編號	英文名稱	中文名稱
JL-FA-01	Amebiasis (AME)	阿米巴病
JL-FA-02	Allergens, Rast scores	過敏原，放射性過敏原吸收實驗。指對特定的人群引起免疫反應或者過敏反應的食品中的蛋白質(zhì)
JL-FA-03	Allergens, Rast scores negative	過敏原，放射性過敏原吸收實驗陰性
JL-FA-04	Anti-cyclic citrullinated peptide Antibody (CCP) Arthritis	抗環(huán)瓜氨酸肽抗體
JL-FA-05	ASCA Saccharomyces Cerevi	人抗釀酒酵母抗體（ASCA）
JL-FA-06	Aspergillis	麴菌病
JL-FA-07	Beta 2 Glycoprotein	β2糖蛋白
JL-FA-08	Beta 2 Glycoprotein IgM	β2糖蛋白 IGM
JL-FA-09	Bordela Pertussis	百日咳桿菌
JL-FA-10	Bordela Pertussis IgM	百日咳桿菌 IGM
JL-FA-11	C-ANCA	C-抗中性粒細胞胞漿抗體（ANCA)
JL-FA-12	Cardiolipin	心肌磷脂
JL-FA-13	Cardiolipin IgA	心肌磷脂 IGA
JL-FA-14	Cardiolipin IgG	心肌磷脂 IGG
JL-FA-15	Cardiolipin IgM	心肌磷脂 IGM
JL-FA-16	Cerebral Spinal Fluid	腦脊髓液
JL-FA-17	Chagas	恰加斯病/南美錐蟲
JL-FA-18	Chlamydia	衣原體
JL-FA-19	Chlamydia IgA	衣原體IGA
JL-FA-20	Chlamydia IgG	衣原體IGG
JL-FA-21	Chlamydia IgM	衣原體IGM
JL-FA-22	Chlamydia Neg	衣原體陰性
JL-FA-23	Clotting Factor C3	凝固因子C3
JL-FA-24	Clotting Factor C4	凝固因子C4
JL-FA-25	Coccidiodes	球孢菌
JL-FA-26	Cytomegalovirus (CMV) Neg	巨細胞病毒抗體陰性
JL-FA-27	CMV IgG	巨細胞病毒 IGG陽性
JL-FA-28	CMV IgM VCA	巨細胞病毒 IGM 陽性
JL-FA-29	C-Reactive Protein (CRP)	C-反應蛋白質(zhì)
JL-FA-30	Dengue Fever	登革熱
JL-FA-31	Dengue Fever IgM	登革熱 IGM
JL-FA-32	DS (Double Stranded) DNA	雙鏈脫氧核糖核酸
JL-FA-33	EBNA (Epstein-Barr nuclear antigen) IgG	EB病毒核抗原 IGG
JL-FA-34	EBNA (Epstein-Barr nuclear antigen) IgM	EB病毒核抗原 IGM
JL-FA-35	Epstein Barr Virus (EBV) Negative Plasma	EB病毒陰性血漿
JL-FA-36	Epstein Barr Virus (EBV) EA IgM	EB病毒早期抗原 IGM
JL-FA-37	Epstein Barr Virus (EBV) VCA IgM	EB病毒殼蛋白 IGM
JL-FA-38	Epstein Barr Virus (EBV) EA IgG	EB病毒早期抗原 IGG
JL-FA-39	EMA (Endomysial Antibodies)	肌內(nèi)膜
JL-FA-40	Gliadin	麩蛋白,麥醇溶蛋白,麥膠蛋白
JL-FA-41	Gliadin IgG	麥醇溶蛋白 IGG
JL-FA-42	Gliadin IgA	麥醇溶蛋白 IGA
JL-FA-43	Glomerular Basement Membrane (GBMA)	腎小球基底膜病
JL-FA-44	Helicobacter pylori IgA	幽門螺旋桿菌IGA
JL-FA-45	Helicobacter pylori IgG	幽門螺旋桿菌IGG
JL-FA-46	Helicobacter pylori IgM	幽門螺旋桿菌IGM
JL-FA-47	Helicobacter pylori Negative	幽門螺旋桿菌陰性
JL-FA-48	Helicobacter pylori Positive Plasma	幽門螺旋桿菌陰性血漿
JL-FA-49	Hepatitis A Virus (HAV) Pos. Plasma	甲型肝炎病毒陽性血漿
JL-FA-50	Hepatitis A Virus (HAV) IgM	甲型肝炎病毒IGM
JL-FA-51	Hepatitis B Core (HBc) IgG	乙型肝炎病毒核心 IGG
JL-FA-52	Hepatitis B Core (HBc) IgM	乙型肝炎病毒核心 IGM
JL-FA-53	Anti Hbe (Antibody to HBV antigen)	乙肝抗體
JL-FA-54	Hepatitis Delta Virus	丁型肝炎病毒
JL-FA-55	HBeAg (HBV e antigen)	乙肝 E抗原
JL-FA-56	anti-HBs (HBV surface antibody)	乙肝表面抗體
JL-FA-57	Hepatitis B (HBsAg) "Chronic"	乙型肝炎（乙肝表面抗原）“慢性病
