9 research outputs found
Formulae Based on Biomathematics to Estimate the Standard Value of Fetal Growth of Japanese
We devised biomathematics-based formulae to estimate the standard values of fetal growth of Japanese after 22 weeks' gestation. The growth rates of bi-parietal diameter (BPD), abdominal circumference (AC), femur length (FL), and estimated fetal body weight (EFBW) at the time of gestation were assumed to be proportional to the product of the value at the time and the rest value of an unknown maximum value, respectively. The EFBW was also assumed to follow a multiple logistic function of BPD, AC and FL to fit the standard values of Japanese fetuses published by the Japan Society of Ultrasonics in Medicine. The Mann-Whitney test was used for statistical analysis. The values as a function of gestational day, t, were as follows: BPD(t)=99.6/(1+exp (2.725−0.01837*t)) (mm); AC(t)=39.7/(1+exp (2.454−0.01379*t)) (cm); FL(t)=79.6/(1+exp (2.851−0.01710*t)) (mm); EFBW(t)=8045.1/(1+exp (6.028−0.06582*BPD(t)−0.1469*AC(t)+ 0.07377*FL(t))) (g). EFBW as a function of BPD, AC and FL was as follows: EFBW=8045.1/(1+exp (4.747+ 0.02584*BPD+0.1010*AC−0.1416*FL)) (g). When the BPD, AC and FL were at −2 standard deviation (SD), −1SD, mean and + 2SD, the EFBW values calculated by the formula were statistically closer to the standard values than conventional formulas with p-values of 4.871×10−7, 4.228×10−7, 9.777×10−7 and 0.028, respectively. The formulae based on biomathematics might be useful to estimate the fetal growth standard values
Neuropeptide Y mediates orexin A-mediated suppression of pulsatile gonadotropin-releasing hormone secretion in ovariectomized rats
Objectives : Reproductive functions are influenced by various feeding regulators.
Orexin, which is one of orexinergic peptides, suppresses the pulsatile secretion of
luteinizing hormone (LH) in bilaterally ovariectomized (OVX) rats. However, the mechanism
of this effect is still not clear. To investigate whether neuropeptide Y (NPY) is involved
in the orexin A-mediated suppression of pulsatile LH secretion, we evaluated the
effects of NPY antibody on the suppressive effect of orexin A. Methods : Orexin A was administered
intracerebroventricularly (icv) and NPY antibody (NPY-Ab) was injected before
icv administration of orexin A in OVX rats. Pulsatile LH secretion was analyzed by
measuring serum LH concentrations in the next 2 h in blood samples drawn at 6-min intervals
by radioimmunoassay. Results : Administration of orexin A significantly reduced
the mean LH concentration and LH pulse frequency. Co-administration of NPY antibody
with orexin A significantly restored the suppressive effect of orexin A on the mean LH
concentration and LH pulse frequency. Conclusion : NPY mediated the suppressive effect
of intracerebroventricularly injected orexin A on pulsatile LH secretion, suggesting that
hypothalamic orexin suppressed pulsatile gonadotropin-releasing hormone (GnRH) secretion
via NPY in the hypothalamus of female rats
Neuropeptide Y mediates orexin A-mediated suppression of pulsatile gonadotropin-releasing hormone secretion in ovariectomized rats
Formulae Based on Biomathematics to Estimate the Standard Value of Fetal Growth of Japanese
Comparison and Problems of Measured Values of LH, FSH, and PRL among Measurement Systems
Orexins, Orexigenic Hypothalamic Neuropeptides, Suppress the Pulsatile Secretion of Luteinizing Hormone in Ovariectomized Female Rats
Clinical subsets associated with different anti-aminoacyl transfer RNA synthetase antibodies and their association with coexisting anti-Ro52
Recurrent CCND3 mutations in MLL-rearranged acute myeloid leukemia
急性骨髄性白血病の新規遺伝子変異を発見 --乳がんの既存薬が治療に有効である可能性--. 京都大学プレスリリース. 2018-11-01.In acute myeloid leukemia (AML), MLL (KMT2A) rearrangements are among the most frequent chromosomal abnormalities; however, knowledge of the genetic landscape of MLL-rearranged AML is limited. In this study, we performed whole-exome sequencing (n = 9) and targeted sequencing (n = 56) of samples from pediatric MLL-rearranged AML patients enrolled in the Japanese Pediatric Leukemia/Lymphoma Study Group AML-05 study. Additionally, we analyzed 105 pediatric t(8;21) AML samples and 30 adult MLL-rearranged AML samples. RNA-sequencing data from 31 patients published in a previous study were also reanalyzed. As a result, we identified 115 mutations in pediatric MLL-rearranged AML patients (2.1 mutations/patient), with mutations in signaling pathway genes being the most frequently detected (60.7%). Mutations in genes associated with epigenetic regulation (21.4%), transcription factors (16.1%), and the cohesin complex (8.9%) were also commonly detected. Novel CCND3 mutations were identified in 5 pediatric MLL-rearranged AML patients (8.9%) and 2 adult MLL-rearranged AML patients (3.3%). Recurrent mutations of CCND1 (n = 3, 2.9%) and CCND2 (n = 8, 7.6%) were found in pediatric t(8;21) AML patients, whereas no CCND3 mutations were found, suggesting that D-type cyclins exhibit a subtype-specific mutation pattern in AML. Treatment of MLL-rearranged AML cell lines with CDK4/6 inhibitors (abemaciclib and palbociclib) blocked G1 to S phase cell-cycle progression and impaired proliferation. Pediatric MLL-MLLT3–rearranged AML patients with coexisting mutations (n = 16) had significantly reduced relapse-free survival and overall survival compared with those without coexisting mutations (n = 9) (P = .048 and .046, respectively). These data provide insights into the genetics of MLL-rearranged AML and suggest therapeutic strategies