion. The number of lysosomes varies considerably. Type 2b is the most common type, with striking basal membrane foldings, abundant rough endoplasmic reticulum cisterns, large Golgi apparatus, numerous mitochondria, lipid droplets, and protein vesicles with 30- to 90-nm-wide casein micelles. The lipid droplets are pinched off with minimal amounts of cytoplasm. Type 2c is composed of alveoli with a cuboidal epithelium and few signs of secretory activity. Increasing expression of peanut-agglutinin-binding sites parallels the maturation and differentiation of the glandular cells. Type 3 lobules are marked by numerous TUNEL-positive nuclei and large lipid droplets and are apparently degenerating structures. Cytokeratin (CK) 14 is usually present in the myoepithelial cells; CK 19 and CK 7 mark ductal and immature alveolar epithelia. Milk protein content varies between 2.6% and 6.3%, and casein micelles range from 35 to 90 nm in diameter. The diameter of intra-alveolar milk fat globules ranges from 5 to 25 micrometer and the membranes bear a filamentous surface coat composed of membrane-anchored mucins; gel-electrophoretic analysis of these mucins from different individuals demonstrates the presence of mucin MUC 1, which is expressed with considerable genetic heterogeneity.

Animals↗

Disparate effects of adhesion and degranulation of platelets on myocardial and coronary function in postischaemic hearts.

OBJECTIVE: Beside the major effect of acute thrombus formation, little is known about the interaction of platelets with the coronary endothelium in an ischaemia-reperfusion situation. The present study was designed to investigate, separately, the consequences of platelet adhesion and degranulation during myocardial reperfusion. METHODS: Isolated guinea pig hearts perfused with Krebs-Henseleit buffer and performing pressure-volume work were used. We infringed myocardial function by imposing ischaemia (20 min of low-flow perfusion with 1 ml/min and 10 min of global ischaemia) and reperfusion (15 min with 5 ml/min). During low-flow perfusion, the coronary endothelium was stimulated by thrombin before and during infusion of a bolus: 10(8) washed human platelets +/- the Arg-Gly-Asp (RGD) analogon lamifiban, the supernatant of 10(8) thrombin-stimulated platelets, fibrinogen (2 microM), lamifiban (2 microM) or Tyrode's solution (control group). The parameter external heart work (EHW), determined pre- and postischaemically, served as criterion for recovery of myocardial function. Additionally, the formation of capillary transudate was measured during the reperfusion phase to assess coronary permeability. Coronary perfusion pressure was monitored continuously and myocardial production of lactate and consumption of pyruvate were measured. Electron microscopy of hearts was performed after platelet application to verify platelet adhesion in the coronary system. RESULTS: Recovery of EHW by hearts without platelet application was 64 +/- 3% and was significantly reduced to 49 +/- 5% by platelet infusion (n = 8 each). Infusion of supernatant of thrombin-stimulated platelets did not impair recovery of heart work. In the reperfusion phase (6th-10th min), hearts that either had received platelets or supernatant of platelets exhibited a significantly reduced production of capillary transudate (70 microliters/min vs. 180 microliters/min for the controls). Intracoronary bolus application of fibrinogen or lamifiban also reduced coronary leak. Coronary perfusion pressure and metabolic parameters were not statistically different between the groups at any time. CONCLUSIONS: Platelet adhesion to the coronary endothelium in a situation of myocardial ischaemia impairs cardiac recovery, whereas constituents released by platelets may have beneficial effects on the integrity of the coronary endothelium. In particular, fibrinogen seems to contribute to the permeability reducing effect, possibly by interaction with endothelial receptors recognising the RGD sequence.

Acetates↗

Apoptosis in restenosis versus stable-angina atherosclerosis: implications for the pathogenesis of restenosis.

