Neurodevelopmental delay up to the age of 4 years in infants born to women with gestational diabetes mellitus: The Japan Environment and Children's Study

Aims/IntroductionThis study aimed to investigate the neurodevelopment of infants born to women with gestational diabetes mellitus (GDM).Materials and MethodsData from the National Birth Cohort in the Japan Environment and Children''s Study from 2011 to 2014 (n = 81,705) were used. Japan uses the GDM guidelines of the International Association of Diabetes and Pregnancy Study Groups. The Japanese translation of the Ages and Stages Questionnaires, third Edition, was used to assess neurodevelopment in the following domains: communication skills, gross motor skills, fine motor skills, problem‐solving ability, and personal and social skills. The survey was carried out every 6 months from the age of 6 months to 4 years (total of eight times). Generalized estimating equations were used to evaluate the association between maternal GDM and neurodevelopmental delay based on odds ratios (ORs) and 95% confidence intervals (95% CIs).ResultsNeurodevelopmental delays, particularly in problem‐solving ability, fine motor skills, and personal and social skills, were significantly higher in infants born to women with GDM than in those born to women without GDM (adjusted OR 1.24, 95% CI 1.12–1.36; adjusted OR 1.15, 95% CI 1.03–1.27; and adjusted OR 1.18, 95% CI 1.04–1.33). Furthermore, stratification showed no significant increase in the adjusted ORs (95% CIs) of girls.ConclusionsNeurodevelopment was significantly delayed up to 4 years‐of‐age among boys born to women with GDM.     

Circularly polarised luminescence from excimer emission of anthracene derivatives complexed with γ-cyclodextrin in the solid state

In this study, we report circularly polarised luminescence (CPL)-active molecules that exhibit high fluorescence quantum yields in the solid state. We developed anthracene derivatives with substituents at the 9 and 10 positions, such as ethyl(anthracene-9-carbonyl)glycinate (9AnGlyEt), N-butylanthracene-9-carboxamide (9AnB), N-benzylanthracene-9-carboxamide (9AnPh), and N⁹,N¹⁰-dibutylanthracene-9,10-dicarboxamide (9,10AnB). These compounds were complexed with γ-cyclodextrin (γ-CD) in the solid state by grinding, and the fluorescence properties of the resulting γ-CD complexes were investigated. The fluorescence quantum yields were enhanced after γ-CD complexation. Among the prepared γ-CD complexes, 9AnGlyEt/γ-CD had the highest fluorescence quantum yield (Φ_f = 0.35), which was enhanced up to 5.8 times after γ-CD complexation. This was probably due to the interaction between the two anthracene molecules in the γ-CD cavity, which prevented fluorescence quenching caused by aggregation of the compounds. Positive CPL of g_CPL = 1.3 × 10⁻³ was observed for 9AnGlyEt/γ-CD based on its excimer emission.

The 9-substituted anthracene derivative forms a spatially restricted dimer in the cavity of γ-cyclodextrin and exhibits circularly polarised luminescence with g_CPL = +1.3 × 10⁻³ in the solid state.     

Mediastinal Cystic Parathyroid Adenoma Diagnosed by Somatostatin Receptor Scintigraphy

A 71-year-old man complained of nausea and loss of appetite for eight months prior to admission. He was transported to a hospital with disorientation and diagnosed with primary hyperparathyroidism by laboratory examinations. However, ultrasonography, computed tomography, and technetium-99m labeled methoxyisobutyl isonitrile (^99mTc-MIBI) with single-photon emission computed tomography did not yield definite results. In contrast, somatostatin receptor scintigraphy successfully identified the lesion responsible for the over-secretion of parathyroid hormone within the middle mediastinum. The tumor was successfully resected by surgery, and a histopathological analysis confirmed the parathyroid adenoma nature of the tumor.     

Poor responses to tyrosine kinase inhibitors in a child with precursor B‐cell acute lymphoblastic leukemia with SNX2‐ABL1 chimeric transcript

In addition to BCR, various rare fusion partners for the ABL1 gene have been reported in leukemia. We have identified the fusion gene SNX2‐ABL1 in a pediatric case of acute lymphoblastic leukemia (ALL), which has only once previously been reported in an adult patient. Cytogenetic analysis detected this fusion gene arising from a t(5;9)(q22;q34) translocation. ALL cells carrying a SNX2‐ABL1 fusion exhibited a BCR‐ABL1+ ALL‐like gene expression profile. The patient poorly responded to dasatinib but partially responded to imatinib. Treatment using tyrosine kinase inhibitors requires further investigation to optimize the genotype‐based treatment stratification for patients with SNX2‐ABL1 fusion.     

