Thermal desorption of structured water layer on epitaxial graphene

Thermal desorption of the structured water layer on graphene was observed in this study via electrical conductivity measurements. Specifically, a structured water layer was formed on the graphene surface via deionized water treatment, following which we examined the thermal desorption process of the layer using sheet resistance measurements. The water molecules acting as a p-type dopant were strongly adsorbed on graphene, forming a solid layer. Consequently, the layer was completely removed from the graphene surface at 300⁡°C. The thermal desorption spectrum of the structured water layer on graphene was quantitatively obtained by converting the measured sheet resistance to carrier density change

Combination Chemotherapy with Low-dose 5-FU, Cisplatin, and Gemcitabine for Gemcitabine-Refractory Pancreatic Cancer

Background : No single agent or combination therapy for advanced pancreatic cancer has been reported superior to single-agent GEM, and an effective second-line chemotherapy option is needed for patients who are resistant to first-line GEM therapy. Methods :We analyzed six patients who had disease progression following first-line gemcitabine therapy. Patients received second-line chemotherapy with low dose cisplatin, 5-fluorouracul or S-1,and gemcitabine every 21 days. Results : Two patients showed a partial response (33.3%) and two showed stable disease. Four patients (66.6%) showed a prolonged survival time with partial responses or stable disease.Median survival times were 7 and 11 months from the start of second-line therapy and the start of first-line gemcitabine therapy,respectively. In addition, all patients reported relief from pain and had a favorable performance status. The major toxicities of leucopenia, stomatitis, and diarrhea were found in one patient each.Conclusion : This second-line chemotherapy regimen is an effective option for patients with gemcitabineresistant pancreatic cancer.Article信州医学雑誌 57(6): 247-253(2009)journal articl

Evolutionary histories of breast cancer and related clones

乳がん発生の進化の歴史を解明 --ゲノム解析による発がんメカニズムの探索--. 京都大学プレスリリース. 2023-07-28.Tracking the ol' mutation trail: Unraveling the long history of breast cancer formation. 京都大学プレスリリース. 2023-08-31.Recent studies have documented frequent evolution of clones carrying common cancer mutations in apparently normal tissues, which are implicated in cancer development1, 2, 3. However, our knowledge is still missing with regard to what additional driver events take place in what order, before one or more of these clones in normal tissues ultimately evolve to cancer. Here, using phylogenetic analyses of multiple microdissected samples from both cancer and non-cancer lesions, we show unique evolutionary histories of breast cancers harbouring der(1;16), a common driver alteration found in roughly 20% of breast cancers. The approximate timing of early evolutionary events was estimated from the mutation rate measured in normal epithelial cells. In der(1;16)(+) cancers, the derivative chromosome was acquired from early puberty to late adolescence, followed by the emergence of a common ancestor by the patient’s early 30s, from which both cancer and non-cancer clones evolved. Replacing the pre-existing mammary epithelium in the following years, these clones occupied a large area within the premenopausal breast tissues by the time of cancer diagnosis. Evolution of multiple independent cancer founders from the non-cancer ancestors was common, contributing to intratumour heterogeneity. The number of driver events did not correlate with histology, suggesting the role of local microenvironments and/or epigenetic driver events. A similar evolutionary pattern was also observed in another case evolving from an AKT1-mutated founder. Taken together, our findings provide new insight into how breast cancer evolves

Novel insight into the correlation between hernia orifice of cystocele and lower urinary tract function: a pilot study

Background It has been hypothesized that women with significant pelvic organ prolapse (POP), particularly of the anterior vaginal wall, may have voiding dysfunction (VD). Although the VD mechanism due to cystocele is not fully understood, different vaginal compartments have rarely been closely examined. This study attempted to further elucidate the correlation between POP and VD through a new subgroup classification using cystoscopy. Methods This study reviewed clinical records of 49 women who underwent cystocele repair. All patients were scheduled for laparoscopic sacrocolpopexy, preoperatively underwent uroflowmetry and postvoid residual urine volume (PVR) measurement, and completed pelvic floor function questionnaires. Bladder examination by cystoscopy was additionally performed using the lithotomy position with the Valsalva maneuver. Results Subjects were divided into four groups according to hernia orifice presence determined by cystoscopy, which included the trigone type, posterior wall type, trigone and urethra type, and trigone and posterior wall type. The posterior wall type had statistically higher PVR values versus the trigone and posterior wall type (P = 0.013). The posterior wall type had statistically lower values for average urine flow rate versus the urethra and trigone type (P = 0.020). There were no significant differences noted in the pelvic floor function questionnaires among the four groups. Conclusions A new bladder defect classification based upon hernia orifice location was associated with lower urinary tract function. Posterior wall hernia presence caused significant voiding function deterioration. This new subgroup classification, which can more clearly identify and indicate bladder function, is also comparable among patients

