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医疗健康有关的英语词汇

医疗健康有关的英语词汇一、常见疾病词汇1. Diabetes (糖尿病)2. Hypertension (高血压)3. Asthma (哮喘)4. Cancer (癌症)5. Heart Disease (心脏病)6. Stroke (中风)7. Arthritis (关节炎)8. Obesity (肥胖症)9. Allergy (过敏)10. Depression (抑郁症)二、身体部位词汇1. Heart (心脏)2. Brain (大脑)3. Liver (肝脏)4. Lung (肺)5. Kidney (肾脏)6. Stomach (胃)7. Intestine (肠道)8. Bone (骨骼)9. Muscle (肌肉)10. Skin (皮肤)三、医疗检查与治疗词汇1. Xray (X光检查)2. CT Scan (CT扫描)3. MRI (磁共振成像)4. Ultrasound (超声波检查)5. Blood Test (血液检查)6. Urine Test (尿液检查)7. Physical Examination (体检)8. Surgery (手术)9. Medication (药物治疗)10. Therapy (治疗)四、医疗人员与设施词汇1. Doctor (医生)2. Nurse (护士)3. Surgeon (外科医生)4. Physician (内科医生)5. Dentist (牙医)6. Hospital (医院)7. Clinic (诊所)8. Pharmacy (药房)9. Ambulance (救护车)10. Health Insurance (医疗保险)五、健康生活习惯词汇1. Exercise (锻炼)2. Diet (饮食)3. Sleep (睡眠)4. Relaxation (放松)5. Meditation (冥想)6. Hydration (补水)7. Quit Smoking (戒烟)8. Limit Alcohol (限酒)9. Preventive Measures (预防措施)10. Healthy Lifestyle (健康生活方式)六、症状描述词汇1. Fever (发烧)2. Cough (咳嗽)3. Sore Throat (喉咙痛)4. Headache (头痛)5. Nausea (恶心)6. Vomiting (呕吐)7. Diarrhea (腹泻)8. Constipation (便秘)9. Fatigue (疲劳)10. Pain (疼痛)七、药物与治疗用品词汇1. Painkiller (止痛药)2. Antibiotic (抗生素)3. Antihistamine (抗组胺药)4. Insulin (胰岛素)5. Aspirin (阿司匹林)6. Tablet (药片)7. Capsule (胶囊)8. Syrup (糖浆)9. Injection (注射)10. Bandage (绷带)八、健康与福祉相关词汇1. Wellness (健康)2. Wellbeing (福祉)3. Prevention (预防)4. Recovery (恢复)5. Rehabilitation (康复)6. Immunization (免疫)7. Vaccination (接种疫苗)8. Nutrition (营养)9. Hygiene (卫生)10. Stress Management (压力管理)九、医疗专业术语词汇1. Appendicitis (阑尾炎)2. Appendectomy (阑尾切除手术)3. Hypoglycemia (低血糖)4. Hyperglycemia (高血糖)5. Hypotension (低血压)6. Hypertrophy (肥大)7. Myocardial Infarction (心肌梗死)8. Osteoporosis (骨质疏松)9. Parkinson's Disease (帕金森病)10. Alzheimer's Disease (阿尔茨海默病)十、医疗保险与费用词汇1. Premium (保险费)2. Deductible (免赔额)3. Copayment (共同支付)4. Coverage (保险覆盖范围)5. Claim (理赔)6. Policy (保险单)7. Provider (医疗服务提供者)8. Outofpocket (自付费用)9. Reimbursement (报销)10. Preexisting Condition (既有疾病)十一、心理健康相关词汇1.心理学 Psychology2.心理咨询 Counseling3.心理治疗 Psychotherapy4.情绪波动 Emotional Fluctuations5.焦虑 Anxiety6.恐慌症 Panic Attack7.强迫症 ObsessiveCompulsive Disorder (OCD)8.创伤后应激障碍 PostTraumatic Stress Disorder (PTSD)9.心理韧性 Psychological Resilience10.自我认知 SelfAwareness十二、替代疗法与补充医学词汇1.针灸 Acupuncture2.按摩 Massage Therapy3.瑜伽 Yoga4.冥想 Meditation5.草药 Herbal Medicine6.顺势疗法 Homeopathy7.营养补充剂 Dietary Supplements8.脊椎按摩 Chiropractic9.能量疗法 Energy Healing10.整骨疗法 Osteopathy十三、医疗程序与手术术语词汇1.活检 Biopsy2.透析 Dialysis3.放疗 Radiation Therapy4.化疗 Chemotherapy5.激光手术 Laser Surgery6.微创手术 Minimally Invasive Surgery7.器官移植 Organ Transplant8.冠状动脉搭桥手术 Coronary Artery Bypass Graft (CABG)9.人工关节置换 Total Joint Replacement10.腹腔镜手术 Laparoscopic Surgery 十四、孕妇与婴儿健康词汇1.妊娠 Pregnancy2.产前检查 Prenatal Care3.分娩 Labor and Delivery4.哺乳 Breastfeeding5.新生儿护理 Newborn Care6.儿科 Pediatrics7.免疫接种 Immunization Schedule8.婴儿食品 Ba Food9.儿童成长发育 Child Development10.产后护理 Postpartum Care十五、健康饮食与营养词汇1.卡路里 Calorie2.蛋白质 Protein3.碳水化合物 Carbohydrates4.脂肪 Fats5.维生素 Vitamins6.矿物质 Minerals7.膳食纤维 Dietary Fiber8.均衡饮食 Balanced Diet9.低脂饮食 LowFat Diet10.素食主义 Vegetarianism通过这些词汇的积累，你将能够更好地理解和沟通医疗健康相关的信息，无论是在专业领域还是日常生活中。

