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  • ¿µ¹®
    ÇѱÛ
  • factor XIII
    Á¦13ÀÎÀÚ
  • granulocyte colony-stimulating factor
    °ú¸³±¸Áý¶ôÀÚ±ØÀÎÀÚ
  • granulocyte-macrophage colony-stimulating factor
    °ú¸³±¸Å«Æ÷½Ä¼¼Æ÷Áý¶ôÀÚ±ØÀÎÀÚ, °ú¸³±¸´ë½Ä±¸Áý¶ôÀÚ±ØÀÎÀÚ
  • growth factor
    ¼ºÀåÀÎÀÚ
  • hyperglycemic-glycogenolytic factor
    °íÇ÷´ç±Û¸®ÄÚ°ÕºÐÇØÀÎÀÚ
  • hematopoietic growth factor
    Ç÷¾×Çü¼º¼ºÀåÀÎÀÚ, Á¶Ç÷¼ºÀåÀÎÀÚ
  • histamine sensitizing factor
    È÷½ºÅ¸¹Î¹Î°¨ÀÎÀÚ
  • host integration factor
    ¼÷ÁÖÅëÇÕÀÎÀÚ
  • human antihemophilic factor
    »ç¶÷Ç×Ç÷¿ìº´ÀÎÀÚ
  • intrinsic factor
    ³»ÀÎÀÎÀÚ, ³»ÀÎÀÚ
  • initiation factor
    ½ÃÀÛÀÎÀÚ
  • insulin-like growth factor
    Àν¶¸°À¯»ç¼ºÀåÀÎÀÚ
  • ketogenic factor
    ÄÉÅæ»ý¼ºÀÎÀÚ
  • labile factor
    1. ºÒ¾ÈÁ¤ÀÎÀÚ 2. ºÒ¾ÈÁ¤¿ä¼Ò
  • leukocyte inhibitory factor
    ¹éÇ÷±¸¾ïÁ¦ÀÎÀÚ
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  • ¿µ¹®
    ÇѱÛ
  • fertility factor
    ¼öÅÂÀÎÀÚ
  • fibrin stabilizing factor
    ¼¶À¯¼Ò¾ÈÁ¤ÀÎÀÚ
  • fibroblast growth factor
    ¼¶À¯¸ð¼¼Æ÷¼ºÀåÀÎÀÚ
  • granulocyte colony-stimulating factor
    °ú¸³±¸Áý¶ôÀÚ±ØÀÎÀÚ
  • granulocyte-macrophage colony-stimulating factor
    °ú¸³±¸Å«Æ÷½Ä¼¼Æ÷Áý¶ôÀÚ±ØÀÎÀÚ
  • growth factor
    ¼ºÀåÀÎÀÚ
  • hematopoietic growth factor
    Ç÷¾×Çü¼º¼ºÀåÀÎÀÚ, Á¶Ç÷¼ºÀåÀÎÀÚ
  • histamine sensitizing factor
    È÷½ºÅ¸¹Î¹Î°¨ÀÎÀÚ
  • host integration factor
    ¼÷ÁÖÅëÇÕÀÎÀÚ
  • hyperglycemic-glycogenolytic factor
    °íÇ÷´ç±Û¸®ÄÚ°ÕºÐÇØÀÎÀÚ
  • insulin-like growth factor
    Àν¶¸°À¯»ç¼ºÀåÀÎÀÚ
  • intrinsic factor
    ³»ÀÎÀÎÀÚ, ³»ÀÎÀÚ
  • ketogenic factor
    ÄÉÅæÇü¼ºÀÎÀÚ
  • labile factor
    ºÒ¾ÈÁ¤ÀÎÀÚ, ºÒ¾ÈÁ¤¿ä¼Ò
  • lactogenic factor
    Á¥ÃËÁøÀÎÀÚ
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  • ¿µ¹®
    ÇѱÛ
  • Factor VIII
    VIII ÀÀ°íÀÎÀÚ(ëêͳì×í­)
  • Factor X activated
    Ȱ¼ºÈ­(üÀàõûù)µÈ X ÀÀ°íÀÎÀÚ(ëêͳì×í­)
  • Factor XI
    XI ÀÀ°íÀÎÀÚ(ëêͳì×í­)
  • Factor XII
    XII ÀÀ°íÀÎÀÚ(ëêͳì×í­)
  • Fibrin-stabilizing factor
    ¼¶À¯¼Ò¾ÈÁ¤ÀÎÀÚ(¡­äÌïÒì×í­)
  • Fibroblast growth factor
    ¼¶À¯¸ð¼¼Æ÷(àéë«Ù½á¬øà)¼ºÀå¿äÀÎ(à÷íþé©ì×)
  • G-CSF (Granulocyte colony-stimulating factor)
    °ú¸³¼¼Æ÷±ºÃËÁøÀÎÀÚ(Î¨Ø£á¬øàÏØõµòäì×í­)
  • GH releasing factor
    ¼ºÀå(à÷íþ)È£¸£¸ó À¯¸®ÀÎÀÚ(ë´×îì×í­).
