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X Ji

Publications and source records attributed to X Ji.

At least 73 records · Page 4Linked to original sources

Crystal structure of a murine glutathione S-transferase in complex with a glutathione conjugate of 4-hydroxynon-2-enal in one subunit and glutathione in the other: evidence of signaling across the dimer interface.

mGSTA4-4, a murine glutathione S-transferase (GST) exhibiting high activity in conjugating the lipid peroxidation product 4-hydroxynon-2-enal (4-HNE) with glutathione (GSH), was crystallized in complex with the GSH conjugate of 4-HNE (GS-Hna). The structure has been solved at 2.6 A resolution, which reveals that the active site of one subunit of the dimeric enzyme binds GS-Hna, whereas the other binds GSH. A marked asymmetry between the two subunits is evident. Most noticeable are the differences in the conformation of arginine residues 69 and 15. In all GST structures published previously, the guanidino groups of R69 residues from both subunits stack at the dimer interface and are related by a (pseudo-) 2-fold axis. In the present structure of mGSTA4-4, however, the two R69 side chains point in opposite directions, although their guanidino groups remain in contact. In the subunit with bound GSH, R69 also interacts with R15, and the guanidino group of R15 points away from the active site, whereas in the subunit that binds GS-Hna, R15 pivots into the active site, which breaks its interaction with R69. According to our previous results [Nanduri et al. (1997) Arch. Biochem. Biophys. 335, 305-310], the availability of R15 in the active site assists the conjugation of 4-HNE with GSH. We propose a model for the catalytic mechanism of mGSTA4-4 in conjugating 4-HNE with GSH-i.e., the guanidino group of R15 is available in the active site of only one subunit at any given time and the stacked pair of R69 residues act as a switch that couples the concerted movement of the two R15 side chains. The alternate occupancy of 4-HNE in the two subunits has been confirmed by our kinetic analysis that shows the negative cooperativity of mGSTA4-4 for 4-HNE. Disruption of the signaling between the subunits by mutating the R69 residues released the negative cooperativity with 4-HNE.

Aldehydes↗

Chiral resolution and stereospecificity of 6-phenyl-4-phenylethynyl- 1,4-dihydropyridines as selective A(3) adenosine receptor antagonists.

Racemic 6-phenyl-4-phenylethynyl-1,4-dihydropyridine derivatives have been shown to be highly selective A(3) adenosine receptor antagonists (Jiang et al. J. Med. Chem. 1997, 40, 2596-2608). Methods for resolving the optical isomers at the C4 position, involving selective crystallization or chromatographic separation of diastereomeric ester derivatives, have been developed. Optically pure glycerol and threitol derivatives were used as chiral auxiliary groups for ester formation at the 3-position, resulting in diastereomeric mixtures of dihydropyridines. Esterification of a 6-phenyl-4-phenylethynyl-1,4-dihydropyridine derivative at the 3-position with a chiral, protected glycerol moiety, (S)-(+)-2, 2-dimethyl-1,3-dioxolane-4-methanol, allowed the selective crystallization of a pure diastereomer, 9. The (1)H NMR spectrum of 9 using the lanthanide shift reagent Eu(fod)(3) indicated optical purity, and the (4S,2'R)-configuration was assigned using X-ray crystallography. The noncrystalline (4R,2'R)-isomer 10 was also isolated and shown to be 3-fold more potent than the (4S,2'R)-isomer in binding to A(3) receptors. The 2,2-dimethyl-1,3-dioxolane moiety also served as a protected form of a diol, which showed selective reactivity versus a 5-ethyl ester in basic transesterification reactions. A racemic 5-carboxylic acid derivative could not be resolved through crystallization of diastereomeric salts. Enantiomers of 5-benzyl 3-ethyl 2-methyl-6-phenyl-4-phenylethynyl-1, 4-dihydropyridine-3,5-dicarboxylate (2) were obtained via an ester derived from (4R,5R)-(-)-2,3-O-isopropylidene-D-threitol at the 3-position, which was resolved using HPLC, and each diastereomer was subsequently deprotected in acidic conditions. The resulting diols were exchanged for ethyl ester groups by base-catalyzed transesterification. The binding of pure enantiomers of 2 at A(3) adenosine receptors indicated a 35-fold stereoselectivity for the (4S)-isomer 21. A receptor docking hypothesis, using a previously derived human A(3) receptor model, shows the bulkier of the two ester groups (5-Bn) of 21 oriented toward the exofacial side and the 4-position phenylethynyl group situated between transmembrane helical domain TM6 and TM7.

