Biomedical subjects

G Yu

Publications and source records attributed to G Yu.

At least 145 records · Page 8Linked to original sources

PubMed1998

Sulfhydryl redox state affects susceptibility to ischemia and sarcoplasmic reticulum Ca2+ release in rat heart. Implications for ischemic preconditioning.

We investigated the effect of sulfhydryl and disulfide reagents on ischemic preconditioning and on sarcoplasmic reticulum Ca2+ release. Isolated working rat hearts were subjected to ischemic preconditioning (three 3-minute periods of global ischemia) or to control aerobic perfusion, which was followed by 30 minutes of global ischemia and 120 minutes of retrograde reperfusion. Necrosis was evaluated on the basis of lactate dehydrogenase release and triphenyltetrazolium chloride staining. In parallel experiments, sarcoplasmic reticulum Ca2+ release and [3H]-ryanodine binding were determined before the sustained ischemia. Ischemic preconditioning was associated with protection versus ischemic injury, decreased Ca2+ release and reduced [3H]-ryanodine binding. The disulfide reducing agent dithiothreitol (1 mmol/L) removed the protection provided by ischemic preconditioning, if added to the perfusion buffer either before or after the preconditioning procedure. In preconditioned hearts, dithiothreitol increased sarcoplasmic reticulum Ca2+ release and ryanodine binding, whereas in control hearts it had no effect on either tissue injury or sarcoplasmic reticulum function. Perfusion of control hearts with the sulfhydryl blocking agents 4,4'-dithiodipyridine (25 micromol/L) and N-ethylmaleimide (16 micromol/L) increased the resistance to ischemia and reduced sarcoplasmic reticulum Ca2+ release and [3H]-ryanodine binding. These effects were not additive with those induced by preconditioning. Sulfhydryl and disulfide reagents produced similar effects on Ca2+ release and [3H]-ryanodine binding if added in vitro to preparations obtained from control and preconditioned hearts. We conclude that ischemic preconditioning is associated with the oxidation of sulfhydryl groups involved in the modulation of sarcoplasmic reticulum Ca2+ release.

Animals↗

PubMed1998

Role of endogenous interferon-gamma on the enhancement of splenic NK cell activity by electroacupuncture stimulation in mice.

Successive electro-acupuncture (EA) stimulation applied to bilateral anterior tibial muscles, where Zusanli (ST36) acupoints are located, once a day (30 min) for 3 successive days significantly enhanced splenic natural killer (NK) cell activity in BALB/c mice. The percentage of splenic NK cells, as measured by flow cytometry, was not affected in these mice. Interferon (IFN)-gamma level in splenic aqueous extract, prepared from the ST36 acupoint-stimulated mice, was significantly higher than that of the controls. In vivo treatment with neutralizing monoclonal antibody against mouse IFN-gamma completely abrogated the increase in splenic NK cell activity induced by ST36 acupoint stimulation. The same stimulation also significantly increased the concentration of splenic beta-endorphin, which coincided with the significant increase in splenic IFN-gamma production. Pre-administration of 10 mg/kg naloxone before initiation of EA stimulation every day reduced the enhancements of NK cell activity and IFN-gamma level. These observations strongly suggest that endogenous IFN-gamma mediates the up-regulation of NK cell activity by EA stimulation at the ST36 acupoints. Furthermore, endogenous beta-endorphin secreted by EA stimulation also plays an important role in the up-regulation of NK cell function, which may be realized through regulating IFN-gamma production.

Animals↗

PubMed1998

Development of novel cell surface CD34-targeted recombinant adenoassociated virus vectors for gene therapy.

Recombinant adenoassociated virus (rAAV) type 2 vectors have been used to transduce a wide variety of cell types, including hematopoietic progenitor cells. For in vivo gene transfer, it is desirable to have an rAAV vector that specifically transduces selected target cells. As a first step toward generating an rAAV vector capable of targeting delivery in vivo, we have engineered a chimeric protein combining the AAV capsid protein and the variable region of a single-chain antibody against human CD34 molecules, a cell surface marker for hematopoietic stem/progenitor cells. Inclusion of the chimeric CD34 single-chain antibody-AAV capsid proteins within an rAAV virion significantly increased the preferential infectivity of rAAV for the CD34+ human myoleukemia cell line KG-1, which is normally refractory to rAAV transduction. Antibodies against the single-chain antibody and the CD34 protein blocked this transduction. This chimeric vector represents a significant improvement in the host range of rAAV and the first step toward specific gene delivery by rAAV vectors to cells of choice, in this case, hematopoietic progenitor cells, for the treatment of human disease.

