Hydrangea (Hydrangea macrophylla) is a unique flower because it is composed of sepals rather than true petals that have the ability to change color. In the early 20th century, it was known that soil acidity and Al³⁺ content could intensify the blue hue of the sepals. In the mid-20th century, the anthocyanin component 3-O-glucosyldelphinidin (1) and the copigment components 5-O-caffeoylquinic, 5-O-p-coumaroylquinic, and 3-O-caffeoylquinic acids (2–4) were reported. Interestingly, all hydrangea colors from red to purple to blue are produced by the same organic components. We were interested in this phenomenon and the chemical mechanisms underlying hydrangea color variation. In this review, we summarize our recent studies on the chemical mechanisms underlying hydrangea sepal color development, including the structure of the blue complex, transporters involved in accumulation of aluminum ion (Al³⁺), and distribution of the blue complex and aluminum ions in living sepal tissue.

The interconversion between spin, charge, and heat currents is being actively studied from the viewpoints of both fundamental physics and thermoelectric applications in the field of spin caloritronics. This field is a branch of spintronics, which has developed rapidly since the discovery of the thermo-spin conversion phenomenon called the spin Seebeck effect. In spin caloritronics, various thermo-spin conversion phenomena and principles have subsequently been discovered and magneto-thermoelectric effects, thermoelectric effects unique to magnetic materials, have received renewed attention with the advances in physical understanding and thermal/thermoelectric measurement techniques. However, the existence of various thermo-spin and magneto-thermoelectric conversion phenomena with similar names may confuse non-specialists. Thus, in this Review, the basic behaviors, spin-charge-heat current conversion symmetries, and functionalities of spin-caloritronic phenomena are summarized, which will help new entrants to learn fundamental physics, materials science, and application studies in spin caloritronics.

N-Glycanase 1 (NGLY1) deficiency is a congenital disorder caused by mutations in the NGLY1 gene. Because systemic Ngly1^−/− mice with a C57BL/6 (B6) background are embryonically lethal, studies on the mechanism of NGLY1 deficiency using mice have been problematic. In this study, B6-Ngly1^−/+ mice were crossed with Japanese wild mice-originated Japanese fancy mouse 1 (JF1) mice to produce viable F₂ Ngly1^−/− mice from (JF1×B6)F₁ Ngly1^−/+ mice. Systemic Ngly1^−/− mice with a JF1 mouse background were also embryonically lethal. Hybrid F1 Ngly1^−/− (JF1/B6F1) mice, however, showed developmental delay and motor dysfunction, similar to that in human patients. JF1/B6F1 Ngly1^−/− mice showed increased levels of plasma and urinary aspartylglycosamine, a potential biomarker for NGLY1 deficiency. JF1/B6F1 Ngly1^−/− mice are a useful isogenic animal model for the preclinical testing of therapeutic options and understanding the precise pathogenic mechanisms responsible for NGLY1 deficiency.