Decreases in programmed cell death (apoptosis) may contribute to restenotic hyperplasia by prolonging the life span of intimal cells. Apoptotic events were compared in restenotic versus primary lesions, by using atherectomy samples from 16 restenotic and 30 primary human peripheral and coronary lesions from patients presenting with stable angina. We used transmission electron microscopy to identify apoptosis, quantify its frequency, distinguish apoptosis from necrosis, and relate these events to cellular composition. Smooth muscle cell (SMC) density was higher in restenotic versus primary lesions (P<0.0001), whereas the number of macrophages was significantly reduced (P<0.01) and the number of lymphocytes was lower, but not significantly (P=0.06). As the main finding, restenotic lesions contained fewer apoptotic cells compared with primary lesions (3% versus 13%, P=0.002), whereas no differences were found for cellular necrosis. With regard to cell type, the lower frequency of apoptotic cells observed in restenotic tissue was attributable to both SMCs and macrophages. The key finding of less apoptosis in restenotic versus primary lesions was in agreement with terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) analysis (2% versus 9%, P<0.001). For all lesions analyzed, significant inverse correlations were observed between the density of SMCs and the frequency of apoptotic cell death (r=-0.60, P<0.001) as well as the density of SMCs and that of macrophages (r=-0.74, P<0.001). No relationship was seen between the frequency of apoptosis and the density of macrophages. In conclusion, the data of the present study indicate that a low level of apoptosis may be an important mechanism leading to restenotic intimal lesion development after interventional procedures.

Adult↗

Isolation and molecular characterization of serous and mucous gland cells of the porcine airways.

Secretory cells of the glands of the airways play important roles in the pathogenesis of several diseases. Little, however, is known about the molecular biology of these cells. Here we describe a procedure for the separation of serous and mucous gland cells and the isolation of genes specifically expressed in these cells. Mucosal tissue was prepared from porcine large airways. Following enzymatic digestion, the cell types were separated by discontinuous Percoll density gradient centrifugation. Cell purity was analyzed by electron microscopy. The cell fractions contained between 75 and 85% mucous and serous cells, respectively. To isolate cell type-specific genes, poly(A)+ RNA was isolated from serous and mucous cell fractions, reverse transcribed and used for differential display polymerase chain reaction (PCR). Out of about a total of 1,700 PCR products identified in horizontal polyacrylamide gels, most bands were found to be common to both cell fractions, indicating that the transcript patterns in cells from both fractions are very similar. Eighteen PCR products, however, were consistently distinct in the two cell fractions, with eight products present only in RNA from the mucous cell fraction and 10 PCR products present only in RNA from the serous cell fraction. Dot-blot analysis of mRNA of serous and mucous cells proved the cell type-specific expression of nine PCR products. Northern blot analysis detected single transcripts for each PCR product. The development of a simple cell separation procedure for secretory cells of the airways, combined with the ability to isolate numerous cell type-specific marker genes, should facilitate the molecular understanding of secretory cells of the airways.

Animals↗

[Immunohistologic study of the localization of ICAM-1 (intercellular cell adhesion molecule 1) in alveolar epithelium in the human lung].

The intercellular cell adhesion molecule 1 (ICAM-1) is expressed in the endothelium of pulmonary blood vessels, in the alveolar epithelium and in the bronchial epithelium. Because of conflicting reports in the literature on the question whether ICAM-1 is exclusively expressed in pneumocytes Type I or also in pneumocytes Type II, the present study aimed at characterising the cell types in normal human alveolar epithelium which show immunoreactivity for ICAM-1. Immunohistochemistry for ICAM-1 was performed on a series of 19 specimens of normal human lung. In addition, double staining procedures of ICAM-1 together with cell type specific antigens were performed. To detect pneumocytes Type II an antibody to cytokeratin 18 (CK 18) was used. Alveolar macrophages were marked by an antibody to the monocyte macrophage-specific leukocyte antigen CD 68. Vascular endothelium was stained by common endothelial markers (Ulex europaeus agglutinin Type I, anti-von Willebrand factor). The alveolar septa showed intense surface staining for ICAM-1 that could be localised predominantly to pneumocytes Type I. There were also single ICAM-1 positive cells having the characteristics of pneumocytes Type II in respect of their morphological appearance and their cytokeratin pattern. For the interpretation of these results the fact had to be considered that pneumocytes Type I can partly cover up pneumocytes Type II. This was confirmed by ultrastructural observations. Our findings suggest that ICAM-1 plays a part in the interaction between intraalveolar leukocytes and the alveolar epithelium.

Adult↗

Localization of a putative progesterone membrane binding protein in porcine hepatocytes.