Antibodies, Anti-Idiotypic↗

PubMed1998

Evidence for an Alzheimer disease susceptibility locus on chromosome 12 and for further locus heterogeneity.

CONTEXT: Alzheimer disease (AD) susceptibility genes have been identified on chromosomes 1, 14, 19, and 21, and a recent study has suggested a locus on chromosome 12. OBJECTIVE: To confirm or refute the existence of a familial AD susceptibility locus on chromosome 12 in an independent sample of familial AD cases. DESIGN: Retrospective cohort study. DNA data for 6 chromosome 12 genetic markers were evaluated using parametric lod score and nonparametric linkage methods and linkage heterogeneity tests. The latter include the admixture test of homogeneity in the total group of families and the predivided sample test in families stratified by the presence or absence of an apolipoprotein E (APOE) epsilon4 allele among affected members. Parametric analyses were repeated assuming autosomal dominant inheritance of AD and either age- and sex-dependent penetrance or zero penetrance for the analysis of unaffected relatives. SETTING: Clinical populations in the continental United States, Canada, Argentina, and Italy. PATIENTS: Fifty-three white families composed of multiple members affected with AD, from whom DNA samples were obtained from 173 patients with AD whose conditions were diagnosed using established criteria and from 146 nondemented relatives. MAIN OUTCOME MEASURE: Presence of an APOE epsilon4 allele among affected family members. RESULTS: Using parametric methods, no evidence for linkage to the region spanned by the chromosome 12 markers could be detected if familial AD is assumed to arise from the same genetic locus in all 53 families. However, significant evidence for linkage was detected in the presence of locus heterogeneity using the admixture test (odds ratio, 15, 135:1). The estimated proportion of linked families within the 53 families examined varied between 0.40 and 0.65, depending on the genetic model assumed and APOE status. The precise location of the AD gene could not be determined, but includes the entire region suggested previously. Nonparametric linkage analysis confirmed linkage to chromosome 12 with the strongest evidence at D12S96 (P<.001). CONCLUSIONS: Our data provide independent confirmation of the existence of an AD susceptibility locus on chromosome 12 and suggest the existence of AD susceptibility genes on other chromosomes. Screening a larger set of families with additional chromosome markers will be necessary for identifying the chromosome 12 AD gene.

Adult↗

PubMed1998

Identification and functional characterization of DR6, a novel death domain-containing TNF receptor.

Tumor nectosis factor (TNF) receptors are key players in inflammation and immune regulation. A new member of this family, termed death receptor-6 (DR6), has been identified. Like other death receptors, DR6 is a type I transmembrane receptor, possesses four extracellular cysteine-rich motifs and a cytoplasmic death domain. DR6 is expressed in most human tissues and abundant transcript was detected in heart, brain, placenta, pancreas, thymus, lymph node and several non-lymphoid cancer cell lines. DR6 interacts with TRADD, which has previously been shown to associate with TNFR1. Furthermore, ectopic expression of DR6 in mammalian cells induces apoptosis and activation of both NF-kappaB and JNK.

Amino Acid Sequence↗

PubMed1998

Absence of association between Alzheimer disease and the -491 regulatory region polymorphism of APOE.

A novel polymorphism (-491 A/T) within the regulatory region on the apolipoprotein E gene has recently been reported to be associated with risk for Alzheimer disease (AD). To test this association in an independent data set, we have examined this polymorphism in a sample of 88 well-characterized AD cases and compared the allele frequency and genotype frequencies for this polymorphism with those observed in 112 cognitively normal subjects drawn from the same ethnic group. These results suggest that in the current data set at least, the -491 A/T polymorphism is not associated with risk for AD, but may be in partial linkage disequilibrium with the APOE epsilon2/epsilon3/epsilon4 polymorphism.

Aged↗

PubMed1998

The presenilin 1 protein is a component of a high molecular weight intracellular complex that contains beta-catenin.

