Risk of Recurrent Ischemic Stroke with Unintended Low-Dose Oral Anticoagulant Therapy and Optimal Timing of Review.

BACKGROUND: Direct oral anticoagulant (DOAC) dose is adjusted according to manufacturer's recommendations when introduced. However, subsequent changes from appropriate DOAC doses to "unintended" inappropriate low-dose DOAC (ILD) due to increased body weight (BW) or decreased serum creatinine concentration might be overlooked. We investigated outcomes in patients receiving appropriate DOAC, "intended" ILD, or unintended ILD, to determine the optimal review time for DOAC doses and associated factors. METHODS: This single-center, retrospective cohort study included inpatients receiving apixaban for stroke prevention between August 2015 and July 2017. Primary outcome was whether starting DOAC dose was selected according to manufacturer's recommendations and whether that dose remained appropriate thereafter. Secondary outcome was the incidence of recurrent ischemic stroke and intracranial bleeding during therapy. Average rates of change in BW, creatinine, and creatinine clearance (CrCl) were evaluated after hospitalization every 10 ± 3 days. RESULTS: During the study period, 120 patients received apixaban; 112 (93.3%) commenced appropriate DOAC doses, and 8 (6.7%) commenced intended ILD doses. Of the 112 patients on appropriate DOAC doses, 7 (6.3%) changed to unintended ILD doses because of increased BW (n = 4) or decreased creatinine (n = 3). The rate of recurrent ischemic stroke differed significantly between the appropriate DOAC dose and the intended or unintended ILD dose group (1.9% [2 of 105] versus 20.0% [3 of 15], P = .014). BW and renal function had stabilized after 20 ± 3 days posthospitalization. CONCLUSIONS: Receiving ILD doses, especially unintended, might be a risk factor for recurrent ischemic stroke and DOAC dose should be reviewed around 20 ± 3 days posthospitalization.

[Successful Use of the i-gel and Dexmedetomidine for Tracheal Resection and Construction Surgery in a Patient with Severe Tracheal Stenosis].

A 51-year-old man, 170 cm, 86 kg, was diagnosed with a tracheal tumor existing just below the glottis occupying more than 80% of his tracheal lumen, and was scheduled for tracheal resection and construction. The patient had a strider due to the severe tracheal stenosis. We could insert i-gel easily under dexmedetomidine sedation. After successful i-gel insertion, tracheotomy and endotracheal intubation were performed. Until ETT insertion, the patient maintained spontaneous respiration without any hypoxic event. Followed by ETT insertion, tracheal resection and construction were performed under general anesthesia. After the operation, the patient was extubated and transferred to the intensive care unit (ICU), where he was given DEX infusion to keep the tracheal anastomosis immobilized. There was no serious complication during the perioparative period.

Design and validation of a method for evaluating medical device cleanliness by recovering and quantifying residual proteins on stainless plates.

We recently reported a method for recovering and quantifying residual proteins bound to surfaces of various medical instruments via thermal coagulation under neutral pH and room temperature. The method effectively recovered and solubilised coagulated proteins at high temperatures in dry and humid conditions, with a protein recovery rate of > 90%. This study validated the previous method by comparing residual protein recovery from test samples using a conventional extraction solution (1% SDS, [pH 11.0]) and proposed solution (1% SDS, 10 mM TCEP, and 10 mM HEPES [pH 7.0]). To mimic soiled medical equipment, pseudo-blood-contaminated stainless steel plates were prepared. Residual protein was recovered using conventional and proposed solutions under varying temperature and humidity conditions. Quantitative protein recovery limits were determined at nine facilities. Compared with the conventional solution, the proposed solution recovered proteins more effectively from samples processed at temperatures > 60 °C. However, low recovery rates were observed for samples processed at 95 °C, possibly owing to differences in protein adhesion due to sample and plate-surface properties. Our findings present a method for quantifying residual proteins on medical instruments exposed to high temperatures during use or disinfection. Further studies should standardise test soiling conditions, materials, and solutions to evaluate cleaning methods.

Potential Mechanisms of COVID-19-related Intracranial Hemorrhage Due to Temporary Depletion of Vitamin K-dependent Coagulation Factors: An Illustrative Case.

Coronavirus disease 2019 (COVID-19)-related intracranial hemorrhage (ICH) is believed to be associated with at least one known risk factor for ICH, such as hypertension, hyperlipidemia, diabetes mellitus, severe pneumonia, or anticoagulation therapy. However, in this study, we report a case of ICH in a 14-year-old boy with mild COVID-19 infection without pneumonia who had no such risk factors. The only abnormal laboratory finding was temporary depletion of vitamin K-dependent coagulation factors. This case indicates that COVID-19 infection may cause simultaneous asymptomatic intracranial microhemorrhages and temporary depletion of vitamin K-dependent coagulation factors. This temporary depletion might transform the intracranial microhemorrhages into symptomatic ICH.

Photo-irradiated titanium dioxide catalyzes site specific DNA damage via generation of hydrogen peroxide.

Titanium dioxide (TiO2) is a potential photosensitizer for photodynamic therapy. In this study, the mechanism of DNA damage catalyzed by photo-irradiated TiO2 was examined using [32P]-5'-end-labeled DNA fragments obtained from human genes. Photo-irradiated TiO2 (anatase and rutile) caused DNA cleavage frequently at the guanine residue in the presence of Cu(II) after E. coli formamidopyrimidine-DNA glycosylase treatment, and the thymine residue was also cleaved after piperidine treatment. Catalase, SOD and bathocuproine, a chelator of Cu(I), inhibited the DNA damage, suggesting the involvement of hydrogen peroxide, superoxide and Cu(I). The photocatalytic generation of Cu(I) from Cu(II) was decreased by the addition of SOD. These findings suggest that the inhibitory effect of SOD on DNA damage is due to the inhibition of the reduction of Cu(II) by superoxide. We also measured the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine, an indicator of oxidative DNA damage, and showed that anatase is more active than rutile. On the other hand, high concentration of anatase caused DNA damage in the absence of Cu(II). Typical free hydroxyl radical scavengers, such as ethanol, mannnitol, sodium formate and DMSO, inhibited the copper-independent DNA photodamage by anatase. In conclusion, photo-irradiated TiO2 particles catalyze the copper-mediated site-specific DNA damage via the formation of hydrogen peroxide rather than that of a free hydroxyl radical. This DNA-damaging mechanism may participate in the phototoxicity of TiO2.