Mannosidase I creates a Man5GlcNAc2-structure on the protein, but note that this has a different structure than the one made on LLO. Next, a GlcNAc residue forms GlcNAc1Man5GlcNAc2, the substrate for a-mannosidase II (aManII). aManII then removes two Man residues, creating the substrate for GlcNAc transferase II, which adds a GlcNAc to the second Man branch. This structure serves as substrate for additional galactosylation, fucosylation and sialylation reactions. Additionally, substitution with more GlcNAc residues can yield tri- and tetra-antennary molecules.Not all structures are fully modified, some remain as high-mannose structures, others as hybrids (one unmodified Man branch and one modified), but the majority become fully modified complex type oligosaccharides.In addition to glycosidase I, mutations have been found:
in MGAT2, in GlcNAc transferase II (CDG-IIa)
in SLC35C1, the GDP-Fuc transporter (CDG-IIc)
in B4GALT1, a galactosyltransferase (CDG-IId)
in COG7, the conserved oligomeric Golgi complex-7 (CDG-IIe)
in SLC35A1, the CMP-sialic acid (NeuAc) transporter (CDG-IIf)However, the use of >100 genes in this process, presumably means that many more defects are to be found. Diagnosis
Classification
Historically, CDGs are classified as Types I and II (CDG-I and CDG-II), depending on the nature and location of the biochemical defect in the metabolic pathway relative to the action of oligosaccharyltransferase. The most commonly used screening method for CDG, analysis of transferrin glycosylation status by isoelectric focusing, ESI-MS, or other techniques, distinguish between these subtypes in so called Type I and Type II patterns.Currently, twenty-two CDG Type-I and fourteen Type-II subtypes of CDG have been described.Since 2009, most researchers use a different nomenclature based on the gene defect (e.g.
Uterine perforation is a potential complication of any intrauterine procedure. It may be associated with injury to surrounding blood vessels or viscera such as the bladder or intestine. If not diagnosed at the time of the procedure it can occasionally result in massive hemorrhage or sepsis; however, the majority of uterine perforations are sub-clinical and safely resolve by themselves without treatment and do not cause any significant long-term damage. Risk factors include cervical stenosis during trans-cervical procedures or decreased strength of the myometrial wall as in pregnancy or menopause. See also
Uterine rupture

References


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