The presenilin (PS) genes associated with Alzheimer disease encode polytopic transmembrane proteins which undergo physiologic endoproteolytic cleavage to generate stable NH2- and COOH-terminal fragments (NTF or CTF) which co-localize in intracellular membranes, but are tightly regulated in their stoichiometry and abundance. We have used linear glycerol velocity and discontinuous sucrose gradient analysis to investigate the distribution and native conformation of PS1 and PS2 during this regulated processing in cultured cells and in brain. The PS1 NTF and CTF co-localize in the endoplasmic reticulum (ER) and in the Golgi apparatus, where they are components of a approximately 250-kDa complex. This complex also contains beta-catenin but not beta-amyloid precursor protein (APP). In contrast, the PS1 holoprotein precursor is predominantly localized to the rough ER and smooth ER, where it is a component of a approximately 180-kDa native complex. PS2 forms similar but independent complexes. Restricted incorporation of the presenilin NTF and CTF along with a potentially functional ligand (beta-catenin) into a multimeric complex in the ER and Golgi apparatus may provide an explanation for the regulated accumulation of the NTF and CTF.

Alzheimer Disease↗

PubMed1998

Detection of a new substrate-derived radical during inactivation of ribonucleotide reductase from Escherichia coli by gemcitabine 5'-diphosphate.

Ribonucleotide reductases (RNRs) play a central role in replication and repair by catalyzing the conversion of nucleotides to deoxynucleotides. Gemcitabine 5'-diphosphate (F2CDP), the nucleoside of which was recently approved by the FDA for treatment of pancreatic cancer, is a potent mechanism-based inhibitor of class I and II RNRs. Inactivation of the Eschericia coli class I RNR is accompanied by loss of two fluorides and one cytosine. This RNR is composed of two homodimeric subunits: R1 and R2. R1 is the site of nucleotide reduction, and R2 contains the essential diferric-tyrosyl radical cofactor. The mechanism of inactivation depends on the availability of reductant. In the presence of reductant [thioredoxin (TR)/thioredoxin reductase (TRR)/NADPH or dithiothreitol], inhibition results from R1 inactivation. In the absence of reductant with prereduced R1 and R2, inhibition results from loss of the essential tyrosyl radical in R2. The same result is obtained with C754S/C759S-R1 in the presence of TR/TRR/NADPH. In both cases, tyrosyl radical loss is accompanied by formation of a new stable radical (0.15-0.25 equiv/RNR). EPR studies in 2H2O, with [U-2H]R1, and examination of the microwave power saturation of the observed signal, indicate by process of elimination that this new radical is nucleotide-based. In contrast to all previously investigated 2'-substituted nucleotide inhibitors of RNR, inactivation is not accompanied by formation of a new protein-associated chromophore under any conditions. The requirement for reductant in the R1 inactivation pathway, the lack of chromophore on the protein, the loss of two fluoride ions, and the stoichiometry of the inactivation all suggest a unique mechanism of RNR inactivation not previously observed with other 2'-substituted nucleotide inhibitors of RNR. This unique mode of inactivation is proposed to be responsible for its observed clinical efficacy.

Chromatography, High Pressure Liquid↗

PubMed1998

TRUNDD, a new member of the TRAIL receptor family that antagonizes TRAIL signalling.

TRAIL/Apo-2L induces rapid apoptosis of a variety of tumor cell lines. A family of tumor necrosis factor receptor-related molecules have been identified as receptors for TRAIL. Herein, we report the identification of another member of the TRAIL receptor family, TRUNDD (TRAIL receptor with a truncated death domain). The TRUNDD transcript was detected in multiple human tissues. TRUNDD is highly homologous to all known TRAIL receptors and has an extracellular TRAIL-binding domain but lacks a functional intracellular death domain and does not induce apoptosis. Consistent with an inhibitory role, ectopic expression of TRUNDD attenuated TRAIL-induced apoptosis in mammalian cells.

Amino Acid Sequence↗

PubMed1998

Squamous cell carcinoma of the tongue in young patients: a matched-pair analysis.

