WordNet

write by means of a keyboard with types; "type the acceptance letter, please" (同)typewrite
a small metal block bearing a raised character on one end; produces a printed character when inked and pressed on paper; "he dropped a case of type, so they made him pick them up"
(biology) the taxonomic group whose characteristics are used to define the next higher taxon
a subdivision of a particular kind of thing; "what type of sculpture do you prefer?"
all of the tokens of the same symbol; "the word `element contains five different types of character"
printed characters; "small type is hard to read"
identify as belonging to a certain type; "Such people can practically be typed" (同)typecast
the 9th letter of the Roman alphabet (同)i
hormone secreted by the isles of Langerhans in the pancreas; regulates storage of glycogen in the liver and accelerates oxidation of sugar in cells
writing done with a typewriter (同)typewriting

PrepTutorEJDIC

〈C〉(…の)『型』,タイプ,類型,種類(kind)《+of+名》 / 〈C〉(その種類の特質を最もよく表している)『典型』,手本,模範《+of+名》 / 〈U〉《集合的に》活字;〈C〉(1個の)活字 / 〈U〉(印刷された)字体,活字 / 〈C〉(貨幣・メダルなどの)模様,図柄 / 〈C〉血液型(blood group) / …‘を'タイプに打つ / (…として)…‘を'分類する《+名+as+名(doing)》 / …‘の'型を決める / タイプライターを打つ
『私は』私が
iodineの化学記号
インシュリン(膵臓(すいぞう)ホルモンで糖尿病治療剤)

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1. 糖尿病におけるインスリン療法の一般原則 general principles of insulin therapy in diabetes mellitus
2. 2型糖尿病におけるインスリン療法 insulin therapy in type 2 diabetes mellitus
3. 成人の1型糖尿病における血糖値マネージメント management of blood glucose in adults with type 1 diabetes mellitus
4. 糖尿病における吸入インスリン療法 inhaled insulin therapy in diabetes mellitus
5. 小児および思春期における1型糖尿病のマネージメント management of type 1 diabetes mellitus in children and adolescents

English Journal

Expression and Purification of Optimized rolGLP-1, A Novel GLP-1 Analog, in Escherichia Coli BL21(DE3) and its Good Glucoregulatory Effect on Type 2 Diabetic Mice.

Ma B, Tu P, Zhao X, Zhang Y, Wang Y, Ma C, Ji Y, Li X, Abbas SA, Li M.Author information Key Laboratory for Bioactive Materials of the Ministry of Education, Institute of Molecular Biology, College of Life Science, Nankai University, Tianjin 300071, P.R. China. mgl@nankai.edu.cn.AbstractGlucagon-like peptide-1 (GLP-1) is an incretin hormone that decreases postprandial glycemic excursions by enhancing insulin secretion but with short half-life due to rapid inactivation by enzymatic N-terminal truncation. Therefore, efforts are being made to improve the stability of GLP-1 via modifying its structure or inhibiting dipeptidylpeptidase IV (DPP IV), which is responsible for its degradation. GLP-M, consisting of 10 tandem repeated rolGLP-1 (GLP-1 analog), has been expressed in Pichia pastoris by our laboratory. Although it had a long effect of maintaining glucose homeostasis, redundant amino acids and purification tag limited its application. Here, optimized rolGLP-1(GLPO) with no redundant amino acids and purification tag was constructed by molecular cloning and site-directed mutagenesis, which was expressed efficiently in Escherichia coli BL21(DE3) with the production of 81.5 mg/L, and confirmed by the results of SDS-PAGE electrophoresis and Western Blotting. Then GLP-O was purified via ion exchange chromatography and gel filtration chromatography. The purity of GLP-O was close to 100%. GLP-O could be cut into single rolGLP-1 by trypsin in vitro, and rolGLP-1 had anti-trypsin activity. After oral administration of GLP-O for 4 weeks, the level of blood glucose in type 2 diabetic mice was lowered effectively, and the oral glucose tolerance of mice was improved significantly. These results settled the foundation for further clinical application of GLP-O.
Current pharmaceutical biotechnology.Curr Pharm Biotechnol.2014 Nov;14(11):985-94.
Glucagon-like peptide-1 (GLP-1) is an incretin hormone that decreases postprandial glycemic excursions by enhancing insulin secretion but with short half-life due to rapid inactivation by enzymatic N-terminal truncation. Therefore, efforts are being made to improve the stability of GLP-1 via modifyi
PMID 24372241

Modulation of the action of insulin by angiotensin-(1-7).

