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Biosynthesis of type 3 capsular polysaccharide in Streptococcus pneumoniae. Enzymatic chain release by an abortive translocation process.

The type 3 polysaccharide synthase from Streptococcus pneumoniae catalyzes sugar transfer from UDP-Glc and UDP-glucuronic acid (GlcUA) to a polymer with the repeating disaccharide unit of [3)-beta-d-GlcUA-(1-->4)-beta-d-Glc-(1-->]. Evidence is presented that release of the polysaccharide chains from S. pneumoniae membranes is time-, temperature-, and pH-dependent and saturable with respect to specific catalytic metabolites. In these studies, the membrane-bound synthase was shown to catalyze a rapid release of enzyme-bound polysaccharide when either UDP-Glc or UDP-GlcUA alone was present in the reaction. Only a slow release of polysaccharide occurred when both UDP sugars were present or when both UDP sugars were absent. Chain size was not a specific determinant in polymer release. The release reaction was saturable with increasing concentrations of UDP-Glc or UDP-GlcUA, with respective apparent K(m) values of 880 and 0.004 micrometer. The apparent V(max) was 48-fold greater with UDP-Glc compared with UDP-GlcUA. The UDP-Glc-actuated reaction was inhibited by UDP-GlcUA with an approximate K(i) of 2 micrometer, and UDP-GlcUA-actuated release was inhibited by UDP-Glc with an approximate K(i) of 5 micrometer. In conjunction with kinetic data regarding the polymerization reaction, these data indicate that UDP-Glc and UDP-GlcUA bind to the same synthase sites in both the biosynthetic reaction and the chain release reaction and that polymer release is catalyzed when one binding site is filled and the concentration of the conjugate UDP-precursor is insufficient to fill the other binding site. The approximate energy of activation values of the biosynthetic and release reactions indicate that release of the polysaccharide occurs by an abortive translocation process. These results are the first to demonstrate a specific enzymatic mechanism for the termination and release of a polysaccharide.

Bacterial Capsules↗

Serum antibodies specific to CD outer membrane protein of Moraxella catarrhalis, P6 outer membrane protein of non-typeable Haemophilus influenzae and capsular polysaccharides of Streptococcus pneumoniae in children with otitis media with effusion.

We measured the levels of serum IgG antibodies to CD outer membrane protein of Moraxella catarrhalis, P6 outer membrane protein of non-typeable Haemophilus influenzae and capsular polysaccharides of Streptococcus pneumoniae in 168 children with otitis media with effusion (OME) who were followed prospectively, using ELISA. Serum IgG antibodies to CD, P6 and pneumococcal capsular polysaccharides were detected in all samples. The anti-pneumococcal polysaccharides antibody level was highest, followed by the anti-P6 antibody level and anti-CD antibody was lowest (median:interquartile ranges were 45.9:19.1-100 microg/ml, 15.6:9.70-23.2 microg/ml and 1.06:0.73-1.87 microg/ml, respectively). In children aged 0-6 years, there were positive correlations among the antibody levels (anti-CD vs anti-P6, r=0.325, p <0.001; anti-CD vs anti-polysaccharide, r=0.397, p <0.0001; anti-P6 vs anti-polysaccharide, r=0.175, p=0.057). However, no relationship was seen in children aged 7-15 years. Children were classified according to severity of OME during the 1-year follow-up. In children aged 0-6 years, the severity of OME correlated inversely with the levels of anti-CD antibody (r=-.23, p=0.012), of anti-P6 antibody (r=-0.292, p=0.0015), and of anti-pneumococcal polysaccharides antibody (r=-0.25, p=0.0064). However, no correlation was found between antibody levels and severity of OME in children aged 7-15 years. These data suggest that persistence and/or recurrence of OME may be due to an insufficient serum antibody response to middle ear pathogens in young children.

Adolescent↗

Incorporation of sulfate into the capsular polysaccharide of the red alga Porphyridium.

The accumulation of sulfate-(35)S by Porphyridium aerugineum cells and subsequent appearance of solubilized capsular polysaccharide-(35)S in the growth medium were examined The uptake of label by the cells was largely light dependent. Pulse-chase experiments using log phase cells revealed a rapid labeling of solubilized capsular polysaccharide, recovered from the medium as the cetylpyridinium chloride precipitate Polyacrylamide gel electrophoresis of the polysaccharide-(35)S showed the sulfate to be firmly bound to an immobile fraction. Sephadex chromatography revealed the molecular weight of the polysaccharide to be in excess of 2 x 10(5). Acid hydrolysis of the polysaccharide-(35)S released sulfate-(35)S ion as evidenced by radioautography of thin layer chromatographs Preliminary electron microscope evidence suggests that the synthesis, movement, and deposition of the capsular polysaccharide on the cell surface are Golgi complex-mediated processes

Acrylamides↗

Form variation in Escherichia coli K1: determined by O-acetylation of the capsular polysaccharide.

