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Pathology

Arginase deficiency typically refers to decreased function of arginase I, the liver isoform of arginase. This deficiency is commonly referred to as hyperargininemia or arginemia. The disorder is hereditary and autosomal recessive. It is characterized by lowered activity of arginase in hepatic cells. Additionally, the disorder is considered to be the rarest of the heritable defects in ureagenesis. Unlike other urea cycle disorders, ureagenesis still persists in subjects with arginase deficiency. A proposed reason for the continuation of arginase function is suggested by increased activity of arginase II in the kidneys of subjects with arginase I deficiency. Researchers believe that buildup of arginine triggers increased expression of arginase II. The enzymes in the kidney will then catalyze ureagenesis, compensating somewhat for a decrease in arginase I activity in the liver. Due to this alternate method of removing excess arginine and ammonia from the bloodstream, subjects with arginase deficiency tend to have longer lifespans than those who have other urea cycle defects.[8]

Symptoms of the disorder include neurological impairment, dementia, retardation of growth, and hyperammonemia. While some symptoms of the disease can be controlled via dietary restrictions and pharmaceutical developments, no cure or completely effective therapy currently exists.

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3 個解答

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  • 1 0 年前
    最佳解答

    臨床發現

    精氨酸酶缺乏症大多是因為精胺酸酶I的機能減失所造成。精胺酸酶I是肺部的精胺酸酶isoform(同樣蛋白質所組成的不同物質,按文義不一定在肺部)。這種缺乏症大多被稱為hyperargininemia或 arginemia。此種失調是由於遺傳因素和體染色體衰退所致。肝細胞內的精胺酸脢活動力降低為其主要特徵。 此外,這種失調症被認定為最罕見的遺傳性尿素分泌缺陷。不像其他尿素循環失調,尿素分泌在精胺酸缺乏患者體內仍能運作。一種解釋是,精氨酸酶的(尿素分泌)功能被"精胺酸酶I缺乏症患者"腎臟內"活動增加的精氨酸酶II"所引發。 研究者相信精胺酸的增進引發了精胺酸脢II的分泌。那些在腎臟內的酵素之後用做催化尿素循環, 多少補償了肺部精胺酸酶I活性的不足。由於這個去除血流中過多精胺酸脢和氨的的替代基制, 精胺酸脢缺乏患者比起有其他尿素循環缺陷患者有更長的壽命。

    失調的症狀包括神經性損傷, 失智症, 發育遲緩, 和hyperammonemia(氨過多,應該是尿毒症). 然而某些這種疾病的症狀可以藉由飲食限制和藥物來控制現在還沒有完全治療的療法.

    (括弧是我下的註解,翻這種文章是種挑戰,維基是就是轉機)

    2010-04-10 17:37:40 補充:

    研究者相信的"精胺酸"增進引發了精胺酸脢II的分泌

    把"精胺酸"改成"α-胺基酸"

    "由於這個去除血流中過多精胺酸脢和氨的的替代基制", 精胺酸脢缺乏患者比起有其他尿素循環缺陷患者有更長的壽命。

    改成

    由於此替代機制去除血流中過多α-胺基酸和氨,精胺酸脢缺乏患者比起有其他尿素循環缺陷患者有更長的壽命。

    沒有什麼大錯誤,應該不會再改。

    2010-04-10 17:39:55 補充:

    啊! 裡面所有的"脢"都改成酶

    2010-04-10 17:52:54 補充:

    按文章所說精胺酸酶出現在肝、肺、腎,身體到處都是蛋白質,精氨酸酶分散在身體各部也是合理的吧?只是還有一型二型,肺有一型,腎有二型。想到你的另一篇性功能障礙,看來一型二型也是遍及全身啊! 不過二型過多會造成陽痿,但是精氨酸缺乏症患者還會在乎陽痿嗎?不懂

    基本上尿素循環有問題就要洗腎了吧? 還有力氣亂搞?