JL-FA-58	HBsAg (HBV surface antigen) Serum	乙肝表面抗原血清
JL-FA-59	HBsAg (AD)	乙肝表面抗原（AD）
JL-FA-60	HBsAg (AY)	乙肝表面抗原（AY）
JL-FA-61	HBV Positive Plasma	乙肝陽性血漿
JL-FA-62	HBV DNA Plasma	乙肝DNA血漿
JL-FA-63	HBV DNA Serum	乙肝DNA血清
JL-FA-64	HBV DNA type A	A型乙肝DNA
JL-FA-65	HBV DNA type B	B型乙肝DNA
JL-FA-66	HBV DNA type C	C型乙肝DNA
JL-FA-67	HBV DNA type D	D型乙肝DNA
JL-FA-68	HBV DNA type E	E型乙肝DNA
JL-FA-69	HBV DNA type F	F型乙肝DNA
JL-FA-70	HBV Antibody HCV Antibody Plasma CO-INFECTED	乙肝和丙肝聯(lián)合感染血漿
JL-FA-71	HCV (Hepatitis C Virus) Antibody	丙型肝炎抗體
JL-FA-72	HCV Core Antigen Positive	丙肝核心抗原陽性
JL-FA-73	HCV RNA PLASMA Genotype 1	基因1型丙肝RNA 血漿
JL-FA-74	HCV RNA PLASMA Genotype 2	基因2型丙肝RNA 血漿
JL-FA-75	HCV RNA PLASMA Genotype 3	基因3型丙肝RNA 血漿
JL-FA-76	HCV RNA PLASMA Genotype 4	基因4型丙肝RNA 血漿
JL-FA-77	HCV RNA PLASMA Genotype 5	基因5型丙肝RNA 血漿
JL-FA-78	HCV RNA PLASMA Genotype 6	基因6型丙肝RNA 血漿
JL-FA-79	HCV Riba single band	丙肝免疫印跡單波段
JL-FA-80	HCV RIBA Pos. (multiple bands)	丙肝免疫印跡陽性多波段
JL-FA-81	HCV Negative	丙肝陰性
JL-FA-82	HCV RNA Pos (quantitative)	丙肝RNA陽性（定量）
JL-FA-83	Hepatitis E	戊型肝炎
JL-FA-84	Herpes Simplex Virus (HSV)1/2 Positive Plasma	單純性皰疹病毒1/2陽性血漿
JL-FA-85	Herpes Simplex Virus (HSV) 1 Negative Plasma	單純性皰疹病毒1 陰性血漿
JL-FA-86	Herpes Simplex Virus (HSV) 1 IgG	單純性皰疹病毒1 IGG
JL-FA-87	Herpes Simplex Virus (HSV 1) IgM	單純性皰疹病毒1 IGM
JL-FA-88	Herpes Simplex Virus (HSV) 2 IgG	單純性皰疹病毒2 IGG
JL-FA-89	Herpes Simplex Virus (HSV) 2 IgM	單純性皰疹病毒2 IGG
JL-FA-90	Histone	組蛋白
JL-FA-91	Human Anti Mouse Ab (HAMA)	人抗鼠抗體
JL-FA-92	Human immunodeficiency virus (HIV) 1 Neg	HIV I 陰性
JL-FA-93	anti Human immunodeficiency virus (HIV) 1 Plasma	抗HIV I 血漿
JL-FA-94	anti Human immunodeficiency virus (HIV) 1 Serum	抗HIV I 血清
JL-FA-95	anti Human immunodeficiency virus (HIV) 2 Western Blot Tested	抗HIV 2 免疫印跡
JL-FA-96	anti Human immunodeficiency virus (HIV) 1/2 2 HIV (+)	抗HIV 1/2 2 HIV陽性
JL-FA-97	Human immunodeficiency virus (HIV) Ag	HIV抗原
JL-FA-98	HIV RNA (quantitative) Plasma	HIV RNA 定量血漿
JL-FA-99	HIV RNA (quantitative) Serum	HIV RNA 定量血清
JL-FA-100	HIV1 Subtype A	HIV1 亞型A
JL-FA-101	HIV1 Subtype B	HIV1 亞型B
JL-FA-102	HIV1 Subtype C	HIV1 亞型C
JL-FA-103	HIV1 Subtype D	HIV1 亞型D
JL-FA-104	HIV1 Subtype E	HIV1 亞型E
JL-FA-105	HIV1 Subtype F	HIV1 亞型F
JL-FA-106	HIV1 Subtype G	HIV1 亞型G
JL-FA-107	HIV1 Subtype H	HIV1 亞型H
JL-FA-108	HIV1 Subtype J	HIV1 亞型J
JL-FA-109	HIV1 Subtype K	HIV1 亞型K
JL-FA-110	HIV1 Group O	HIV1 亞型O
JL-FA-111	Human immunodeficiency virus (HIV) 2 Antibody Plasma	HIV 2 抗體血漿