Animals↗

Structure and function of residue 104 and water molecules in the xenobiotic substrate-binding site in human glutathione S-transferase P1-1.

Two variants of human class pi glutathione (GSH) S-transferase 1-1 with either isoleucine or valine in position 104 (hGSTP1-1[I104] and hGSTP1-1[V104]) have distinct activity toward (+)-anti-7, 8-dihydroxy-9,10-oxy-7,8,9,10-tetrahydrobenzo[a]pyrene [(+)-anti-BPDE]. To elucidate their structure-function relationship, we determined the crystal structures of the two variants in complex with GSBpd, the GSH conjugate of (+)-anti-BPDE, at 2.1 and 2.0 A resolution, respectively. The crystal structures reveal that residue 104 in the xenobiotic substrate-binding site (H-site) dictates the binding modes of the product molecule GSBpd with the following three consequences. First, the distance between the hydroxyl group of Y7 and the sulfur atom of GSBpd is 5.9 A in the hGSTP1-1[I104].GSBpd complex versus 3.2 A in the V104 variant. Second, one of the hydroxyl groups of GSBpd forms a direct hydrogen bond with R13 in hGSTP1-1[V104].GSBpd; in contrast, this hydrogen bond is not observed in the I104 complex. Third, in the hydrophilic portion of the H-site of the I104 complex, five H-site water molecules [Ji, X., et al. (1997) Biochemistry 36, 9690-9702] are observed, whereas in the V104 complex, two of the five have been displaced by the Bpd moiety of GSBpd. Although there is no direct hydrogen bond between Y108 (OH) and the hydroxyl groups of GSBpd, indirect hydrogen bonds mediated by water molecules are observed in both complexes, supporting the previously suggested role of the hydroxyl group of Y108 as an electrophilic participant in the addition of GSH to epoxides.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗

Amino acid substitutions at positions 207 and 221 contribute to catalytic differences between murine glutathione S-transferase Al-1 and A2-2 toward (+)-anti-7,8-dihydroxy-9,10-epoxy-7,8,9, 10-tetrahydrobenzo[a]pyrene.

We have previously identified a novel Alpha class murine glutathione (GSH) S-transferase isoenzyme (designated mGSTAl-2) which is exceptionally efficient in catalyzing the GSH conjugation of (+)-anti-7,8-dihydroxy-9,10-epoxy-7,8,9,10-tetrahydrobenzo[a]pyrene [(+)-anti-BPDE], the ultimate carcinogen of widespread environmental pollutant benzo[a]pyrene. Furthermore, we have demonstrated that the Al-type subunit of this isoenzyme is significantly more active toward (+)-anti-BPDE than the other subunit (mGSTA2). To establish the basis for catalytic differences between mGSTAl and mGSTA2, which differ in their primary structures by 10 amino acids [distributed in three sections (I-III) as clusters of two (residues 65 and 95), three (residues 157, 162, and 169), and five (residues 207, 213, 218, 221, and 222) amino acids], three chimeric enzymes were expressed and tested for their activity toward (+)-anti-BPDE. These studies revealed that amino acid substitution(s) in section III determined the high catalytic activity of mGSTAl. Molecular modeling studies suggested that amino acid substitutions at positions 207 and/or 221, but not at positions 213, 218, and 222, may be responsible for such a difference. To test this possibility, amino acids at positions 207 and 221 of mGSTAl were mutated with the equivalent residues of mGSTA2. Kinetic analysis of the wild type and the mutant enzymes revealed that both methionine-207 and isoleucine-221 are critical for higher activity of mGSTA1-1 toward (+)-anti-BPDE compared with that of mGSTA2-2.

Amino Acid Substitution↗

Crystal structure of ERA: a GTPase-dependent cell cycle regulator containing an RNA binding motif.

