BackgroundThe accuracy, safety and feasibility of, the compounding robot APOTECAchemo were evaluated in the clinical practice of Japan.MethodsAccuracy and precision of robotic preparations by APOTECAchemo was evaluated in 20 preparations of fluorouracil (FU) and cyclophosphamide (CPA) infusions by four pharmacists. Environmental and product contaminations with FU and CPA were evaluated by wipe testing. Robotic performance was compared with manual preparation in a biological safety cabinet. The number of robotic products, total compounding time and total pre-reconstitution time of lyophilized drugs between January 1, 2014 to December 31, 2015 were investigated.ResultsRobotic preparation resulted more accurate and precise (mean absolute dose error and coefficient of variation were 0.83 and 1.04% for FU and 0.52 and 0.59% for CPA) than those of manual preparation (respective values were 1.20 and 1.46% for FU and 1.70 and 2.20% for CPA). Drug residue was not detected from any of the prepared infusion bags with the robotic preparation, whereas FU was detected in two of four analyzed infusion bags with manual preparation. Average total time to make single anticancer drug preparation (compounding plus reconstitution of lyophilized drugs) was 6.11 min in the second half of 2015. During the study period, the highest percentage of production covered by APOTECAchemo was 70.4% of the total inpatient pharmacy activity.ConclusionRobotic preparation using APOTECAchemo should give substantial advantages in drug compounding for accuracy and safety and was able to be successfully worked in Mie university hospital.

No abstract

No abstract

We have demonstrated for the first time that a second‐generation antihistamine ameliorates nocturnal scratching behavior in atopic dermatitis patients using a modified wristwatch‐type acoustic scratching counting system that we have recently developed. We also analyzed the sleep quality by simultaneous recording of electroencephalogram, and found that sleep quality was unaffected.

We have previously reported a novel homozygous 4-bp deletion in DDHD1 as the responsible variant for spastic paraplegia type 28 (SPG28;OMIM#609340). The variant causes a frameshift, resulting in a functionally null allele in the patient. DDHD1 encodes phospholipase A1 (PLA1) catalyzing phosphatidylinositol to lysophosphatidylinositol (LPI). To clarify the pathogenic mechanism of SPG28, we established Ddhd1 knockout mice (Ddhd1[−/−]) carrying a 5-bp deletion in Ddhd1, resulting in a premature termination of translation at a position similar to that of the patient. We observed a significant decrease in foot–base angle (FBA) in aged Ddhd1(−/−) (24 months of age) and a significant decrease of LPI 20:4 (sn-2) in Ddhd1(−/−) cerebra (26 months of age). These changes of FBA were not observed in 14 months of age. We also observed significant changes of expression levels of 22 genes in the Ddhd1(−/−) cerebra (26 months of age). GO terms relating to the nervous system and cell–cell communications were significantly enriched. We conclude that the reduced signaling of LPI 20:4 (sn-2) by PLA1 dysfunction is responsible for the locomotive abnormality in SPG28, further suggesting that the reduction of downstream signaling such as GPR55 which is agonized by LPI is involved in the pathogenesis of SPG28.