N-Acetylglucosamine-6-O-sulfotransferase catalyzes the transfer of sulfate from 3'-phosphoadenosine 5'-phosphosulfate to position 6 of a non-reducing N-acetylglucosamine (GlcNAc) residue. We have cloned human GlcNAc-6-O-sulfotransferase cDNA, based on the sequence homology to cloned cDNA of mouse GlcNAc-6-O-sulfotransferase. The predicted protein sequence of the human enzyme was highly homologous to that of the mouse enzyme; in the 363 amino acid stretch of the catalytic region, the two proteins were nearly identical except for conservative changes in 3 amino acid residues. The expressed enzyme transferred sulfate to GlcNAcbeta1-3Galbeta1-4GlcNAcbeta1-3Galbeta1-4Gl cNAc. Co-transfection of the enzyme cDNA and fucosyltransferase VII cDNA into COS-7 cells resulted in cell surface expression of 6-sulfo sialyl Lewis X. Fluorescence in situ hybridization analysis revealed that the GlcNAc-6-O-sulfotransferase gene is located on human chromosome 7q31. mRNA of the human enzyme was strongly expressed in the bone marrow, peripheral blood leukocytes, spleen, brain, spinal cord, ovary, and placenta, and moderate levels of expression were observed in many organs including lymph nodes and thymus. In situ hybridization with the mouse system showed that the transcript was localized in specific regions of the brain, i.e. pyramidal cells in the CA3 subregion of the hippocampus, cerebellar nucleus and Purkinje cells. Among human tumor cells, strong expression of the mRNA was found in MOLT-4 and Jarkat lymphoblastic leukemia cells, Raji lymphoma cells, K-562 chronic myelogeneous leukemia cells, U251 glioma cells, and G361 melanoma cells. Carbohydrate structures synthesized by the sulfotransferase may be involved in various aspects of the differentiation and behavior of blood cells, their progenitor cells, and neurons in the central nervous system.

ObjectivesHypernatraemia is one of the major electrolyte disorders associated with mortality among critically ill patients in intensive care units (ICUs). It is unclear whether this applies to patients with cerebrovascular diseases in whom high sodium concentrations may be allowed in order to prevent cerebral oedema. This study aimed to examine the association between ICU-acquired hypernatraemia and the prognosis of patients with cerebrovascular diseases.DesignA retrospective cohort study.SettingThe incidence of ICU-acquired hypernatraemia was assessed retrospectively in a single tertiary care facility in Japan.ParticipantsAdult patients (≥18 years old) whose length of stay in ICU was >2 days and those whose serum sodium concentrations were 130–149 mEq/L on admission to ICU were included.Outcome measures28-day in-hospital mortality risk was assessed by Cox regression analysis. Hypernatraemia was defined as serum sodium concentration ≥150 mEq/L. Using multivariate analysis, we examined whether ICU-acquired hypernatraemia and the main symptom present at ICU admission were associated with time to death among ICU patients. We also evaluated how the maximum and minimum sodium concentrations during ICU stay were associated with mortality, using restricted cubic splines.ResultsOf 1756 patients, 121 developed ICU-acquired hypernatraemia. Multivariate Cox proportional hazard analysis revealed an association between ICU-acquired hypernatraemia and 28-day mortality (adjusted HR, 3.07 (95% CI 2.12 to 4.44)). The interaction between ICU-acquired hypernatraemia and cerebrovascular disease was significantly associated with 28-day mortality (HR, 3.03 (95% CI 1.29 to 7.15)). The restricted cubic splines analysis of maximum serum sodium concentration in ICU patients determined a threshold maximum of 147 mEq/L. There was no significant association between minimum sodium concentration and mortality.ConclusionsICU-acquired hypernatraemia was associated with an increased mortality rate among critically ill patients with cerebrovascular diseases; the threshold maximum serum sodium concentration associated with mortality was 147 mEq/L.

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Multiple studies have shown that Staphylococcus aureus bacteremia (SAB) has been a major cause of death in hemodialysis patients. We examined whether SAB is a risk for mortality among chronic hemodialysis patients in Japan where the standard vascular access is arteriovenous fistula (AVF). This was a multicenter, retrospective study of maintenance hemodialysis patients with bloodstream infection (BSI) from 2011 to 2013 at tertiary care centers in Japan. The endpoint was hospital mortality. Our cohort contained 32 SAB cases (14 MRSA and 18 MSSA) and 42 non-SAB cases. Hospital mortality was higher among SAB cases than non-SAB cases (46.9% vs. 23.8%, P = 0.038). In patients with BSI, SAB was significantly associated with hospital mortality after adjustment for potential confounders, including type of vascular access (OR 3.26). S. aureus was the leading cause of BSI and hospital mortality among this cohort. Therefore, initial empiric treatment should cover for S. aureus.