Metabolites of alveolarEchinococcus as determined by [31P]- and [1H]-nuclear magnetic resonance spectroscopy

[³¹P]-Nuclear magnetic resonance (NMR) in vivo spectra ofEchinococcus multilocularis cysts growing subcutaneously inMeriones unguiculatus showed prominent signals due to phosphomonoesters (PME), phosphodiesters (PDE), inorganic phosphate (Pi) and the , and phosphate groups of adenosine triphosphate (ATP). The internal pH of the parasite cysts was 6.7–6.8. The³¹P spectra of extracts of these subcutaneous cysts showed peaks identified as glucose-6-phosphate (Glu-6-P), glycerol-3-phosphate (Gly-3-P), phosphorylethanolamine (PE), adenosine-5-monophosphate (5-AMP), nicotinamide adenine dinucleotide phosphate (NADP), phosphorylcholine (PC), Pi, glycerolphosphorylethanolamine (GPE), glycerolphosphorylcholine (GPC), phosphoenolpyruvate (PEP), adenosine diphosphate (ADP), ATP and diphosphodiesters (DPDE). These metabolites were also detected at comparable concentrations in the extracts of intraperitoneally grown cysts. In addition, significantly more phosphocreatine (PCr), probably of host origin, was detected in the subcutaneous cysts than in the intraperitoneal cysts. [¹H]-NMR spectra of cyst extracts revealed that parasites grown in the abdominal cavity contained significantly less glucose but significantly more succinate, acetate, alanine and -hydroxybutyrate. Glycogen, creatine, glycine, taurine, betaine, cholines and lactate were present at similar concentrations in cyst material from both locations.     

Glycine-like immunoreactivity in the cerebellum of rat and Senegalese baboon,Papio papio: a comparison with the distribution of GABA-like immunoreactivity and with [3H]glycine and [3H]GABA uptake

Summary An antiserum against conjugated glycine was characterized and applied to cerebellar sections of rats and baboons that had been perfusion-fixed with glutaraldehyde. After immunosorbent purification the serum reacted with brain protein-glutaraldehyde-glycine conjugates, but did not stain similar test conjugates prepared from other amino acids, including GABA and -alanine. In the rat cerebellum the glycine antiserum selectively labelled a subpopulation of Golgi neurons. Adjacent Vibratome sections treated with an antiserum against conjugated GABA revealed an about equally large subpopulation of immunopositive Golgi cells. A proportion of the Golgi cells that were cleaved by the plane of section contained both immunoreactivities. Additional evidence for a colocalization of glycine and GABA was obtained by postembedding staining of alternate semithin sections with the GABA antiserum and glycine antiserum, respectively. The ability of the antisera to distinguish between fixed glycine and GABA was corroborated by preincubation of the antisera with glutaraldehyde-amino acid fixation complexes: glycine complexes abolished staining with the glycine antiserum but had no effect on the GABA antiserum. The opposite effects were obtained with the GABA complexes. Matching the distributions of the respective immunoreactivities, [³H]glycine uptake was restricted to glomerulus-like structures in the granule cell layer whereas [³H]GABA uptake also occurred in punctate and fibrous profiles in the molecular layer. The baboon showed a distribution of glycine-like immunoreactivity similar to that in the rat, except that a few immunopositive neurons occurred in the molecular layer. The latter neurons were interpreted as outlying Golgi neurons; however, the possibility that they represent a subpopulation of basket cells could not be excluded. The Purkinje cells were negative in both species. Glial cells were weakly stained with the glycine antiserum but were strongly immunopositive after incubation with an antiserum raised against conjugates of the structurally similar amino acid -alanine. The present data suggest that glycine and GABA occur in about equally large subpopulations of Golgi neurons. A subpopulation of the Golgi neurons appears to contain both glycine and GABA.     