ERA forms a unique family of GTPase. It is widely conserved and essential in bacteria. ERA functions in cell cycle control by coupling cell division with growth rate. ERA homologues also are found in eukaryotes. Here we report the crystal structure of ERA from Escherichia coli. The structure has been determined at 2.4-A resolution. It reveals a two-domain arrangement of the molecule: an N-terminal domain that resembles p21 Ras and a C-terminal domain that is unique. Structure-based topological search of the C domain fails to reveal any meaningful match, although sequence analysis suggests that it contains a KH domain. KH domains are RNA binding motifs that usually occur in tandem repeats and exhibit low sequence similarity except for the well-conserved segment VIGxxGxxIK. We have identified a betaalphaalphabeta fold that contains the VIGxxGxxIK sequence and is shared by the C domain of ERA and the KH domain. We propose that this betaalphaalphabeta fold is the RNA binding motif, the minimum structural requirement for RNA binding. ERA dimerizes in crystal. The dimer formation involves a significantly distorted switch II region, which may shed light on how ERA protein regulates downstream events.

Bacterial Proteins↗

3D imaging of the 58 kDa cell binding subunit of the Helicobacter pylori cytotoxin.

Pathogenic strains of Helicobacter pylori produce a potent exotoxin, VacA, which intoxicates gastric epithelial cells and leads to peptic ulcer. The toxin is released from the bacteria as a high molecular mass homo-oligomer of a 95 kDa polypeptide which undergoes specific proteolytic cleavage to 37 kDa and 58 kDa subunits. We have engineered a strain of H. pylori to delete the gene sequence coding for the 37 kDa subunit. The remaining 58 kDa subunit is expressed efficiently and exported as a soluble dimer that is non-toxic but binds target cells in a manner similar to the holotoxin. A 3D reconstruction of the molecule from electron micrographs of quick-freeze, deep-etched preparations reveals the contribution of each building block to the structure and permits the reconstruction of the oligomeric holotoxin starting from individual subunits. In this model P58 subunits are assembled in a ring structure with P37 subunits laying on the top. The data indicate that the 58 kDa subunit is capable of folding autonomously into a discrete structure recognizable within the holotoxin and containing the cell binding domain.

Bacterial Proteins↗

Purification, characterization and crystallization of ERA, an essential GTPase from Escherichia coli.

ERA is an essential GTPase widely conserved in bacteria. Homologues of ERA are also present in higher eukaryotic cells. ERA is involved in bacterial cell cycle control at a point preceding cell division. In order to aid the functional investigation of ERA and to facilitate structure-function studies, we have undertaken the X-ray crystallographic analysis of this protein. Here, we report the purification and crystallization procedures and results. The purified ERA exhibits nucleotide-binding activity and GTP-hydrolytic activity. ERA is one of the very few multi-domain GTPases crystallized to date.

Bacterial Proteins↗

Opsonic complement component C3 in the solitary ascidian, Halocynthia roretzi.

The recent identification of two mannose-binding lectin-associated serine protease clones from Halocynthia roretzi, an ascidian, suggested the presence of a complement system in urochordates. To elucidate the structure and function of this possibly primitive complement system, we have isolated cDNA clones for ascidian C3 (AsC3) and purified AsC3 protein from body fluid. The deduced primary structure of AsC3 shows overall similarity to mammalian C3, including a typical thioester site with the His residue required for nucleophilic activation of the thioester. AsC3 has a two-subunit chain structure, and the alpha-chain is cleaved at a specific site near to the N terminus upon activation. Ascidian body fluid contains an opsonic activity which enhances phagocytosis of yeast by ascidian blood cells, and Ab against AsC3 inhibits this opsonic activity. These results indicate that the complement system played a pivotal role in innate immunity by enhancing phagocytosis before the emergence of the vertebrates and well ahead of the establishment of adaptive immunity, which is believed to have occurred at about the time of the appearance of cartilaginous fish.

Amino Acid Sequence↗

Cysteines beta93 and beta112 as probes of conformational and functional events at the human hemoglobin subunit interfaces.

