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PubMed1962

Studies on the cornea. I. The fine structure of the rabbit cornea and the uptake and transport of colloidal particles by the cornea in vivo.

Physiological studies have demonstrated that ions, as well as large molecules such as hemoglobin or fluorescein, can diffuse across and within the cornea. Most of the substrates for corneal metabolism are obtained from aqueous humor filling the anterior chamber. In order to receive its nutrients and in order to maintain its normal conditions of hydration, the avascular cornea must transport relatively large amounts of solute and solvent across the cellular layers which cover this structure. It has been suggested in the past that there may be a morphological basis for the transport of large amounts of solvents and solutes by cells by the mechanism of pinocytosis. The use of electron-opaque markers to study fluid movements at the electron microscope magnification level was described by Wissig (29). The present study describes the fine structure of the normal rabbit cornea and the pathways of transport of colloidal particles by the cornea in vivo. Rabbit corneas were exposed in vivo to suspensions of saccharated iron oxide, thorium dioxide, or ferritin by injection of the material into the anterior chamber. In other experiments thorium dioxide or saccharated iron oxide was injected into the corneal stroma, producing a small bleb. Particles presented at the aqueous humor surface of the rabbit corneal endothelium are first attached to the cell surface and then pinocytosed. It appears that the particles are carried around the terminal bar by an intracellular pathway involving the pinocytosis of the particles and their subsequent transport in vesicles to the lateral cell margin basal to the terminal bar. Particles introduced at the basal surface of the endothelium (via blebs in the corneal stroma) are apparently carried through the endothelial cells in membrane-bounded vesicles without appearing in the intercellular space. There appears to be free diffusion of these particles through Descemet's membrane and the corneal stroma. The stromal cells take up large quantities of the particles when blebs are injected into the stroma.

Animals↗
PubMed1962

The effect of insulin, alloxan diabetes, and anoxia on the ultrastructure of the rat heart.

Hearts from normal and alloxan diabetic rats were perfused in vitro with a bicarbonate-buffered medium containing glucose. Transport of glucose through the cell membrane was stimulated with insulin or by induction of anaerobiosis. The organs were rapidly fixed and examined by electron microscopy. Transport stimulation was not associated with any increase in the number of sarcolemmal invaginations or subsarcolemmal cytoplasmic vesicles. It was concluded that glucose transport and the effects of insulin or anoxia do not involve pinocytosis. The relationship of pinocytosis to glucose transport is discussed. The appearance of numerous lipid inclusions at the Z line level of the sarcomeres in the diabetic and anoxic myocardia is described.

Animals↗
PubMed1964

OOCYTE DIFFERENTIATION AND VITELLOGENESIS IN THE ROACH PERIPLANETA AMERICANA.

The ovary of the roach Periplaneta americana has been studied by techniques of light and electron microscopy. Each ovariole (panoistic type) contains a linear array of oocytes in varying stages of development. Newly formed oocytes become encased by a layer of follicle cells and begin pinocytosis. All subsequent growth stages of the oocytes are dependent, in part, on this phenomenon. All of the pinocytotic caveolae show an unique surface modification; i.e., on their internal surface they have an amorphous or filamentous substance and their external surface is studded with many fine radially oriented spike-like projections. The pinosomes of early oocytes do not contain a demonstrable internal structure; they are thought to contain nutritive substances for the developing oocytes rather than yolk precursors. When the oocyte enters its last stage of growth, characterized by yolk deposition, the caveolae become filled with a dense material which is thought to be the precursors of yolk. Hence the conclusion is drawn that yolk formation is independent of any cytoplasmic organelle system of the oocyte and that the precursors of this deutoplasmic substance are manufactured outside the ovary and are internalized by the process of pinocytosis. Under the phase-contrast microscope the nucleoli of early oocytes are large irregular masses and show the phenomenon of nucleolar emission (fragmentation). These "emissions" become randomly dispersed in the nucleoplasm and some of them come to be intimately associated with the fenestrated nuclear envelope. After this process ceases, the main nucleolar mass becomes vacuolated. Electron micrographs suggest that the constituent particles of the nucleolar emissions migrate from the nucleus through patent pores of the nuclear envelope.

Animals↗
PubMed1965

Protein uptake in the oocytes of the cecropia moth.

