Anomalous V2 of the left pulmonary vein detected using three-dimensional computed tomography in a patient with lung cancer : A case report

We report one of the rare anatomical variations of the pulmonary vein wherein the left V2 drained into the inferior pulmonary vein. A 63-year-old man was referred to our hospital because of an abnormal shadow in the left lower lung field that was noted on chest X-ray. Computed tomography (CT) revealed a tumor in the left lower lobe. A biopsied tumor specimen was diagnosed as an adenocarcinoma, and thus, left lower lobectomy was performed. Preoperative three-dimensional CT revealed that an anomalous V2 of the left lung drained from the superior segment into the inferior pulmonary vein. This variation type was confirmed during thoracoscopic left lower lobectomy. We were able to perform left lower lobectomy with the preservation of the anomalous V2. The postoperative course was uneventful, and the patient was discharged on postoperative day 12. It is important to identify anatomical variations of the pulmonary vein and reliably preserve and process the affected area to prevent postoperative complications

The basis of clinicopathological heterogeneity in TDP-43 proteinopathy

Transactive response DNA-binding protein 43 kDa (TDP-43) was identified as a major disease-associated component in the brain of patients with amyotrophic lateral sclerosis (ALS), as well as the largest subset of patients with frontotemporal lobar degeneration with ubiquitinated inclusions (FTLD-U), which characteristically exhibits cytoplasmic inclusions that are positive for ubiquitin but negative for tau and α-synuclein. TDP-43 pathology occurs in distinct brain regions, involves disparate brain networks, and features accumulation of misfolded proteins in various cell types and in different neuroanatomical regions. The clinical phenotypes of ALS and FTLD-TDP (FTLD with abnormal intracellular accumulations of TDP-43) correlate with characteristic distribution patterns of the underlying pathology across specific brain regions with disease progression. Recent studies support the idea that pathological protein spreads from neuron to neuron via axonal transport in a hierarchical manner. However, little is known to date about the basis of the selective cellular and regional vulnerability, although the information would have important implications for the development of targeted and personalized therapies. Here, we aim to summarize recent advances in the neuropathology, genetics and animal models of TDP-43 proteinopathy, and their relationship to clinical phenotypes for the underlying selective neuronal and regional susceptibilities. Finally, we attempt to integrate these findings into the emerging picture of TDP-43 proteinopathy, and to highlight key issues for future therapy and research

12(S)-Hydroxyeicosatetraenoic acid induces cAMP production via increasing intracellular calcium concentration

AbstractWe have found that a 12-lipoxygenase metabolite of arachidonic acid, 12(S)-hydroxy-5Z,8Z,10E,14Z-eicosatetraenoic acid (12-HETE), induces cAMP production in human normal fibroblast TIG-1 cells. This phenomenon was not observed in other cells tested including human embryonic kidney HEK293 cells. We have speculated that this specific response might be influenced by the kinds of isoform of adenylyl cyclase (AC) present in cells. We found that TIG-1 cells specifically expressed type VIII AC. As type VIII AC is known to be activated by an increase of calcium concentration, we determined the change of intracellular Ca2+ concentration after the addition of 12-HETE. It was elevated not only in TIG-1 cells, but also HEK293 cells, which did not respond to 12-HETE to produce cAMP. The addition of a calcium ionophore elevated the concentration of intracellular cAMP in TIG-1 cells, but it was without effect in HEK293 cells. To show that the expression of this particular isoform of AC is responsible for the positive response to 12-HETE, we transfected this AC isoform into HEK293 cells. The type VIII AC-transfected cells, in contrast to the mock-transfected ones, became very responsive to 12-HETE to produce cAMP. Taken all together the data would strongly suggest that 12-HETE specifically activates type VIII AC via increasing intracellular Ca2+ concentration