  • GH releasing factor
    ¼ºÀåÈ£¸£¸óÀ¯¸®ÀÎÀÚ.
  • Growth factor
    ¼ºÀåÀÎÀÚ(à÷íþì×í­)
  • Hageman factor
    ÇϰԸ¸ÀÎÀÚ
  • Hydrostatic factor
    Á¤¼öÀÎÀÚ(ð¡â©ì×í­)
  • IGF-I(insulin-like growth factor-I)
    Àν¶¸° À¯»ç ¼ºÀåÀÎÀÚ-1
  • Luteinization -inhibiting factor
    Ȳüȭ¾ïÁ¦¿äÀÎ(üÜô÷ûùåäð¤é©ì×)
  • Macrophage colony-stimulating factor
    ´ë½Ä¼¼Æ÷Áý¶ôÇü¼ºÃËÁøÀÎÀÚ(ÓÞãÝá¬øàó¢Õªû¡à÷õµòäì×í­)à÷õµòäì×?
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  • ¿µ¹®
    ÇѱÛ
  • dietary deficiency
    ½ÄÀ̼º ¿µ¾ç°áÇÌ(ãÝìÈàõç½å×ÌÀù¹).
  • diphosphatase deficiency
    µðÆ÷½ºÆÄŸÁ¦°áÇÌ(Áõ)
  • disaccaridase deficiency
    ÀÌ´çºÐÇØÈ¿¼Ò°áÇÌ(ì£ÓØÝÂú°ý£áÈÌÀù¹)
  • disaccharidase deficiency
    ÀÌ´ç·ùºÐÇØÈ¿¼Ò°áÇÌÁõ
  • disaccharide deficiency
    ÀÌź´ç°áÇÌ
  • dissacharidase deficiency syndrome
    ÀÌ´ç·ùºÐÇØÈ¿¼Ò °áÇÌÁõÈıº(¡­ÌÀù¹ñøý¦ÏØ ).
  • electrolyte deficiency syndrome
    ÀüÇØÁú °áÇÌÁõÈıº(ï³ú°òõÌÀù¹ñøý¦ÏØ).
  • enzyme deficiency
    È¿¼Ò°áÇÌ(Áõ)
  • erythrocyte enzyme deficiency
    ÀûÇ÷±¸È¿¼Ò°áÇÌÁõ
  • erythropoietin deficiency anemia
    ¿¡¸®Æ®·ÎÆ÷¿¡Æ¾ °áÇ̼º ºóÇ÷, ÀûÇ÷
  • familial apolipoprotein CII deficiency
    °¡Á·¼º ¾ÆÆ÷Áö¹æ´Ü¹é CII °áÇÌÁõ
  • fat deficiency disease
    Áö¹æ°áÇÌÁõ.
