Juntendo medical journal最新文献_第3页

Insulin Resistance-related Gray Matter Volume Reduction is Associated with the Default Mode Network. 胰岛素抵抗相关的灰质体积减少与默认模式网络有关

Juntendo medical journal Pub Date : 2025-01-30 eCollection Date: 2025-01-01 DOI: 10.14789/ejmj.JMJ24-0044-OT

Saki Asano, Akitoshi Ogawa, Takahiro Osada, Satoshi Oka, Koji Nakajima, Yasushi Oshima, Sakae Tanaka, Hideyoshi Kaga, Yoshifumi Tamura, Hirotaka Watada, Ryuzo Kawamori, Seiki Konishi

引用次数: 0

Mechanisms of Itch in Atopic Dermatitis. 特应性皮炎的瘙痒机制。

Juntendo medical journal Pub Date : 2025-01-30 eCollection Date: 2025-01-01 DOI: 10.14789/ejmj.JMJ24-0036-R

Yayoi Kamata, Mitsutoshi Tominaga, Kenji Takamori

{"title":"Mechanisms of Itch in Atopic Dermatitis.","authors":"Yayoi Kamata, Mitsutoshi Tominaga, Kenji Takamori","doi":"10.14789/ejmj.JMJ24-0036-R","DOIUrl":"10.14789/ejmj.JMJ24-0036-R","url":null,"abstract":"Atopic dermatitis (AD) is a common inflammatory skin disease characterized by recurrent eczematous lesions and intense itch. The pathological mechanism of AD involves a complex interaction between skin barrier dysfunction and a predominantly T helper (Th) 2-skewed immune dysregulation. The dysfunctional skin barrier in AD enhances antigen penetration, exacerbating allergic reactions. Scratching further damages the skin barrier, worsens dryness and increases the release of pro-inflammatory mediators, perpetuating the itch-scratch cycle. Breaking this cycle with appropriate treatments is vital. Th2 cells secrete interleukin (IL)-4, IL-13 and IL-31 which play keys roles in AD pathogenesis. IL-31 directly induces pruritus, while IL-4 and IL-13 enhance itching. An increased density of intraepidermal nerve fibers has been observed in AD lesions in a disease-state-dependent manner. In normal skin, both semaphorin 3A (Sema3A; a nerve repulsion factor) and nerve growth factor (NGF; a nerve elongation factor) are expressed. However, in AD lesions, Sema3A expression decreases while NGF expression increases. These findings suggest that epidermal nerve density is regulated by a fine balance between Sema3A and NGF, with Sema3A playing a key role in itch sensitivity in AD. In healthy skin, Sema3A is produced during the early-stage of differentiation of keratinocytes and moves into the upper epidermis. The levels of Sema3A and the density of epidermal nerve fibers may vary depending on the disease state of AD. Our future research will focus on the regulatory mechanisms of Sema3A in skin, and potential clinical applications.","PeriodicalId":520470,"journal":{"name":"Juntendo medical journal","volume":"71 1","pages":"43-50"},"PeriodicalIF":0.0,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915750/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143665836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Clinical and Basic Research on Dopa-Responsive Dystonia: Neuropathological and Neurochemical Findings. 多巴反应性肌张力障碍的临床和基础研究：神经病理和神经化学的发现。

Juntendo medical journal Pub Date : 2025-01-30 eCollection Date: 2025-01-01 DOI: 10.14789/ejmj.JMJ24-0023-R

