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1. 小児における運動過多な運動障害 hyperkinetic movement disorders in children
2. 家族性アルドステロン症 familial hyperaldosteronism
3. 心房細動患者における洞調律維持のための抗不整脈薬：臨床試験 antiarrhythmic drugs to maintain sinus rhythm in patients with atrial fibrillation clinical trials
4. 原発性アルドステロン症の病態生理および臨床的特徴 pathophysiology and clinical features of primary aldosteronism
5. 原発性アルドステロン症の治療 treatment of primary aldosteronism

English Journal

Abnormal Regulation of Renin Angiotensin Aldosterone System Is Associated With Right Ventricular Dysfunction in Hypertension.

Gregori M1, Tocci G2, Giammarioli B3, Befani A3, Ciavarella GM3, Ferrucci A3, Paneni F2.Author information 1Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy. Electronic address: gremao@libero.it.2Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy; Istituto di Ricerca a Carattere Scientifico (IRCCS) Neuromed, Pozzilli, Italy.3Division of Cardiology, Department of Clinical and Molecular Medicine, University of Rome "Sapienza", Rome, Italy.AbstractBACKGROUND: Right ventricular dysfunction (RVD) is a major predictor of cardiovascular mortality. Inadequate suppression of the renin-angiotensin-aldosterone system (RAAS) after postural manoeuvres favours alterations of left ventricular (LV) function. The effects of RAAS dysregulation on RV performance remain elusive. The present study investigated RV function in hypertensive patients with or without altered RAAS activation.
The Canadian journal of cardiology.Can J Cardiol.2014 Feb;30(2):188-94. doi: 10.1016/j.cjca.2013.11.009. Epub 2013 Nov 15.
BACKGROUND: Right ventricular dysfunction (RVD) is a major predictor of cardiovascular mortality. Inadequate suppression of the renin-angiotensin-aldosterone system (RAAS) after postural manoeuvres favours alterations of left ventricular (LV) function. The effects of RAAS dysregulation on RV perform
PMID 24461920

Resolving pathobiological mechanisms relating to Huntington disease: gait, balance, and involuntary movements in mice with targeted ablation of striatal D1 dopamine receptor cells.

Kim HA1, Jiang L1, Madsen H1, Parish CL1, Massalas J1, Smardencas A1, O'Leary C2, Gantois I1, O'Tuathaigh C3, Waddington JL3, Ehrlich ME4, Lawrence AJ1, Drago J5.Author information 1Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Australia.2Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Australia; Molecular and Cellular Therapeutics, RCSI Research Institute, Royal College of Surgeons in Ireland, Dublin 2, Ireland.3Molecular and Cellular Therapeutics, RCSI Research Institute, Royal College of Surgeons in Ireland, Dublin 2, Ireland.4Department of Neurology, Mount Sinai School of Medicine, New York, NY, USA.5Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Australia. Electronic address: john.drago@florey.edu.au.AbstractProgressive cell loss is observed in the striatum, cerebral cortex, thalamus, hypothalamus, subthalamic nucleus and hippocampus in Huntington disease. In the striatum, dopamine-responsive medium spiny neurons are preferentially lost. Clinical features include involuntary movements, gait and orofacial impairments in addition to cognitive deficits and psychosis, anxiety and mood disorders. We utilized the Cre-LoxP system to generate mutant mice with selective postnatal ablation of D1 dopamine receptor-expressing striatal neurons to determine which elements of the complex Huntington disease phenotype relate to loss of this neuronal subpopulation. Mutant mice had reduced body weight, locomotor slowing, reduced rearing, ataxia, a short stride length wide-based erratic gait, impairment in orofacial movements and displayed haloperidol-suppressible tic-like movements. The mutation was associated with an anxiolytic profile. Mutant mice had significant striatal-specific atrophy and astrogliosis. D1-expressing cell number was reduced throughout the rostrocaudal extent of the dorsal striatum consistent with partial destruction of the striatonigral pathway. Additional striatal changes included up-regulated D2 and enkephalin mRNA, and an increased density of D2 and preproenkephalin-expressing projection neurons, and striatal neuropeptide Y and cholinergic interneurons. These data suggest that striatal D1-cell-ablation alone may account for the involuntary movements and locomotor, balance and orofacial deficits seen not only in HD but also in HD phenocopy syndromes with striatal atrophy. Therapeutic strategies would therefore need to target striatal D1 cells to ameliorate deficits especially when the clinical presentation is dominated by a bradykinetic/ataxic phenotype with involuntary movements.
Neurobiology of disease.Neurobiol Dis.2014 Feb;62:323-37. doi: 10.1016/j.nbd.2013.09.015. Epub 2013 Oct 14.
Progressive cell loss is observed in the striatum, cerebral cortex, thalamus, hypothalamus, subthalamic nucleus and hippocampus in Huntington disease. In the striatum, dopamine-responsive medium spiny neurons are preferentially lost. Clinical features include involuntary movements, gait and orofacia
PMID 24135007