JL-FA-112	Human immunodeficiency virus (HIV) 2 Antibody Serum	HIV 2 抗體血清
JL-FA-113	HPV (Human Papiloma Virus) Negative	人乳狀瘤病毒HPV陰性
JL-FA-114	HPV (Human Papiloma Virus) Positive	人乳狀瘤病毒HPV陽性
JL-FA-115	Human immunodeficiency virus (HIV) Antibody HCV Antibody Plasma COINFECTED	HIV 抗體 HCV
JL-FA-116	Human T-cell Lymphotropic Virus (HTLV) I/II	人嗜T淋巴細胞病毒(HTLV) I/II
JL-FA-117	Human T-cell Lymphotropic Virus (HTLV) I	人嗜T淋巴細胞病毒(HTLV) I
JL-FA-118	Human T-cell Lymphotropic Virus (HTLV) II	人嗜T淋巴細胞病毒(HTLV) II
JL-FA-119	Jo-1	多發(fā)性肌炎抗原JO-1
JL-FA-120	IgE < 5,000 Ku/L	IgE < 5,000 Ku/L
JL-FA-121	Legionella	軍團桿菌屬
JL-FA-122	Leptospira	軍團桿菌屬
JL-FA-123	Lyme Disease	萊姆(氏)病:蜱傳播的全身性疾病,常在夏季發(fā)生
JL-FA-124	Lyme IgG	萊姆(氏)病 IGG
JL-FA-125	Lyme IgM	萊姆(氏)病 IGM
JL-FA-126	Lyme Disease Neg	萊姆(氏)病陰性
JL-FA-127	Malaria	瘧疾
JL-FA-128	Mononucleosis (infectious)	單核細胞增多癥（有傳染性的）
JL-FA-129	Mononucleosis Negative	單核細胞增多癥陰性
JL-FA-130	Measles Negative	麻疹陰性
JL-FA-131	Measles IgG	麻疹 IGG
JL-FA-132	Measles IgM	麻疹 IGM
JL-FA-133	Microsomal Anti-thyroid peroxidase antibody (TPO) Positive Plasma Standard Titer (typically 1,000-3,000 IU/mL)	微粒體抗甲狀腺過氧化物酶抗體
JL-FA-134	Microsomal Anti-thyroid peroxidase antibody (TPO) Negative Plasma	微粒體抗甲狀腺過氧化物酶抗體
JL-FA-135	Anti-mitochondrial antibody (AMA)	抗線粒體抗體
JL-FA-136	Multiple Sclerosis	多發(fā)性硬化癥
JL-FA-137	Mumps IgG	流行性腮腺炎 IGG
JL-FA-138	Mumps Ab IgM	流行性腮腺炎抗體 IGM
JL-FA-139	Mumps Antibody Negative Plasma	流行性腮腺炎抗體陰性血漿
JL-FA-140	Mumps Antibody Negative Serum	流行性腮腺炎抗體陰性血清
JL-FA-141	Myeloma Plasma	骨髓瘤血漿
JL-FA-142	Myeloma IgA	骨髓瘤IGA
JL-FA-143	Myeloma IgE	骨髓瘤IGE
JL-FA-144	Myeloma IgG	骨髓瘤IGG
JL-FA-145	Myeloma IgM	骨髓瘤IGM
JL-FA-146	Mycoplasma	支原體
JL-FA-147	Mycoplasma Negative	支原體陰性
JL-FA-148	Mycoplasma IgG	支原體IGG
JL-FA-149	Mycoplasma IgM	支原體IGM
JL-FA-150	Mycoplasma PCR	支原體PCR
JL-FA-151	Normal Human Plasma	正常人血漿
JL-FA-152	Normal Human Serum	正常人血清
JL-FA-153	Nuclear Antibody Centromere	核抗體著絲粒
JL-FA-154	Nuclear Antibody, Speckled ANA	核抗體，斑點抗核抗體
JL-FA-155	Nuclear Antibody, Nucleolar ANA	核抗體,核仁抗核抗體
JL-FA-156	Nuclear Antibody, Homogeneous ANA	核抗體，同質(zhì)抗核抗體
JL-FA-157	Nuclear Antiobody, Speckled. (ANA) Negative	核抗體，斑點?？购丝贵w陰性
JL-FA-158	P-ANCA (associated neutrophil cytoplasmic antibodies)	相關(guān)的嗜中性粒細胞胞漿抗體
JL-FA-159	Parietal Cell Antibody (PCA)	胃)壁細胞抗體
JL-FA-160	Parvo positive plasma	細小病毒陽性血漿
JL-FA-161	Parvo IgM	細小病毒 IGM
JL-FA-162	Parvo IgG	細小病毒 IGG
JL-FA-163	Parvo Negative Plasma	細小病毒陰性血漿
JL-FA-164	Parvo DNA positive	細小病毒 DNA 陽性
