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  • ¿µ¹®
    ÇѱÛ
  • lymphocyte activating factor
    ¸²ÇÁ±¸È°¼ºÀÎÀÚ
  • lymphocyte inhibitory factor
    ¸²ÇÁ±¸¾ïÁ¦ÀÎÀÚ
  • lactogenic factor
    Á¥ÃËÁøÀÎÀÚ
  • lymphocytosis stimulating factor
    ¸²ÇÁ±¸Áõ°¡ÀÚ±ØÀÎÀÚ
  • migration inhibition factor
    À̵¿ÀúÁöÀÎÀÚ
  • mitogenic factor
    ºÐ¿­ÃËÁøÀÎÀÚ
  • myocardial depressant factor
    ½É(Àå)±Ù(À°)¾ïÁ¦ÀÎÀÚ
  • macrophage aggregating factor
    Å«Æ÷½Ä¼¼Æ÷ÀÀÁýÀÎÀÚ, ´ë½Ä¼¼Æ÷ÀÀÁýÀÎÀÚ
  • macrophage arming factor
    Å«Æ÷½Ä¼¼Æ÷¹«ÀåÀÎÀÚ, ´ë½Ä¼¼Æ÷¹«ÀåÀÎÀÚ
  • macrophage chemotactic factor
    Å«Æ÷½Ä¼¼Æ÷È­Çнò¸²ÀÎÀÚ, ´ë½Ä¼¼Æ÷È­Çнò¸²ÀÎÀÚ
  • macrophage colony-stimulating factor
    Å«Æ÷½Ä¼¼Æ÷Áý¶ôÀÚ±ØÀÎÀÚ, ´ë½Ä¼¼Æ÷Áý¶ôÀÚ±ØÀÎÀÚ
  • macrophage migration inhibitory factor
    Å«Æ÷½Ä¼¼Æ÷À̵¿ÀúÁöÀÎÀÚ, ´ë½Ä¼¼Æ÷À̵¿ÀúÁöÀÎÀÚ
  • macrophage-activating factor
    Å«Æ÷½Ä¼¼Æ÷Ȱ¼ºÀÎÀÚ, ´ë½Ä¼¼Æ÷Ȱ¼ºÀÎÀÚ
  • macrophage-derived growth factor
    Å«Æ÷½Ä¼¼Æ÷À¯·¡¼ºÀåÀÎÀÚ, ´ë½Ä¼¼Æ÷À¯·¡¼ºÀåÀÎÀÚ
  • nerve growth factor
    ½Å°æ¼ºÀåÀÎÀÚ
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  • ¿µ¹®
    ÇѱÛ
  • luteotrophic hormone inhibitory factor
    ȲüÀÚ±ØÈ£¸£¸ó¾ïÁ¦ÀÎÀÚ
  • lymphocyte activating factor
    ¸²ÇÁ±¸È°¼ºÀÎÀÚ
  • lymphocyte inhibitory factor
    ¸²ÇÁ±¸¾ïÁ¦ÀÎÀÚ
  • lymphocytosis stimulating factor
    ¸²ÇÁ±¸Áõ°¡ÀÚ±ØÀÎÀÚ
  • macrophage aggregating factor
    Å«Æ÷½Ä¼¼Æ÷ÀÀÁýÀÎÀÚ
  • macrophage arming factor
    Å«Æ÷½Ä¼¼Æ÷¹«ÀåÀÎÀÚ
  • macrophage chemotactic factor
    Å«Æ÷½Ä¼¼Æ÷È­ÇÐÁÖ¼ºÀÎÀÚ, Å«Æ÷½Ä¼¼Æ÷È­Çнò¸²ÀÎÀÚ
  • macrophage colony-stimulating factor
    Å«Æ÷½Ä¼¼Æ÷Áý¶ôÀÚ±ØÀÎÀÚ
  • macrophage migration inhibitory factor
    Å«Æ÷½Ä¼¼Æ÷À̵¿ÀúÁöÀÎÀÚ
  • macrophage-activating factor
    Å«Æ÷½Ä¼¼Æ÷Ȱ¼ºÀÎÀÚ
  • macrophage-derived growth factor
    Å«Æ÷½Ä¼¼Æ÷À¯·¡¼ºÀåÀÎÀÚ
  • migration inhibition factor
    Æ÷½Ä¼¼Æ÷À̵¿ÀúÇØÀÎÀÚ
  • mitogenic factor
    ºÐ¿­ÃËÁøÀÎÀÚ
  • myocardial depressant factor
    ½ÉÀå±Ù¾ïÁ¦ÀÎÀÚ
  • nerve growth factor
    ½Å°æ¼ºÀåÀÎÀÚ
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  • ¿µ¹®
    ÇѱÛ
  • 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×?
