Publications by authors named "Yoshitake Shiraishi"

Article Synopsis
  • The human cerebrum is rich in cortico-cortical association fibers, particularly short-range U-fibers located in the white matter beneath gray matter.
  • This study focused on the properties of U-fiber regions in the ferret cerebrum using various advanced techniques.
  • Researchers identified two subregions within U-fibers (outer and inner), discovering that outer U-fiber regions have smaller axons and thinner myelin, suggesting a complex functional organization.
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  • Lipid peroxidation, particularly involving the product 4-hydroxy-2-nonenal (HNE), plays a crucial role in causing cell death in hepatocytes during nonalcoholic steatohepatitis (NASH).
  • Research using various models, including cell lines and animal studies, revealed that HNE triggers hepatocyte death by damaging lysosomes through the activation of a specific receptor (GPR120) and enzyme (μ-calpain).
  • Blocking GPR120 or using a compound called Alda-1 can prevent HNE-induced damage and improve liver conditions, providing potential new therapeutic approaches for NASH.
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produces botulinum neurotoxin complexes that cause botulism. Previous studies elucidated the molecular pathogenesis of botulinum neurotoxin complexes; however, it currently remains unclear whether other components of the bacterium affect host cells. Recent studies provided insights into the role of bacterial membrane vesicles (MVs) produced by some bacterial species in host immunity and pathology.

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CD38 is an enzyme that catalyzes the synthesis of cyclic adenosine diphosphate-ribose from nicotinamide adenine dinucleotide (NAD). We recently reported that this molecule regulates the maturation and differentiation of glial cells such as astrocytes and oligodendrocytes (OLs) in the developing brain. To analyze its role in the demyelinating situation, we employed cuprizone (CPZ)-induced demyelination model in mice, which is characterized by oligodendrocyte-specific apoptosis, followed by the strong glial activation, demyelination, and repopulation of OLs.

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Article Synopsis
  • Oxytocin plays a key role in childbirth by stimulating uterine contractions, enabling lactation, and promoting maternal bonding behaviors, with mice lacking oxytocin or its receptor showing failure to nurture.
  • This maternal behavior can be restored in some cases with oxytocin replacement, indicating that the hormone can enter the brain and influence behavior despite general restrictions on polypeptides crossing the blood-brain barrier.
  • Research highlights that receptor for advanced glycation end-products (RAGE) on brain capillary cells is crucial for transporting oxytocin into the brain, and without RAGE, male mice exhibit issues with maternal bonding and increased hyperactivity, underscoring RAGE’s importance in oxytocin's parenting and social bonding effects.
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Background Diabetic gastropathy is a complex neuromuscular dysfunction of the stomach that commonly occurs in diabetes mellitus. Diabetic patients often present with upper gastrointestinal symptoms, such as epigastric discomfort or pain. The aim of this study was to assess gastric sensation in streptozocin-induced diabetes mellitus (DM) rats and to determine the contribution of C-C motif chemokine receptor 2 (CCR2) signaling to gastric hyperalgesia.

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Glial development is critical for the function of the central nervous system. CD38 is a multifunctional molecule with ADP-ribosyl cyclase activity. While critical roles of CD38 in the adult brain such as oxytocin release and social behavior have been reported, those in the developing brain remain largely unknown.

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CD38, a transmembrane glycoprotein with ADP-ribosyl cyclase activity, catalyses the formation of Ca2+ signalling molecules, but its role in the neuroendocrine system is unknown. Here we show that adult CD38 knockout (CD38-/-) female and male mice show marked defects in maternal nurturing and social behaviour, respectively, with higher locomotor activity. Consistently, the plasma level of oxytocin (OT), but not vasopressin, was strongly decreased in CD38-/- mice.

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