BACKGROUND: Tongue cancer is seen with increasing frequency in young individuals. There is controversy concerning the clinical course and outcome for oral tongue cancer in young patients. METHODS: A retrospective review of 36 patients under 40 years of age with squamous cell carcinoma of the tongue was performed. These patients were matched to an older population. The 5-year disease-free survival; rates of local, regional, and distant failure; and rate of second primary tumor were determined for both populations. RESULTS: The 5-year disease-free survival for the young patients was 62% versus 69% in the older population (p = .30). Ten of 36 (28%) of younger patients recurred locally versus five of 36 (14%) of the older patients (p = .11). Nine of 36 (25%) younger patients recurred regionally in the younger group versus six of 36 (17%) patients in the older group (p = .25). Sixteen of 36 (44%) of the younger patients had locoregional failure versus eight of 36 (22%) of the older patients (p < .05). The rates of metastatic disease and second primary lesions were similar in both populations. CONCLUSIONS: In this series, younger patients with squamous cell carcinoma of the oral tongue had a higher rate of locoregional recurrence rate than did older patients. This did not translate into a survival difference.

Adult↗

PubMed1998

Serum levels of phospholipid fatty acids in mothers and their babies in relation to allergic disease.

UNLABELLED: The fatty acid composition of serum phospholipids was analysed by gas chromatography in 26 non-allergic and 32 allergic mothers at the time of delivery. In 47 of them the levels were compared with those in the cord blood of their babies. The children were then followed for 6 years with regard to the development of allergic disease. There was an inverse relationship between the levels of linoleic acid (LA, C18:2n-6) and its metabolic products arachidonic acid (AA, C20:4n-6) (r = -0.63, P < 0.001), and C22:4 (r = -0.50, P < 0.01) in the non-allergic, but not in allergic mothers (r = 0.25 and r = -0.39, respectively). Comparing the fatty acid levels in maternal and umbilical cord serum, a significant correlation was observed between the LA levels in serum of non-allergic mothers and their babies (r = 0.53, P < 0.05). Furthermore, the maternal dihomo-gamma-linolenic acid (DHGLA, C20:3n-6) levels correlated with the cord serum levels of AA (r = 0.65, P < 0.01) and C22:4 (r = 0.65, P < 0.01) and with docosahexaenoic acid (DHA, C22:6n-3, r = 0.65, P < 0.01). None of these relationships were seen when comparing the fatty acid levels in the allergic mothers and their babies. In the mothers of children who did not develop any allergic manifestations during the first 6 years of life, the AA levels correlated with C22:4 (r = 0.53, P < 0.001) and eicosapentaenoic acid (EPA, C20:5n-3) (r = 0.56, P < 0.001). Similar findings were recorded within the n-3 series of fatty acids, i.e. the levels of docosapentaenoic acid (DPA, C22:5n-3) correlated with DHA (r = 0.61, P < 0.001). None of these correlations were significant in the 20 mothers whose babies developed allergic disease (r = 0.42, 0.28 and 0.44 respectively). Taken together, the findings indicate that there is an abnormal metabolism relationship between some of the long-chain polyunsaturated fatty acids in allergic mothers, affecting their infants. Furthermore, the findings suggest an association between the fatty acid composition in maternal serum and the appearance of allergic disease in their children during the first 6 years of life. CONCLUSION: The proportions of various long-chain polyunsaturated fatty acids were altered in the serum phospholipids of allergic pregnant mothers and in mothers whose babies developed allergic disease over the first 6 years of life, indicating that atopy is associated with a disturbed fatty acid metabolism.

Adult↗

PubMed1998

Conformational changes and anticoagulant activity of chondroitin sulfate following its O-sulfonation.

Chondroitin sulfate from bovine tracheal cartilage, with the basic structure (4-O-sulfo-D-GalpNAc beta-1-->4-D-GlcpA)n, was chemically modified by O-sulfonation. Depending on the reaction conditions, the products showed a different degree of O-sulfonation. A fully O-sulfonated chondroitin sulfate, having no free hydroxyl groups, and a sulfo ester group:disaccharide unit ratio of 4.0 was prepared. This chondroitin sulfate derivative was shown by 1H NMR spectroscopy to have a uronate residue with an altered conformation. Usually, the uronate residue in chondroitin sulfate resides in the 4C1 form. Fully O-sulfonated chondroitin sulfate had an uronate residue in the 1C4 form at 30 degrees C, similar to the preferred conformation of the 2-O-sulfo-iduronate residue most commonly found in heparin. The 2S0 form of the uronate residue was also found in fully O-sulfonated chondroitin sulfate at 60 degrees C. The anti-factor IIa activity of fully O-sulfonated chondroitin sulfate was 40 units/mg. This value is similar to the activities reported for various low-molecular-weight heparins, and substantially higher than those previously reported for partially O-sulfonated chondroitin sulfates having an average sulfate group/disaccharide unit of 2.5 to 3.3. The anti-factor Xa activity of the fully O-sulfonated chondroitin sulfate was 12 units/mg. This value is considerably lower than the activities reported for various low-molecular-weight heparins, consistent with the critical importance of an antithrombin III pentasaccharide binding site for anti-factor Xa activity. These findings suggest that the conformational change of glucuronic acid residue in chondroitin sulfate resulting from its full O-sulfonation can result in enhanced anticoagulant activity, particularly as measured by anti-factor IIa assay.