The formation of yolk spheres in the oocyte of the cecropia moth, Hyalophora cecropia (L.), is known immunologically to result largely from uptake of a sex-limited blood protein. Recent electron microscope analyses of insect and other animal oocytes have demonstrated fine structural configurations consistent with uptake of proteins by pinocytosis. An electron microscope analysis of the cecropia ovary confirms the presence of similar structural modifications. With the exception of two apparently amorphous layers, the basement lamella on the outer surface of the follicular epithelium and the vitelline membrane on the inner, there is free access of blood to the oocyte surface between follicle cells. Dense material is found in the interfollicular cell space and adsorbed to the outer surface of the much folded oocyte membrane. Pits in the oocyte membrane and vesicles immediately under it are lined with the same dense material not unlike the yolk spheres in appearance. Introduction of ferritin into the blood of a developing cecropia moth and its localization adsorbed to the surface of the oocyte, and within the vesicles and yolk spheres of the oocyte cortex, is experimental evidence that the structural modifications of the oocyte cortex represent stages in the pinocytosis of blood proteins which arrive at the oocyte surface largely by an intercellular route. Small tubules attached to the yolk spheres are provisionally interpreted as a manifestation of oocyte-synthesized protein being contributed to the yolk spheres.

Bombyx↗
PubMed1967

Studies on protein uptake by isolated tumor cells. 3. Apparent stimulations due to pH, hypertonicity, polycations, or dehydration and their relation to the enhanced penetration of infectious nucleic acids.

Fixation of (131)I-serum albumin by Ehrlich ascites tumor cells in suspensions and sarcoma S-180 monolayers was measured under experimental conditions. Anaerobic incubation and inhibitors of the oxidative metabolism critically restricted the range of glucose concentrations capable of supporting cell life; in glucose concentrations higher than 10(-2)M, Ehrlich cells suffered from their own acid production; in concentrations 10(-2)M, lower than they underwent damage by starvation. Both types of damage were accompanied by increased albumin fixation unrelated to pinocytosis. Different procedures recommended to enhance the uptake of infectious viral RNA by animal cells in culture were tested for their ability to increase albumin uptake. They enhanced the penetration of both albumin and vital dyes and decreased the viability of cell populations. Their effect, therefore, is related to cell damage. It was postulated that reversible damage to cells favors RNA infection by leading to abnormal uptake processes and by decreasing intracellular digestion. This abnormal uptake is different from pinocytosis and also from the massive fixation of albumin to dead cells. The latter phenomenon is due to adsorption by intracellular sites exposed by disruption of the cell membrane. Polycations are able to induce all three forms of fixation depending on the experimental conditions.

Adsorption↗
PubMed1959

The ingestion of proteins and colloidal materials by columnar absorptive cells of the small intestine in suckling rats and mice.

Proteins and colloidal materials, administered orally to suckling rats and mice, were ingested by columnar absorptive cells of the jejunum and ileum, but not of the duodenum. Bovine gamma globulin and ovalbumin were identified in the apical cytoplasm by staining with fluorescent antibody; trypan blue, Evans blue, saccharated iron oxide, and colloidal gold were detected intracellularly by their color, specific staining, and appearance in the electron microscope. Each substance was segregated in membrane-enclosed vacuoles, apparently part of a system of potentially interconnecting vacuoles and tubules in the apical cytoplasm which is continuous in places with the apical cell membrane. We postulate that ingestion of foreign materials was accomplished by pinocytosis, that is, by invagination of the apical cell membrane to form vacuoles containing material from the intestinal lumen. Approximately 18 days after birth columnar absorptive cells lost the ability to ingest proteins and colloids, and no longer contained large vacuoles and numerous tubules. At this age rats and mice lose the ability to absorb antibodies from the intestine in an immunologically intact form, and we conclude that cellular ingestion is part of the mechanism of absorption of intact proteins in suckling animals. Particulate fat apparently is absorbed in both newborn and adult animals by micropinocytosis. Thus adult animals may not have lost the capacity for pinocytosis, but rather have become selective as to what substances provoke it. Cortisone acetate, administered subcutaneously to rats 8 to 10 days old alters the columnar absorptive cells within 72 hours so that they resemble the cells in adult animals and no longer ingest proteins.

Animals↗
PubMed1980

Chemotactic peptide receptor modulation in polymorphonuclear leukocytes.