The chemical basis for the alternating antigenic change called form variation noted for the Escherichia coli K1-capsular polysaccharide has been shown by 13C nuclear magnetic resonance to be a result of random O-acetylation of C7 and C9 carbons of the alpha-2-8-linked sialic acid homopolymer. A serologic method (antiserum agar) was developed to identify and isolate the form variants. The O-acetyl positive and O-acetyl negative K1 polysaccharides had unique biochemical and immunologic properties. The O-acetyl-positive variants resisted neuraminidase hydrolysis in contrast to the susceptibility of the O-acetyl negative variant to this enzyme. In addition, O-acetylation altered the antigenicity of the O-acetyl polysaccharides. When injected as whole organisms, O-acetyl positive organisms produced anti-K1 -antibodies in rabbits specific for this polysaccharide variant. O-acetyl negative organisms were comparatively less immunogenic; however, antibodies induced by these organisms reacted with both K1 polysaccharide variants. Burros, injected with either variant, produced antibodies reactive with both K1 polysaccharides.

Acetylation↗

Antibody recognition of the type 14 pneumococcal capsule. Evidence for a conformational epitope in a neutral polysaccharide.

Oligosaccharides consisting of one or more tetrasaccharide repeating units were derived from the capsular polysaccharide of type 14 pneumococcus (Pn14) by endo-beta-galactosidase digestion. The relative affinity of anticapsular antibody binding to derivative oligosaccharides of different chain lengths was measured in a Pn 14 ELISA inhibition assay. The concentration of inhibiting antigen required to achieve 50% inhibition of IgG binding increased progressively from 5.6 x 10(-4) M to 7.0 x 10(-11) M as the inhibiting saccharide chain length increased from 1 tetrasaccharide repeating unit to 2,500 repeating units. These data indicate that antibodies directed against the Pn14 polysaccharide recognize a conformational epitope fully expressed only in high molecular weight forms of the antigen. Similar results were found for inhibition of Fab fragment binding, suggesting that recognition of the conformational epitope is largely dependent on the intrinsic affinity of the Fab combining region. Unlike previously reported polysaccharides for which conformational epitopes have been described, the Pn14 polysaccharide does not contain negatively charged residues, indicating that expression of conformational determinants is not limited to acidic polysaccharides. Antibody recognition of conformational epitopes may be a common mechanism by which the host immune response discriminates between bacterial polysaccharides and host oligosaccharides of similar structure.

Animals↗

Induction of immunologic refractoriness in adults by meningococcal C polysaccharide vaccination.

Thirty-four adults were vaccinated with 1/50 of the usual dose of meningococcal polysaccharide vaccine (1 microg of A, C, Y, and W135 polysaccharides, given intramuscularly). This dose was selected as a probe to assess B cell memory. The probe elicited meningococcal C bactericidal antibody responses in all 18 adults who had been vaccinated 4 years earlier with an investigational meningococcal A and C oligosaccharide-protein conjugate vaccine and in the majority of the 11 subjects vaccinated for the first time. In contrast, the responses of the 5 adults given a full dose of licensed polysaccharide vaccine 4 years earlier were <1/10 of those of the other 2 groups. Thus, adults previously given a full dose of meningococcal polysaccharide vaccine show evidence of immunologic refractoriness to group C polysaccharide, whereas refractoriness is not observed after conjugate vaccination. These findings have implications for the use of meningococcal polysaccharide vaccine when the risk of disease is low.

Adult↗

Maternal immunization and the immune response of neonates to pneumococcal polysaccharides.

The effect of maternal immunization on the immune response of neonates to pneumococcal polysaccharides and the characterization of IgG receptor molecules have been reviewed and studied. Maternal immunization with pneumococcal 19F polysaccharide during gestation and/or lactation induces a significantly stronger response in offspring. When young mice born to pregnant mice immunized with a polysaccharide-protein conjugate (e.g., 19F polysaccharide-human IgG) are given an additional dose of polysaccharide-protein conjugate immunogen, they develop an antibody response stronger than that of young mice not receiving additional immunogen. Injection of female mice (before their mating) with type 19F or type 3 polysaccharide may also induce a stronger antibody response in offspring. Combined passive immunization with immunoglobulin and active immunization do not cause suppression or observable harmful immunologic effects; rather, such immunization may elicit sufficient 19F antibody formation for protection against infection during early life. IgG receptor molecules have been isolated from rabbit yolk-sac membranes, and their physicochemical properties have been characterized.