Animals↗

PubMed1998

Pretreatment and biodegradability enhancement of DSD acid manufacturing wastewater.

Two advanced oxidation processes, Fenton's reagent oxidation and ozonation, were used for pretreatment of a 4,4'-diaminostilbene-2,2'-disulfonic acid (DSD-acid) manufacturing wastewater on a laboratory scale. The results showed that both methods are suitable for partial removal of chemical oxygen demand (COD) and color as well as the enhancement of biodegradability of DSD-acid manufacturing wastewater before the conventional biological treatment. Fenton's reagent oxidation by 9.0 g/L H2O2 and 150 mg/L Fe2+ and ozonation by 7.5 g/L O3 led to an improved biodegradability (BOD5/COD = 0.3). Fenton's reagent oxidation in combination with Fe3+ coagulation has shown to effectively remove COD and color. About 90% of COD and 95% of color removals were obtained at the optimum condition, oxidation by 150 mg/L Fe2+ and 2 g/L H2O2, followed by two-stage coagulation with 5 g/L and 2 g/L FeCl3, respectively.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗

PubMed1998

Amyloid-beta-protein isoforms in brain of subjects with PS1-linked, beta APP-linked and sporadic Alzheimer disease.

To determine whether similar abnormalities of various soluble full-length and N-terminal truncated Abeta peptides occur in postmortem cerebral cortex of affected PS1 mutation carriers, we examined the amounts of two amyloid species ending at residue 40 or at residues 42(43) using sandwich ELISA systems. Our results indicate that PS1 mutations effect a dramatic accumulation in brain of the highly insoluble potentially neurotoxic long-tailed isoforms of the Abeta peptide such as Abeta1-42(43) and Abetax-42(43). This enhancing effect of PS1 mutation on Abetax-42(43) deposition was highly similar to that of a betaAPP mutation (Val717Ile) but the effects on Abetax-40 production were significantly different between these two causal genes. In contrast to previous studies of soluble Abeta in plasma and in supernatants from cultured fibroblasts of subjects with PS1 mutations, our studies also show that there is an increase in insoluble Abetax-40 peptides in brain of subjects with PS1 mutations.

Adult↗

PubMed1998

Experimental studies on traumatic facial nerve injury.

PURPOSE: The purpose of this study was to investigate the outcome of different injuries to the facial nerve. MATERIALS AND METHODS: Six patterns of injuries (exposure, compression, crushing, stretching, division and post-division anastomosis) were produced in the buccal branches of the facial nerve in 60 rabbits. Electroneuronography (ENoG) and histology at definite time were used to evaluate the results. RESULTS AND CONCLUSIONS: Exposure and compression injuries produced a neuropraxic injury and rapid recovery. Crushing and stretching injuries resulted in axonotmesis and whilst complete recovery can take place it may be very slow. Division and post-division anastomosis fall into neurotmesis injury and do not completely recover within six months; the former recovers slower and later than the latter.

Animals↗

PubMed1998

Analysis of mammalian origin specification in ORC-depleted Xenopus egg extracts.