Effect of leukotriene C4D4 antagonist on colonic damage induced by intracolonic administration of trinitrobenzene sulfonic acid in rats

We examined the effects of eicosanoid antagonists on colonic damage induced by trinitrobenzene sulfonic acid (TNB) in a rat inflammatory bowel model. TNB (30 mg) dissolved in 0.25 ml of 50% ethanol, was given intrarectally. The appropriate doses of ONO-1078 (a leukotriene C₄D₄ antagonist), ONO-4057 (a leukotriene B₄ antagonist), and OKY-046 (a thromboxane A₂ synthetase inhibitor) were given to obtain the same blood level, either 4 h before (pre-treatment model) or 24 h after (the post-treatment model) the administration of TNB (n=8 in all groups). Drugs were given once daily for 6 days through a gastric feeding tube. Autopsy was performed on the 7th day. Colonie damage was assessed in terms of colonie damage scores, and myeloperoxidase (MPO) activity and eicosanoid concentrations in colonie tissues were measured. Compared with the group given TNB alone, the colonie damage score was reduced to 10% in the pre-treatment model with ONO-1078, but the score was not reduced in other groups, MPO activity was not changed in any group. The concentration of leukotriene C₄ was reduced with ONO-1078 treatment, in both pre- and post-treatment models. These results demonstrated that a leukotriene C₄D₄ antagonist reduced colonie inflammation; however, its anti-inflammatory effect was limited in this colitis model.     

The role of mineralocorticoid receptor expression in brain remodeling after cerebral ischemia

Mineralocorticoid receptors (MRs) are classically known to be expressed in the distal collecting duct of the kidney. Recently it was reported that MR is identified in the heart and vasculature. Although MR expression is also found in the brain, it is restricted to the hippocampus and cerebral cortex under normal condition, and the role played by MRs in brain remodeling after cerebral ischemia remains unclear. In the present study, we used the mouse 20-min middle cerebral artery occlusion model to examine the time course of MR expression and activity in the ischemic brain. We found that MR-positive cells remarkably increased in the ischemic striatum, in which MR expression is not observed under normal conditions, during the acute and, especially, subacute phases after stroke and that the majority of MR-expressing cells were astrocytes that migrated to the ischemic core. Treatment with the MR antagonist spironolactone markedly suppressed superoxide production within the infarct area during this period. Quantitative real-time RT-PCR revealed that spironolactone stimulated the expression of neuroprotective or angiogenic factors, such as basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), whereas immunohistochemical analysis showed astrocytes to be cells expressing bFGF and VEGF. Thereby the incidence of apoptosis was reduced. The up-regulated bFGF and VEGF expression also appeared to promote endogenous angiogenesis and blood flow within the infarct area and to increase the number of neuroblasts migrating toward the ischemic striatum. By these beneficial effects, the infarct volume was significantly reduced in spironolactone-treated mice. Spironolactone may thus provide therapeutic neuroprotective effects in the ischemic brain after stroke.     

Permissive role of thyrotropin on thyroid radioiodine uptake during the recovery phase of subacute thyroiditis

Serial measurements of serum triiodothyronine (T₃), thyroxine (T₄), thyrotropin (TSH), and 4-hr thyroidal ¹³¹I uptake were carried out in nine patients with subacute thyroiditis. In the acute phase, suppressed TSH and ¹³¹I uptake were observed simultaneously with the elevations of T₃ and T₄. Thyrotropin-releasing hormone (TRH) failed to increase TSH in all patients studied. The mean value of an increment in serum TSH was only 1.8 μU/ml during the recovery phase when ¹³¹I uptake was normal or hyper-normal. In addition, and elevated ¹³¹I uptake was not necessarily associated with an immediate increase in the serum T₃ and T₄. These observations suggest that the resumption of the iodide pump may be more important than an increment in TSH in producing normal or hypernormal ¹³¹I uptake during the recovery phase. There appears to be a dissociation between the reestablishment of ¹³¹I uptake and the resumption of the mechanism of hormonal synthesis and secretion in the thyroid.     

Long‐term persistent fetomaternal hemorrhage

It is not clear that how long the affected fetuses can tolerate fetomaternal hemorrhage (FMH). Incidental serial measurements of the fetal peak systolic velocity of the middle cerebral artery and the retrospective analysis of stocked blood available incidentally indicated that our patient had suffered from FMH for at least 2 weeks prior to delivery.