Three variants of tetrameric human hemoglobin, with changes at the alpha1beta2/alpha2beta1-interface, at the alpha1beta1/alpha2beta2-interface, and at both interfaces, have been constructed. At alpha1beta2/alpha2beta1-interface the beta93 cysteine was replaced by alanine (betaC93A), and at the alpha1beta1/alpha2beta2-interface the beta112 cysteine was replaced by glycine (betaC112G). The alpha1beta2 interface variant, betaC93A, and the alpha1beta1/alpha1beta2 double mutant, beta(C93A+C112G), were crystallized in the T-state, and the structures determined at 2. 0 and 1.8 A resolution, respectively. A comparison of the structures with that of natural hemoglobin A shows the absence of detectable changes in the tertiary folding of the protein or in the T-state quaternary assembly. At the beta112 site, the void left by the removal of the cysteine side chain is filled by a water molecule, and the functional characteristics of betaC112G are essentially those of human hemoglobin A. At the beta93 site, water molecules do not replace the cysteine side chain, and the alanine substitution increases the conformational freedom of beta146His, weakening the important interaction of this residue with beta94Asp. As a result, when Cl- is present in the solution, at a concentration 100 mM, the Bohr effect of the two mutants carrying the beta93Cys-->Ala substitution, betaC93A and beta(C93A+C112G), is significantly modified being practically absent below pH 7.4. Based on the crystallographic data, we attribute these effects to the competition between beta94Asp and Cl- in the salt link with beta146His in T-state hemoglobin. These results point to an interplay between the betaHis146-betaAsp94 salt bridge and the Cl- in solution regulated by the Cys present at position beta93, indicating yet another role of beta93 Cys in the regulation of hemoglobin function.

Amino Acid Substitution↗

Crystal structure of 6-hydroxymethyl-7,8-dihydropterin pyrophosphokinase, a potential target for the development of novel antimicrobial agents.

BACKGROUND: Folate cofactors are essential for life. Mammals derive folates from their diet, whereas most microorganisms must synthesize folates de novo. Enzymes of the folate pathway therefore provide ideal targets for the development of antimicrobial agents. 6-Hydroxymethyl-7,8-dihydropterin pyrophosphokinase (HPPK) catalyzes the transfer of pyrophosphate from ATP to 6-hydroxymethyl-7,8-dihydropterin (HP), the first reaction in the folate biosynthetic pathway. RESULTS: The crystal structure of HPPK from Escherichia coli has been determined at 1.5 A resolution with a crystallographic R factor of 0.182. The HPPK molecule has a novel three-layered alpha beta alpha fold that creates a valley approximately 26 A long, 10 A wide and 10 A deep. The active center of HPPK is located in the valley and the substrate-binding sites have been identified with the aid of NMR spectroscopy. The HP-binding site is located at one end of the valley, near Asn55, and is sandwiched between two aromatic sidechains. The ATP-binding site is located at the other end of the valley. The adenine base of ATP is positioned near Leu111 and the ribose and the triphosphate extend across and reach the vicinity of HP. CONCLUSIONS: The HPPK structure provides a framework to elucidate structure/function relationships of the enzyme and to analyze mechanisms of pyrophosphoryl transfer. Furthermore, this work may prove useful in the structure-based design of new antimicrobial agents.

Adenosine Triphosphate↗

Beta- and gamma-catenin mutations, but not E-cadherin inactivation, underlie T-cell factor/lymphoid enhancer factor transcriptional deregulation in gastric and pancreatic cancer.

Adenomatous polyposis coli (APC) mutations are present in >70% of colon cancers. The APC protein binds to beta-catenin (beta-cat), a protein first identified because of its role in E-cadherin (E-cad) cell adhesion. In some colon cancers lacking APC defects, mutations in presumptive glycogen synthase kinase 3beta phosphorylation sites near the beta-cat NH2 terminus appear to render beta-cat resistant to regulation by APC and glycogen synthase kinase 3beta. In cells with APC or beta-cat defects, beta-cat is stabilized and, in turn, binds to and activates T-cell factor (Tcf)/lymphoid enhancer factor (Lef) transcription factors. To further explore the role of APC, beta-cat, Tcf, and E-cad defects in gastrointestinal cancers, we assessed gastric and pancreatic cancers for constitutive Tcf transcriptional activity (CTTA). Two of four gastric and two of eight pancreatic cancer lines showed CTTA. One gastric and one pancreatic cancer had mutations in the NH2-terminal phosphorylation sites of beta-cat. The other gastric cancer with CTTA had a missense mutation at serine 28 of gamma-cat, a potential phosphorylation site in this beta-cat-related protein. Although E-cad is an important binding partner for beta-cat and gamma-cat, E-cad inactivation did not result in CTTA. The beta-cat and gamma-cat mutant proteins identified in our studies strongly activated Tcf transcription in vitro, whereas beta-cat mutant proteins with large NH2-terminal deletions had only modest effects on Tcf. Our results suggest a role for Tcf deregulation in gastric and pancreatic cancer, resulting from beta-cat and gamma-cat mutations in some cases and, in others, from yet to be defined defects. Furthermore, these data imply that the consequences of APC and beta-cat mutations are distinct from the effects of E-cad inactivation.

