Rituximab, an anti-CD20 monoclonal antibody, can cause infusion reactions (IRs), especially during the initial rituximab infusion therapy. Generally, patients are administered a histamine H
We previously showed by in vitro experiments that the cysteine residue (Cys111) near the dimer interface is critical for monomerization and resultant aggregate formation of mutant Cu, Zn-superoxide dismutase (SOD1) protein, which is toxic to motor neurons in familial amyotrophic lateral sclerosis (ALS). To verify the importance of Cys111 in the mutant SOD1-associated ALS pathogenesis in vivo, we analyzed the disease phenotype of SOD1 transgenic mice harboring H46R mutation alone (H46R mice) or H46R/C111S double mutations (H46R/C111S mice). Behavioral, histological and biochemical analyses of the spinal cord showed that the onset and progression of the disease phenotype were delayed in H46R/C111S mice compared with H46R mice. We found that peroxidized Cys111 of H46R SOD1 plays a role in promoting formation of high molecular weight insoluble SOD1 species that is correlated with the progression of the motor neuron disease phenotype. These results support that Cys111 is a critical residue for the neuronal toxicity of mutant SOD1 in vivo, and the blockage of peroxidation of this residue in mutant SOD1 may constitute a future target for developing ALS treatment.
We began to print the laboratory data of each patient on their in-hospital prescription in April, 2010 and further introduced a prescription checking system associated with laboratory data in December, 2014. This study evaluated the changed prescriptions based on prescription queries and the usefulness of using prescriptions with laboratory data as well as the prescription checking system. We examined the number of changed in-hospital prescriptions after the prescription queries in three periods: before and after using prescriptions with laboratory data (from June, 2009 to November, 2009 and from June, 2010 to November, 2010, respectively), and after the introduction of the prescription checking system (from September, 2016 to August, 2017). Although there were no changed prescriptions based on the laboratory data before using prescriptions with laboratory data, 6.6％ of changed prescriptions were based on laboratory data after using prescriptions with laboratory data. In addition, the changed prescription ratio based on laboratory data significantly increased after the introduction of the prescription checking system compared with that after using prescriptions with laboratory data (8.9％ versus 6.6％, P = 0.015). In conclusion, using prescriptions with laboratory data and the prescription checking system associated with laboratory data were useful for checking prescriptions effectively in order to avoid adverse drug reactions.
This study was done to evaluate the effects of soy protein hydrolyzate with bound phospholipids (c-SPHP), on the serum cholesterol levels in hypercholesterolemic subjects over a three-month period. Subjects were Taiwanese adlut male volunteers whose serum total cholesterol levels were above 220 mg/dl. Twenty-one subjects were divided into three groups randomly, and each group was given c-SPHP zero, 3, or 6 g per day. Test diets were orally administered in a powdered dringk form that contained c-SPHP or casein hydrolyzate (placebo). The subjects were given the test diet four times daily. The study consisted of a two-week pre-feeding period, a three-month feeding period, followed by a two-week post-feeding period. After 3 months of c-SPHP administration, 3 g per day, serum total cholesterol decreased significantly from the initial level (15.0%, p<0.01) and compared with the placebo group (p<0.05). Furthermore, LDL-cholesterol decreased significantly (27.7%, p<0.01) and the LDL/HDL ratio also decreased significantly (47.4%, p<0.01) from the initial levels. These effects of c-SPHP were dose-dependent. This study suggests that c-SPHP has remarkable improving effecs on the serum cholesterol levels in hypercholesterolemic subjects.
Abstract The present study reports the design of a novel bioanode to deeply oxidize glucose in an enzymatic biofuel cell (EFC). This enzymatic glucose cell utilizes three co‐immobilized enzymes: NAD‐dependent glucose dehydrogenase (GDH), NAD(P) + ‐dependent gluconate‐5‐dehydrogenase (Ga5DH), and diaphorase (DI). Glucose is oxidized to gluconate by NAD‐dependent GDH, gaining two electrons per glucose; the gluconate obtained as a by‐product is oxidized at the C5 carbon to 5‐keto‐gluconate by Ga5DH. Operation of our bioanode enabled the oxidation of glucose in two stages, resulting in the gain of four electrons. The three‐enzyme EFC provides a maximum power density of 10.51 ± 1.72 μW cm –2 , which is about 1.6 times higher than the maximum power density of an EFC using a bioanode based on the co‐immobilization of two enzymes (GDH and DI). Our results hold promise for increasing the current density of EFCs, and for application in glucose biosensor.
e15622 Background: Signal transducer and activator of transcription (STAT) 3 has been reported to be a mediator for keratinocyte toxicity induced by molecular-targeted drugs. Our purpose was to assess the association between single nucleotide polymorphisms (SNPs) in the STAT3 gene and hand-foot skin reaction (HFSR) in metastatic renal cell carcinoma (mRCC) patients treated with multi-kinase inhibitors (MKIs). Methods: Sixty-five mRCC patients treated with MKIs (sunitinib, sorafenib, or axitinib) were genotyped for rs4796793 in the 5′ region of the STAT3 gene. We retrospectively analyzed 60 patients whose first MKI therapy lasted for more than 4 months, regardless of the presence or absence of HFSR, and who developed HFSR within 4 months before treatment failure. Results: MKIs sunitinib, sorafenib, and axitinib were given to 35, 16, and 9 patients, respectively. HFSR was observed in 46 patients. Genotypes GG, GC, and CC at rs4796793 were found in 9, 27, and 24 patients, respectively. A significant association was found between the alleles of rs4796793 and HFSR (G vs C; odds ratio (OR), 4.33; 95% confidence interval (CI), 1.80–10.45; p < 0.001). The GG genotype at rs4796793 had the highest OR compared with GC + CC genotypes (OR, 10.75; 95% CI, 2.38–48.07; p < 0.001). In time-to-event analysis, the median time to developing HFSR in patients with GC + CC genotypes at rs4796793 was 21 days whereas the median time for patients with the GG genotype was not reached in 4 months. Kaplan–Meier analysis demonstrated a statistically significant difference between the two groups (p = 0.0095) . Conclusions: SNPs in the STAT3 gene correlate with development of HFSR in mRCC patients treated with MKIs. The wild-type homozygous genotype (GG) of STAT3-associated SNP could be considered a prognostic biomarker of resistance to HFSR related to MKIs in mRCC.