持続可能な地球環境のためのプラネタリーヘルス : 未来を切り開く学際融合研究

はじめに…i 学長挨拶…ii 大学間パネルプログラム…1 開会挨拶 金子慎治　広島大学理事・副学長（グローバル化担当）…3 田中純子　広島大学理事・副学長（霞地区・教員人事・広報担当）…5 司会 李漢沫　広島大学教授…6 来賓挨拶 黒川清　日本医療政策機構　代表理事…7 趣旨説明 鹿嶋小緒里　広島大学IDEC国際連携機構プラネタリーヘルスイノベーションサイエンスセンター(PHIS)センター長…9 基調講演 モデレーター 丸山史人　広島大学教授…12 基調講演 アントニー　プラセンシア　ISGlobal所長…16 パネルディスカッション モデレーター 中村安秀　公益社団法人日本WHO協会理事長…26 パネリスト 鈴木定彦　北海道大学ディスティングイッシュトプロフェッサー…28 中村桂子　東京医科歯科大学教授…31 橋爪真弘　東京大学教授…34 渡辺知保　長崎大学プラネタリーヘルス学環長…37 藤原章正　広島大学教授…41 広島プラネタリーヘルス宣言2023…44 閉会挨拶 新福洋子　広島大学副学長（国際広報担当）…48 開催報告…49 実行委員会…52 編集後記…53Preface…i Message from the President of Hiroshima University…ii The 6 University Panel Symposium Program…2 Opening Remarks KANEKO Shinji, Executive Vice President of Hiroshima University…3 TANAKA Junko, Executive Vice President of Hiroshima University…5 Chair LEE Han Soo, Professor, Hiroshima University…6 Guest Speech KUROKAWA Kiyoshi, Chairman, Health and Global Policy Institute…7 Introduction KASHIMA Saori, Director, PHIS, Hiroshima University…9 Keynote Lecture Moderator MARUYAMA Fumito, Professor, Hiroshima University…12 Lecturer Antoni Plasència, General Director of IS Global…16 Panel Discussion Moderator NAKAMURA Yasuhide, President, Friends of WHO Japan…26 Panelists: SUZUKI Yasuhiko, Distinguished Professor, Hokkaido University…28 NAKAMURA Keiko, Professor, Tokyo Medical and Dental University…31 HASHIZUME Masahiro, Professor, The University of Tokyo…34 WATANABE Chiho, Dean, Interfaculty Initiative in Planetary Health, Nagasaki University…37 FUJIWARA Akimasa, Professor, Hiroshima University…41 Hiroshima PH Declaration 2023…44 Closing Remarks SHIMPUKU Yoko, Vice President of Hiroshima University…48 Symposium Report…49 Organizing Committee…52 Editor's Note…53主催：広島大学IDEC 国際連携機構・広島大学 共催：長崎大学 後援：日本医療政策機構、（公財）日本WHO 協会、プラネタリーヘルスアライアンス、プラネタリーヘルスアライアンス日本支部、フューチャー・アース（Future Earth）、東広島市、広島大学先進理工系科学研究科G7 広島サミットに向けたプラネタリーヘルス大学間パネル: The University Panel Symposium on Planetary Health for the G7 Hiroshima Summit. 広島大学創立 75+75 周年記念事業. 旭硝子ブループラネット地球環境特別研究助成キックオフ

Frequent mutations that converge on the NFKBIZ pathway in ulcerative colitis

潰瘍性大腸炎による上皮再構築メカニズムと発がんとの関係を解明 --IL-17シグナル経路に変異を獲得した上皮細胞は発がん過程で陰性に選択される--. 京都大学プレスリリース. 2019-12-20.Chronic inflammation is accompanied by recurring cycles of tissue destruction and repair and is associated with an increased risk of cancer1, 2, 3. However, how such cycles affect the clonal composition of tissues, particularly in terms of cancer development, remains unknown. Here we show that in patients with ulcerative colitis, the inflamed intestine undergoes widespread remodelling by pervasive clones, many of which are positively selected by acquiring mutations that commonly involve the NFKBIZ, TRAF3IP2, ZC3H12A, PIGR and HNRNPF genes and are implicated in the downregulation of IL-17 and other pro-inflammatory signals. Mutational profiles vary substantially between colitis-associated cancer and non-dysplastic tissues in ulcerative colitis, which indicates that there are distinct mechanisms of positive selection in both tissues. In particular, mutations in NFKBIZ are highly prevalent in the epithelium of patients with ulcerative colitis but rarely found in both sporadic and colitis-associated cancer, indicating that NFKBIZ-mutant cells are selected against during colorectal carcinogenesis. In further support of this negative selection, we found that tumour formation was significantly attenuated in Nfkbiz-mutant mice and cell competition was compromised by disruption of NFKBIZ in human colorectal cancer cells. Our results highlight common and discrete mechanisms of clonal selection in inflammatory tissues, which reveal unexpected cancer vulnerabilities that could potentially be exploited for therapeutics in colorectal cancer