Adenomatous Polyposis Coli Protein↗

Enhancing effects of silkworm expressed recombinant human macrophage colony-stimulating factor on hematopoietic recovery of irradiation-injured mice.

OBJECTIVE: To study the hematopoietic enhancing effects of recombinant human macrophage colony-stimulating factor (rhM-CSF) expressed in silkworm. METHOD: Balb/c mice were irradiated with sublethal dose of 60 Co gamma-rays and then administered intraperitoneally with silkworm expressed rhM-CSF (1000 U per individual for 7 days) in treatment group or with normal saline (for 7 days as well) in control group. The hematopoietic recovery of irradiation mice was observed by comparing peripheral white blood cell (WBC) counts, differential counts of WBC and bone marrow hematopoietic progenitor cell colony forming assay in soft agar at different time after irradiation. RESULTS: The total WBC counts (x 10(9)/L) of treatment group at day 15 and 20 after irradiation(3.42 +/- 1.20, 5.56 +/- 2.50, respectively) were significantly higher than those of control group (2.03 +/- 0.90, 3.72 +/- 2.30; both P < 0.05). On days 10, 15, 20, 25 and 30 after irradiation, the monocyte counts (x 10(9)/L) of treatment group (0.08 +/- 0.06, 0.16 +/- 0.10, 0.48 +/- 0.35, 0.47 +/- 0.21 and 0.33 +/- 0.17, respectively) were all significantly higher than those of control group (0.025 +/- 0.016, 0.05 +/- 0.04, 0.23 +/- 0.16, 0.33 +/- 0.19 and 0.17 +/- 0.13; all P < 0.05). On days 15, 20 and 25, the granulocyte count (X 10(9)/L) of treatment group (1.03 +/- 0.61, 2.18 +/- 1.19 and 3.28 +/- 1.09) were also higher than those of control group (0.62 +/- 0.37, 1.40 +/- 0.99 and 2.20 +/- 0.74; all P < 0.05). On day 9 after irradiation, the bone marrow CFU-GM yield of control group (19 +/- 11/10(6) cells) was significantly lower than that of treatment group (78 +/- 30/10(6) cells, P < 0.05). CONCLUSION: rhM-CSF expressed in silkworm could accelerate hematopoietic recovery in irradiated mice.

Animals↗

[The genotype of vac A gene of Helicobacter pylori (Hp) and its correlation with the gastroduodenal diseases associated with Hp].

OBJECTIVE: To analyze the expression of vac A gene of Helicobacter pylori (Hp) isolated from Chinese patients and to find out the relationship between the genotype of Hp vac A and the gastroduodenal diseases associated with Hp. METHODS: Clones of Hp obtained from patients with gastroduodenal diseases were cultured and mRNA extraction was performed with reverse transcriptase polymerase chain reaction (RT-PCR). RESULTS: 92% of the strains isolated in Shanghai (China) was found to be s1/m2. Strains expressing s1/m1 forms were obtained in 4 cases. s2 form was not found. CONCLUSION: The overwhelming majority of strains isolated from Shanghai patients expresses s1/m2 from. The s1/m2 genotype is dispersed in all of the gastroduodenal diseases associated with Hp.

Adolescent↗

[Multivariate analysis of prognostic factors after hepatectomy for primary liver cancer].

OBJECTIVE: To determine the prognostic factors for primary liver cancer (PLC) after hepatectomy. METHODS: 182 patients who underwent hepatectomy for PLC from 1988 to 1996 were included for univariate and Cox multivariate analysis. 20 factors contributed to the long-term survival rate (SR) and the disease-free SR were analysed. RESULTS: The cumulative SR (n = 182) in 5 years was 43.3%. The 5-year SR and disease-free SR in the curative resection (CR) group (n = 156) were 48.0%, 24.9%, respectively. Multivariate analysis revealed that classification of CR and differentiation grade were significant factors for the long-term SR, and classification of CR and Child-Pugh's classification were significant factors for the disease-free SR. The 5-year SR and disease-free SR for pathological CR, clinical CR and non-CR (palliative resection) groups were 61.1%, 20.4%, 0 and 28.8%, 15.5%, 0, respectively. CONCLUSIONS: The classification of CR is the determining prognostic factor. Pathological CR is the first option for patients with requirements. To control liver disease and improve adjuvant therapy are essential to decreasing the recurrence and metastasis rates.