Distribution of opiate receptors within visual structures of the cat brain

Summary The distributions of , , and opiate receptors within visual regions in the cat cortex, thalamus and midbrain were determined by in vitro autoradiography. The overall distribution of receptors was examined using [³H]-etorphine, a ligand that nonselectively labels all types of opiate receptors. [³H]-[D-Ala², N-Me-Phe⁴, Gly(ol)⁵]-enkephalin (DAGO) was used to selectively label receptors, [³H]-[D-Pen^2,5]-enkephalin (DPDPE) for receptors, and [³H]-bremazocine for receptors. Each of the areas examined showed clear opiate receptor binding with [³H]-etorphine and a differential distribution of , , and receptors. Compared to other cortical regions, opiate binding in layers 3 and 4 of areas 17 and 18 was sparse. In the adjacent areas a more uniform distribution across layers was observed. The density of opiate receptors was greater in cortex than in subcortical structures, whereas the reverse was the case for receptors. Nevertheless, all three types of opiate receptors were found in the ventral and dorsal subdivisions of the lateral geniculate (LGN), the pulvinar complex, and the suprageniculate nucleus. In the midbrain, the superficial layers of the superior colliculus were heavily labelled with the , receptor ligand, and modestly with the ligand. Compared with other midbrain and diencephalic areas, binding was low in the superior colliculus. These results suggest that the diverse effects of opiates on visual perception are mediated by the unique distributions of opiate receptor types throughout the visual areas in the brain.     

Apparent superiority of H2-receptor stimulation and simultaneousβ-blockade over conventional treatment withβ-sympathomimetic drugs in post-acute myocardial infarction: Cardiac effects of impromidine — a new specific H2-receptor agonist — in the surviving catecholamine-insensitive myocardium

Left ventricular infarction (AMI) was produced in experimental animals and the contractile response to -adrenergic and H₂-histaminergic stimulation by isoproterenol and impromidine tested in the isolated perfused heart preparation. Adenylate cyclase activity as well as binding characteristics of [³H]-dihydroalprenolol ([³H]-DHA), [³H]-methyl-tiotidine ([³H]-TIOT) and [³H]-quinuclidinyl benzilate ([³H]-QNB) to cardiac ₁-, H₂- and cholinergic muscarinic receptors were determined in sarcolemmal membrane preparations of the right ventricle of the same hearts. In addition, an attempt was made to elucidate the therapeutic value of post-AMI treatment with impromidine in the presence and absence of-sympathomimetic, in contrast to administration of prenalterol and the conventional therapy with -sympathomimetic drugs, e.g. dobutamine. Three days post-AMI the dose-response curve for isoproterenol of right ventriculardP/dt _max was significantly depressed, while the inotropic effect of impromidine was not impaired. Stimulation of adenylate cyclase activity by isoproterenol was reduced by 80% whereas impromidine and NaF stimulation rates were unaltered. Receptor-binding studies indicated a 90% loss and 10-times lowered affinity (K _D) of the remaining -receptors while specific [³H]-TIOT- and [³H]-QNB-binding was unchanged.Administration of dobutamine increased mortality rates and extension of infarct size, led to a further decrease in contractile response to isoproterenol, induced complete insensitivity of adenylate cyclase to isoproterenol stimulation and caused pronounced additional reduction of number and affinity of [³H]-DHA-binding sites. In contrast, all above alterations were prevented by treatment with either prenalterol or combined administration of impromidine plus metoprolol. It is concluded, that these alterations in the non-ischemic, uninvolved myocardium post-AMI are the result of catecholamine-induced specific damage of sarcolemmal -receptors. Furthermore, treatment with H₂-agonists in combination with -blocking agents may have beneficial effects, whereas conventional therapy with -sympathomimetic drugs tends to worsen the already depressed function of the -adrenergic stimulation mechanism.Supported by grants Ba 666/1 and Ba 666/2-2 from the Deutsche Forschungsgemeinschaft (DFG).Data presented in this paper are part of a doctoral thesis by Dr S.B. Felix.     

Binding of [3H]cimetidine to rat brain tissue

Binding of [³H]cimetidine to rat brain tissue was investigated, and a saturable binding with dissociation constant 0.22±0.05 M found. This binding is inhibited by a range of imidazole-derived histamine H₂-receptor antagonists, but not by a number of non-imidazole H₂-receptor antagonists. It is concluded that the [³H]cimetidine binding site in rat brain tissue that is labelled in these experiments is not the histamine H₂-receptor.     