  • folate deficiency
    ¿±»ê°áÇÌ(ç¨ß«ÌÀù¹)
  • folic acid deficiency
    ¿±»ê°áÇÌÁõ.
  • folic acid deficiency
    ¿±»ê°áÇÌ(ç¨ß«ÌÀù¹)
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  • ¿µ¹®
    ÇѱÛ
  • factor ¥°
    ÀÎÀÚ(ì×í­) I
  • factor ¥±
    ÀÎÀÚ(ì×í­) II
  • factor ¥²
    ÀÎÀÚ(ì×í­) III
  • factor ¥³
    ÀÎÀÚ(ì×í­) IV
  • factor ¥´
    ÀÎÀÚ(ì×í­) V
  • factor ¥¶
    ÀÎÀÚ(ì×í­) VII
  • factor ¥·
    ÀÎÀÚ(ì×í­) VIII
  • factor ¥¸
    ÀÎÀÚ(ì×í­) IX
  • factor ¥¹
    ÀÎÀÚ(ì×í­) X
  • factor XI
    ÀÎÀÚ(ì×í­) XI
  • factor XII
    ÀÎÀÚ(ì×í­) XII
  • factor XIII
    ÀÎÀÚ(ì×í­) XIII
  • factor XIV
    ÀÎÀÚ(ì×í­) XIV
  • factor F
    ÀÎÀÚ(ì×í­) F
  • factor G
    ÀÎÀÚ(ì×í­) G
KMLE ÀÇÇоà¾î »çÀü À¯»ç °Ë»ö °á°ú : 5 ÆäÀÌÁö: 6
APF acidulated phosphofluoride; American Psychological Foundation; anabolism-promoting factor; animal pr...
EPF early pregnancy factor; endocarditis parietalis fibroplastica; endothelial proliferating factor; est...
HF Hageman factor; haplotype frequency; hard filled [capsule]; hay fever; head of fetus; head forward; ...
IF idiopathic fibroplasia; idiopathic flushing; immersion foot; immunofluorescence; indirect fluorescen...
KAF conglutinogen-activating factor; killer-assisting factor; kinase activating factor
KMLE ÀÚµ¿ÃßÃâ ÀÇÇоà¾î »çÀü À¯»ç °Ë»ö °á°ú : 5 ÆäÀÌÁö: 6
LPD Luteal phase deficiency
MPHD Multiple Pituitary Hormone Deficiency
MSD Multiple Sulfatase Deficiency
MAIDS Murine acquired immune deficiency syndrome
NOD/SCID Nonobese diabetic/severe combined immune deficiency
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  • ¿µ¹®
    ÇѱÛ
    ¼³¸í
  • cavity-gas calibration factor
    °­-±âü ±³Á¤ °è¼ö
  • certainty factor
    È®½Ç ¿äÀÎ
  • chamber calibration factor
    Àü¸®ÇÔ ÃøÁ¤ °è¼ö, »óÀÚ ÃøÁ¤ °è¼ö
  • circumstance factor
    »óȲ ÀÎÀÚ
  • clotting factor
    ÀÀÇ÷ ÀÎÀÚ, ÀÀ°í ÀÎÀÚ
  • clumping factor
    ÀÀ±« ÀÎÀÚ
  • coagulase-reacting factor
    Ç÷Àå ÀÀ°í È¿¼Ò ¹ÝÀÀ ÀÎÀÚ
  • coagulation factor
    ÀÀÇ÷ ÀÎÀÚ, ÀÀ°í ÀÎÀÚ
  • coagulation factor inhibitor
    ÀÀ°í ÀÎÀÚ ¾ïÁ¦Á¦
  • colicin factor
    Äݸ®½Å ÀÎÀÚ
  • colony stimulating factor
    ±ºÃ¼ ÀÚ±Ø ¿ä¼Ò, Áý¶ô ÀÚ±Ø ÀÎÀÚ
    ¹ß´Þ ´Ü°èÀÇ Àü±¸Àû ¼¼Æ÷°¡ Áý¶ôÀ» Çü¼ºÇÏ´Â °úÁ¤¿¡´Â À̰ÍÀÇ ÀÛ¿ëÀÌ ÇÊ¿äÇÏ´Ù´Â °ÍÀÌ ÀνĵǾú´Ù. ÀÌ ÀÎÀÚ´Â ¼¶À¯¾Æ¼¼Æ÷, ³»ÇǼ¼Æ÷, ´ë½Ä¼¼Æ÷ µî¿¡¼­ »ý»êµÇ¸ç ¼º¼÷ÇÑ ¸é¿ª°è ¼¼Æ÷ÀÇ ÀÛ¿ë¿¡µµ ¿µÇâÀ» ³¢Ä£´Ù.
