Disease relevance of NAG-(3-1)GCU-(4-1)NAG-(3-1)GCU

• To investigate the role of AIF in the apoptotic process in vivo, we induced retinal detachment (RD) by subretinal injection of sodium hyaluronate, either in Brown Norway rats or in C3H mice [1].
• Pseudogout following intraarticular injection of sodium hyaluronate [2].
• Intra-articular sodium hyaluronate in osteoarthritis of the knee [3].
• Histological examination revealed accelerated epithelial healing of the vesical mucosa and inhibited vesical fibrosis in the group treated with 0.4% sodium hyaluronate [4].
• Intravesical sodium hyaluronate has been used to treat interstitial cystitis due to its possible replenishment of bladder glycosaminoglycans [5].

High impact information on NAG-(3-1)GCU-(4-1)NAG-(3-1)GCU

• Partial degradation products of sodium hyaluronate produced by the action of testicular hyaluronidase induced an angiogenic response (formation of new blood vessels) on the chick chorioallantoic membrane [6].
• Recent animal studies show that endothelial cells in liver sinusoids are the main site for removal of sodium hyaluronate from the circulation [7].
• Fragmented HA, but not Healon, increased MCP-1 mRNA within 30 min with a peak after 2 h [8].
• Healon and human umbilical cord HA are ineffective because their molecular weight is too large, while smaller HA derived from these larger molecules or normally present in bovine vitreous humor preparations stimulates the chondrogenic differentiation of stage 24 limb mesenchymal cells in culture [9].
• When limb mesenchymal cells are plated onto HA from bovine vitreous humor, human umbilical cord, or large molecular weight HA (Healon), increased chondrogenesis is observed only on the bovine vitreous humor HA [9].

Chemical compound and disease context of NAG-(3-1)GCU-(4-1)NAG-(3-1)GCU

• CONCLUSION: Sodium hyaluronate enhances tumour metastatic potential in vitro and in vivo, which suggests that use of sodium hyaluronate to prevent adhesions in colorectal cancer surgery may also potentiate intraperitoneal tumour growth [10].
• PURPOSE: To evaluate the effect of sodium hyaluronate on epithelial healing of the vesical mucosa and vesical fibrosis, and clarify the effect of the sodium hyaluronate solution concentration, we administered sodium hyaluronate in the bladder of rabbits with acetic acid induced cystitis [4].
• The clinical efficacy and tolerability of sodium hyaluronate, a high-molecular-weight hyaluronic acid preparation, in the treatment of patients with periarthritis of the shoulder was investigated in a multicenter, cooperative study [11].
• PURPOSE: The aim of the study was to assess the impact of sodium hyaluronate and carboxymethylcellulose membrane (Seprafilm) on postoperative intestinal obstruction as judged by the rates of bowel obstruction and laparotomy for bowel obstruction [12].
• CONCLUSIONS: The results observed in this investigation indicate that the addition of lidocaine to the sodium hyaluronate in VisThesia does not induce additional toxicity nor does it result in increased endothelial cell loss when compared with other, similar OVDs [13].

Biological context of NAG-(3-1)GCU-(4-1)NAG-(3-1)GCU

• Aqueous humor replacement with 1% sodium hyaluronate resulted in mild, transient elevations of intraocular pressure compared to eyes that were injected with balanced salt solution [14].
• With regard to postoperative inflammatory reaction and wound healing, no side effects have been observed after use of Healon [15].
• RESULTS: The patient achieved a visual acuity of 20/20 in the involved eye after descemetopexy with sodium hyaluronate and air combined with suturing [16].
• RESULTS: In vitro sodium hyaluronate increased tumour cell proliferation and motility significantly [10].
• Sodium hyaluronate-induced tumour cell motility appeared to be CD44 receptor dependent, whereas sodium hyaluronate-induced tumour cell proliferation was CD44 receptor independent [10].

Anatomical context of NAG-(3-1)GCU-(4-1)NAG-(3-1)GCU

• If Healon was injected into the anterior chamber, the thickness and staining intensity of this layer increased conspicuously [17].
• Sodium hyaluronate (HA) protects the corneal endothelium during cataract surgery [17].
• A highly viscous agent, eg, sodium hyaluronate 1%, in a thin layer produced extensive endothelial cell damage because it transmitted excessive shear force to the endothelium [18].
• The effect of sodium hyaluronate on the corneal epithelium. An ultrastructural study [19].
• METHODS: After tunnelization of the sclera, different formulations based on POE were injected (100 microL) into the suprachoroidal space of pigmented rabbits and compared with 1% sodium hyaluronate [20].

Associations of NAG-(3-1)GCU-(4-1)NAG-(3-1)GCU with other chemical compounds

• The effect of sodium hyaluronate and sodium chondroitin sulfate on the coagulation system in vitro [21].
• METHODS: Human colorectal tumour cell lines SW480, SW620 and SW707 were treated with sodium hyaluronate (10-500 microg/ml) and carboxymethylcellulose (0.125-1 per cent), and tumour cell proliferation and motility were determined in vitro [10].
• Reaction of high molecular weight sodium hyaluronate (NaHA, MW approximately 2 x 10(6] with EDC at pH 4.75, either in the presence or absence of a primary diamine, gave the N-acylurea and O-acylisourea as NaHA-carbodiimide adducts [22].
• DESIGN: A review of the literature based on a MEDLINE search through June 2004, using the terms HA, sodium hyaluronate, hyaluronic acid, hylan, hylan G-F 20, OA, disease modification, structure modifying and joint structure [23].
• PURPOSE: To investigate the morphological effects of Viscoat (sodium hyaluronate 3.0%-chondroitin sulfate 4.0%) on lens epithelial cells (LECs) [24].

Gene context of NAG-(3-1)GCU-(4-1)NAG-(3-1)GCU

• Sodium hyaluronate is the ligand for CD44, a cell surface adhesion molecule which has been found on normal human corneal epithelial cells [25].
• Among OA patients in whom remarkable improvement was noted in hydrarthrosis, the synovial fluid IL-6 and IL-8 levels at the initial examination were relatively higher, and were markedly decreased after treatment with sodium hyaluronate (NaHA) [26].
• The uPA concentration was significantly decreased by sodium hyaluronate in the medium but not in cell lysates (P<.0001) [27].
• Cells were treated with TNF-alpha, a cytokine typically involved in peritoneal inflammation, and sodium hyaluronate was added in a final concentration of 0.1%, 0.2%, or 0.4% [27].
• Sodium hyaluronate significantly decreased PAI-1 concentration in the medium and reduced its gene expression 500-fold (P =.04), while PAI-1 concentration in cell lysates did not change [27].

Analytical, diagnostic and therapeutic context of NAG-(3-1)GCU-(4-1)NAG-(3-1)GCU

• Sodium hyaluronate 1% protected the feline endothelium against cell loss incurred by contact with hyaluronate-coated intraocular lenses compared to endothelial contact with lenses that were not coated with sodium hyaluronate [14].
• The use of intraoperative 1% sodium hyaluronate, however, did not protect against endothelial cell loss incurred by penetrating keratoplasty or prevent subsequent skin graft-induced corneal homograft rejections [14].
• Preparation and circular dichroism analysis of sodium hyaluronate oligosaccharides and chondroitin [28].
• The effect of sodium hyaluronate (NaHa) 1% and 0.1% was studied on 14-day chick embryo corneal epithelium by scanning electron microscopy [19].
• Homograft rejections were milder, however, in some eyes that received grafts coated with 1% sodium hyaluronate [14].

References