  • NGF=>nerve growth factor
    ½Å°æ¼ºÀåÀÎÀÚ
  • PAF =platelet activating factor
    Ç÷¼ÒÆÇȰ¼ºÀÎÀÚ.
  • PAF= platelet activating factor
    Ç÷¼ÒÆÇ Ȱ¼ºÀÎÀÚ.
  • Q factor
    Å¥ ÀÎÀÚ
  • Q-factor
    Å¥-ÀÎÀÚ (ì×í­)
  • R factor
    ³»¼ºÀÎÀÚ.
  • R factor
    ³»¼ºÀÎÀÚ.
  • Rh factor
    RhÀÎÀÚ.
  • Stuart-Prower factor
    ½ºÆ©¾îÆ®-ÇÁ¶ó¿ö ÀÎÀÚ
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  • ¿µ¹®
    ÇѱÛ
  • color vision deficiency
    »ö°¢ÀÌ»ó
  • combined immunity deficiency syndrome
    º¹Çո鿪°áÇÌÁõÈıº.
  • combined immunity deficiency synsdrome
    º¹Çո鿪°áÇÌÁõÈıº.
  • complement deficiency
    º¸Ã¼°áÇÌ
  • congenital deficiency of glucuronyl transfe ra se
    ¼±Ãµ¼º ±Û·çÄí·Ð»ê Àü À§È¿¼Ò°áÇÌÁõ(¡­ï®êÈý£áÈÌÀù¹ñø).
  • copper deficiency
    ±¸¸®°áÇÌÁõ(¡­ÌÀù¹ñø)
  • cytochrome C oxidase deficiency
    ½ÃƮũ·Ò C ¿Á½Ã´ÙÁ¦(»êÈ­È¿¼Ò)°áÇÌ
  • cytochrome b5 reductase deficiency
    ½ÃÅäÅ©·Ò b5 ȯ¿øÈ¿¼Ò °áÇÌ
  • cytogenetic deficiency
    ¼¼Æ÷¹ß»ý°áÇÌ
  • deficiency
    °áÇÌ(Áõ)(ÌÀù¹ñø)
  • deficiency
    °áÇÌ
  • deficiency (monstrous tumor)
    °áÇÌ (±«¹°Á¾)
  • deficiency (nanismus)
    °áÇÌ(³­ÀåÀÌÁõ)
  • deficiency state, complement
    º¸Ã¼°áÇÌÁõ
  • diabetes mellitus,insulin deficiency
    Àν¶¸° °áÇÌÁõ(¡­ÌÀù¹ñø)
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  • ¿µ¹®
    ÇѱÛ
  • leukocyte inhibitory factor
    ¹éÇ÷±¸ÀúÇØÀÎÀÚ(ÛÜúìϹîÁúªì×í­)
  • Lewis factor
    ·çÀ̽ºÀÎÀÚ(ì×í­)
  • lipoprotein tissue factor
    ÁöÁú´Ü¹éÁú(ò·òõÓ±ÛÜòõ) Á¶Á÷ÀÎÀÚ(ðÚòÄì×í­)
  • liver filtrate factor
    °£ ¿©°ú ÀÎÀÚ(ÊÜÕëΦì×í­)
  • LLD factor
    LLD ÀÎÀÚ(ì×í­)
  • L-L factor
    "L-L ÀÎÀÚ(ì×í­), (å²) Laki-Lorand ÀÎÀÚ(ì×í­)"
  • lymph node permeability factor
    ¸²ÇÁÀý(ï½)Åõ°úÀÎÀÚ(÷âΦì×í­)
  • lymphocyte-derived chemotactic factor
    ¸²ÇÁ±¸-À¯µµ(ë¯Óô) È­ÇÐÁÖ¼ºÀÎÀÚ(ûùùÊñËà÷ì×í­)
  • macrophage activation factor
    ´ë½Ä¼¼Æ÷Ȱ¼ºÀÎÀÚ(ÓÞãÝá¬øàüÀàõì×í­)