Differential effects of interleukin-1α and β on the arachidonic acid cascade in human synovial cells and chondrocytes in culture

The effects of interleukin-1 and were tested on the [³H]-arachidonic acid release and the prostaglandin synthesis by human cultured synovial cells and chondrocytes. Both forms of interleukin-1 stimulated the arachidonic acid release but interleukin-1 was more potent than IL-1. Human synovial cells and chondrocytes synthesized three types of prostaglandins upon stimulation with interleukin-1 or : prostaglandin E₂, F₂ and 6-keto-prostaglandin F₁. Regarding the synthesis of these prostaglandins, IL-1 was again more potent than IL-1. A comparison between interleukin-1-stimulated synovial cells and chondrocytes revealed neither significant quantitative nor qualitative differences in both the arachidonic acid release and the prostaglandin synthesis.     

Anterograde transport of opioid receptors in rat vagus nerves and dorsal roots of spinal nerves: pharmacology and sensitivity to sodium and guanine nucleotides

Summary We have utilized the technique of in vitro autoradiography to ascertain that opioid receptors are transported in the rat vagus nerve and in the rat dorsal spinal root fibers. In the dorsal roots, opioid receptors accumulated on both sides of the ligatures. In the vagus nerve, a distal accumulation of binding sites was difficult to detect, however, proximal to the ligatures, vagal receptors accumulated in a linear fashion during the first 12 h of ligation. At longer periods after ligation, accumulation was less than expected and the receptors appeared to migrate retrogradely. The receptor transport could be blocked by intravagal colchicine injection and the receptor translocation could be elicited in isolated vagal nerve segments suggesting that the receptors move by fast transport. Sodium chloride, present in the incubation medium, inhibited [³H]dihydromorphine ([³H]DHM) binding to receptors adjacent to and far from the proximal aspect of the ligature with IC₅₀'s of 42 mM and 51 mM, respectively. The addition of GTP in the incubation medium also inhibited [³H]DHM binding to proximal and far proximal receptors with IC₅₀'s of 0.27 M and 1.0 M, respectively. The presence of GTP also inhibited [³H]naloxone ([³H]Nal) binding to proximal and far proximal receptors with IC⁵⁰'s of 0.34 M and 0.66 M, respectively. The transported vagal opioid receptors bound the ligands in a stereospecific manner. Using [³H]DHM, [³H]D-ala²-D-leu⁵-enkephalin ([³H]DADL), and [³H]ethylketocyclazocine ([³H]EKC), we found that most of the transported vagal receptors have mupharmacology although kappa and delta receptors are present.     

Distribution of α2-macroglobulin in normal,inflammatory, and tumor tissues in rats

Distribution of uptake and catabolism of intravenously administered¹²⁵l-labeled rat ₂-macroglobulin(¹²⁵I-₂MG) were examined in normal, inflammatory, and tumor tissues of rats. Clearance of intravenously administered [¹²⁵l]₂MG from the circulation was rapid. Accumulation of this compound into inflammatory tissue was 2–3 times more extensive than in normal tissues. The accumulation into sarcoma tissue was much less. Radioactivity in TCA-PTA precipitates remained fairly constant for the first 12 h in inflammatory tissue and for the first 24 h in sarcoma. These patterns of accumulation were never observed in the normal tissues. As the kidney preferentially accumulated large amounts of [¹²⁵l]₂MG in the nondegraded form and its degradation products, the tissue may play a special role in the metabolism of ₂MG. Rapid clearance from the circulation and relatively small amounts of accumulation in tissues suggest that ₂MG may function as a protease inhibitor, mainly in the circulation rather than in the tissues.     

Tityusγ toxin,a high affinity effector of the Na+ channel in muscle,with a selectivity for channels in the surface membrane

Toxin from the venom ofTityus serrulatus scorpion produces a partial block of the surface Na⁺ channel in frog muscle. This block occurs with no change in the voltage-dependence or in the kinetics of the remaining surface Na⁺ current. The partial blockade of Na⁺ channel activity occurs with no change in tubular Na⁺ currents nor in twitch tension. The maximum effect of the toxin is attained at concentrations as low as 3×10^–10 M. Hyperpolarization to potentials more negative than the resting potential (E=–90 mV) reduces or abolishes the effect of the toxin.Radioiodinated toxin binds to frog muscle membranes with a very high affinity corresponding to a dissociation constant of about 1×10^–11 M. Data obtained with both rabbit and frog muscle indicate that toxin is specific for Na⁺ channels in surface membranes. Toxin does not seem to bind to Na⁺ channels in T-tubule membranes. The biochemical data are in good agreement with electrophysiological studies and data on contraction. There is oneTityus toxin binding site per tetrodotoxin binding site in surface membranes. Competition experiments have confirmed thatTityus toxin binds to a new toxin receptor site on the Na⁺ channel structure. This site is the same that the toxin II fromCentruroides suffusus binding site, but this toxin has 100 times less affinity for the Na⁺ channel thanTityus toxin.     