A putative membrane bound steroid receptor was localized using a peptide specific antibody. Surprisingly, the distribution of immunocytochemical staining in porcine hepatocytes cells provides evidence for the localization to endomembranes (endoplasmic reticulum, Golgi apparatus). Immunofluorescence experiments with HEK cells, which were transfected with a pcDNA3.1 vector containing the coding sequence of the putative progesterone binding protein shows staining within the cells supporting these results. Additionally, 3H-progesterone binding and glucose-6-phosphatase activity as marker enzyme for endoplasmic reticulum were closely correlated in subcellular fractions of porcine liver cells.

Animals↗

Lectins and antibodies to blood group antigens as markers for the basal cells of the human respiratory epithelium.

We used a pattern of 30 lectins and antibodies against antigens of the ABO-blood group system to find specific and sensitive markers for the basal cells of the human respiratory surface epithelium. Three lectins always stained the basal cells: Aaptos papillata agglutinin I (APA I), peanut agglutinin (PNA), and wheat germ agglutinin (WGA): Other lectins and the antibodies gave positive results only in tissue of secretors (blood group antigens in secretions) and these were dependent on the ABO-blood group. Griffonia simplicifolia agglutinin (GSA I B4) bound to basal cells of humans with blood group B and AB, Helix pomatia agglutinin (HPA), Soy bean agglutinin (SBA), and Dolichos biflorus agglutinin (DBA) bound to blood group A and AB, Lens tetragonolobus agglutinin (LTA) and Ulex europaeus agglutinin I (UEA) bound to secretors in every case, and strongly to blood group O. The antibodies bound to basal cells only in the tissue of secretors, dependent on the ABO-blood group. The results show that lectins and antibodies may be used as markers for the detection of basal cells in the human respiratory epithelium. Furthermore they suggest that the glycosylation of some glycocomponents of the basal cells is under the control of the genes of the secretor- and ABO-blood group system.

ABO Blood-Group System↗

Histological, histochemical, and fine structural observations on the lymph node of the common seal (Phoca vitulina) and the grey seal (Halichoerus grypus).

BACKGROUND: The recent seal death epizootic prompted interest in their immune system, for which no current morphological data were available. METHODS: Lymph nodes from adult harbor seals (Phoca vitulina) and grey seals (Halichoerus grypus) were investigated by light microscopy, electron microscopy, and lectin histochemistry. RESULTS: No significant differences in the lymph node morphology were found between the two species, and the overall organization of the nodes comprises of capsule, trabeculae, cortex, paracortex, and medulla. Capsule and trabeculae are composed of tightly packed collagen and elastic fibrils and are rich in fibroblasts, myofibroblasts, and smooth muscle cells. Unmyelinated nerve fibers are common. The cortex contains numerous secondary follicles with well-developed germinal centers and paracortical areas with high endothelial venules. Antigen-presenting cells and phagocytic macrophages were abundantly present. The medullary cords contain numerous plasma cells. Fibroblastic reticulum cells are common throughout the parenchyma and transverse the sinus. Marginal, radial, and medullary sinuses are lined by littoral cells. The visceral lining of the sinuses is marked by macrophages and by numerous mast cells. CONCLUSIONS: The morphology of seal lymph nodes does not differ significantly from that of terrestrial mammals. Earlier functional conclusions concerning seal lymph nodes are substantiated by this morphological study.

Animals↗

Histophysiological observations on the external auditory meatus, middle, and inner ear of the Weddell seal (Leptonychotes weddelli).

The external auditory meatus, middle, and inner ear of the deep-diving Weddell seal (Leptonychotes weddelli) were studied with light microscopic, histological, and histochemical techniques in order to contribute to the open discussion on the orientation of this seal in the darkness of the deep Antarctic seas. The external auditory meatus is characterized by a well-developed venous plexus, single apocrine ceruminous, and numerous holocrine sebaceous glands and an incomplete tube of elastic cartilage. The tympanic membrane is comprised of two layers of radially and concentrically arranged collagen fibers and by elastic fibers which are concentrated in the outer part of the ear drum. The tympanic cavity is lined by a pseudostratified prismatic ciliated epithelium with goblet cells; a plexus of wide venous vessels marks the subepithelial lamina propria. The cochlea is about 10 mm high and forms about two and a half turns. The richly pigmented stria vascularis is well vascularized, while the cell-rich prominentia spiralis contains only single small blood vessels. The organ of Corti contains one row of inner and three rows of outer hair cells. Cells of Hensen, Claudius, and Boettcher are present. The basilar membrane is of comparatively uniform simple structure and is composed of abundant glycoproteins, proteoglycans, collagenous fibers, and the loose tissue of the tympanal layer. The spiral ligament is built up by abundant proteoglycans and a complex system of radial and concentric collagen fibers; close to the osseous wall of the bony cochlea it contains fine elastic fibers. The inner zone of the osseous wall of the cochlea strikingly contains hyaline cartilage. The thin lamina spiralis ossea is covered by a limbus spiralis with interdental cells secreting the lamina tectoria, which has a fibrous texture and contains glycoproteins and negatively charged components.