    2010-04-10 18:04:18 補充:

    把增進"引發"的引發給去掉,精氨酸酶ii一般人體內也有。

    2010-04-10 18:19:02 補充:

    aginase是精胺酸酶 aginine是阿法鍵氨基酸 是代謝廢物

    精氨酸酶專門消化aginine

    但是精胺酸酶太多會把L-aginine這種產生nitron oxide synthase必要的基質都吃了

    所以男的無法勃起 女的沒有性欲

    抱歉,精胺酸酶怎麼搶NO synthase 我不會翻。你另一篇的coexpress翻成共同製造或分泌會比較對

  • 匿名使用者
    1 0 年前

    Pathology

    Arginase deficiency typically refers to decreased function of arginase I, the liver isoform of arginase.

    This deficiency is commonly referred to as hyperargininemia or arginemia.

    The disorder is hereditary and autosomal recessive.

    It is characterized by lowered activity of arginase in hepatic cells.

    Additionally, the disorder is considered to be the rarest of the heritable defects in ureagenesis.

    Unlike other urea cycle disorders, ureagenesis still persists in subjects with arginase deficiency.

    A proposed reason for the continuation of arginase function is suggested by increased activity of arginase II in the kidneys of subjects with arginase I deficiency.

    Researchers believe that buildup of arginine triggers increased expression of arginase II.

    The enzymes in the kidney will then catalyze ureagenesis, compensating somewhat for a decrease in arginase I activity in the liver.

    Due to this alternate method of removing excess arginine and ammonia from the bloodstream, subjects with arginase deficiency tend to have longer lifespans than those who have other urea cycle defects.[8]

    Symptoms of the disorder include neurological impairment, dementia, retardation of growth, and hyperammonemia.

    While some symptoms of the disease can be controlled via dietary restrictions and pharmaceutical developments, no cure or completely effective therapy currently exists.

    病理

    精氨酸酶缺乏症通常是指功能下降的精氨酸我,肝臟亞型的精氨酸酶。

    這種缺陷通常被稱為 hyperargininemia或arginemia。

    這種疾病是常染色體隱性遺傳和。

    它的特點是精氨酸酶的活性降低肝細胞。

    此外,這種疾病被認為是最稀有的遺傳缺陷ureagenesis。

    不像其他的尿素循環障礙,ureagenesis仍然堅持學科與精氨酸酶缺乏症。

    擬議的理由繼續對精氨酸酶的功能,建議通過增加活性精氨酸酶II在腎臟科與精氨酸我的不足。

    研究人員認為,建設引發的精氨酸精氨酸酶表達增加二。

    在腎臟的酶會催化ureagenesis,補償有所下降,精氨酸酶的活性在我的肝臟。

    由於這種替代方法去除多餘的精氨酸及氨從血液中,研究對象與精氨酸酶缺乏症往往有較長的壽命比那些誰還有其他尿素循環障礙。[8]

    這種疾病的症狀包括神經系統受損,癡呆,遲緩的增長,高血氨症。

    雖然某些症狀的疾病,可通過控制飲食和醫藥的發展限制,無法治愈或完全有效的治療目前存在。

    希望這樣的回答能幫助到你!!!

    參考資料: 我的無名((留個腳印吧))http://www.wretch.cc/blog/aa45214zz
  • 1 0 年前

    病理

    精氨酸酶缺乏症通常是指功能下降的精氨酸我,肝臟亞型的精氨酸酶。這種缺陷通常被稱為 hyperargininemia或arginemia。這種疾病是常染色體隱性遺傳和。它的特點是精氨酸酶的活性降低肝細胞。此外,這種疾病被認為是最稀有的遺傳缺陷ureagenesis。不像其他的尿素循環障礙,ureagenesis仍然堅持學科與精氨酸酶缺乏症。擬議的理由繼續對精氨酸酶的功能,建議通過增加活性精氨酸酶II在腎臟科與精氨酸我的不足。研究人員認為,建設引發的精氨酸精氨酸酶表達增加二。在腎臟的酶會催化ureagenesis,補償有所下降,精氨酸酶的活性在我的肝臟。由於這種替代方法去除多餘的精氨酸及氨從血液中,研究對象與精氨酸酶缺乏症往往有較長的壽命比那些誰還有其他尿素循環障礙。[8]

    這種疾病的症狀包括神經系統受損,癡呆,遲緩的增長,高血氨症。雖然某些症狀的疾病,可通過控制飲食和醫藥的發展限制,無法治愈或完全有效的治療目前存在。

    哈哈哈哈哈哈

    2010-04-10 14:56:03 補充:

    厲害吧

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