Sequence specificity of mutations induced by benzo[a]pyrene-7,8-diol-9,10-epoxide at endogenousaprt gene in CHO cells

We have determined the spectrum of mutations induced, by±trans-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a] pyrene (BPDE) at the endogenous aprt locus in an hemizigous Chinese hamster ovary cell line exposed to 0.7 M BPDE. Southern analysis of 59 independent mutants revealed no major genomic alterations, indicating that gene inactivation was the result of a point mutation. This conclusion was confirmed by the cloning and sequencing of 21 of these mutants. The predominant mutation, the GCTTA transversion, comprised 62% of the spectrum, but other base pair substitutions and frameshifts were recovered. An examination of the target sequences for BPDE mutation revealed that mutations were localized within runs of GC base pairs. However, approximately half of these GC runs involved a particular sequence—a run of guanines flanked by adenine residues. Of seven such sites within the coding sequence ofaprt, mutations were clustered within five of them. This class of sequence occurs at codon 61 of the human C-Ha-ras1 protooncogene and may account for the selective activation of this codon by BPDE.     

Electron microscopic localization of [125I]alpha-bungarotoxin binding sites in the outer plexiform layer of the goldfish retina.

Summary Light and electron microscope autoradiography were performed on goldfish (Carassius auratus) retinas incubated in [¹²⁵I] labelled -bungarotoxin. The toxin was bound preferentially to membrane receptors in the inner and outer plexiform layers. Binding was suppressed by 10^–5 M nicotine or 10^–5 M native -bungarotoxin. Electron microscopic analysis of the outer plexiform layer (OPL) strongly suggested that -bungarotoxin binding sites were located on small bipolar cell dendritic processes that invaginated rod and cone synaptic terminals, and on large bipolar cell dendritic processes more proximally situated in the OPL. Large horizontal cell processes in the OPL and horizontal cell processes that invaginated rod and cone synaptic terminals did not appear to be labelled.     

The contractile behaviour of EGTA- and detergent-treated heart muscle

Summary Tension responses of rat ventricular trabeculae subjected to successive treatment with EGTA and Triton X-100 are described in order to investigate the effects of chemical skinning techniques. In some preparations the alkaloid saponin was also used before Triton. Ultrastructural evidence is cited that the EGTA-treatment fails to render cells hyperpermeable, i.e. freely permeable to small ions, whereas both saponin and Triton do so. In this paper we show that contractile responses like those described previously for the EGTA-treated tissue can be obtained. However, more detailed examination shows that such behaviour is quantitatively distinct from that of conventionally skinned fibres in a way that is incompatible with the notion of hyperpermeability. The Ca-sensitivity after treatment with either EGTA, saponin or Triton is identical in our hands. However, this is not explained by free access of Ca (and EGTA) to the intracellular space in the EGTA-treated preparation: contractures develop with very different time courses, being fastest after Triton and only marginally slower when first exposed to saponin but a factor of five times slower after EGTA-treatment alone. This applies to contractures evoked direct from Ca²⁺ concentration 10^–9 m to the test Ca²⁺ concentration at constant total buffer concentration.EGTA-treated fibres develop tension when ATP or creatine phosphate (CrP) are removed from the bath. However, responses to ADP and to CrP changes persist with millimolar levels of ATP present, quite unlike the Triton-skinned muscle. Exposure to each of a variety of solutions for 24h produce preparations showing similar behaviour: whatever the explanation for the EGTA-skinning phenomenon it is not dependent upon low bathing Ca²⁺ concentration. On the basis of the functional characteristics described here, and the structural results cited, we conclude that the cell membrane continues to function as a selective permeability barrier after EGTA-treatment: this treatment does not produce a model of a selectively skinned cardiac cell.     

