Effects of Parity and Postpartum Depression on Mother-Infant Bonding in the First Month Postpartum: A Retrospective Study.

Objective This study aimed to examine the relationship between parity, postpartum depression (PPD), and mother-infant bonding (MIB) failure in the first month postpartum. Methods The study included 1,509 Japanese patients (748 primiparous and 761 multiparous). MIB was assessed using the Mother-to-Infant Bonding Scale Japanese version (MIBS-J), which was translated in 2012, and its subscales, including lack of affection (LA) and anger and rejection (AR).

Cerebellar Hypoperfusion in Two Patients with Cornelia de Lange Syndrome with Novel Variants.

Introduction: Cornelia de Lange syndrome (CdLS) is a rare congenital malformation characterized by distinctive facial features, short stature, and limb defects. In addition, half of the patients with CdLS exhibit repetitive self-injurious behaviors (SIBs) related to intellectual disability with autistic traits. CdLS is caused by pathogenic variants of genes encoding the cohesin complex pathway, with 70% of these variants identified in the nipped-B-like () gene.

The Effectiveness of Perampanel for Myoclonic Seizures in Down Syndrome with Isodicentric Chromosome 21.

Epileptic seizures are common in the elderly Down syndrome population. We encountered a patient with Down syndrome in whom karyotyping showed the rare isodicentric chromosome 21 and who suffered from myoclonic seizures. A 52-year-old woman with Down syndrome experienced sudden onset of drowsiness and frequent myoclonic jerks in the upper body.

Mitochondrial function is required for extracellular ATP-induced NLRP3 inflammasome activation.

The NLRP3 inflammasome plays a critical role in the processing and release of inflammatory cytokines, such as interleukin-1β (IL-1β) and IL-18. Accumulating evidence suggests that mitochondria are common mediators of NLRP3 inflammasome activation induced by a wide range of inflammatory stimuli; however, the precise role of mitochondria is still not fully understood. Here, we show that mitochondrial function is required for extracellular ATP-induced NLRP3 inflammasome activation.

TNF-α Induces Caspase-1 Activation Independently of Simultaneously Induced NLRP3 in 3T3-L1 Cells.

The intracellular cysteine protease caspase-1 is critically involved in obesity-induced inflammation in adipose tissue. A substantial body of evidence from immune cells, such as macrophages, has shown that caspase-1 activation depends largely on a protein complex, called the NLRP3 inflammasome, which consists of the NOD-like receptor (NLR) family protein NLRP3, the adaptor protein ASC, and caspase-1 itself. However, it is not fully understood how caspase-1 activation is regulated within adipocytes upon inflammatory stimuli.