はっ水性微細凹凸面上の流動抵抗低減に関する研究

金沢大学理工研究域ミクロンオーダーの規則的な凹凸形状を表面構造に持ち強いはっ水性を有する流路壁面で,流動抵抗の低減を実現するための基礎研究として,表面近傍の状態の観測や流れの計測を行った.本年度は,ニッケル製メッシュを型に用いて,数十ミクロンオーダの微細凹凸をアクリル樹脂表面上に加熱成型することにより,半導体プロセス技術を用いない安価な微細凹凸面作成法を考案した.前年度の数値解析で示唆された凹凸のスケールが大きいほど抵抗低減効果が大きいという推測により,この加熱成型法で数種類の凹凸サイズの試験面を作製した.表面のはっ水性は市販のはっ水剤を塗布することにより付与した.実験では,水滴の接触角,水中での空気層保持機能の経時変化や空気層の面積,及び層流域での流動抵抗を測定した.試験した微細凹凸面の中で凹凸が最も大きい100ミクロン間隔,50ミクロン角の突起を有する試験面において2%の流動抵抗低減を見出した.また,水中での空気保持機能に対しては凹凸のスケールのほか凸部と凹部の面積割合が影響し,表面上の水滴接触角により評価されるはっ水性と水中での空気保持機能との間の相違も見出した.凹部の比率が最も大きい突起間隔50ミクロン,14ミクロン角の微細凹凸面において水滴接触角が最大になったものの,突起のサイズに比べ間隔が過大であったため水中において凹部への浸水を生じさせ気体層を保持が不可能であった.本研究により,微細凹凸を有するはっ水面における流動抵抗低減現象の凹凸サイズ・形状と抵抗低減割合に関連性があることを示す事が出来た.ただし,抵抗低減割合は従来の研究などに比べ顕著ではなく,より望ましい微細凹凸サイズ・形状を精査することが今後の課題である.研究課題/領域番号:13750139, 研究期間(年度):2001-2002出典：「はっ水性微細凹凸面上の流動抵抗低減に関する研究」研究成果報告書　課題番号13750139（KAKEN：科学研究費助成事業データベース（国立情報学研究所））（ https://kaken.nii.ac.jp/ja/grant/KAKENHI-PROJECT-13750139/）を加工して作

Potent prion-like behaviors of pathogenic α-synuclein and evaluation of inactivation methods

The concept that abnormal protein aggregates show prion-like propagation between cells has been considered to explain the onset and progression of many neurodegenerative diseases. Indeed, both synthetic amyloid-like fibrils and pathogenic proteins extracted from patients’ brains induce self-templated amplification and cell-to-cell transmission in vitro and in vivo. However, it is unclear whether exposure to exogenous prion-like proteins can potentially cause these diseases in humans. Here, we investigated in detail the prion-like seeding activities of several kinds of pathogenic α-synuclein (α-syn), including synthetic fibrils and detergent-insoluble fractions extracted from brains of patients with α-synucleinopathies. Exposure to synthetic α-syn fibrils at concentrations above 100 pg/mL caused seeded aggregation of α-syn in SH-SY5Y cells, and seeded aggregation was also observed in C57BL/6 J mice after intracerebral inoculation of at least 0.1 μg/animal. α-Syn aggregates extracted from brains of multiple system atrophy (MSA) patients showed higher seeding activity than those extracted from patients with dementia with Lewy bodies (DLB), and their potency was similar to that of synthetic α-syn fibrils. We also examined the effects of various methods that have been reported to inactivate abnormal prion proteins (PrPSc), including autoclaving at various temperatures, exposure to sodium dodecyl sulfate (SDS), and combined treatments. The combination of autoclaving and 1% SDS substantially reduced the seeding activities of synthetic α-syn fibrils and α-syn aggregates extracted from MSA brains. However, single treatment with 1% SDS or generally used sterilization conditions proved insufficient to prevent accumulation of pathological α-syn. In conclusion, α-syn aggregates derived from MSA patients showed a potent prion-like seeding activity, which could be efficiently reduced by combined use of SDS and autoclaving