The binding of the chemotactic peptide N-formylnorleucylleucylphenylalanine (FNLLP) to its receptor on rabbit polymorphonuclear leukocytes (PMNs) modulates the number of available peptide receptors. Incubation with FNLLP decreases subsequent binding capacity, a phenomenon that has been termed receptor down regulation. Down regulation of the chemotactic peptide receptor is concentration dependent in both the rate and extent of receptor loss. The dose response parallels that of FNLLP binding to the recptor. The time-course is rapid; even at concentrations of FNLLP as low as 3 x 10(-9) M, the new equilibrium concentration of receptors is reached within 15 min. Down regulation is temperature dependent, but does occur even at 4 degrees C. Concomitant with down regulation, some of the peptide becomes irreversibly cell associated. At 4 degrees C, there is a small accumulation of nondissociable peptide that rapidly reaches a plateau. At higher temperatures, accumulation of nondissociable peptide continues after the rceptor number has reached equilibrium, and the amount accumulated can exceed the initial number of receptors by as much as 300%. The dose response of peptide uptake at 37 degrees C reflects that of binding, suggesting that it is receptor mediated. This uptake may occur via a pinocytosis mechanism. Although PMNs have not been considered to be pinocytic, the addition of FNLLP causes a fourfold stimulation of the rate of pinocytosis as measured by the uptake of [3H]sucrose.

Adaptation, Physiological↗
PubMed1980

Contractile basis of ameboid movement. VII. Aequorin luminescence during ameboid movement, endocytosis, and capping.

Aequorin luminescence has been utilized to determine the spatial and temporal fluctuations of the free calcium ion concentration [Ca++] in Chaos carolinensis during ameboid movement, pinocytosis, and capping. The [Ca++] increases above approximately 10(-7) M during normal ameboid movement. Three types of luminescent signals are detected in cells: continuous luminescence, spontaneous pulses, and stimulated pulses. Continuous luminescence is localized in the tails of actively motile cells, and spontaneous pulses occur primarily over the anterior regions of cells. We are sometimes able to correlate the spontaneous pulses with extending pseudopods, whereas stimulated pulses are induced by mechanical damage, electrical stimulation, concanavalin A-induced capping, and pinocytosis. The localization of both distinct actin structures and sites where [Ca++] increases suggests cellular sites of contractile activity. The independent evidence from localizing actin structures and the distribution of [Ca++] can also be viewed in relation to the solation-contraction coupling hypothesis defined in vitro.

Actins↗
PubMed1980

Phorbol myristate acetate stimulates microtubule and 10-nm filament extension and lysosome redistribution in mouse macrophages.

Phorbol myristate acetate (PMA) stimulates cell spreading and fluid-phase pinocytosis in mouse peritoneal macrophages. Colchicine (10(-5) M) and cytochalasin B (10(-5) M) abolish PMA stimulated pinocytosis but have little effect on cellular spreading (Phaire-Washington et al., 1980, J. Cell Biol., 86:634-640). We report here that PMA also alters the organization of the cytoskeleton and the distrubution of organelles in these cells. Neither control nor PMA-treated macrophages contain actin cables. PMA-treated resident thioglycolate-elicited macrophages exhibit beneath their substrate-adherent membranes many randomly distributed punctate foci that stain brightly for actin. The appearance and distribution of these actin-containing foci are not altered by colchicine (10(-5) M) or cytochalasin B (10(-5) M). In thioglycolate-elicited macrophages PMA causes the extension and radial organization of microtubules and 10-nm filaments and promotes the movement of secondary lysosomes from their perinuclear location to the peripheral cytoplasm. Depending upon the concentration of PMA used, 45-71% of thioglycolate-elicited macrophages and 32-44% of proteose-peptone-elicited macrophages and numerous lysosomes, radiating from the centrosphere region, arranged linearly along microtubule and 10-nm filament bundles. Colchicine (10(-5) M) and podophyllotoxin (10(-5) M) prevent the radial redistribution of microtubules, 10-nm filaments, and lysosomes in these cells. Cytochalasins B and D (10(-5) M) have no inhibitory effects on these processes. These findings indicate that microtubules and 10-nm filaments respond in a coordinated fashion to PMA and to agents that inhibit microtubule function; they suggest that these cytoskeletal elements regulate the movement and distribution of lysosomes in the macrophage cytoplasm.