Adaptation, Physiological↗

Endovascular catheter-delivered photodynamic therapy in an experimental response to injury model.

BACKGROUND: The effectiveness of local endovascular photodynamic therapy (PDT) in preventing tissue hyperplasia was evaluated in a vascular injury model. METHODS: Standardized unidirectional arterial injury with a directional atherectomy catheter was performed in porcine arteries (n = 180). Animals (n = 72) were randomly allocated to unidirectional injury only (Group 1), injury followed by drug delivery of photosensitizer with a porous balloon (Group 2), or by local exposure to monochromatic light (Group 3). In Group 4, injury was followed by local drug delivery of photosensitizer and subsequent exposure to light (PDT). Up to 21 days after treatment, all experimental vessels were excised, fixed and processed for histology, immunohistochemistry and transmission electron microscopy. RESULTS: After vascular injury an inflammatory and myoproliferative response was observed in Groups 1, 2 and 3 (mean tissue hyperplasia/media ratio 1.0 +/- 0.5 at 21 days; area tissue hyperplasia: 1.57 +/- 0.9 mm2). Proliferation in injured vascular segments (Group 1-3) reached a maximum at 7 days, with 6%. Only in Group 4, after injury followed by photodynamic therapy, was there no significant vascular response (mean tissue hyperplasia/media ratio 0.3 +/- 0.2: area tissue hyperplasia: 0.1 +/- 0.05 mm2 p < 0.001, proliferating cells 0.3%). CONCLUSION: Vascular response after unidirectional injury was suppressed only by endovascular photodynamic therapy.

Animals↗

[Decreased apoptosis as a pathogenic factor in intimal hyperplasia of human arteriosclerosis lesions].

Restenosis remains a persistent problem following intravascular reconstruction. Smooth muscle cell proliferation, extracellular matrix production and remodeling are accepted mechanisms of restenotic lesion formation. Decreased programmed cell death (apoptosis) may also contribute to restenosis by prolonging the life span of intimal cells, with their subsequent accumulation and development of hyperplastic lesions. The objectives of the present study were as follows: i) to identify cell death, ii) to distinguish and quantify apoptosis from necrosis, and iii) to compare restenotic with primary lesions. To this end, human atherectomy specimens from 25 primary and 14 restenotic coronary and peripheral lesions were studied by TUNEL test (TdT-mediated dUTP Nick End Labeling; detection of cell death by the presence of fragmented DNA), transmission electron microscopy and morphometric analysis. Intimal hyperplasia was more consistent with restenosis than with primary lesion origin, and was mainly attributed to increased smooth muscle cell density (649 vs. 219 cells/mm2; p < 0.001). The main finding of the present study is that hypercellular restenotic tissue contains fewer TUNEL+ cells than hypocellular plaques (14% vs. 27%; p < 0.05). Most importantly, ultrastructural evaluation revealed a markedly reduced portion of intimal plaque cells, especially smooth muscle cells exhibiting distinct morphologic signs of apoptosis (3% vs. 13%; p < 0.001). In contrast, incidence of necroses did not differ between both lesion types (0.13 vs. 0.12 necroses/ cell; p = 0.49). Thus, our data indicate apoptosis and not necrosis to be the crucial cell death form to account for the apparent discrepancy found in both lesion types with reduced apoptosis in cell-rich restenoses. The findings of the present study suggest that decreased apoptosis is an important regulatory mechanism ultimately leading to intimal hyperplasia as commonly found in human restenosis post angioplasty.

Aged↗

[Increased apoptosis and necrosis of coronary plaques in unstable angina].