Dominici FP1, Burghi V1, Muñoz MC1, Giani JF2.Author information 1*IQUIFIB, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires, Argentina.2†Department of Biomedical Sciences and Department of Pathology and Laboratory Medicine, Cedars-Sinai Medical Center, Los Angeles, CA, U.S.A.AbstractThe prevalence of Type 2 diabetes mellitus is predicted to increase dramatically over the coming years and the clinical implications and healthcare costs from this disease are overwhelming. In many cases, this pathological condition is linked to a cluster of metabolic disorders, such as obesity, systemic hypertension and dyslipidaemia, defined as the metabolic syndrome. Insulin resistance has been proposed as the key mediator of all of these features and contributes to the associated high cardiovascular morbidity and mortality. Although the molecular mechanisms behind insulin resistance are not completely understood, a negative cross-talk between AngII (angiotensin II) and the insulin signalling pathway has been the focus of great interest in the last decade. Indeed, substantial evidence has shown that anti-hypertensive drugs that block the RAS (renin-angiotensin system) may also act to prevent diabetes. Despite its long history, new components within the RAS continue to be discovered. Among them, Ang-(1-7) [angiotensin-(1-7)] has gained special attention as a counter-regulatory hormone opposing many of the AngII-related deleterious effects. Specifically, we and others have demonstrated that Ang-(1-7) improves the action of insulin and opposes the negative effect that AngII exerts at this level. In the present review, we provide evidence showing that insulin and Ang-(1-7) share a common intracellular signalling pathway. We also address the molecular mechanisms behind the beneficial effects of Ang-(1-7) on AngII-mediated insulin resistance. Finally, we discuss potential therapeutic approaches leading to modulation of the ACE2 (angiotensin-converting enzyme 2)/Ang-(1-7)/Mas receptor axis as a very attractive strategy in the therapy of the metabolic syndrome and diabetes-associated diseases.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 May 1;126(9):613-30. doi: 10.1042/CS20130333.
The prevalence of Type 2 diabetes mellitus is predicted to increase dramatically over the coming years and the clinical implications and healthcare costs from this disease are overwhelming. In many cases, this pathological condition is linked to a cluster of metabolic disorders, such as obesity, sy
PMID 24450744

Role of angiotensin-converting enzyme 2 (ACE2) in diabetic cardiovascular complications.

Patel VB, Parajuli N, Oudit GY.AbstractDiabetes mellitus results in severe cardiovascular complications, and heart disease and failure remain the major causes of death in patients with diabetes. Given the increasing global tide of obesity and diabetes, the clinical burden of diabetes-induced cardiovascular disease is reaching epidemic proportions. Therefore urgent actions are needed to stem the tide of diabetes which entails new prevention and treatment tools. Clinical and pharmacological studies have demonstrated that AngII (angiotensin II), the major effector peptide of the RAS (renin-angiotensin system), is a critical promoter of insulin resistance and diabetes mellitus. The role of RAS and AngII has been implicated in the progression of diabetic cardiovascular complications and AT1R (AngII type 1 receptor) blockers and ACE (angiotensin-converting enzyme) inhibitors have shown clinical benefits. ACE2, the recently discovered homologue of ACE, is a monocarboxypeptidase which converts AngII into Ang-(1-7) [angiotensin-(1-7)] which, by virtue of its actions on the MasR (Mas receptor), opposes the effects of AngII. In animal models of diabetes, an early increase in ACE2 expression and activity occurs, whereas ACE2 mRNA and protein levels have been found to decrease in older STZ (streptozotocin)-induced diabetic rats. Using the Akita mouse model of Type 1 diabetes, we have recently shown that loss of ACE2 disrupts the balance of the RAS in a diabetic state and leads to AngII/AT1R-dependent systolic dysfunction and impaired vascular function. In the present review, we will discuss the role of the RAS in the pathophysiology and treatment of diabetes and its complications with particular emphasis on potential benefits of the ACE2/Ang-(1-7)/MasR axis activation.
Clinical science (London, England : 1979).Clin Sci (Lond).2014 Apr;126(7):471-82. doi: 10.1042/CS20130344.
Diabetes mellitus results in severe cardiovascular complications, and heart disease and failure remain the major causes of death in patients with diabetes. Given the increasing global tide of obesity and diabetes, the clinical burden of diabetes-induced cardiovascular disease is reaching epidemic pr
PMID 24329564

Japanese Journal

非妊時の自己管理が良好ではなかった1型糖尿病をもつ女性の妊娠前から妊娠中期における経験と思い

福島千恵子,杉浦絹子,Fukushma Chieko,Sugiura Kinuko
三重看護学誌 14(1), 11-17, 2012-03-15
… 娠前は計画妊娠への援助，妊娠初期は妊娠継続するか否かの自己決定を支える援助と妊娠中の自己管理の受け入れへの援助，妊娠中期は妊娠期特有の管理への戸惑いと無力感及び不安の表出への援助であると考えられた．In this study, we conducted research for the purpose of clarifying the experiences and emotion from the pre-pregnancy to puerperal period of women with type 1 diabetes mellitus in terms of self-controlling of diabetes, and considering what kind of care is …
NAID 120003974432

High-fat diet-induced reduction of peroxisome proliferator-activated receptor-γ coactivator-1α messenger RNA levels and oxidative capacity in the soleus muscle of rats with metabolic syndrome.

Nagatomo Fumiko,Fujino Hidemi,Kondo Hiroyo,Takeda Isao,Tsuda Kinsuke,Ishihara Akihiko
Nutrition research (New York, N.Y.) 32(2), 144-151, 2012-02
… Animal models of type 2 diabetes exhibit reduced peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) messenger RNA (mRNA) levels, which are associated with decreased oxidative capacity, in skeletal muscles. … We hypothesized that a high-fat diet decreases PGC-1α mRNA levels in skeletal muscles of rats with metabolic syndrome, reducing muscle oxidative capacity and accelerating metabolic syndrome or inducing type 2 diabetes. …
NAID 120003988288