Animals↗

Cross-antigenicity and immunogenicity between capsular polysaccharides of group C Neisseria meningitidis and of Escherichia coli K92.

Antibodies to capsular polysaccharides of group C Neisseria meningitidis are often found in sera of young adults despite infrequent nasopharyngeal carriage and low rate of attack of N. meningitidis in the United States. Thus, experiments were designed for detection of bacteria cross-reactive with N. meningitidis. Among 3,264 cultures of stool, urine, blood, and cerebrospinal fluid, only 14 strains were found to be cross-reactive; all were Escherichia coli possessing the K92 capsular polysaccharide. The somatic O-antigens were 16, 13, 23, and 73; the flagellar antigens were H4 and 34. All K92 strains of E. coli showed the expected fermentations, were sensitive to common antibiotics, and lacked enteropathogenicity. Antigens of both E. coli K92 and group C N. meningitidis are capsular, acidic polysaccharides composed of sialic acid. The K92 polysaccharide is N- but not O-acetylated, sensitive to neuraminidase, and linked by alpha-2,8- alternating with alpha-2,9-ketosidic bonds. The K92 polysaccharides from all E. coli studied had similar biophysical and immunological properties. Intravenous injection of formalin-treated K92 organisms induced precipitating and bactericidal antibodies to polysaccharides of N. meningitidis. E. coli K92 strains may provide an alternative immunogen for prophylaxis against disease due to group C N. meningitidis in infants and young children.

Adult↗

Lipopolysaccharide-derived serotype polysaccharides from Neisseria meningitidis group B.

Three immunologically distinct types of polysaccharides have been isolated by diethylaminoethyl (DEAE) chromatography from the lipopolysaccharide extracts of group B Neisseria meningitidis. All types contain a set of common determinants, as well as distinct ones; all of these determinants are detectable by either immunodiffusion or enzyme-linked immunosorbent assay (ELISA). The polysaccharides elute from a Sepharose 4B column in the range of 2-3 x 10(5) daltons and have isoelectric points from 4.2 to 4.3. Their antigenicity is destroyed by oxidation but is unaffected by neuraminidase, lysozyme, or trypsin. One type of polysaccharide cross-reacts with the Gc2 polysaccharide of Neisseria gonorrhoeae in immunodiffusion systems. Chemical analysis indicates that these polysaccharides contain hexoses, hexosamines, 2-keto-3-deoxyoctonate, ethanolamine, and heptose; analysis of amino acids indicates protein contents of less than 0.05%. In contrast to the lipopolysaccharide from which they are derived, these polysaccharides contain no lipid A and less than 0.5% fatty acids. All three types are precipitated by wheat germ agglutinin but not by concanavalin A or fucose-binding protein. Specific inhibition of this precipitation can be achieved with N-acetyl glucosamine. These antigens may be the bases of a lipopolysaccharide-derived typing system for group B N. meningitidis.

Animals↗

Sulfated polysaccharides inhibit lymphocyte-to-epithelial transmission of human immunodeficiency virus-1.