In acute coronary syndromes, arteriosclerotic plaques are characterized by inflammation and decreased smooth muscle cell density. The underlying pathogenic processes remain unclear. Among others, increased programmed cell death (apoptosis) is postulated. Coronary atherectomy specimens from 26 patients with unstable angina (group 1) and from 24 patients with stable angina (group 2) were examined, using immunohistochemistry (TUNEL test to detect fragmented DNA) and transmission electron microscopy. The objectives of the present study were to evaluate plaque group differences in the cellular composition, to detect and quantify cell death, and to differentiate between apoptosis and necrosis. Group 1 lesions contained more macrophages and lymphocytes as well as significantly (p = 0.01) less smooth muscle cells compared with group 2 lesions, whereas both revealed a comparable cell density. All plaques showed signals for fragmented DNA. TUNEL-positive cells were seen more frequently in lesions with unstable angina (p = 0.04). Ultrastructural analysis revealed signs of programmed cell death, such as nuclear alterations, cellular condensation due to lost adhesion, and apoptotic bodies. Importantly, group I lesions comprised significantly more apoptotic SMCs and apoptotic macrophages compared with group 2 lesions (28% vs. 16%; p = 0.02). Also, cellular necroses were found to be increased in lesions with unstable angina (18% vs. 8%; p = 0.02). The density of macrophages showed a positive correlation to the incidence of cellular necroses in group 1 lesions (r = 0.44; p = 0.02), but not in group 2 lesions. In both plaque groups, this determinant was independent from cellular apoptosis, also at high levels as found with unstable angina. The present study on coronary atherectomy specimens with unstable angina reveals intimal macrophage infiltration and the density of apoptotic as well as necrotic intimal cells to be increased, whereas the content of intact SMCs was reduced. Increased, macrophage-independent apoptosis strongly points to the presence of one or several pro-apoptotic intimal factor(s) predisposing to plaque rupture. Implications of our findings may be directed to identify this (these) factor(s) and to modulate endogenous apoptotic activity with the ultimate goal to raise regional smooth muscle cell density.

Angina, Unstable↗

Sulphated polyanions in cytoplasm and nuclei of epithelial cells of Branchiostoma demonstrated by the cationic dye Cupromeronic Blue.

The intracellular occurrence and distribution of sulphated polyanions, interpreted to represent mucins, were studied in secretory epithelial cells in the primitive chordates Branchiostoma lanceolatum and B. floridae at the electron microscopical level by using Cupromeronic Blue (CMB). CMB-precipitates were mainly found within two potential types of mucin vesicles (apical and basal) and Golgi cisterns. The mucin vesicles form a distinct population of secretory granules different from another nonmucin granule population. Within the epidermal cells the staining intensity of the Golgi cisterns with CMB increased from the cis to the trans compartment. The pharyngeal mucous cells showed staining only in the trans Golgi compartment. These findings indicate, that CMB can be used for intracellular localization of mucins and that sulphation of the mucins in the investigated cells may occur within different compartments of the Golgi complex. Apparently the mucin is secreted apically but only in the epidermis it forms a dense layer covering the apical microvilli. In the Branchiostoma epidermal cells a layer of specialized basal vesicles occurred, containing unusually large and branched CMB-precipitates which possibly serve mechanical functions. In the nuclei CMB-precipitates were regularly demonstrated in the euchromatin of the cell types studied.

Animals↗

Use of antibodies directed against blood group substances and lectins together with glycosidase digestion to study the composition and cellular distribution of glycoproteins in the large human airways.