Acid Phosphatase↗
PubMed1975

Anti-immunoglobulin-induced histamine secretion by rat peritoneal mast cells studied by immunoferritin electron microscopy.

We have used ferritin-conjugated divalent and monovalent anti-Ig antibodies to study simultaneously, histamine secretion and the ultrastructural distribution and redistribution of Ig receptors on rat peritoneal mast cells. We conclude that (a) divalent anti-Ig is required for both receptor redistribution and for calcium-dependent degranulation and histamine release, (b) divalent anti-Ig induces patching and pinocytosis but not capping of Ig molecules, (c) neither capping nor pinocytosis are required for triggering and if clustering is necessary, then less than 10 Ig molecules are required per cluster, and (d) degranulation (and histamine release) is not an all or none response of the mast cell.

Animals↗
PubMed1986

Effect of the amino acid analog hadacidin on intracellular membrane flow and the cell surface in Dictyostelium discoideum. A transmission- and scanning-electron-microscope study.

We examined the effect of the amino acid analog hadacidin (N-formyl-N-hydroxy glycine) on the process of endocytosis in the slime mold Dictyostelium discoideum. Endocytosis was followed using iron-dextran and transmission electron microscopy. In cells taken from the mid-log growth stage, iron-dextran was found to be distributed in small, medium, and large vesicles at a density lower than that present in the incubation medium, thus suggesting the fusion of small, iron-dextran-containing pinosomal vesicles with intracellular vesicles not containing iron-dextran. In cells treated with hadacidin, more small vesicles were present than in untreated cells, there being a reduction in the number of larger-sized vesicles; in these vesicles, iron-dextran was present at a density similar to that of the medium. This result is consistent with the conclusion that, while pinocytosis had continued, the fusion of vesicles and dilution of the vesicle contents had been inhibited. Also, the large number of small pinosomal vesicles in the drug-treated cells suggested that the recycling of vesicles to the surface had been inhibited. The observation that pinocytosis but not recycling continued after drug treatment raised the question of the origin of the membrane needed for the formation of pinosomes. Measurements of the cell surface revealed no difference between drug-treated and untreated cells, indicating that, when the membrane was internalized for pinosomes, the cell size remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Membrane↗
PubMed1972

The fluid mosaic model of the structure of cell membranes.

A fluid mosaic model is presented for the gross organization and structure of the proteins and lipids of biological membranes. The model is consistent with the restrictions imposed by thermodynamics. In this model, the proteins that are integral to the membrane are a heterogeneous set of globular molecules, each arranged in an amphipathic structure, that is, with the ionic and highly polar groups protruding from the membrane into the aqueous phase, and the nonpolar groups largely buried in the hydrophobic interior of the membrane. These globular molecules are partially embedded in a matrix of phospholipid. The bulk of the phospholipid is organized as a discontinuous, fluid bilayer, although a small fraction of the lipid may interact specifically with the membrane proteins. The fluid mosaic structure is therefore formally analogous to a two-dimensional oriented solution of integral proteins (or lipoproteins) in the viscous phospholipid bilayer solvent. Recent experiments with a wide variety of techniqes and several different membrane systems are described, all of which abet consistent with, and add much detail to, the fluid mosaic model. It therefore seems appropriate to suggest possible mechanisms for various membrane functions and membrane-mediated phenomena in the light of the model. As examples, experimentally testable mechanisms are suggested for cell surface changes in malignant transformation, and for cooperative effects exhibited in the interactions of membranes with some specific ligands. Note added in proof: Since this article was written, we have obtained electron microscopic evidence (69) that the concanavalin A binding sites on the membranes of SV40 virus-transformed mouse fibroblasts (3T3 cells) are more clustered than the sites on the membranes of normal cells, as predicted by the hypothesis represented in Fig. 7B. T-here has also appeared a study by Taylor et al. (70) showing the remarkable effects produced on lymphocytes by the addition of antibodies directed to their surface immunoglobulin molecules. The antibodies induce a redistribution and pinocytosis of these surface immunoglobulins, so that within about 30 minutes at 37 degrees C the surface immunoglobulins are completely swept out of the membrane. These effects do not occur, however, if the bivalent antibodies are replaced by their univalent Fab fragments or if the antibody experiments are carried out at 0 degrees C instead of 37 degrees C. These and related results strongly indicate that the bivalent antibodies produce an aggregation of the surface immunoglobulin molecules in the plane of the membrane, which can occur only if the immunoglobulin molecules are free to diffuse in the membrane. This aggregation then appears to trigger off the pinocytosis of the membrane components by some unknown mechanism. Such membrane transformations may be of crucial importance in the induction of an antibody response to an antigen, as well as iv other processes of cell differentiation.