We have previously suggested that sulfated polysaccharides could be used in a vaginal formulation to inhibit infection by human immunodeficiency virus (HIV-1). This supposition was based on studies in which we developed and employed an in vitro model to simulate the mechanism of HIV-1 transmission during coitus. We found that adhesion of mononuclear cells to epithelia was the initial step in infection and speculated that blocking adhesion would prevent HIV-1 transmission. We observed that certain sulfated polysaccharides prevented adhesion of lymphoma cell lines to epithelial cell lines, which were derived from the genital tract, in concentrations of a few milligrams per milliliter; and we theorized that sulfated polysaccharides could thus be used as active ingredients in a topical "microbicide." In the present in vitro study, evidence is presented that a number of sulfated polysaccharides, including carrageenan, dextran sulfate, heparin, fucoidan, and pentosan polysulfate, are capable of blocking infection by mechanisms other than adhesion at concentrations of a thousand times lower than the dosages that are needed to block cell adhesion. One of these compounds, iota carrageenan, is capable not only of blocking infection of epithelia at concentrations of 1-2 micrograms, but of blocking adhesion to a far greater extent than the other sulfated polysaccharides tested. For this reason, as well as for considerations of safety, stability, and gelling properties, we suggest that iota carrageenan may be the best choice of the sulfated polysaccharides tested for use as a vaginal microbicide. The same in vitro model was employed to decipher the cell surface molecules involved in lymphocyte-to-epithelial adhesion. To accomplish this, we screened for the presence of cell adhesion molecules (CAMs), carbohydrates, proteoglycans, and carbohydrate-binding sites. HIV-1-infected lymphocytic cells expressed a CAM profile typical of activated, infected cells (e.g., HLA-DR+, CD4-, LFA-1+, ICAM-1+, LFA-3+, CD2+) whereas epithelia expressed few CAMs (LFA-3, ICAM-1, VLA-5, CD44, CD26, sLEX). Both cell types expressed heparan sulfate and chondroitin sulfate proteoglycans. A variety of sugars (mannose, fucose, galactose, Nac-galactosamine, Nac-glucosamine) were also present, but these cells expressed few carbohydrate-binding sites; lymphocytes bound beta-galactose. We were unable to block the adhesion with anti-CAM antibodies or with exogenous sugars. When enzymes were used against sulfated cell surface molecules, chondroitinase was found to block the adhesion. Our evidence suggests that this CAM-independent adhesion may be a lectin-glycosaminoglycan interaction.

Acquired Immunodeficiency Syndrome↗

Comparison of cell-wall polysaccharides from Nectria cinnabarina with those from the group of Nectria with Sesquicillium anamorphs.

Alkali-extractable and water-soluble polysaccharides were purified from cell walls of five species of Sesquicillium or its teleomorphs, Nectria lasiacidis and Nectria impariphialis, and from Nectria cinnabarina, the type species of Nectria, a heterogeneous genus that belongs to the Hypocreales. Methylation and NMR analyses for determination of linkage types and structure were performed and indicated differences between the polysaccharides purified during the present study and those isolated from other nectrioid fungi, namely the presence of 5-O-substituted galactofuranose (-->5)-Galf-(1-->) in the main chain together with 2,6-di-O-substituted galactofuranose (-->2,6)-Galf-(1-->) residues in Sesquicillium buxi and Sesquicillium pseudosetosum. The polysaccharide from N. impariphialis was similar to those obtained from the above species, although an additional residue of 6-O-substituted glucopyranose (-->6)-Glcp-(1-->), was detected in some side chains. In N. lasiacidis and Sesquicillium candelabrum the polysaccharide contained an additional branching point of 5,6-di-O-substituted galactofuranose (-->5,6)-Galf-(1-->) linked to terminal N-acetylglucosamine GlcNAc-(1-->). These chains were linked to a small mannan core. All these polysaccharides showed major differences to the polysaccharide of N. cinnabarina, which was formed by a main chain of (1-->6)-beta-linked galactofuranose units almost fully branched at positions 2-O by either single residues of glucopyranose or acidic chains containing glucuronic acid and mannose.

Ascomycota↗

RppA, a transducer homologue, and MmrA, a multidrug transporter homologue, are involved in the biogenesis and/or assembly of polysaccharide in Myxococcus xanthus.

Myxococcus xanthus cells move by gliding, and form multicellular fruiting bodies under conditions of starvation. The authors cloned a gene, designated rppA (for receptor for polysaccharide production), which encodes a methyl-accepting protein homologous to the chemotaxis transducers in eubacteria. The rppA gene was co-transcribed with mmrA, a gene homologous to various multidrug transporter genes. The rppA or mmrA single mutants showed almost identical phenotypes to the wild-type strain; however, the rppA-mmrA double mutant exhibited reduced colony expansion, cell-cell agglutination and cellular reversal frequency. The double-mutant cells also showed less binding to Congo red, which mainly binds to fibril polysaccharide, than wild-type cells. Analysis of total polysaccharide in stationary-phase cells demonstrated that in the double mutant, polysaccharide levels were decreased by about 30 % as compared with the wild-type strain. These results indicated that RppA and MmrA play a role in the biogenesis and/or assembly of polysaccharide, and the phenotypes of the double mutant may be due to the reduction in fibril polysaccharide.

ATP Binding Cassette Transporter, Subfamily B↗

Cell-wall lipopolysaccharide of the 'Shigella-like' Escherichia coli 0124. Structure of the polysaccharide chain.