Some 30 lectins in combination with glycosidase digestion and immunohistochemistry with 5 antibodies directed against antigens of the ABO and Lewis blood group systems were used to analyse the distribution and synthesis of glycoconjugates in the epithelium of the large airways in man. Both mucous gland cells and goblet cells were labelled by 12 of 30 lectins and by the antibodies, dependent on the ABO, Lewis, and secretor status. The corresponding binding patterns of the serous gland cells differed markedly from those of goblet and mucous gland cells and in general were not dependent on the ABO, Lewis, and secretor status. After digestion with neuraminidase and fucosidase, binding of soy bean agglutinin and peanut agglutinin to goblet and mucous gland cells was increased. Binding of peanut agglutinin to serous gland cells was stronger only after the digestion with neuraminidase. Digestion with O-glycosidase after the use of neuraminidase or fucosidase resulted in a decrease of peanut agglutinin binding to goblet and mucous gland cells. The present results show that the secretory products of goblet and mucous gland cells on the one hand and those of serous cells on the other differ considerably with respect to their terminal glycosylation. The glycosyltransferases coded by genes of the ABO and Lewis blood group and secretor systems are active only in goblet and mucous gland cells, resulting in the presence of the corresponding antigens. Precursor substances of blood group antigens types 1, 2, and 3 are found only in these cell types. In serous gland cells, blood group systems do not influence the glycosylation of glycoproteins. The results of the digestion with O-glycosidase indicates the presence of O-glycosylation in mucous gland and goblet cells, but not in serous gland cells.

ABO Blood-Group System↗

[Electron microscopy studies of vascular innervation of nasal mucosa in the human].

BACKGROUND: The distribution of neural structures in human nasal vasculature is still not completely understood. To date, immunocytochemical and histochemical studies of the innervation pattern and neurotransmitter distribution have only been performed using light microscopy. The aim of this study was to verify these results by electron microscopy and to obtain new knowledge of the innervation of the individual vessel types. The target was to determine the role of the different vessels in the swelling mechanism in human nasal mucosa. MATERIAL AND METHODS: Specimens were prefixed in glutaraldehyde and postfixed in osmium tetroxide. After dehydration they were embedded in araldite. Ultrathin sections were cut, contrasted with uranylacetate and lead citrate, and studied under EM. RESULTS: Nasal vasculature is controlled by a dense innervation. Amyelinated longitudinal nerve bundles and smaller axon conglomerates are detected in the arterial adventitia. Capacitance vessels (veins) in general show few nerve structures, which, in contrast to arteries, are also located between the smooth muscle cells. Cushion veins, however, reveal a stronger innervation pattern especially in their muscular swelling. In contrast to smaller arterioles, no axons can de demonstrated in capillaries. CONCLUSION: The density of innervation in arteries and cushion veins seems to indicate that these vessel types are the central neural control point for the swelling mechanism in human nasal mucosa. Capillary function, however, does not seem to be directly influenced by the autonomic nervous system.

Arteries↗

Ultrastructural characteristics of human atherectomy tissue from coronary and lower extremity arterial stenoses.

In animal studies, smooth muscle cell phenotype conversion has been suggested to be an essential prerequisite for subsequent migratory and proliferative events leading to (neo)intima formation. To determine ultrastructural characteristics of individual smooth muscle cells and to relate them to specific lesion types and intimal cell density, we compared atherectomy samples from 17 restenotic and 32 primary coronary and peripheral lesions using transmission electron microscopy and histology. Ultrastructural analysis of cell-rich tissue, predominantly of restenotic origin, revealed smooth muscle cells full of synthetic organelles. Moreover, these cells were frequently found to be surrounded by loose extracellular matrix and partially fragmented basement membrane components. In contrast, plaques exhibiting low cell density, as exclusively seen with primary lesions, displayed an extensive buildup of extracellular matrix containing sparse numbers of microfilament-rich smooth muscle cells. The central finding of our study is a morphometrically quantitated, twofold greater (p <0.001) volume fraction of synthetic organelles (VS) within smooth muscle cells in restenotic versus primary plaques, indicating a more dedifferentiated cellular phenotype as a typical feature of restenotic lesions. Equally enhanced VS values were seen for restenotic coronary and peripheral plaques. No VS decrease was observed during time after angioplasty (2.2 to 30 months) regardless of previous revascularization procedures (balloon angioplasty or atherectomy). Despite intra- and interlesional variability, VS and intimal cell density were strongly correlated (r = 0.74; p <0.001). This correlation was observed more often with clinical restenoses and, importantly, in a portion (10% to 15%) of primary lesions. Data from restenotic lesions indicate that a dedifferentiated smooth muscle cell phenotype, pericellular matrix disintegration, and intimal hypercellularity are long-lasting biologic responses to previous smooth muscle cell injury. Similar tissue characteristics expressed in several primary lesions suggest that comparable pathogenic mechanisms are related to the progression and/or acuity of chronic lesions.

Adult↗