Applicability of the ATP assay in monitoring the cleanliness of hospital environments.

BACKGROUND: The adenosine triphosphate (ATP) assay is widely used for simple and rapid evaluation of the cleanliness of environmental surfaces. However, there remain concerns regarding the reliability of the ATP assay in hospital settings. This study aimed to assess whether the ATP assay could detect inadequate cleaning within hospital environments as well as monitor the effectiveness of routine cleaning. METHODS: The cleanliness of seven types of high-touch surfaces in operating rooms that were routinely cleaned was evaluated by testing the ATP assay and aerobic colony counts (ACC). For pressure redistribution mattresses (Soft-nurse®) that were found to be particularly at risk of infection, cleaning methods were improved, and the effectiveness of these improvements was monitored using the same two methods. RESULTS: The ATP assay quantitatively detected contamination on seven high-touch surfaces but showed no correlation with ACC. However, a significant positive correlation between luminescence and ACC was found on one specific surface, allowing for determining a theoretical cutoff value. Additionally, the ATP assay effectively identified the risk of future infection, which the ACC test could not assess. CONCLUSIONS: The ATP assay can monitor the effectiveness of routine cleaning by setting a theoretical cutoff value for each subject. The method provides quantitative and meaningful values when used with an understanding of its limitations.

Beta-hydroxybutyrate, an endogenous NLRP3 inflammasome inhibitor, attenuates anxiety-related behavior in a rodent post-traumatic stress disorder model.

Accumulating evidence suggests that elevated inflammation contributes to the pathophysiology of post-traumatic stress disorder (PTSD) and that anti-inflammatory drugs might be a new treatment strategy for PTSD. It has been reported that beta-hydroxybutyrate (BHB), one of the main ketone bodies produced, can have an anti-inflammatory and antidepressant effect. Here, we investigated the potential anti-anxiety and anti-inflammatory effects of BHB using a rodent PTSD model, induced by single prolonged stress (SPS). Male, Sprague-Dawley rats were employed in this study. Repeated administration of BHB attenuated SPS-induced anxiety-related behaviors evaluated by the elevated plus maze test. SPS increased the serum levels of TNF-α and IL-1ß. In contrast, BHB administration partially attenuated the increase of serum TNF-α. These findings demonstrate that BHB exerts its anxiolytic effects, possibly by inhibiting systemic TNF-α. Hence, BHB may be a novel therapeutic candidate for the treatment of PTSD.

A case of successful pregnancy following multidrug treatment including rituximab and intravenous immunoglobulin for primary antiphospholipid antibody syndrome refractory to conventional treatment.

Antiphospholipid antibody syndrome (APS) is defined by the presence of clinical symptoms caused by antiphospholipid antibodies. When APS occurs during pregnancy, it is conventionally treated with low-dose aspirin or heparin. In cases refractory to conventional treatment, intravenous immunoglobulin (IvIg) is sometimes added. We present the case of an APS patient with severe thrombocytopenia who experienced a successful pregnancy after treatment that included intravenous rituximab and IvIg. As far as we know, this is the first report demonstrating a positive pregnancy outcome in this context. Physicians may consider prescribing not only IvIg but also rituximab during the first trimester of pregnancy in APS patients with severe obstetrical complications and thrombocytopenia refractory to conventional treatment.

Prefrontal cortex infusion of beta-hydroxybutyrate, an endogenous NLRP3 inflammasome inhibitor, produces antidepressant-like effects in a rodent model of depression.

AIMS: Neuroinflammation is deeply related to the pathophysiology of depression. Beta-hydroxybutyrate (BHB), which is an endogenous ketone body, exerts anti-inflammatory effects, and peripheral administration of BHB induces antidepressant effects in an animal model of depression; however, it is unclear whether BHB specifically mediates these actions in the brain. Thus, we administered BHB directly into the brain in a rodent model of depression using a chronic unpredictable stress (CUS) paradigm. METHODS: BHB was continuously microinjected into the prefrontal cortex (PFC) using osmotic pumps for 21 days. Behavioral testing included the forced swim test (FST) and the open field test (OFT); the levels of pro-inflammatory cytokines, such as interleukin 1ß (IL-1ß) and tumor necrosis factor α (TNF-α), were quantified in the PFC, and the concentration of corticosterone in blood serum was measured. RESULTS: BHB administration into the PFC significantly decreased immobility time in the FST, without significantly altering locomotor activity assessed in the OFT. Also, CUS significantly increased the levels of TNF-α in the PFC and decreased serum corticosterone levels; these changes were attenuated by BHB administration. These findings suggest that a small amount of BHB administered into the PFC directly produces antidepressant effects, possibly through anti-inflammatory mechanisms, and can improve hypothalamus-pituitary-adrenal axis responses. CONCLUSION: BHB may be a novel therapeutic candidate for the treatment of depression based on the neuro-inflammatory hypothesis, and the PFC is a region implicated in the antidepressant action of BHB.

Destabilisation of the c-kit1 G-quadruplex structure by N6-methyladenosine modification.

N6-methyladenine (m6dA) has been recently discovered in eukaryotic genomic DNA. However, there have been few reports on its biological roles. G-quadruplex (G4) is a non-canonical nucleic acid structure formed by the stacking of G-tetrads. G4-forming sequences are enriched with cis-regulatory elements in genomic DNA and the G4 structures have important roles in various cellular functions. We previously reported that CpG methylation stabilized vascular endothelial growth factor (VEGF) G4 structure. Here we report that m6dA modification destabilizes the human c-kit1 G4 structure. These results suggest that epigenetic modifications may affect G4 formation in order to regulate the biological functions.