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Sense of agency (SoA) is a feeling of controlling one’s own action. Recognition memory can improve for stimuli that involve SoA perhaps because of the self-reference effect. Recognition memory consists of recollection (i.e., detailed memory of stimuli) and familiarity (i.e., a feeling that stimuli are in memory). The self-reference effect is often observed in the recollection. Here, we investigated whether SoA particularly improves the recollection process. Participants pressed a key to produce an outcome (i.e., box movement followed by word presentation in Experiment 1 or word presentation in Experiment 2) and rated their SoA over the outcome. The outcome was spatially congruent or incongruent with the action. The participants learned the words intentionally (Experiment 1) or incidentally (Experiment 2). Performances of recollection and familiarity were assessed using the remember/know procedure. Our results suggest that the participants’ SoA was successfully manipulated. However, contrary to our hypothesis and previous findings, we found no effects of voluntary action and action–outcome congruence on recollection and familiarity processes of recognition memory, regardless of the latency of word presentation and learning strategies. Further studies are needed to replicate and elucidate the relationship between the SoA and recognition memory.

The rubber hand illusion (RHI) is an illusion where the synchronized stroking of a rubber hand, placed in front of a participant, along with their concealed real hand results in a sense of ownership over the rubber hand. The questionnaire used to subjectively measure the RHI incorporated control and illusion statements to address demand characteristics. However, Lush (2020) demonstrated participants expected the illusion upon viewing a video of the RHI procedure despite the absence of tactile stimuli, indicating a lack of control over demand characteristics. In our study, Experiment 1, conducted with a Japanese sample (n = 27), was a preliminary direct replication of Lush (2020). Experiment 2, involving a larger sample (n = 185), also directly replicated Lush’s study and further investigated the influence of condition order on expectancies for the RHI. In both experiments, participants showed stronger agreement with the illusion statement expectancies in the synchronous condition compared to the asynchronous condition. However, this difference was not observed in the control statement expectancies, thereby replicating the outcomes of the original study. In Experiment 2, the group exposed to the asynchronous condition first showed stronger agreement with the illusion statement expectancies in that condition than those exposed to the synchronous condition first. As the RHI has been defined as the difference in direct and indirect measures between synchronous and asynchronous conditions, our results suggest that the methods in the RHI paradigm insufficiently control demand characteristics and order effects; thus, findings based on these methods are confounded by these effects.

Preventing rejection is a major challenge in transplantation medicine, even when using pluripotent stem cell-derived grafts. In iPS cell (iPSC)-based transplantation, to reduce the risk of rejection, it is thought to be optimal that preparing the cells from donors whose human leukocyte antigen-haplotype are homozygous. Generally, this approach is referred to as major histocompatibility complex (MHC) homo-to-hetero transplantation, which is MHC-matched but minor antigen-mismatched. To investigate the immune response in the MHC homo-to-hetero transplantation, we established a murine experimental system in which MHC-matched but minor antigen-mismatched tissue (skin) grafts were transplanted into MHC-heterozygous recipients. Unexpectedly, only minor antigen-mismatched grafts were rejected at the same time points as rejection of fully allogeneic grafts. A vigorous anti-donor type T cell response was detected in vitro and conventional immunosuppressants targeting T cell activation had limited effects on controlling rejection. However, anti-donor antibodies were not detected only in the minor antigen-mismatched transplantation. This murine transplantation model can be used to further analyze immunological subjects for MHC homo-to-hetero iPSC-based transplantation.

Mitochondrial DNA (mtDNA) mutations occur frequently in cancer cells, and some of them are often homoplasmic. Targeting such mtDNA mutations could be a new method for killing cancer cells with minimal impact on normal cells. Pyrrole‐imidazole polyamides (PIPs) are cell‐permeable minor groove binders that show sequence‐specific binding to double‐stranded DNA and inhibit the transcription of target genes. PIP conjugated with the lipophilic triphenylphosphonium (TPP) cation can be delivered to mitochondria without uptake into the nucleus. Here, we investigated the feasibility of the use of PIP‐TPP to target a mtDNA mutation in order to kill cancer cells that harbor the mutation. We synthesized hairpin‐type PIP‐TPP targeting the A3243G mutation and examined its effects on the survival of HeLa cybrid cells with or without the mutation (HeLamtA3243G cells or HeLamtHeLa cells, respectively). A surface plasmon resonance assay demonstrated that PIP‐TPP showed approximately 60‐fold higher binding affinity for the mutant G‐containing synthetic double‐stranded DNA than for the wild‐type A‐containing DNA. When added to cells, it localized in mitochondria and induced mitochondrial reactive oxygen species production, extensive mitophagy, and apoptosis in HeLamtA3243G cells, while only slightly exerting these effects in HeLamtHeLa cells. These results suggest that PIP‐TPPs targeting mtDNA mutations could be potential chemotherapeutic drugs to treat cancers without severe adverse effects. Pyrrole‐imidazole polyamide (PIP) conjugated with triphenylphosphonium (TPP) targeting mtDNA mutations induced extensive mitophagy and apoptosis in cancer cells harboring the mutation. Thus, they could be potential chemotherapeutic drugs to treat cancers.