  • competence inducing factor
    Àû°Ý À¯¹ß ÀÎÀÚ
  • complementary factor
    º¸Ãæ ÀÎÀÚ
  • complicating factor
    º¹ÇÕ ¿äÀÎ
  • constitutional factor
    ±¸¼º ¿ä¼Ò, üÁú ¿äÀÎ
CancerWEB ¿µ¿µ ÀÇÇлçÀü À¯»ç °Ë»ö °á°ú : 15 ÆäÀÌÁö: 6
myophosphorylase deficiency glycogenosis Glycogenosis due to muscle glycogen phosphorylase deficiency, resulting in accumulation of glycogen of normal chemical structure in muscle.
Synonym: McArdle's disease, McArdle's syndrome, McArdle-Schmid-Pearson disease, myophosphorylase deficiency glycogenosis.
(05 Mar 2000)
potassium deficiency A condition due to decreased dietary intake of potassium, as in starvation or failure to administer in intravenous solutions, or to gastrointestinal loss in diarrhoea, chronic laxative abuse, vomiting, gastric suction, or bowel diversion. Severe potassium deficiency may produce muscular weakness and lead to paralysis and respiratory failure. Muscular malfunction may result in hypoventilation, paralytic ileus, hypotension, muscle twitches, tetany, and rhabomyolysis. Nephropathy from potassium deficit impairs the concentrating mechanism, producing polyuria and decreased maximal urinary concentrating ability with secondary polydipsia. (merck manual, 16th ed)
(12 Dec 1998)
hepatophosphorylase deficiency glycogenosis Glycogenosis due to hepatic glycogen phosphorylase deficiency, resulting in accumulation of glycogen of normal chemical structure in liver and leukocytes.
Synonym: hepatophosphorylase deficiency glycogenosis, Hers' disease.
(05 Mar 2000)
protein c deficiency Protein C is a protein in plasma that enters into the cascade of biochemical events leading to the formation of a clot. Deficiency of protein c results in thrombotic (clotting) disease and excess platelets with recurrent thrombophlebitis (inflammation of the vein that occurs when a clot forms). The clot can break loose and travel through the blood stream (thromboembolism) to the lungs causing a pulmonary embolism, brain causing a stroke (cerebrovascular accident), heart causing an early heart attack, skin causing what in the newborn is called neonatal purpura fulminans, the adrenal gland causing haemorrhage with abdominal pain, abnormally low blood pressure (hypotension), and salt loss. Protein c deficiency is due to possession of one gene (heterozygosity) in chromosome band 2q13-14. The possession of two such genes (homozygosity) is usually lethal.
(12 Dec 1998)
protein deficiency A nutritional condition produced by a deficiency of proteins in the diet, characterised by adaptive enzyme changes in the liver, increase in amino acid synthetases, and diminution of urea formation, thus conserving nitrogen and reducing its loss in the urine. Growth, immune response, repair, and production of enzymes and hormones are all impaired in severe protein deficiency. Protein deficiency may also arise in the face of adequate protein intake if the protein is of poor quality (i.e., the content of one or more amino acids is inadequate and thus becomes the limiting factor in protein utilization).
