WordNet

sprinkle as if with salt; "the rebels had salted the fields with mines and traps"
a compound formed by replacing hydrogen in an acid by a metal (or a radical that acts like a metal)
preserve with salt; "people used to salt meats on ships"
the taste experience when common salt is taken into the mouth (同)saltiness, salinity
white crystalline form of especially sodium chloride used to season and preserve food (同)table_salt, common salt
(of speech) painful or bitter; "salt scorn"- Shakespeare; "a salt apology"
add salt to
add zest or liveliness to; "She salts her lectures with jokes"
(used especially of meats) preserved in salt (同)salt-cured, brine-cured
the act of adding salt to food

PrepTutorEJDIC

〈U〉『塩』食塩 / 〈U〉(化学で)塩 / 《複数形で》薬用塩類(Epsom salt[s],smelling salts) / 〈U〉生気(刺激,興趣)を与えるもの / 〈C〉《話》(特に老練な)水夫 / 塩の,塩を含んでいる;塩気のある,塩辛い / 塩漬けにした / (土地が)塩につかった / 塩信でできた,塩水の中で育つ / 〈食べ物〉‘を'塩で味をつける;〈肉・魚など〉‘を'塩漬けにして保存する《+『名』+『down』,+『down』+『名』》 / 《受動態で》(…で)〈言葉・話なで〉‘を'ぴりっとさせる,‘に'味をつける《+『名』+『with』+『名』》
衰弱(荒廃)させる
塩で味をつけて,塩味の;塩漬けの
Strategic Arms Limitation Talks戦略兵器制限交渉

UpToDate Contents

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1. 中枢性塩類喪失 cerebral salt wasting
2. 低ナトリウム血症を有する成人の評価 evaluation of adults with hyponatremia
3. バーター症候群およびギテルマン症候群 bartter and gitelman syndromes
4. 成人における体液量減少の病因、臨床症状、および診断 etiology clinical manifestations and diagnosis of volume depletion in adults
5. 多尿および尿崩症の診断 diagnosis of polyuria and diabetes insipidus

English Journal

Mineralocorticoid receptor antagonizes Dot1a-Af9 complex to increase αENaC transcription.

Zhang X1, Zhou Q, Chen L, Berger S, Wu H, Xiao Z, Pearce D, Zhou X, Zhang W.Author information 1Dept. of Internal Medicine, Univ. of Texas Medical School at Houston, 6431 Fannin, MSB 5.135, Houston, TX 77030. wenzheng.zhang@uth.tmc.edu.AbstractAldosterone is a major regulator of Na(+) absorption and acts by activating the mineralocorticoid receptor (MR) to stimulate the epithelial Na(+) channel (ENaC). MR(-/-) mice exhibited pseudohypoaldosteronism type 1 (hyponatremia, hyperkalemia, salt wasting, and high levels of aldosterone) and died around postnatal day 10. However, if and how MR regulates ENaC transcription remain incompletely understood. Our earlier work demonstrated that aldosterone activates αENaC transcription by reducing expression of Dot1a and Af9 and by impairing Dot1a-Af9 interaction. Most recently, we reported identification of a major Af9 binding site in the αENaC promoter and upregulation of αENaC mRNA expression in mouse kidneys lacking Dot1a. Despite these findings, the putative antagonism between the MR/aldosterone and Dot1a-Af9 complexes has never been addressed. The molecular defects leading to PHA-1 in MR(-/-) mice remain elusive. Here, we report that MR competes with Dot1a to bind Af9. MR/aldosterone and Dot1a-Af9 complexes mutually counterbalance ENaC mRNA expression in inner medullary collecting duct 3 (IMCD3) cells. Real-time RT-quantitative PCR revealed that 5-day-old MR(-/-) vs. MR(+/+) mice had significantly lower αENaC mRNA levels. This change was associated with an increased Af9 binding and H3 K79 hypermethylation in the αENaC promoter. Therefore, this study identified MR as a novel binding partner and regulator of Af9 and a novel mechanism coupling MR-mediated activation with relief of Dot1a-Af9-mediated repression via MR-Af9 interaction. Impaired ENaC expression due to failure to inhibit Dot1a-Af9 may play an important role in the early stages of PHA-1 (before postnatal day 8) in MR(-/-) mice.
American journal of physiology. Renal physiology.Am J Physiol Renal Physiol.2013 Nov 15;305(10):F1436-44. doi: 10.1152/ajprenal.00202.2013. Epub 2013 Sep 11.
Aldosterone is a major regulator of Na(+) absorption and acts by activating the mineralocorticoid receptor (MR) to stimulate the epithelial Na(+) channel (ENaC). MR(-/-) mice exhibited pseudohypoaldosteronism type 1 (hyponatremia, hyperkalemia, salt wasting, and high levels of aldosterone) and died
PMID 24026182

Development of contrast-induced nephropathy in subarachnoid hemorrhage: a single center perspective.