JL-FA-165	Phospholipid Positive Plasma	磷脂陽性血漿
JL-FA-166	Prothrombin	凝血酶原,凝血因子
JL-FA-167	Rheumatoid Factor (RF) <1000 IU/mL	類風濕因子<1000 IU/mL
JL-FA-168	Rheumatoid Factor (RF) 1001-2000 IU/mL	類風濕因子1001-2000 IU/mL
JL-FA-169	Rheumatoid Factor (RF) 2001-4000 IU/mL	類風濕因子 2001-4000 IU/mL
JL-FA-170	Rheumatoid Factor (RF) 4001-5000 IU/mL	類風濕因子 4001-5000 IU/mL
JL-FA-171	Rheumatoid Factor (RF) >5000 IU/mL	類風濕因子>5000 IU/mL
JL-FA-172	Ribonucleoprotein (RNP) Positive	核糖核蛋白陽性
JL-FA-173	Rubella Chimeric	風疹
JL-FA-174	Rubella Negative	風疹陰性
JL-FA-175	Rubella IgG	風疹I(lǐng)GG
JL-FA-176	Rubella IgM	風疹I(lǐng)GM
JL-FA-177	Rubeola Negative Plasma	風疹陰性血漿
JL-FA-178	Rubeola IgG	風疹I(lǐng)GG
JL-FA-179	Scleroderma (Scl-70) Pos	膠原沉著病,硬皮病,硬皮癥陽性
JL-FA-180	Scleroderma (Scl-70) Negative	硬皮病陰性
JL-FA-181	Sickle Cell Fresh Whole Blood	鐮刀形紅細胞新鮮全血
JL-FA-182	Smith (SM)	抗Smith抗體陽性血清（SLE的特征性抗體）
JL-FA-183	SMITH RNP	抗RNP抗體陽性血清（SLE的特征性抗體）
JL-FA-184	Smooth Muscle (ASMA)	抗平滑肌抗體陽性血清
JL-FA-185	Sjogren syndrome antigen A (SSA) Positive	舍格倫綜合征或干燥綜合征抗原A 陽性
JL-FA-186	Sjogren syndrome antigen B (SSB) Positive	舍格倫綜合征抗原B 陽性
JL-FA-187	Sjogren syndrome antigen B (SSB) Negative	舍格倫綜合征抗原B陰性
JL-FA-188	Streptolysin O Ab (ASO)	鏈球菌溶血素O抗體
JL-FA-189	Syphilis (RPR - Rapid Plasma Reagin) Positive Plasma	梅毒（梅毒-快速血漿反應）陽性血漿
JL-FA-190	Syphilis (RPR - Rapid Plasma Reagin) Negative Plasma	梅毒（梅毒-快速血漿反應）陰性血漿
JL-FA-191	Syphilis/ATA/T. pallidum IgG	梅毒ATA/T，蒼白球IGG
JL-FA-192	Syphilis/ATA/T. pallidum IgM	梅毒ATA/T，蒼白球IGM
JL-FA-193	Systemic Lupus Erythematosus (SLE) Positive	全身性紅斑狼瘡陽性
JL-FA-194	Systemic Lupus Erythematosus (SLE) Negative	全身性紅斑狼瘡陰性
JL-FA-195	TG/TPO Positive (Standard Titer 1,000 - 3000 IU/mL)	甲狀腺球蛋白/甲狀腺過氧化物酶陽性
JL-FA-196	TG/TPO Negative	甲狀腺球蛋白/甲狀腺過氧化物酶陰性
JL-FA-197	TTG (Tissue Transglutaminase)	組織轉(zhuǎn)谷氨酰胺酶
JL-FA-198	TTG (Tissue Transglutaminase) IgA	組織轉(zhuǎn)谷氨酰胺酶 IGA
JL-FA-199	ToRCH (Toxo, Rubella, CMV, HSV) Positive	優(yōu)生優(yōu)育（弓形蟲，風疹，巨細胞，單胞）陽性
JL-FA-200	ToRCH (Toxo, Rubella, CMV, HSV) Negative	優(yōu)生優(yōu)育（弓形蟲，風疹，巨細胞，單胞）陰性
JL-FA-201	Toxoplasmosis (Toxo)	弓形蟲病
JL-FA-202	Toxoplasmosis (Toxo) IgG	弓形蟲病IGG
JL-FA-203	Toxoplasmosis (Toxo) IgM	弓形蟲病IGM
JL-FA-204	Thyroglobulin (TG) Positive Plasma	甲狀腺球蛋白陽性血漿
JL-FA-205	Thyroglobulin (TG) Negative	甲狀腺球蛋白陰性
JL-FA-206	Varicella-Zoster Virus (VZV) Negative	水痘-帶狀皰疹病毒陰性
JL-FA-207	Varicella-Zoster Virus (VZV) IgG	水痘-帶狀皰疹病毒IGG
JL-FA-208	Varicella-Zoster Virus (VZV) IgM	水痘-帶狀皰疹病毒IGM
JL-FA-209	West Nile Virus (WNV)	西尼羅河腦炎病毒