Expression of growth factor receptors in injured nervous tissue. II. Induction of specific platelet-derived growth factor binding in the injured PNS is associated with a breakdown in the blood-nerve barrier and endoneurial interstitial oedema

Summary We have studied the expression of the platelet-derived growth factor (PDGF) receptors in the injured chick PNS using [¹²⁵I]-iodinated PDGF as a radioactive probe to map autoradiographically thein situ distribution of specific [¹²⁵I]PDGF binding.Crush or transection of the sciatic nerve led to a rapid and massive induction of specific [¹²⁵I]PDGF binding on fibroblast-like cells of the injured endoneurium, already observed 2 h postoperatively. It is initially characterized by a symmetrical appearance both below and above the site of injury, spreading throughout the distal part of the lesioned nerve 1 to 2 days postoperatively. Comparison with distribution of specific [¹²⁵I]-nerve growth factor (-NGF) binding (see preceding paper) revealed a number of important differences: unlike the specific [¹²⁵I]-NGF binding, which rapidly disappears after reinnervation of the distal nerve, this was not observed in the case of [¹²⁵I]PDGF binding. [¹²⁵I]PDGF binding also correlated poorly with the extent of axonal injury. The segmental removal of the perineurium, resulting in heavy interstitial oedema without widespread axonal injury, led to a strong, local induction of [¹²⁵I]PDGF binding, while causing moderate -NGF binding to only the few degenerating nerve fibre tubes. These results suggest the existence of different pathophysiological mechanisms that regulate the expression of PDGF and -NGF receptors in the lesioned and regenerating PNS.     

Histamine H3-receptor activation inhibits acetylcholine release from the guinea pig myenteric plexus

The role of histamine H₃-receptors in the control of acetylcholine release from peripheral cholinergic neurons was evaluated in the isolated guinea pig ileum, previously loaded with³H-choline. When tested in the presence of H₁- and H₂-blockade, histamine (0.1–100 mol/l) and (R)-methylhistamine (0.01–1 mol/l) dose-dependently reduced the electrically-evoked choline outflow, with (R)-methylhistamine being a partial agonist. Selective H₃-receptor blocking drugs, thioperamide (0.1 mol/l) and impromidine (0.1 mol/l) reversed the histamine-induced inhibitory, effect. These data suggest that intestinal cholinergic nerves are endowed with histamine H₃-receptors whose activation produces an inhibitory effect upon acetylcholine release. The practical implications of these findings are obvious.     

ATP-sensitive K-channels in HIT T15 β-cells studied by patch-clamp methods, 86Rb efflux and glibenclamide binding

ATP-sensitive K-channels in the cloned -cell line HIT T15 were studied by patch-clamp methods; by measurement of ⁸⁶Rb efflux; and by [³H]glibenclamide binding to isolated membrane preparations. In inside-out patches a 50 pS K-channel was found which was blocked by ATP or tolbutamide applied to the intracellular membrane surface. A minimum estimate of about 500 channels per -cell was obtained by combining whole-cell and single-channel data. The rate of efflux of ⁸⁶Rb from ⁸⁶RbCl-loaded HIT cells was markedly increased by intracellular ATP-depletion; ⁸⁶Rb-efflux was progressively inhibited by increasing concentrations of glibenclamide or tolbutamide. In non-ATP-depleted cells, diazoxide elicited a concentration-dependent stimulation of ⁸⁶Rb-efflux which was completely blocked by 1 M glibenclamide. Isolated membranes showed dose-dependent saturable binding of [³H]glibenclamide to both high (K _d=1.12 nM) and low (K _d=136 nM) affinity binding sites. We estimate about 5000 high-affinity binding sites per cell. [³H]-glibenclamide binding was inhibited by tolbutamide (IC₅₀=125 M) but was not affected by diazoxide. ADP (0.5 or 1.0 mM) markedly reduced binding; other nucleotides tested were ineffective.     

The influence of negative staining on the infectivity of vaccinia virus

Summary The specific infectivity of [³H]-thymidine-labeled vaccinia virus in electron microscopic specimens after negative staining has been determined by correlating infectivity with radioactivity counts as the criterion for morphological preservation.     