BACKGROUND: Xenopus egg extracts initiate replication specifically at the Chinese Hamster Ovary (CHO) cell dihydrofolate reductase (DHFR) origin with CHO G1-phase nuclei as a substrate, providing that these nuclei have intact nuclear envelopes and are isolated from cells that have passed through a distinct transition (origin decision point; ODP) early in G1-phase. With intact pre-ODP nuclei, or with post-ODP nuclei that have permeabilized nuclear envelopes, replication initiates efficiently but, at apparently random sites. We have investigated whether the Xenopus embryonic origin recognition complex (XORC) influences origin specification in this system. RESULTS: Xenopus egg extracts were immunodepleted of XORC, eliminating their ability to assemble pre-initiation complexes. These extracts were deficient in the replication of CHO metaphase chromosomes but supported efficient DNA replication within both pre- and post-ODP hamster G1-phase nuclei, even after permeabilization and extraction of soluble nuclear proteins. XORC-depleted extracts initiated replication specifically at the DHFR origin with intact post-ODP nuclei but still initiated at apparently random sites with intact pre-ODP nuclei or permeabilized post-ODP nuclei. CONCLUSIONS: Xenopus embryonic ORC is clearly not required for random origin site selection in Xenopus egg extracts. We conclude that a modification of Chinese Hamster chromatin takes place shortly after metaphase that complements a lack of XORC activity. This modification most likely represents an interaction of mammalian ORC with chromatin that is required for replication but, that is not sufficient for origin specification.

Animals↗

PubMed1998

Fatty acid composition in colostrum and mature milk from non-atopic and atopic mothers during the first 6 months of lactation.

The fatty acid composition of total lipids was analysed in colostrum and mature human milk samples obtained at 1, 3, 4 and 6 months from 17 non-atopic and at 1 and 3 months from 17 atopic mothers. The relative levels of linoleic acid and alpha-linolenic acid increased up to 3 months after delivery and then declined. In contrast, the levels of their metabolites were higher in colostrum than in mature milk. The levels of dihomo-gamma-linolenic acid, eicosapentaenoic acid, docosapentaenoic acid and docosahexaenoic acid were all lower in atopic than non-atopic mothers in milk samples obtained after 1 month of lactation (all p < 0.05). The ratio of total n-6 to n-3 long-chain polyunsaturated fatty acids (LCP) in milk at 1 and 3 months was higher in atopic than non-atopic mothers (all p < 0.05). Lower levels of the monounsaturated fatty acids (MUFA) were also observed in atopic mothers, as compared to non-atopic mothers. In the non-atopic mothers, the levels of individual n-6 LCP correlated and also correlated with n-3 LCP in colostrum and early mature milk (r = 0.60-0.92, all p < 0.01). These correlations within n-6 and between n-6 and n-3 LCP were mostly absent in atopic mothers. The findings suggest that the LCP metabolism in human milk is disturbed in atopic mothers, as indicated by the lower relative levels of some LCP at 1 month, higher ratios of n-6 to n-3 LCP and poor correlations between the levels of the various compounds during the first 3 months of lactation.

Colostrum↗

PubMed1998

Determination of the structure of oligosaccharides prepared from acharan sulfate.

The fine structure of acharan sulfate, a recently discovered glycosaminoglycan isolated from Achatina fulica , was examined. This glycosaminoglycan has a major disaccharide repeating unit of -->4)-alpha-D-GlcNpAc(1-->4)-alpha-L-IdoAp2S(1--> (where GlcNpAc is N -acetylglucosamine, IdoAp is iduronic acid, and S is sulfate) making it structurally related to both heparin and heparan sulfate. Using heparin lyases prepared from Flavobacterium heparinum and a newly isolated heparinase from Bacteroides stercoris , the controlled enzymatic depolymerization of acharan sulfate was undertaken to prepare a mixture of oligosaccharides. Fractionation of this mixture of oligosaccharides by strong-anion-exchange high performance liquid chromatography afforded oligosaccharides that capillary electrophoresis established were sufficiently pure for structural characterization. Electrospray ionization mass spectrometry identified two series of oligosaccharides, one derived from acharan sulfate's major repeating unit and a second minor group of undersulfated oligosaccharides. Proton nuclear magnetic resonance spectroscopy established the structure of these two classes of oligosaccharides to be DeltaUAp2S(1-->[4)-alpha-D-GlcNpAc(1-->4)-alpha-L-IdoAp2S (1-->]n4)- D-GlcNpAcalpha,beta (where n = 0,1,2,3 and DeltaUAp is 4-deoxy-alpha-L- threo -hex-4-enopyranosyluronic acid) and DeltaUAp(1-->[4)- alpha-D-GlcNpAc(1-->4)-alpha-L-IdoAp2S(1-->]m-D-GlcNpAcal pha,beta (where m = 1,2,3). These results suggest the presence of minor sequence variants in acharan sulfate containing unsulfated iduronic acid having the structure -->4)-alpha-D-GlcNpAc(1-->4)-alpha-L-IdoAp(1-->.

Animals↗