JL-FA-210	West Nile Virus (WNV) IgM	西尼羅河腦炎病毒IGM

美國

“這項發(fā)現(xiàn)是我的實驗室20年來的研究結(jié)果，” 加州大學圣地亞哥分校醫(yī)學院細胞和分子系的教授史蒂文·f·道迪博士說。“它*抗原抗體了一個傳統(tǒng)的認知，即一個稱為p16-細胞周期蛋白D通路(癌癥中zui常見的遺傳通路突變)促進所有腫瘤細胞的細胞周期進程的一個基本方面。”這項研究結(jié)果發(fā)表于《eLife》雜志上。
細胞周期蛋白D是在細胞復制的*階段期間合成的，被認為有助于促進復雜的，多階段的過程，其中包括與視網(wǎng)膜母細胞瘤(Rb)蛋白的相互作用，Rb蛋白的功能是通過抑制細胞周期進程防止細胞過度生長，直到細胞準備分裂。RB是一個抑癌基因。
幾個主要的癌癥相關(guān)的Rb突變和功能失調(diào)，以及細胞周期蛋白D一直被描述為促進癌癥的一個致癌基因，因為它被認為是通過一種叫做磷酸化的過程，使Rb的抑癌功能失活。
道迪和他的同事們精心計算細胞周期進程期間的磷酸鹽添加到Rb的數(shù)量。這多達14個，但科學家發(fā)現(xiàn)，細胞周期蛋白D只增加了一個單磷酸，且只有細胞周期進程的早期G1期的14個位點中的一個，基本上有14個不同亞型的Rb。單磷酸鹽的作用是激活RB，不使它失活，這個認知已超過了20年。
研究人員說，這項研究從根本上改變了對G1期細胞周期調(diào)控和許多癌癥相關(guān)的分子起源的理解。非常重要的是要明白一個基因通路的實際功能和中斷它的后果，尤其是細胞周期蛋白D的多種藥物抑制劑用于抗原抗體癌的臨床試驗測試這種情況下。
據(jù)認為，當器官一旦*形成，腎細胞就不能夠繁殖了。但新的研究表明，腎臟在人類的整個生命中能夠進行再生和自我修復。
美國斯坦福大學干細胞生物學和再生醫(yī)學研究所，以及以色列賽克勒醫(yī)學院的研究人員展示了，腎臟如何不斷增長以及自我更新的驚人能力，這項發(fā)現(xiàn)抗原抗體了數(shù)十年來認為腎臟不能夠再生的*理論，它也打開了通向修復腎臟甚至增長的新方法。
“這些基本理論對腎臟疾病和腎臟再生有直接的影響，”論文的主要作者Yuval Rinkevich博士說。這項研究發(fā)表于2014年5月15日的《Cell Reports》雜志上。
Cell Reports:腎臟的再生能力貫穿人的一生
長期以來，人們一直認為，腎細胞在器官一旦*形成的時候就喪失了再生的能力。這項新的研究表明，腎臟在人類的整個生命中都能夠進行再生和自我修復。
“這項研究告訴我們，腎臟決不是一個靜態(tài)的器官，” 本文的高級作者、賽克勒醫(yī)學院的兒科系副教授本杰明·德克爾博士說。“令人難以置信，腎臟可以自己恢復活力，并繼續(xù)生成專門的腎細胞。”
本文的另一個高級作者是病理學和發(fā)育生物學的教授和斯坦福研究所的主任歐文·韋斯曼博士。

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"This finding is the result of two decades of my laboratory's research," said Dr. Steven F. Dodi, a professor of cellular and molecular medicine at the University of California San Diego School of Medicine. "It's a compley traditional understanding of antigen-antibody, a fundamental aspect of what is known as the p16-cyclin D pathway, the most common genetic pathway mutation in cancer, that promotes the cell cycle progression of all tumor cells." The study Results published in the "eLife" magazine.
Cyclin D, which is synthesized during the first phase of cell replication, is thought to contribute to the promotion of a complex, multi-stage process including the interaction with retinoblastoma (Rb) proteins whose function is Prevent cell overgrowth by inhibiting cell cycle progression until the cell is ready for division. RB is a tumor suppressor gene.
Several major cancer-associated Rb mutations and dysfunctions, as well as cyclin D, have long been described as an oncogene that promotes cancer as it is thought to cause the tumor suppressor function of Rb through a process called phosphorylation live.