Adenocarcinoma rarely manifests as a bulky, invasive mediastinal tumor. Even more unusual is when such a tumor, initially diagnosed as another malignancy on biopsy, is later identified as an adenocarcinoma of unknown primary origin. A 46-year-old man with no prior history of malignancy was diagnosed with primary mediastinal seminoma and received chemotherapy before being referred to our hospital. At referral, the tumor had shrunk to half its original size, measuring 7 cm in maximum diameter. Due to its extensive invasion, we performed a combined resection, including the resection and reconstruction of the superior vena cava, achieving complete tumor removal. However, the resected specimen showed extensive necrosis, making it unidentifiable as a tumor. This prompted a reexamination of the pretreatment biopsy, which led to a revised diagnosis of \"adenocarcinoma not otherwise specified with clear cell features.\" Immunohistochemical staining suggested a lung cancer profile, but systemic examination failed to identify the primary site, resulting in a final diagnosis of carcinoma of unknown primary. The cancer recurred 26 months after surgery, and the patient underwent repeated chemotherapy up to the fourth line. He survived for 92 months after surgery before passing away. This case highlights the diagnostic challenges posed by invasive mediastinal adenocarcinoma of unknown primary. It also demonstrates that multidisciplinary treatment - combining induction chemotherapy, curative surgery, and post-recurrence chemotherapy - can enable long-term survival, even in such complex cases.

Prenatal alcohol exposure causes many detrimental alcohol-induced defects in children, collectively known as fetal alcohol spectrum disorders (FASD). This study aimed to evaluate a rat model of FASD, in which alcohol was administered at progressively increasing doses during late pregnancy, using preclinical magnetic resonance (MR) imaging (MRI) and MR spectroscopy (MRS). Wistar rats were orally administered 2.5 mL/day of ethanol (25% concentration) on gestational day 15, and postnatal fetuses were used as FASD models. Four groups were used: a control group (non-treatment group) and three groups of FASD model rats that received one, two, or four doses of ethanol, respectively, during the embryonic period. Body weight was measured every other week until eight weeks of age. MRI and MRS were performed at 4 and 8 weeks of age. The volume of each brain region was measured using acquired T2-weighted images. At 4 weeks of age, body weight and cortex volume were significantly lower in the three FASD model groups (2.5 × 1: 304 ± 6 mm3, p < 0.05; 2.5 × 2: 302 ± 8 mm3, p < 0.01; 2.5 × 4: 305 ± 6 mm3, p < 0.05) than they were in the non-treatment group (non-treatment: 313 ± 6 mm3). The FASD model group that received four doses of alcohol (2.5 × 4: 0.72 ± 0.09, p < 0.05) had lower Taurine/Cr values than the non-treatment group did (non-treatment: 0.91 ± 0.15), an effect that continued at 8 weeks of age (non-treatment: 0.63 ± 0.09; 2.5 × 4: 0.52 ± 0.09, p < 0.05). This study is the first to assess brain metabolites and volume over time using MRI and MRS. Decreases in brain volume and taurine levels were observed at 4 and 8 weeks of age, suggesting that the effects of alcohol persisted beyond adulthood.

Background INF2 mutations cause focal segmental glomerulosclerosis (FSGS) and Charcot–Marie–Tooth disease (CMT). Accurate genetic diagnosis is critical, as INF2‐related FSGS is typically resistant to immunotherapy yet rarely recurs after transplantation, and its associated neuropathy can mimic treatable immune‐mediated disorders such as chronic inflammatory demyelinating polyradiculoneuropathy (CIDP). Methods We performed a multicenter study investigating 3329 Japanese patients with inherited peripheral neuropathies/CMT who underwent gene panel sequencing or whole‐exome analysis between 2007 and 2024. Clinical data, including electrophysiological assessments, were obtained from the patients' medical records. Results We identified six pathogenic INF2 variants in eight patients, all of which were located within the diaphanous inhibitory domain. Structural modeling revealed clustering of variants near the diaphanous autoregulatory domain‐binding pocket, which is critical for INF2 autoinhibition. Clinically, all cases were sporadic, with a median age at neurological onset of 9 years. All patients exhibited lower limb weakness, and 6/8 (75%) had sensory disturbances. All patients also developed kidney dysfunction, with 7/8 (88%) progressing to end‐stage renal disease at a median age of 15 years. Furthermore, all patients showed demyelinating neuropathy, and 2/8 (25%) received immunotherapy due to suspected immune‐mediated neuropathy. Conclusion Although INF2 variants are a rare cause of CMT in Japan, they should be considered in pediatric patients with demyelinating neuropathy and early‐onset proteinuria, even in the absence of a family history. Blood and urine tests assessing renal dysfunction can provide guidance for appropriate genetic testing.