Agglutination↗
PubMed1991

Effects of cytochalasin D and methylamine on intracellular growth of Legionella pneumophila in amoebae and human monocyte-like cells.

A cloned and axenically cultured strain of Hartmannella vermiformis was used as a model to study intracellular multiplication of Legionella pneumophila in amoebae. The growth of L. pneumophilia in both H. vermiformis and a human monocyte-like cell line (U937) was investigated with cytoskeletal and metabolic inhibitors. L. pneumophila replicated only intracellularly in these cellular models, and electron microscopy showed ultrastructural similarities in the initial phase of multiplication. Treatment of amoebae with an inhibitor of microfilament-dependent phagocytosis (cytochalasin D, 0.5 or 1.0 micrograms/ml) did not inhibit intracellular growth of L. pneumophila; however, intracellular multiplication was inhibited by treatment of U937 monocytes with the same concentrations of cytochalasin D. Methylamine (10 to 100 mM), an inhibitor of adsorptive pinocytosis, inhibited the replication of L. pneumophila in amoebae in a dose-dependent manner. All doses of methylamine tested (10 to 50 mM) inhibited growth of L. pneumophila in U937 monocytes. Cytochalasin D and methylamine had no effect on the multiplication of L. pneumophila in culture medium or on the viability of amoebae or U937 monocytes. Intracellular replication of L. pneumophila in H. vermiformis may be accomplished by a cytochalasin D-independent mechanism, such as adsorptive pinocytosis. In contrast, both cytochalasin D- and methylamine-sensitive mechanisms may be essential for the intracellular multiplication of L. pneumophila in U937 monocytes.

Analysis of Variance↗
PubMed1975

Effects of contrast agents on the blood-brain barrier. An electron microscopic study.

To determine if contrast agents after the blood-brain barrier by opening tight junctions between endothelial cells and by increasing pinocytosis, the distribution of horseradish peroxidase (HRP) was evaluated after intracarotid injections of contrast media. HRP did not cross the endothelium of cerebral blood vessels. Tight junctions remained closed. There was increased endothelial cell pinocytosis and swelling of astrocyte end-feet.

Animals↗
PubMed2000

Role of thyroglobulin endocytic pathways in the control of thyroid hormone release.

Thyroglobulin (Tg), the thyroid hormone precursor, is synthesized by thyrocytes and secreted into the colloid. Hormone release requires uptake of Tg by thyrocytes and degradation in lysosomes. This process must be precisely regulated. Tg uptake occurs mainly by micropinocytosis, which can result from both fluid-phase pinocytosis and receptor-mediated endocytosis. Because Tg is highly concentrated in the colloid, fluid-phase pinocytosis or low-affinity receptors should provide sufficient Tg uptake for hormone release; high-affinity receptors may serve to target Tg away from lysosomes, through recycling into the colloid or by transcytosis into the bloodstream. Several apical receptors have been suggested to play roles in Tg uptake and intracellular trafficking. A thyroid asialoglycoprotein receptor may internalize and recycle immature forms of Tg back to the colloid, a function also attributed to an as yet unidentified N-acetylglucosamine receptor. Megalin mediates Tg uptake by thyrocytes, especially under intense thyroid-stimulating hormone stimulation, resulting in transcytosis of Tg from the colloid to the bloodstream, a function that prevents excessive hormone release.

Animals↗
PubMed2000

Different pathways of degradation of SP-A and saturated phosphatidylcholine by alveolar macrophages.

