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any of various organs that synthesize substances needed by the body and release it through ducts or directly into the bloodstream (同)secretory organ, secretor, secreter

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(生物体内の)腺(せん)

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1. 唾液腺腫瘍：疫学、診断、評価、および病期分類 salivary gland tumors epidemiology diagnosis evaluation and staging
2. 唾石症 salivary gland stones
3. 唾液腺腫瘍：限局性疾患の治療 salivary gland tumors treatment of locoregional disease
4. シェーグレン症候群の臨床症状：外分泌腺障害 clinical manifestations of sjogrens syndrome exocrine gland disease
5. シェーグレン症候群の分類および診断 classification and diagnosis of sjogrens syndrome

English Journal

Enhanced toxicity of 'bulk' titanium dioxide compared to 'fresh' and 'aged' nano-TiO2 in marine mussels (Mytilus galloprovincialis).

D'Agata A, Fasulo S, Dallas LJ, Fisher AS, Maisano M, Readman JW, Jha AN.Author information Department of Biological and Environmental Sciences, University of Messina , Viale F. Stagno d'Alcontres 31, S. Agata - 98166, Messina , Italy.AbstractAbstract Marine bivalves (Mytilus galloprovincialis) were exposed to titanium dioxide (10 mg L(-1)) either as engineered nanoparticles (nTiO2; fresh, or aged under simulated sunlight for 7 days) or the bulk equivalent. Inductively coupled plasma-optical emission spectrometry analyses of mussel tissues showed higher Ti accumulation (>10-fold) in the digestive gland compared to gills. Nano-sized TiO2 showed greater accumulation than bulk, irrespective of ageing, particularly in digestive gland (>sixfold higher). Despite this, transcriptional expression of metallothionein genes, histology and histochemical analysis suggested that the bulk material was more toxic. Haemocytes showed significantly enhanced DNA damage, determined by the modified comet assay, for all treatments compared to the control, but no significant differences between the treatments. Our integrated study suggests that for this ecologically relevant organism photocatalytic ageing of nTiO2 does not significantly alter toxicity, and that bulk TiO2 may be less ecotoxicologically inert than previously assumed.
Nanotoxicology.Nanotoxicology.2014 Aug;8:549-58. doi: 10.3109/17435390.2013.807446. Epub 2013 Jun 13.
Abstract Marine bivalves (Mytilus galloprovincialis) were exposed to titanium dioxide (10 mg L(-1)) either as engineered nanoparticles (nTiO2; fresh, or aged under simulated sunlight for 7 days) or the bulk equivalent. Inductively coupled plasma-optical emission spectrometry analyses of mussel tissu
PMID 23697396

Loss of PPARγ expression in mammary secretory epithelial cells creates a pro-breast tumorigenic environment.

Apostoli AJ, Skelhorne-Gross GE, Rubino RE, Peterson NT, Di Lena MA, Schneider MM, Sengupta SK, Nicol CJ.Author information Department of Pathology and Molecular Medicine, Queen's University, Kingston, ON, Canada.AbstractBreast cancer is the leading cause of new cancer diagnoses among women. Using peroxisome proliferator-activated receptor (PPAR)γ((+/-)) mice, we showed normal expression of PPARγ was critical to stop 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast tumorigenesis. PPARγ is expressed in many breast cell types including mammary secretory epithelial (MSE) cells. MSEs proliferate as required during pregnancy, and undergo apoptosis or reversible transdifferentiation during involution once lactation is complete. Thus, MSE-specific loss of PPARγ was hypothesized to enhance DMBA-mediated breast tumorigenesis. To test this, MSE cell-specific PPARγ knockout (PPARγ-MSE KO) and control (PPARγ-WT) mice were generated, mated and allowed to nurse for three days. One week after involution, dams were treated with DMBA to initiate breast tumors, and randomized on week 7 to continue receiving a normal chow diet (DMBA Only: PPARγ-WT, n = 15; PPARγ-MSE KO, n = 25) or one supplemented with a PPARγ activating drug (DMBA + ROSI: PPARγ-WT, n = 17; PPARγ-MSE KO, n = 24), and monitored for changes in breast tumor outcomes. PPARγ-MSE KOs had significantly lower overall survival and decreased mammary tumor latency as compared to PPARγ-WT controls. PPARγ activation significantly reduced DMBA-mediated malignant mammary tumor volumes irrespective of genotype. MSE-specific PPARγ loss resulted in decreased mammary gland expression of PTEN and Bax, increased superoxide anion production, and elevated serum eotaxin and RANTES, creating a protumorigenic environment. Moreover, PPARγ activation in MSEs delayed mammary tumor growth in part by down-regulating Cox-1, Cox-2 and cyclin D1. Collectively, these studies highlight a protective role of MSE-specific PPARγ during breast tumorigenesis, and support a novel chemotherapeutic role of PPARγ activation in breast cancer.
International journal of cancer. Journal international du cancer.Int J Cancer.2014 Mar 1;134(5):1055-66. doi: 10.1002/ijc.28432. Epub 2013 Sep 19.
Breast cancer is the leading cause of new cancer diagnoses among women. Using peroxisome proliferator-activated receptor (PPAR)γ((+/-)) mice, we showed normal expression of PPARγ was critical to stop 7,12-dimethylbenz[a]anthracene (DMBA)-induced breast tumorigenesis. PPARγ is expressed in many br
PMID 23934545

