Glycemic variability is associated with sural nerve conduction velocity in outpatients with type 2 diabetes: Usefulness of a new point-of-care device for nerve conduction studies.

AIMS/INTRODUCTION: Although several studies have shown the association between continuous glucose monitoring (CGM)-derived glycemic variability (GV) and diabetic peripheral neuropathy, no studies have focused on outpatients or used NC-stat®/DPNCheck™, a new point-of-care device for nerve conduction study (NCS). We investigated the association between CGM-derived GV and NCS using DPNCheck™ in outpatients with type 2 diabetes, and further analyzed the difference in results between patients with and without well-controlled HbA1c levels. MATERIALS AND METHODS: All outpatients with type 2 diabetes using the CGM device (FreeStyle Libre Pro®) between 2017 and 2022 were investigated. Sural nerve conduction was evaluated by sensory nerve action potential (SNAP) amplitude and sensory conduction velocity (SCV) using DPNCheck™. Associations of CGM-derived GV metrics with SNAP amplitude and SCV were investigated. RESULTS: In total, 304 outpatients with type 2 diabetes were included. In a linear regression model, most CGM-derived GV metrics except for the mean amplitude of glucose excursion and low blood glucose index were significantly associated with SCV, but not with SNAP amplitude. The significant associations of most CGM-derived GV metrics with SCV remained after adjustment for possible confounding factors, but not after adjustment for glycated hemoglobin (HbA1c). Most CGM-derived GV metrics were significantly associated with SCV after adjustment for HbA1c in patients with a HbA1c ≤ 6.9%, but not in those with a HbA1c ≥ 7.0%. CONCLUSIONS: In outpatients with type 2 diabetes, multiple CGM-derived GV metrics were significantly associated with SCV obtained by DPNCheck™. GV may have independent impacts on peripheral nerve function, particularly in patients with well-controlled HbA1c levels.

A retrospective study of the risk factors for linezolid-induced thrombocytopenia and anemia.

Myelosuppression is major treatment-related adverse events of linezolid therapy and result in treatment termination in some cases. We aimed to identify the risk factors for linezolid-induced thrombocytopenia and anemia. We retrospectively retrieved demographic and laboratory data from the medical records of 221 Japanese patients who were undergoing linezolid therapy. Thrombocytopenia and anemia were defined as an unexplained reduction of >30% in the patient's platelet count and hemoglobin level, respectively, from the baseline. Thrombocytopenia developed in 48.4% of patients, and anemia developed in 10.4% of patients during linezolid therapy. In multivariate analysis, creatinine clearance (adjusted odds ratio = 0.94 [0.92-0.95], P < 0.001), hemodialysis (3.32 [1.14-9.67], P = 0.011), and the duration of linezolid therapy (1.14 [1.07-1.21], P < 0.001) were found to be significant risk factors for linezolid-induced thrombocytopenia. Patients with creatinine clearance rates of <60 mL/min and those on hemodialysis were found to be at high risk of linezolid-induced thrombocytopenia. In addition, a high incidence of linezolid-induced thrombocytopenia was even detected among the patients that had received linezolid therapy for <7 days. As for anemia, the duration of linezolid therapy (1.04 [1.01-1.07], P = 0.011) was shown to be a risk factor for anemia, and a high incidence of anemia was seen among the patients who received linezolid for >15 days. In conclusion, we recommend that among patients receiving linezolid therapy the platelet counts of those with risk factors for linezolid-induced thrombocytopenia should be monitored closely throughout treatment, and the hemoglobin levels of patients that receive linezolid for >15 days should be carefully monitored on a weekly basis to detect anemia.

Discovery of novel transcription control relationships with gene regulatory networks generated from multiple-disruption full genome expression libraries.

Gene regulatory networks elucidated from strategic, genome-wide experimental data can aid in the discovery of novel gene function information and expression regulation events from observation of transcriptional regulation among genes of known and unknown biological function. To create a reliable and comprehensive data set for the elucidation of transcription regulation networks, we conducted systematic genome-wide disruption expression experiments of yeast on 118 genes with known involvement in transcription regulation. We report several novel regulatory relationships between known transcription factors and other genes with previously unknown biological function discovered with this expression library. Here we report the downstream regulatory subnetworks for UME6 and MET28. The elucidated network topology among these genes demonstrates MET28's role as a nodal point between genes involved in cell division and those involved in DNA repair mechanisms.