(12 Dec 1998)
protein s deficiency An autosomal dominant disorder showing decreased levels of plasma protein s antigen or activity, associated with venous thrombosis and pulmonary embolism. Protein s is a vitamin k-dependent plasma protein that inhibits blood clotting by serving as a cofactor for activated protein c (also a vitamin k-dependent protein), and the clinical manifestations of its deficiency are virtually identical to those of protein c deficiency. Treatment with heparin for acute thrombotic processes is usually followed by maintenance administration of coumarin drugs for the prevention of recurrent thrombosis.
(12 Dec 1998)
prothrombin deficiency A congenital or acquired disorder of blood clotting where there is a deficiency of factor II (prothrombin), one of 20 necessary plasma proteins for normal blood coagulation. Acquired factor II deficiency may result from vitamin K deficiency, severe liver disease and anticoagulant drugs.
Symptoms include abnormal bleeding, nosebleeds, abnormal menstrual bleeding, easy bruising and umbilical cord bleeding at birth. Treatment involves the infusion of fresh frozen plasma. Vitamin K may be administered in select cases.
(27 Sep 1997)
proximal femoral focal deficiency A congenital defect in which variable portions of the upper end of the femur are reduced or absent.
(05 Mar 2000)
pseudocholinesterase deficiency An autosomal dominant disorder manifested by exaggerated responses to drugs ordinarily hydrolyzed by serum pseudocholinesterase (e.g., succinylcholine); believed to entail production of a variant enzyme that is less active than the normal enzyme in hydrolyzing appropriate substrates, but also abnormally resistant to the effects of anticholinesterases.
(05 Mar 2000)
secondary antibody deficiency Immunodeficiency in which there is no evident defect in the lymphoid tissues, but rather hypercatabolism or loss of immunoglobulins such as occurs in familial idiopathic hypercatabolic hypoproteinaemia or in defects associated with the nephrotic syndrome.
Synonym: secondary agammaglobulinaemia, secondary antibody deficiency, secondary hypogammaglobulinaemia.
(05 Mar 2000)
selective immunoglobulin A deficiency <immunology> An inherited disorder in which there is a markedly reduced or absent IgA, resulting in immature IgA-bearing B-cells.
(05 Mar 2000)
selenium deficiency deficiency of the essential mineral selenium causes keshan disease, a fatal form of cardiomyopathy (disease of the heart muscle) first observed in keshan province in china and since found elsewhere. According to the national academy of sciences, the recommended dietary allowances of selenium are 70 milligrams per day for men and 55 milligrams per day for women. Food sources of selenium include seafoods, some meats such as kidney and liver, and some grains and seeds
(12 Dec 1998)
pyridoxine deficiency A nutritional condition produced by a deficiency of pyridoxine in the diet, characterised by dermatitis, glossitis, cheilosis, and stomatitis. Marked deficiency causes irritability, weakness, depression, dizziness, peripheral neuropathy, and seizures. In infants and children typical manifestations are diarrhoea, anaemia, and seizures. Increasingly recognised as a cause is prolonged therapy with certain medications, among them isoniazid, cycloserine, and l-dopa.
(12 Dec 1998)
pyruvate carboxylase deficiency An autosomal recessive pyruvate metabolism disorder resulting from absent or deficient expression of pyruvate carboxylase activity. Decreased production of oxaloacetate leads to decreased gluconeogenesis, thereby causing fasting hypoglycaemia, lactic acid acidosis, and decreased synthesis of amino acid neurotransmitters. Clinical presentations include acidosis, ataxia, mental retardation; sometimes co-occurs with leigh disease.
(12 Dec 1998)
pyruvate dehydrogenase complex deficiency An autosomal recessive pyruvate metabolism disorder resulting from deficient enzyme activity in one of several proteins of pyruvate dehydrogenase complex, resulting in deficiency of acetyl CoA. Deficiency in acetyl CoA product reduces the synthesis of acetylcholine, thereby causing neurological abnormalities. Clinical presentations include lactic acidosis, mental retardation, and ataxia.
(12 Dec 1998)
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