From Escherichia coli 0124 two lipopolysaccharide preparations were obtained with phenol/water extraction and cetavlon precipitation. Polyacrylamide gel electrophoresis in the presence of sodium dodecylsulfate and chemical analysis showed that the two preparations from E. coli 0124 and the corresponding preparations from Shigella dysenteriae type 3 reacted alike. The O-specific polysaccharide moiety was characterized with proton magnetic resonance spectroscopy, optical rotation and paper electrophoresis. The constituents were determined by gas chromatography and ion-exchange chromatography. The polysaccharide contained glucose (Glc), galactose (Gal), galactosamine (GalN) and 4-O-(1'-carboxyethyl)-D-glucopyranose (glucolactilic acid, GlcLA) in the molar ratios of 1:2:1:1. Glucolactilic acid, which has a structure similar to muramic acid, was first found in Sh. dysenteriae. The polysaccharide from E. coli 0124 and oligosaccharides obtained from it by partial acid hydrolysis were subjected to methylation analysis using the method of combined gas chromatography--mass spectrometry. The results indicated that the pentasaccharide repeating unit of the polysaccharide is (see article). In the polysaccharide the repeating units are joined through galactofuranosidic linkages. This structure is identical with that of the somatic polysaccharide of Sh. dysenterae type 3.

Cell Wall↗

An extracellular polysaccharide produced by Zoogloea ramigera 115.

A weakly acidic polysaccharide was purified from the extracellular zoogloeal matrix produced by Zoogloeal ramigera 115. The purified polysaccharide was homogeneous as judged by sedimentation analysis, and the average molecular weight was estimated to be about 10(5) by gel permeation chromatography of the fully methylated preparation. The polysaccharide was composed of D-glucose, D-galactose and pyruvic acid in an approximate molar ratio 11:3:1.5. On the basis of methylation, periodate oxidation, Smith degradation and partial hydrolysis, the following highly branched structure was deduced for the polysaccharide: a long chain mainly consisting of beta 1 leads to 4-linked glucose residues branching at the C-3 or C-6 position of galactose residues which are present in beta 1 leads to 4 or beta 1 leads to 3 linkages as the minor component of the long chain; pyruvic acid residues, the sole acidic component, are linked to the nonreducing end and/or 1,3-linked glucose residues through 4,6-ketal linkages. The purified polysaccharide was not readily soluble in water and had a high affinity for several metallic ions (e.g, 0.25 mumol Fe3+/mg, and 0.17 mumol Fe2+ mg). Upon addition of metallic ions (1 mM) to a gelatinous aqueous solution of the polysaccharide (K+ form, 0.125%), more than 80% of it immediately coprecipitated out with them.

Chemical Phenomena↗

Somatic antigens of Pseudomonas aeruginosa. The structure of O-specific polysaccharide chains of lipopolysaccharides of P. aeruginosa O3 (Lányi), O25 (Wokatsch) and Fisher immunotypes 3 and 7.

O-specific polysaccharides, obtained on mild acid degradation of lipopolysacchrides of the serologically related strains Pseudomonas aeruginosa O3 (Lányi classification), O25 (Wokatsch classification) and immunotypes 3 and 7 (Fisher classification), are built up of trisaccharide repeating units involving 2-acetamido-2,6-dideoxy-D-galactose (N-acetyl-D-fucosamine), 2,3-diacetamido-2,3-dideoxy-D-mannuronic acid or 2,3-diacetamido-2,3-dideoxy-L-guluronic acid and 3-acetamidino-2-acetamido-2,3-dideoxy-D-mannuronic acid or 3-acetamidino-2-acetamido-2,3-dideoxy-L-guluronic acid. Lányi O3(a),3d,3f and Wokatsch O25 polysaccharides contain also O-acetyl groups. On the basis of solvolysis with anhydrous hydrogen fluoride, resulting in trisaccharide fragments with N-acetylfucosamine residue at the reducing terminus, chemical modifications of the acetamidino group (alkaline hydrolysis to the acetamido group or reductive deamination to the ethylamino group), as well as analysis by 1H-NMR (including nuclear Overhauser effect experiments) and 13C-NMR spectroscopy, and fast-atom bombardment mass spectrometry, it was concluded that the repeating units of the polysaccharides have the following structures: (Formula: see text) where HexNAcAmA = alpha-L-GulNAcAmA (approximately 70%) or beta-D-ManNacAMA (approximately 30%). Lányi O3(a),3d,3f polysaccharide involves two types of repeating units, which differ from each other only in the configuration at C-5 of the 3-acetamidino-2-acetamido-2,3-dideoxyuronic acid residue. Lányi O3(a),3c,O3a,3d,3e and Fisher immunotypes 3 and 7 polysaccharides contain, together with the major repeating units shown above, a small proportion of units in which the derivative of alpha-L-guluronic acid is replaced by the corresponding beta-D-manno isomer. The data obtained provide the opportunity to substantiate the serological interrelations between these strains of P. aeruginosa by the presence in the O-specific polysaccharides of common monosaccharides or disaccharide fragments. The distinctions between them stem from the presence or absence of the O-acetyl group, a different configuration of the glycosidic linkage of the N-acetylfucosamine residue and/or a different configuration at C-5 of one or both derivatives of diaminouronic acids.

