WordNet

rain, hail, or snow hard and be very windy, often with thunder or lightning; "If it storms, well need shelter"
a violent commotion or disturbance; "the storms that had characterized their relationship had died away"; "it was only a tempest in a teapot" (同)tempest
a violent weather condition with winds 64-72 knots (11 on the Beaufort scale) and precipitation and thunder and lightning (同)violent storm
a direct and violent assault on a stronghold
take by force; "Storm the fort" (同)force
attack by storm; attack suddenly (同)surprise
blow hard; "It was storming all night"
of or relating to or affected by hyperthyroidism

PrepTutorEJDIC

『あらし』,暴風[雨],荒天 / (感情・言動などの)『あらし』,激発《+『of』+『名』》 / (一般に)激動,波乱,騒動 / (弾丸などが)雨あられと飛ぶこと《+『of』+『名』》 / 《itを主語にして》〈天候が〉『荒れる』 / 猛然と突進する;激しく怒る / …‘を'強襲する,急襲する

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1. 甲状腺クリーゼ thyroid storm
2. 甲状腺機能亢進症およびバセドウ病の神経学的症状 neurologic manifestations of hyperthyroidism and graves disease
3. エレクトリカルストームおよびインセサント型心室頻拍 electrical storm and incessant ventricular tachycardia
4. 甲状腺中毒性周期性四肢麻痺 thyrotoxic periodic paralysis
5. 小児臓器提供候補者（ポテンシャルドナー）のマネージメント management of the potential pediatric organ donor

English Journal

Acute pericarditis: unique comorbidity of thyrotoxic crisis with Graves' disease.

Inami T1, Seino Y2, Goda H3, Okazaki H3, Shirakabe A3, Yamamoto M3, Okajima F4, Emoto N4, Hata N3, Shimizu W5.Author information 1Department of Cardiology, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan. Electronic address: t-inami@nms.ac.jp.2Department of Cardiology, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan.3Department of Intensive Care Unit, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan.4Department of Endocrinolgy, Nippon Medical School Chiba Hokusoh Hospital, Chiba, Japan.5Department of Cardiovascular Medicine, Nippon Medical School, Tokyo, Japan.KEYWORDS: Acute pericarditis, Graves' disease, Thyroid crisis
International journal of cardiology.Int J Cardiol.2014 Feb 15;171(3):e129-30. doi: 10.1016/j.ijcard.2013.12.042. Epub 2013 Dec 28.
PMID 24411211

Fetal cell carcinogenesis of the thyroid: A modified theory based on recent evidence [My Opinion].

Takano T.Author information Department of Laboratory Medicine, Osaka University Graduate School of Medicine, Suita 565-0871, Japan.AbstractThyroid cancer cells were believed to be generated by multi-step carcinogenesis, in which cancer cells are derived from thyrocytes, via multiple incidences of damage to their genome, especially in oncogenes or anti-oncogenes that accelerate proliferation or foster malignant phenotypes, such as the ability to invade the surrounding tissue or metastasize to distant organs, until a new hypothesis, fetal cell carcinogenesis, was presented. In fetal cell carcinogenesis, thyroid tumor cells are assumed to be derived from three types of fetal thyroid cell which only exist in fetuses or young children, namely, thyroid stem cells (TSCs), thyroblasts and prothyrocytes, by proliferation without differentiation. Genomic alternations, such as RET/PTC and PAX8-PPARgamma1 rearrangements and a mutation in the BRAF gene, play an oncogenic role by preventing thyroid fetal cells from differentiating. Fetal cell carcinogenesis effectively explains recent molecular and clinical evidence regarding thyroid cancer, including thyroid cancer initiating cells (TCICs), and it underscores the importance of identifying a stem cells and clarifying the molecular mechanism of organ development in cancer research. It introduces three important concepts, the reverse approach, stem cell crisis and mature and immature cancers. Further, it implies that analysis of a small population of cells in a cancer tissue will be a key technique in establishing future laboratory tests. In the contrary, mass analysis such as gene expression profiling, whole genomic scan, and proteomics analysis may have definite limitations since they can only provide information based on many cells.
Endocrine journal.Endocr J.2014 Jan 22. [Epub ahead of print]
Thyroid cancer cells were believed to be generated by multi-step carcinogenesis, in which cancer cells are derived from thyrocytes, via multiple incidences of damage to their genome, especially in oncogenes or anti-oncogenes that accelerate proliferation or foster malignant phenotypes, such as the a
PMID 24452016

Glucose variability before and after treatment of a patient with Graves' disease complicated by diabetes mellitus: Assessment by continuous glucose monitoring.

Torimoto K1, Okada Y, Arao T, Mori H, Yamamoto S, Narisawa M, Kurozumi A, Tanaka Y.Author information 1First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushyu 807-8555, Japan.AbstractA 48-year-old woman was diagnosed and treated for Graves' disease (GD) in 1999 but she discontinued treatment at her own discretion. In 2011, she was admitted to a local hospital for management of thyrotoxic crisis. Treatment with propylthiouracil, iodide potassium (KI), and prednisolone (PSL) was started, which resulted in improvement of the general condition. PSL and KI were discontinued before she was transferred to our hospital. At the local hospital, fasting plasma glucose (FPG) was 212 mg/dL and hemoglobin A1c concentration was 11.2%; intensive insulin therapy had been instituted. Upon admission to our hospital, FPG level was 122 mg/dL, but insulin secretion was compromised, suggesting aggravation of thyroid function and deterioration of glycemic control. The FPG level increased to 173 mg/dL; continuous glucose monitoring (CGM) identified dawn phenomenon at approximately 0400 h. Resumption of KI resulted in improvement of FPG and disappearance of the dawn phenomenon, as assessed by CGM. These results indicate that in patients with compromised insulin secretion, hyperthyroidism can induce elevation of not only postprandial blood glucose, but also FPG level due to the dawn phenomenon and that the dawn phenomenon can be alleviated with improvement in thyroid function. To our knowledge, no studies have assessed glucose variability by CGM before and after treatment of Graves' disease. The observations made in this case shed light on the understanding of abnormal glucose metabolism associated with Graves' disease.
Endocrine journal.Endocr J.2014 Jan 11. [Epub ahead of print]
A 48-year-old woman was diagnosed and treated for Graves' disease (GD) in 1999 but she discontinued treatment at her own discretion. In 2011, she was admitted to a local hospital for management of thyrotoxic crisis. Treatment with propylthiouracil, iodide potassium (KI), and prednisolone (PSL) was s
PMID 24420389