Adolescent↗

[Clinic and immunophenotypic studies on midline malignant histiocytosis].

OBJECTIVE: To understand the clinic opatholgic changes of midline malignant histiocytosis (MMH), and to explain the source of atypical lymphoid cells (ALC) of MMH, so as to search after the relation between MMH and malignant lymphoma. METHOD: Histopathologic section of 39 cases of MMH were taken HE staining and the histopathologic changes were obsered under microscope. The immunohistochemical staining was also used to examine the immunophenotype of ALC. RESULT: 1. Pathologic changes of MMH: coaglation necrosis and mixed inflammatory cells infiltration, with epithelial infiltration which distributed around the center of blood vessel were their characteristics. 2. Immunohistochemical staining result: 28 in 39 cases of MMH (71.8%) expressed the immunophenvtype of T-cell; among them 13 (33.3%) were finded both positive reaction to CD3 and CD57 antigens with ALCs at the same time. CONCLUSION: According to immunophenotypic studies, most ALCs came from proliferation and infiltration of atypical T cell. ALCs of MMH expressed not only T-cell markers (CD3), but also NK-associated antigen (CD57). MMH was a mucosa related peripheral T/NK cell lymphoma originally.

Adult↗

[Establishment of A + G ligation mediated polymerase chain reaction and its application in in vivo footprinting study].

OBJECTIVE: To establish a new ligation mediated PCR method for the work in in vivo footprinting study of some regions of low G-residue content or some regions of G-residue free. METHODS: The A > G chemical cleavage method of Maxam-Gilbert sequencing was modified for ligation mediated PCR after A + G chemical cleavage and separate the PCR products by sequencing PAGE. RESULTS: A new A + G ligation mediated method was established and could be used in vivo footprinting study. CONCLUSIONS: Our results indicated that the newly developed method could analyze the DNA-Protein interaction at both A-residue and G-residue, enabled us to get more information and enlarged the scope of its application.

Animals↗

[A preliminary report of a new technique: non-penetrating trabecular surgery].

OBJECTIVE: To evaluate the clinical effect of nonpenetrating trabecular surgery with sodium hyaluronate gel implant in Primary Open-Angle Glaucoma(POAG). METHODS: Twenty-four eyes of 22 patients with medically uncontrolled POAG were underwent nonpenetrating trabecular surgery with hyaluronate gel implant. The procedure was performed involing excising a deep-sclera tissue that flush with innerwall of Schlemm' s canal without opening the anterior chamber, then placing a 3 mm x 4.5 mm x 0.5 mm or 3.5 mm x 3.5 mm x 3.5 mm sodium hyaluronate gel implant under the scleral flap respectively. The postoperative Intraocular Pressure (IOP), Inflammation and fitering bleb were analysised. All of patients were undertaken ultrasound biomicroscopy (UBM) to evaluate the surgery site on postoperative 1-3 months. Mean follow-up was 3.9 +/- 2.2 months. RESULTS: The IOP decreased from a mean preoperative value of 24.4 +/- 9.1 mmHg to a mean postoperative value of 15.1 +/- 3.7 mmHg (P < 0.01). The number of anti-glaucomatous medications by topically or systemically was reduced from preoperative sorts of 2.8 +/- 1.4 to postoperative sorts of 0.7 +/- 1.0 (P < 0.01). The visual acuity remained stable, 6 eyes had IOP elevated and 2 eyes had occured hyphema. The complications such as flat chamber, inflammation and detachment of choroid were not observed. The UBM showed that the hyaluronate gel implant wasn't degraded and a transparent liquid space was formed under the scleral flap in all of patients on postoperatively 1-3 month. The filtering blebs were formed in some patients. CONCLUSION: Nonpenetrating trabecular surgery with hyaluronate gel implant can effectively lower IOP and reduce the number of anti-glaucomatous medications. No severe complications occured. With a simple postoperative nursing, it can be performed in clinic. It is proved to be a promising and new special technique to treat glaucoma.

Adolescent↗