Expression and significance of notch signaling pathway in salivary adenoid cystic carcinoma.

Bell D, Hanna EY, Miele L, Roberts D, Weber RS, El-Naggar AK.Author information Department of Pathology, The University of Texas MD Anderson Cancer Center, Houston, TX. Electronic address: diana.bell@mdanderson.org.AbstractNotch signaling plays a role in stem cell biology, tumor formation, angiogenesis, and cell death. Targeting Notch pathway could serve as a therapeutic strategy in cancer. Little is known about the differential role of various components of the Notch pathway in salivary adenoid cystic carcinoma (AdCC). To investigate the association of the Notch pathway in AdCC carcinogenesis, we analyzed the Notch receptor (Notch-1, Notch-2, Notch-4) and Notch ligand (Jagged-1, Delta) expressions. The results showed elevated expression levels of all 5 proteins in AdCC tissue relative to normal salivary gland tissues. Jagged-1/Notch-2 coexpression was significantly associated with increased patient survival rate. The elevated expression level of these Notch receptors and ligands in AdCC points to Notch signaling as a key player in AdCC pathogenesis. Our data provide evidence for a relationship between Jagged-1/Notch-2 coexpression and better overall patient survival with AdCC. Targeting Notch signaling pathway may provide therapeutic benefits for these patients.
Annals of diagnostic pathology.Ann Diagn Pathol.2014 Feb;18(1):10-3. doi: 10.1016/j.anndiagpath.2013.10.001. Epub 2013 Oct 10.
Notch signaling plays a role in stem cell biology, tumor formation, angiogenesis, and cell death. Targeting Notch pathway could serve as a therapeutic strategy in cancer. Little is known about the differential role of various components of the Notch pathway in salivary adenoid cystic carcinoma (AdCC
PMID 24238845

Japanese Journal

ヒト胃および十二指腸粘膜生検組織内ペプシノーゲン活性　　サクシニルアルブミンを基質とした測定法による:サクシニルアルブミンを基質とした測定法による

三木一正,一瀬雅夫,降旗千恵,張景明,丹羽寛文,岡博,織旧敏次,松島泰次郎
日本消化機病學會雜誌. 乙 78(11), 2079-2086, 1981
当科外来•入院患者95例の延100回の上部消化管内視鏡検査時に,病変部に加え幽門•胃角•体中部小弯胃粘膜および十二指腸球部粘膜を内視鏡直視下にほぼ同一部位で2個ずつ生検採取し,1個を腸上皮化生の有無等,病理組織検索用に,他の1個をペプシノーゲン(Pg)測定用とし,計355個の生検材料よりPg測定用試料の抽出を行なつた.Pg活性測定はサクシニルアルブミンを基質とする方法で行ないmg蛋白当りPg活性値 …
NAID 130001062803

多発早期胃癌診断に関する臨床的研究―第1報―

大田由己子,黒川きみえ,丸山正隆,渡辺伸一郎,白鳥敬子,鈴木博孝
日本消化器内視鏡学会雑誌 22(10), 1413-1420, 1980
多発早期胃癌(多発群)診断の問題にっいて検討するために,まず多発群を,単発早期胃癌(単発群)と比較し,臨床病理組織学的検索を行なった.多発群の頻度は,1968年から1977年までに切除された胃癌症例中,2.1%で,男女比は7.6:1,年齢分布は61.1±9.7(mean±SD)歳であった.単発群では,陥凹性病変が過半数を占めていたが,多発群ではこの傾向はみられず,むしろ隆起性病変が44.0%で,多 …
NAID 130004251182

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