Alveolar macrophages degrade surfactant protein (SP) A and saturated phosphatidycholine [dipalmitoylphosphatidylcholine (DPPC)]. To clarify this process, using rabbit alveolar macrophages, we analyzed the effect of drugs known to affect phagocytosis, pinocytosis, clathrin-mediated uptake, caveolae, the cytoskeleton, lysosomal pH, protein kinase C, and phosphatidylinositol 3-kinase (PI3K) on the degradation of SP-A and DPPC. We found the following: 1) SP-A binds to the plasma membrane, is rapidly internalized, and then moves toward degradative compartments. Uptake could be clathrin mediated, whereas phagocytosis, pinocytosis, or the use of caveolae are less likely. An intact cytoskeleton and an acidic milieu are necessary for the degradation of SP-A. 2) Stimulation of protein kinase C increases the degradation of SP-A. 3) PI3K influences the degradation of SP-A by regulating both the speed of internalization and subsequent intracellular steps, but its inhibition does not prevent SP-A from reaching the lysosomal compartment. 4) The degradation of DPPC is unaffected by most of the treatments able to influence the degradation of SP-A. Thus it appears that DPPC is degraded by alveolar macrophages through mechanisms very different from those utilized for the degradation of SP-A.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1994

Linkage of azurophil granule secretion in neutrophils to chloride ion transport and endosomal transcytosis.

Neutrophils contain at least two types of secretory granules. The present work links the secretion of the (lysosomal type) azurophil granules, but not that of specific granules, to endosomal transport mechanisms. (a) Selective stimulation of azurophil granule secretion by the Na-ionophore Monensin, or nonselective stimulation by FMLP after cytochalasin B pretreatment elicited marked pinocytic activity in parallel with azurophil granule release, whereas FMLP alone, selective for specific granules, elicited little fluid pinocytosis. (b) Pinosomes thus formed fused with azurophil granules, suggesting that exocytosis of azurophil granules might occur via endosomal organelles. This hypothesis was tested by determining the effect on the endosomal pathway(s) of two treatments that selectively prevent the release of azurophil granule contents without interfering with specific granule secretion, namely replacement of Cl- with gluconate- or the addition of zinc. Replacement of Cl- was found to impair the pinocytosis process itself, whereas ZnSO4 appeared to prevent the fusion between endosomes and azurophil granules. These data support the concept that the (lysosomal type) azurophil granules, but not the specific granules, are secreted through the endosomal pathway.

Chlorides↗
PubMed1985

Estrogen regulates low density lipoprotein metabolism by cultured swine granulosa cells.

To test estrogen's possible regulation of lipoprotein metabolism by granulosa cells, swine granulosa cells were cultured under serum-free conditions in the presence or absence of estradiol. Treatment with estradiol significantly enhanced high affinity, saturable, [125I]iodo-low density lipoprotein (LDL) binding with a median 2.85-fold (range 2.3- to 5.6-fold, n = six experiments) increase in the calculated number of LDL receptors and no change in the apparent dissociation constant (Kd) for LDL binding (Kd = 3.4 +/- 0.92 micrograms/ml in control and 4.0 +/- 0.87 micrograms/ml human LDL in estradiol-treated cultures). Estradiol also significantly increased [125I]iodo-LDL internalization by granulosa cells and augmented the maximal rate of LDL degradation by 2.0 to 2.5-fold without altering the apparent Michaelis-Menten constant (Km) for this process. Estrogen's dose-dependent enhancement of [125I]iodo-LDL binding, internalization, and degradation could be observed at minimum estradiol concentrations of approximately 100 ng/ml and was accompanied by increased progesterone secretion by granulosa cells. Further studies indicated that estrogen's stimulation of LDL internalization and degradation was not simply attributable to increased rates of nonspecific bulk fluid-phase pinocytosis (assessed with [125I]iodo-polyvinylpyrrolidone) or increased steroidogenesis per se (tested by blocking cholesterol side-chain cleavage with aminoglutethimide). We conclude that estradiol amplifies LDL binding by swine granulosa cells by increasing the number of high affinity, saturable LDL receptors with no alteration in their apparent affinity. Moreover, estrogen action is accompanied by enhanced rates of progesterone production in the presence of LDL, and increased rates of LDL internalization and degradation, which could not be accounted for simply by accelerated nonspecific bulk fluid-phase pinocytosis. We suggest that the significant facilitative actions of estradiol on lipoprotein binding and metabolism are likely to assist in preparing granulosa cells for the increased rates of progesterone biosynthesis ultimately required in functional corpora lutea.

Animals↗