Yoshiaki Furukawa

{"title":"Clinical and Basic Research on Dopa-Responsive Dystonia: Neuropathological and Neurochemical Findings.","authors":"Yoshiaki Furukawa","doi":"10.14789/ejmj.JMJ24-0023-R","DOIUrl":"10.14789/ejmj.JMJ24-0023-R","url":null,"abstract":"Dopa-responsive dystonia (DRD) is a clinical syndrome characterized by childhood-onset dystonia and a dramatic and sustained response to low doses of levodopa. Typically, DRD presents with gait disturbance due to foot dystonia, later development of parkinsonism, and diurnal fluctuation of symptoms. Since the discovery of mutations responsible for DRD in GCH1, coding for GTP cyclohydrolase 1 (GTPCH) that catalyzes the rate-limiting step in tetrahydrobiopterin (BH4: the cofactor for tyrosine hydroxylase [TH]) biosynthesis, and in TH, coding for TH in catecholamine biosynthesis, our understanding of this syndrome has greatly increased. However, the underlying mechanisms of phenotypic heterogeneity are still unknown and physicians should learn from genetic, pathological, and biochemical findings of DRD. Neuropathological studies have shown a normal population of cells with decreased melanin and no Lewy bodies in the substantia nigra of classic GTPCH-deficient and TH-deficient DRD. Neurochemical investigations in GTPCH-deficient DRD have indicated that dopamine reduction in the striatum is caused not only by decreased TH activity resulting from low cofactor content but also by actual loss of TH protein without nerve terminal loss. This striatal TH protein loss may be due to a diminished regulatory effect of BH4 on stability of TH molecules. Neurochemical findings in an asymptomatic GCH1 mutation carrier versus symptomatic cases suggest that there may be additional genetic and/or environmental factors modulating the regulatory BH4 effect on TH stability and that the extent of striatal protein loss in TH (rather than that in GTPCH) may be critical in determining the symptomatic state of GTPCH-deficient DRD.","PeriodicalId":520470,"journal":{"name":"Juntendo medical journal","volume":"71 1","pages":"2-10"},"PeriodicalIF":0.0,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915469/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143665832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Development of Functional Recovery Therapy for Post-Stroke Sequelae: Towards a Future without Stroke Aftereffects. 脑卒中后后遗症功能恢复疗法的发展：迈向无脑卒中后遗症的未来。

Juntendo medical journal Pub Date : 2025-01-17 eCollection Date: 2025-01-01 DOI: 10.14789/ejmj.JMJ24-0026-P

Nobukazu Miyamoto, Nobutaka Hattori

{"title":"Development of Functional Recovery Therapy for Post-Stroke Sequelae: Towards a Future without Stroke Aftereffects.","authors":"Nobukazu Miyamoto, Nobutaka Hattori","doi":"10.14789/ejmj.JMJ24-0026-P","DOIUrl":"10.14789/ejmj.JMJ24-0026-P","url":null,"abstract":"Stroke remains a leading cause of mortality and morbidity globally, posing significant challenges to healthcare systems due to its impact on Activities of Daily Living, Quality of Life, and healthcare costs. Current treatments primarily focus on acute management through thrombolytic therapy and thrombectomy, but only a limited number of patients benefit, underscoring the need for effective therapies to aid chronic stroke recovery. Despite ongoing clinical trials, cell therapy faces substantial logistical and cost-related hurdles, limiting its widespread adoption. Strategies to minimalize post-stroke sequelae emphasize preventing cerebral infarction deterioration, utilizing predictive scoring systems for focused treatment, and exploring drug repositioning. The complex interplay within the Neurovascular Unit and Oligovascular Niche highlights the role of various cell types and neurotrophic factors in stroke pathophysiology and recovery phases. Notably, microglia and astrocytes exhibit dual phenotypes ─ either inflammatory or protective ─ depending on the environment, influencing neural damage or repair processes post-stroke. Mitochondrial therapy emerges as a promising avenue, leveraging the organelles' ability to migrate between cells and mitigate inflammatory responses. Studies suggest that mitochondria transferred from astrocytes or other sources could transform inflammatory astrocytes into protective ones, thereby promoting white matter integrity and potentially reducing dementia progression associated with stroke sequelae. In conclusion, addressing stroke's multifaceted challenges requires innovative therapeutic approaches targeting inflammatory mechanisms and enhancing neuroprotection. Early detection and intervention, coupled with advancements in mitochondrial therapy and understanding intercellular interactions, hold promise for improving stroke outcomes and reducing long-term neurological complications.","PeriodicalId":520470,"journal":{"name":"Juntendo medical journal","volume":"71 1","pages":"26-31"},"PeriodicalIF":0.0,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11915467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143665833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0