Prognostic Factors Affecting Disease-Specific Survival in Patients with Recurrent and/or Metastatic Differentiated Thyroid Carcinoma Detected by Positron Emission Tomography/Computed Tomography.

Akkas BE, Demirel BB, Vural GU.Author information Ankara Oncology Research and Training Hospital , Department of Nuclear Medicine, Ankara, Turkey .AbstractAim: We aimed to analyze the prognostic factors affecting disease-specific survival in patients with recurrent and/or metastatic differentiated thyroid carcinoma. Methods: Seventy-seven patients with recurrent/metastatic differentiated thyroid carcinoma who were previously treated with total thyroidectomy followed by radioactive iodine therapy were enrolled. Recurrent/metastatic disease was detected by positron emission tomography/computed tomography. At the time of last follow-up (mean 4.8±1.3 years), patients were grouped as having (i) clinical remission (n=17), (ii) stable disease (n=22), or (iii) progressive disease (n=38). We retrospectively examined the prognostic impact of clinical factors (age, sex, TNM stage), histopathological factors of the primary tumor (tumor size, histology, the presence of vascular invasion, extrathyroidal spread, and lymph node metastasis), serum thyroglobulin levels, and metabolic parameters of recurrent/metastatic disease such as radioactive iodine avidity, F18-fluorodeoxyglucose uptake (SUVmax) in metastatic deposits, number and location of F18-fluorodeoxyglucose-avid lesions (locoregional vs. distant), and the impact of surgery on disease-specific survival. Results: Lack of vascular invasion (p=0.04), presence of surgically amenable recurrence/metastasis (p=0.0001), and suppressible on-therapy serum thyroglobulin levels at the time of recurrent/metastatic disease (p=0.01) were strong predictors of clinical remission and good prognosis on multivariate analysis. Lesional SUVmax, number or location of F18-fluorodeoxyglucose-avid lesions, and TNM stage did not correlate with clinical outcome. Clinical remission could only be achieved by curative surgery. Patients without curative surgery for recurrence/metastasis had a 43 times higher risk to develop progressive disease than patients with disease amenable to surgery. Conclusions: Curative surgery is an essential therapeutic modality to achieve clinical remission in metastatic/recurrent differentiated thyroid carcinoma. Positron emission tomography/computed tomography is a powerful method to detect surgically resectable disease for the selection of patients who may benefit from curative surgery.
Thyroid : official journal of the American Thyroid Association.Thyroid.2014 Feb;24(2):287-95. doi: 10.1089/thy.2013.0195. Epub 2013 Aug 24.
Aim: We aimed to analyze the prognostic factors affecting disease-specific survival in patients with recurrent and/or metastatic differentiated thyroid carcinoma. Methods: Seventy-seven patients with recurrent/metastatic differentiated thyroid carcinoma who were previously treated with total thyroid
PMID 23750862

Japanese Journal

2004年新潟県中越地震で被害を免れたRC造校舎の入力地震動と地震時応答に関する研究

土方勝一郎,杉山達也,徳光亮一,山添正稔,古山田耕司,岡野創,宮本裕司
日本建築学会構造系論文集 73(631), 1519-1527, 2008-09-30
… Next, simulation analyses were performed using the strong motions and the suppressible factors of structure damage were verified on the basis of the analyses results. …
NAID 110006894636

研究紹介カキ'刀根早生'果実の流通中の熟柿化現象の原因究明と防止技術の開発

稲葉昭次
岡山大学農学部学術報告 96, 71-77, 2007-02
… We clarified the mechanism of this fruit softening and developed a completely suppressible technique based on that mechanism. …
NAID 120002311154

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★リンクテーブル★

リンク元	「repressible」「抑圧可能」
拡張検索	「glucocorticoid suppressible hyperaldosteronism」「nonsuppressible insulin-like activity」「dexamethasone suppressible hyperaldosteronism」