Morphometric observations on the rat heart after high-dose treatment with cortisol

Summary Male Wistar rats were treated with high cortisol doses for 1 week. The dose administered daily was 15 mg per animal in group 1 (7 animals) and 30 mg in group 2 (7 animals). 7 rats served as control group. After cortisol treatment the body weights decreased due to skeletal muscle catabolism and the heart weights increased. Morphometric analysis of the left ventricular posterior papillary muscles gave evidence that the increased heart weights resulted from an increased number of mitochondria and an increased volume of the cytoplasm, whereas the myofibrillar mass was not affected. The surface area of inner mitochondrial membranes (+cristae mitochondriales) per myofibrillar unit volume increased from 15.7 ²/³ to 21.3 ²/³ in group 1 and 21.4 ²/³ in group 2. Ultrastructural changes indicating myocardial cell damage were absent. Similar quantitative results have been reported to occur in the early phase of cardiac overload. For elucidating the hemodynamic effects of glucocorticoid a second experiment was performed: 7 Wistar rats were treated with cortisol in the same way as group 1, 7 others of the same body weight served as control. The systolic arterial pressure was significantly elevated in the cortisol group. Though myocardial tissue is known to be able to accumulate large quantities of glucocorticoids our results indicate that the application of high cortisol doses for a short time does not produce myocardial cell damage and does not suppress the myocardial adaption to the glucocorticoid-induced hypertension, i.e. hypertrophy. On the contrary, it seems to be possible that the adaption process is itself facilitated or accelerated by the presence of high cortisol concentrations in the heart. This thesis is supported by the considerably higher relative heart weights in the cortisol groups and is in agreement with observations reported by other authors.Dedicated to Professor Dr. W. Doerr on the occasion of his 65th birthdayThe results have been partially reported in 1977 (cf. G. Mall and H. Reinhard, Verh. Dtsch. Ges. Path. 61, 445)This investigation was supported by the Sonderforschungsbereich 90 of the Deutsche Forschungsgemeinschaft.     

Transformation of ψ − Saccharomyces cerevisiae to ψ + with DNA co-purified with 3 μm circles

Summary DNA enriched for supercoiled plasmids prepared from the 3 m plasmid-enriched, [ ⁺], [2 m°] strain 6-1G-P188 and from the [2 m⁺] [⁺] strain LL20 can be used to transform a ^– recipient strain to ⁺. Fractionation of the former preparation by electrophoresis showed that the 3 Mm plasmid band contained the transforming activity.     

Targeted gene replacement at the endogenousAPRT locus in CHO cells

We demonstrate the feasibility of targeted gene replacement at an endogenous, chromosomal gene locus in cultured mammalian cells, employing a two-step strategy similar to an approach routinely used for genetic manipulation in yeast. Utilizing an APRT⁺ recombinant generated by targeted integration of plasmid sequences (including a functional copy of the gpt gene) at the CHO APRT locus, we have been able to select gpt^– pop-out recombinants that have arisen by intrachromosomal recombination between APRT direct repeats at the targeted integration site. Reciprocal exchanges leading to pop-out of integrated plasmid/gpt gene sequences occur at a rate of 6.3×10^–6 per cell generation. Depending on the site of crossover, such pop-out events result in either replacement or restoration of the original APRT target gene sequence.     

Phenotypic characteristics of lewis lung carcinoma cells

We studied adhesive properties and physiological activity in vivo of cells from Lewis lung carcinoma and its metastases. These cells differed in tumorogenic activity and metastatic potential in the syngeneic system. In vivo non-metastasizing cells are characterized by a lower content of surface lectins to tetrasaccharides SiaLe^x [Neu5Ac2-3Gal1-4(Fuc1-3) GlcNAc] and SiaLe^a [Neu5Ac2-3Gal1-3(Fuc1-4)GlcNAc] and trisaccharide HSO₃Le^x [HSO₃2-3Gal1-4(Fuc1-3)GlcNAc] compared to cells forming metastases in the syngeneic system. Metastatic cells with low tumorogenic activity weakly expressed lectins to disaccharide ligands 6-SiaLac [Neu5Ac2-6Gal1-4Glc], 6-HSO₃LacNAc, and A-di [GalNAc 1-3Gal] and trisaccharides H-type 1 [Fuc1-2Gal1-3GlcNAc and Le^x [Fuc1-3(Gal 1-4)GlcNAc] compared to cells that initiated tumor formation in the syngeneic system (similarly to transplanted tumors). We hypothesized that cell receptors to these carbohydrate determinates are involved in the development and growth of primary tumors, while lectins to SiaLe^x, SiaLe^a, and HSO₃Le^x play a role in the progress of tumor process and metastasizing.