Lamina Densa Malformation Involved in Histogenesis of Primary Localized Cutaneous Amyloidosis

Skin lesions of lichenoid amyloidosis and macular amyloidosis were immunohistochemically investigated using five monoclonal antibodies against basement membrane zone (BMZ) components. A hemidesmosomal component did not contribute to amyloid deposits, but components of the lamina densa and anchoring fibrils were associated with amyloid deposits in the uppermost dermis. Immunoelectron microscopy revealed that these BMZ components were not only aggregated in the BMZ and dermis, but were also involved in the individual amyloid islets. The lamina densa was disrupted in the interface areas just above the amyloid deposits, where cytoplasm of the basal cells directly faced the aggregate of amyloid filaments. Aggregates of some BMZ components were continuous to the amyloid islets from the lamina densa area. These findings suggest that a lamina densa malformation is involved in amyloid production in the interface of the BMZ, and support the secretion theory rather than the fibrillar body theory of amyloidogenesis in these types of primary localized cutaneous amyloidosis

Rhotekin regulates axon regeneration through the talin-Vinculin-Vinexin axis in Caenorhabditis elegans.

Axon regeneration requires actomyosin interaction, which generates contractile force and pulls the regenerating axon forward. In Caenorhabditis elegans, TLN-1/talin promotes axon regeneration through multiple down-stream events. One is the activation of the PAT-3/integrin-RHO-1/RhoA GTPase-LET-502/ROCK (Rho-associated coiled-coil kinase)-regulatory non-muscle myosin light-chain (MLC) phosphorylation signaling pathway, which is dependent on the MLC scaffolding protein ALP-1/ALP-Enigma. The other is mediated by the F-actin-binding protein DEB-1/vinculin and is independent of the MLC phosphorylation pathway. In this study, we identified the svh-7/rtkn-1 gene, encoding a homolog of the RhoA-binding protein Rhotekin, as a regulator of axon regeneration in motor neurons. However, we found that RTKN-1 does not function in the RhoA-ROCK-MLC phosphorylation pathway in the regulation of axon regeneration. We show that RTKN-1 interacts with ALP-1 and the vinculin-binding protein SORB-1/vinexin, and that SORB-1 acts with DEB-1 to promote axon regeneration. Thus, RTKN-1 links the DEB-1-SORB-1 complex to ALP-1 and physically connects phosphorylated MLC on ALP-1 to the actin cytoskeleton. These results suggest that TLN-1 signaling pathways coordinate MLC phosphorylation and recruitment of phosphorylated MLC to the actin cytoskeleton during axon regeneration

前立腺癌における血清γ-セミノプロティンの測定

前立腺癌の新しいマーカーとして, γ-セミノプロテイン(γ-Sm)と前立腺性酸性ホスファターゼ(PAP)とを比較評価した.未治療前立腺癌におけるγ-SMおよびPAPのsensitivityは, それぞれ81%, 67%であった.γ-Smはすべての病期で前立腺肥大症と比較して陽性率が高かった.前立腺癌ではγ-SmとPAPは相関を示さなかった.γ-SmとPAPを同時に測定することにより, 感度が上昇した.γ-SmおよびPAPのspecificityはそれぞれ87%と90%であった.内分泌療法を施行した病期D2において, γ-SmはPAPよりもより多く正常化した.以上より, γ-Smは前立腺癌のもう1つの有用なマーカーであるといえるSerum gamma-seminoprotein (gamma-Sm) was evaluated as a new marker for prostatic cancer in comparison with prostatic acid phosphatase (PAP). The sensitivity of gamma-Sm and PAP for untreated prostatic cancer was 81% and 67%, respectively. gamma-Sm showed a higher positive rate over all stages than in benign prostatic hypertrophy (BPH). There was no correlation between gamma-Sm and PAP in prostatic cancer. Improved sensitivity was obtained by simultaneous measurement of gamma-Sm and PAP. Specificity of gamma-Sm and PAP for BPH was 87% and 90%, respectively. gamma-Sm normalized after endocrine therapy for stage D2 more often than did PAP. These results indicate that gamma-Sm is another useful marker to evaluate prostatic cancer

上皮・間質間の作用からみたホルモン療法抵抗性前立腺癌の増殖機構に関する研究

科学研究費補助金研究成果報告書研究種目: 基盤研究(C)研究期間: 1997～1998課題番号: 09671624研究代表者: 吉貴 達寛（滋賀医科大学・医学部・講師）研究分担者: 林田 英資（滋賀医科大学・医学部・助手）研究分担者: 金 哲将（滋賀医科大学・医学部・助手）研究分担者: 濱口 晃一（滋賀医科大学・医学部・助手

Structural diversity of cancer-related and non-cancer-related prostate-specific antigen

科学研究費補助金研究成果報告書研究種目: 基盤研究(C)研究期間: 2002～2003課題番号: 14571496研究代表者: 吉貴 達寛（滋賀医科大学・医学部・助教授）研究分担者: 若林 賢彦（滋賀医科大学・医学部・講師）研究分担者: 上仁 数義（滋賀医科大学・医学部・助手）研究分担者: 片岡 晃（滋賀医科大学・医学部・助手

Significance and development of Urine uroplakin III mRNA measurement in vesicoureteral reflux

科学研究費補助金研究成果報告書研究種目: 基盤研究(C)研究期間: 2005～2006課題番号: 17591673研究代表者: 上仁 数義（滋賀医科大学・医学部・助手）研究分担者: 吉貴 達寛（滋賀医科大学・医学部・助教授）研究分担者: 成田 充弘（滋賀医科大学・医学部・講師）研究分担者: 影山 進（滋賀医科大学・医学部・助手）研究分担者: 坂野 祐司（滋賀医科大学・医学部・助手

SEARCH FOR SPECIFIC GENE ALTERATIONS IN RENAL CELL CARCINOMAS WITH RAPID GROWING FEATURES

科学研究費補助金研究成果報告書研究種目: 基盤研究(C)研究期間: 1999～2000課題番号: 11671551研究代表者: 岡本 圭生（滋賀医科大学・医学部・助手）研究分担者: 岡田 裕作（滋賀医科大学・医学部・教授）研究分担者: 吉貴 達寛（滋賀医科大学・医学部・助教授）研究分担者: 金 哲将（滋賀医科大学・医学部・助手）研究分担者: 片岡 晃（滋賀医科大学・医学部・助手

Identification of gene on chromosome 14q arm responsible for the development of rapid type human renal cell carcinoma

科学研究費補助金研究成果報告書研究種目: 基盤研究(B)研究期間: 2001～2003課題番号: 13470332研究代表者: 岡本 圭生（滋賀医科大学・医学部・助手）研究分担者: 岡田 裕作（滋賀医科大学・医学部・教授）研究分担者: 金 哲将（滋賀医科大学・医学部・講師）研究分担者: 吉貴 達寛（滋賀医科大学・医学部・助教授）研究協力者: 川上 享弘（滋賀医科大学・医学部・助手