Dodi and his colleagues carefully calculated the amount of phosphate added to the Rb during the cell cycle progression. This is up to 14, but scientists have found that cyclin D only adds one monophosphate and that only one of 14 sites in the early G1 phase of the cell cycle process has essentially 14 different subtypes of Rb. The role of monophosphates is to activate RB without inactivating it, a fact that has been recognized for more than 20 years.
The researchers say the study fundamentally changed the understanding of the molecular origins of G1-phase cell cycle regulation and many cancers. It is very important to understand the actual function of a gene pathway and to disrupt its consequences, especially in the case of a clinical trial of multiple drug inhibitors of cyclin D for antigen-antibody cancer.
It is believed that when the organ is fully formed, the kidney cells can not reproduce. But new research shows that the kidneys are able to regenerate and repair themselves throughout human life.
Researchers at the Stem Cell Biology and Regenerative Medicine Institute at Stanford University in the United States and at the Scythian Institute of Medicine in Israel demonstrated how the kidneys are constantly growing and the amazing ability to self-renew, the antigenic antibody that for decades has not been able to regenerate the kidneys The accepted theory, it also opened up new ways to repair the kidneys and even growth.
"These basic theories have a direct impact on kidney disease and kidney regeneration," said lead author Yuval Rinkevich, PhD. The study was published in Cell Reports on May 15, 2014.
Cell Reports: The ability of the kidneys to regenerate throughout one's entire life
It has long been believed that kidney cells lose their ability to regenerate once the organ is fully formed. This new study shows that the kidneys are able to regenerate and repair themselves throughout human life.
"This study ls us that the kidney is by no means a static organ," said Benjamin Dinkel, a senior author of the article and associate professor of pediatrics at Seckler School of Medicine. "It's incredible that the kidneys can regain their own vitality and continue to produce specialized kidney cells."
Another top author of this article is a professor of pathology and developmental biology and Dr. Irving Weissman, director of the Stanford Institute.

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