Carbohydrate Conformation↗

Effect of hypertonic solutes upon the polysaccharide capsule in Cryptococcus neoformans.

The polysaccharide capsule is a characteristic virulence factor in the yeast-pathogen, Cryptococcus neoformans. Growth in hypertonic growth media results in yeast cells with visibly smaller capsules. We investigated this suppression quantitatively, using a chemical assay for cell-bound and dissolved capsular polysaccharide. Molar NaCl suppressed production of cell-bound polysaccharide by a factor of 2.5- to 5-fold. The possibility of salt-induced physico-chemical contraction of capsular gel was tested by dialysis of fixed cells from hypotonic medium against medium containing 1 M NaCl and against the original medium again, while capsular thickness, packed cell volume and cell-bound polysaccharide were followed. We detected a physical contraction of gel following dialysis against medium containing 1 M NaCl. Mutants which gave mucoid colonies on hypertonic agar were isolated. One of these gave twice as much polysaccharide as the wild type when cultivated in medium containing 1 M NaCl. The hypercapsular trait was passed through serial outcrosses to the wild type and segregated as a chromosomal gene. This mutant may represent a gene which regulates production of capsular polysaccharide.

Cryptococcus↗

Effectiveness of microporous polysaccharide hemospheres for achieving hemostasis in mohs micrographic surgery.

BACKGROUND: Microporous polysaccharide hemospheres consist of controlled-porosity spherical particles manufactured from bioinert plant polysaccharide. Microporous polysaccharide hemospheres facilitate hemostasis by rapidly absorbing the fluid component of blood, concentrating platelets and clotting factors to accelerate blood clotting. OBJECTIVE: The objective was to compare a microporous polysaccharide hemosphere bandage and electrocautery in achieving hemostasis. METHODS: Twenty-four patients with a total of 48 stages of Mohs micrographic surgery were included. Patients were stratified by whether or not they were taking anticoagulant medications. Within each group, patients were randomized to receive either the microporous polysaccharide hemosphere bandage or electrocautery. Outcomes included bleeding through the dressing (early time point) and active bleeding upon dressing removal (late time point). RESULTS: Nineteen patients not taking anticoagulants had 40 stages, of which 18 received the study bandage and 22 received electrocautery. The remaining 5 patients on anticoagulants had 8 stages, of which 4 received the study bandage and 4 received electrocautery. In both total and subgroup analysis, there was a higher incidence of bleeding through the dressing with the study bandage (p<0.05), but no increase in the incidence of active bleeding upon dressing removal (p>0.05). CONCLUSION: The microporous polysaccharide hemosphere study bandage had an increased incidence of bleeding through the dressing compared to electrocautery, but did not have an increased incidence of active bleeding upon dressing removal.

Aged↗

Antrodia camphorata polysaccharides exhibit anti-hepatitis B virus effects.

Polysaccharides were extracted from fruiting bodies and cultured mycelia from five Antrodia camphorata strains. Polysaccharide profiles of the five strains, as determined by high-performance anion-exchange chromatography, showed varying yields and composition of neutral sugars. A. camphorata fruiting bodies also had different polysaccharide patterns compared to the cultured mycelium. Analysis of 26-day-old mycelia showed that the neutral sugars galactose, glucose, mannose, and galactosamine were predominant. All mycelia polysaccharide preparations exhibited anti-hepatitis B virus activity. Polysaccharides from strain B86 at a concentration of 50 microg ml(-1) showed the highest level of anti-hepatitis B surface antigen effect, which was higher than alpha-interferon at a dosage of 1000 U ml(-1). Only strains B86 and 35398 had substantial anti-hepatitis B e antigen activities. None of the polysaccharides exhibited cytotoxic effects.

Antiviral Agents↗