  • macrophage inhibition factor
    ´ë½Ä¼¼Æ÷ÀúÇØÀÎÀÚ(ÓÞãÝá¬øàîÁúªì×í­)
  • maize factor
    ¿Á¼ö¼ö ÀÎÀÚ(ì×í­)
  • maturation factor
    ¼º¼÷ÀÎÀÚ(à÷âÙì×í­)
  • migration enhancement factor
    À̵¿Ç×Áø ÀÎÀÚ(ì¹ÔÑùñòäì×í­)
  • migration inhibition factor
    À̵¿ÀúÇØ ÀÎÀÚ(ì¹ÔÑîÁúªì×í­)
  • mitogenic factor
    ºÐ¿­ÃËÁøÀÎÀÚ(ÝÂÖ®õµòäì×í­)
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ANF alpha-naphthoflavone; American Nurses' Foundation; antineuritic factor; antinuclear factor; atrial n...
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...
KMLE ÀÚµ¿ÃßÃâ ÀÇÇоà¾î »çÀü À¯»ç °Ë»ö °á°ú : 5 ÆäÀÌÁö: 9
CVID Common Variable Immuno-Deficiency
EFAD Essential fatty acid deficiency
GH-D GH deficiency
G6PD Glucose-6-Phosphate dehydrogenase deficiency
GKD Glycerol kinase deficiency
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  • ¿µ¹®
    ÇѱÛ
    ¼³¸í
  • cooperative factor
    Çùµ¿ ÀÎÀÚ
  • coronary risk factor
    °ü»ó µ¿¸Æ Áúȯ À§Çè ¿äÀÎ
  • cothromboplastin factor VII
    ÄÚÆ®·Ò º¸ÇÃ¶ó½ºÆ¾
  • coupling factor
    ¹è¿ì ÀÎÀÚ
  • covering factor
    ÇǺ¹ ÀÎÀÚ
  • cultural and ethnic factor
    ¹®È­ ¹ÎÁ·Àû ¿äÀÎ
  • cytotoxic factor
    ¼¼Æ÷ µ¶¼º ÀÎÀÚ
  • D and C ÀÚ±ÃÀÇ °æºÎ È®Àå°ú ³»¸· ¼ÒÆÄ.

    D factor

    D-ÀÎÀÚ
  • Decay accelerating factor
    ºØ±« °¡¼Ó ¿ä¼Ò
  • diabetogenic factor
    ´ç´¢ À¯¹ß ÀÎÀÚ
  • differentiation factor
    °¨º° ¿äÀÎ, °¨º° ¿ä¼Ò, °¨º° ÀÎÀÚ
  • diffusion factor
    È®»ê ÀÎÀÚ
  • dilution factor
    Èñ¼® ÀÎÀÚ
  • dose modifying factor
    ¼±·® ¼ö½Ä °è¼ö
  • drug resistance factor
    ¾àÁ¦ ³»¼º ÀÎÀÚ
CancerWEB ¿µ¿µ ÀÇÇлçÀü À¯»ç °Ë»ö °á°ú : 15 ÆäÀÌÁö: 9
polyendocrine deficiency syndrome <syndrome> Polyglandular deficiency syndrome, associated pathologic dysfunction of several endocrine glands, as in Schmidt's syndrome.
(05 Mar 2000)
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)
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