Ray B1, Rickert KL, Welch BG, White JA, Klinger DR, Boudreaux BP, Whittemore BA, Gu E.Author information 1Division of Neurocritical Care, Department of Neurological Surgery and Neurology & Neurotherapeutics, University of Texas-Southwestern Medical Center, Dallas, TX, USA, docbappa@gmail.com.AbstractBACKGROUND AND PURPOSE: The use of iodinated contrast-enhanced imaging studies is increasing in acute cerebrovascular diseases, especially in subarachnoid hemorrhage (SAH). In SAH, such studies are essential for both diagnosis and treatment of the cause and sequela of hemorrhage. These patients are often subjected to multiple contrast studies such as computed tomographic angiography, computed tomographic perfusion, and cerebral angiography. They are also predisposed to intravascular volume depletion as a part of the disease process from cerebral salt wasting (CSW) and as a result of multiple contrast exposure can develop contrast-induced nephropathy (CIN). Data regarding CIN in this population are scarce. We aimed to examine the incidence of CIN in SAH and identify potential associative risk factors.
Neurocritical care.Neurocrit Care.2013 Oct;19(2):150-6. doi: 10.1007/s12028-013-9850-1.
BACKGROUND AND PURPOSE: The use of iodinated contrast-enhanced imaging studies is increasing in acute cerebrovascular diseases, especially in subarachnoid hemorrhage (SAH). In SAH, such studies are essential for both diagnosis and treatment of the cause and sequela of hemorrhage. These patients are
PMID 23653268

Heterozygous disruption of renal outer medullary potassium channel in rats is associated with reduced blood pressure.

Zhou X1, Zhang Z, Shin MK, Horwitz SB, Levorse JM, Zhu L, Sharif-Rodriguez W, Streltsov DY, Dajee M, Hernandez M, Pan Y, Urosevic-Price O, Wang L, Forrest G, Szeto D, Zhu Y, Cui Y, Michael B, Balogh LA, Welling PA, Wade JB, Roy S, Sullivan KA.Author information 1Department of Cardiovascular Diseases, Merck Research Laboratories, 126 E Lincoln Ave, Rahway, NJ 07065, USA. xiaoyan_zhou@merck.comAbstractThe renal outer medullary potassium channel (ROMK, KCNJ1) mediates potassium recycling and facilitates sodium reabsorption through the Na(+)/K(+)/2Cl(-) cotransporter in the loop of Henle and potassium secretion at the cortical collecting duct. Human genetic studies indicate that ROMK homozygous loss-of-function mutations cause type II Bartter syndrome, featuring polyuria, renal salt wasting, and hypotension; humans heterozygous for ROMK mutations identified in the Framingham Heart Study have reduced blood pressure. ROMK null mice recapitulate many of the features of type II Bartter syndrome. We have generated an ROMK knockout rat model in Dahl salt-sensitive background by using zinc finger nuclease technology and investigated the effects of knocking out ROMK on systemic and renal hemodynamics and kidney histology in the Dahl salt-sensitive rats. The ROMK(-/-) pups recapitulated features identified in the ROMK null mice. The ROMK(+/-) rats, when challenged with a 4% salt diet, exhibited a reduced blood pressure compared with their ROMK(+/+) littermates. More importantly, when challenged with an 8% salt diet, the Dahl salt-sensitive rats with 50% less ROMK expression showed increased protection from salt-induced blood pressure elevation and signs of protection from renal injury. Our findings in ROMK knockout Dahl salt-sensitive rats, together with the previous reports in humans and mice, underscore a critical role of ROMK in blood pressure regulation.
Hypertension.Hypertension.2013 Aug;62(2):288-94. doi: 10.1161/HYPERTENSIONAHA.111.01051. Epub 2013 Jun 10.
The renal outer medullary potassium channel (ROMK, KCNJ1) mediates potassium recycling and facilitates sodium reabsorption through the Na(+)/K(+)/2Cl(-) cotransporter in the loop of Henle and potassium secretion at the cortical collecting duct. Human genetic studies indicate that ROMK homozygous los
PMID 23753405

Japanese Journal

造血幹細胞移植後に発症したHHV-6脳炎に対し foscarnet 投与後合併した塩類喪失性腎症

名島悠峰,大橋一輝,安藤稔 [他],越田晃,山下卓也,秋山秀樹,坂巻壽
臨床血液 = The Japanese Journal of Clinical Hematology 49(1), 40-45, 2008-01-30
NAID 10021256944

化学放射線療法を契機に抗利尿ホルモン不適切分泌症候群を発症した顆粒球コロニー刺激因子産生肺腺癌の1例

花岡淳,大内政嗣,井上修平,手塚則明,澤井聡,藤野昇三
肺癌 45(4), 357-362, 2005-08-20
背景.肺癌患者の治療経過中に低Na血症が出現することがあり, 稀ではあるが抗腫瘍薬投与により抗利尿ホルモン不適切分泌症候群(SIADH)が原因となることがある.症例.71歳男性.胸部異常陰影と顔面・上肢の浮腫で入院となった.胸部CTで右上葉の腫瘤影と縦隔リンパ節腫大を認め, 経気管支肺生検で低分化型肺腺癌の診断を得た.入院時より末梢血白血球数増多を認め, 血漿顆粒球コロニー刺激因子(G-CSF)高 …
NAID 110003143639