The BF mode on the Sysmex XN could be an alternative method for the manual counts in the BF analysis with a few drawbacks. However, if a concentration of HF-BF cells is greater than the given threshold, microscopic examination should be subsequently performed.

Sepsis patients demonstrated significant changes in routine and CPD items related to RBC, neutrophils, lymphocytes, and platelets when compared to NCs. Increase in CPD items NE-SFL and NE-WY, which may indicate neutrophil immaturity or activation, could be useful for the detection of sepsis patients, in conjunction with currently used surrogate sepsis biomarkers. However, these items did not efficiently contribute to the discrimination of sepsis severity or predict mortality.

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BackgroundPrimary Sjogren’s syndrome (pSS) is a chronic autoimmune disease with low quality of life caused by various constitutional symptoms and glandular dysfunction. Although fatigue is one of the most frequent symptoms in pSS, its etiology or biomarkers are poorly elucidated.ObjectivesWe investigated potential relationship between severity of fatigue and the kynurenine pathway in pSS.MethodsClinical data and blood samples of 81 patients were obtained from a prospective cohort for pSS and compared with age- and sex-matched healthy controls (HC). Severity of fatigue was defined according to the fatigue domain scores in the ESSPRI. Potential biomarkers related to the kynurenine pathway were determined using ELISA.ResultsOf the total, 44 patients were defined as the “severe fatigue (ESSPRI fatigue ≥ 5)” group, whereas 37 as the “less fatigue (ESSPRI fatigue < 5)”. Serum tryptophan levels in the severe fatigue group were significantly lower while those of kynurenine were higher. Serum interferon gamma, IDO1, and quinolinic acid levels were mostly higher in the less fatigue group. Kynurenine/tryptophan ratios were distinctly higher in the severe fatigue group than both HC and the less fatigue group (p < 0.001). This ratio showed a strong degree of positive correlation (r = 0.624, p < 0.001) with severity of fatigue in pSS while the other markers showed fair degrees of correlation.ConclusionSerum markers related to the kynurenine pathway, especially the kynurenine/tryptophan ratio, may be associated with severity of fatigue in pSS. These results can provide guidance for further investigations on fatigue in pSS.Figure 1.Serum levels of tryptophan, its metabolites, and related enzymatic activities in patients with primary Sjogren’s syndrome (pSS) and healthy controls (HC). (A) Interferon gamma; (B) tryptophan; (C) indoleamine-2,3-dioxygenase 1 (IDO1); (D) L-kynurenine; (E) quinolinic acid; (F) ratio of L-kynurenine to tryptophan. All data were measured using enzyme-linked immunosorbent assay. The bars indicate the median and interquartile range. * p < 0.05, **p < 0.01, ***p < 0.001.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsNone Declared.

Background: We investigated the effects of sevoflurane exposure on the expression of matrix metalloproteinase (MMP), expression and ablation of natural killer group 2, member D (NKG2D) ligands (UL16-binding proteins 1–3 and major histocompatibility complex class I chain-related molecules A/B), and natural killer (NK) cell-mediated cytotoxicity in breast cancer cells.Methods: Three human breast cancer cell lines (MCF-7, MDA-MB-453, and HCC-70) were incubated with 0 (control), 600 (S6), or 1200 μM (S12) sevoflurane for 4 h. The gene expression of NKG2D ligands and their protein expression on cancer cell surfaces were measured using multiplex polymerase chain reaction (PCR) and flow cytometry, respectively. Protein expression of MMP-1 and -2 and the concentration of soluble NKG2D ligands were analyzed using western blotting and enzyme-linked immunosorbent assays, respectively. Results: Sevoflurane downregulated the mRNA and protein expression of the NKG2D ligand in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells but did not affect the expression of MMP-1 or -2 or the concentration of soluble NKG2D ligands in the MCF-7, MDA-MB-453, and HCC-70 cells. Sevoflurane attenuated NK cell-mediated cancer cell lysis in a dose-dependent manner in MCF-7, MDA-MB-453, and HCC-70 cells (P = 0.040, P = 0.040, and P = 0.040, respectively).Conclusions: Our results demonstrate that sevoflurane exposure attenuates NK cell-mediated cytotoxicity in breast cancer cells in a dose-dependent manner. This could be attributed to a sevoflurane-induced decrease in the transcription of NKG2D ligands rather than sevoflurane-induced changes in MMP expression and their proteolytic activity.