医学英语后缀汇总

本资料由►爱医生◄提供/content/%E5%8C%BB%E5%AD%A6%E8%8B%B1%E8%AF%AD%E5%90%8E%E7%B C%80%E6%B1%87%E6%80%BB后缀在缀合法中只起改变词性的作用，不改变词根的含意。

现将常用后缀分一般英语后缀及"医学英语后缀两部分来说明。

因词性不同、后缀可分为名词性、形容词等。

一、名词性后缀1、-age为抽象名词后缀，表示行为，状态和全体总称，percentage百分数，百分率，voltage电压，伏特数，lavage灌洗，洗，出法，gavage管词法，curettage刮除法，shortage 不足，缺少。

2、-cy表示抽象名词，accuracy准确，精确度，infancy婴儿期。

3、-ence、-ance表示性质和动作，difference不同，interference干扰，干预，influence影响，感化，occurrence发出，出现，violence激烈，暴力，existence存在，significance意义，意味。

4、-ency、-ancy抽象名词后缀，difficiency不足，不全，tendency趋势，趋向，frequency频率，pregnancy 妊娠，emergency紧急，急救，fluency流利，流畅，sufficiency 足够，充足，constancy坚定，经久不变。

5、-er表示……人、……者，diameter直径，receiver接收者，接受者，carrier携带者，beginner初学者，创始人，reader读者，shutter 快门，goiter甲状腺肿。

6、-ics 表示……科学，psdiatrics儿科学，psychiatrics精神病学，obstetrics 产科学，orthopdics矫形科学，auristrics耳科学，gnathostomatics口腔生理学，andriatrics男性医学，男性科。

成人斯蒂尔病

出现率（%）
96-100 71-97 59-92 55-88 44-85 35-85 52-62
实验室检查
RF及ANA阴性血培养阴性血清铁蛋白明显升高（常≥1000ug/ml） C反应蛋白常高于10倍正常上限 IL-18可用于诊断和监测病情活动
放射学检查
多数正常
病程长者可出现软骨侵蚀、关节间隙狭窄腕、颈椎、髋、膝均可受累 5~33%的患者进展迅速

感染恶性肿瘤其它风湿病
诊断：符合5条标准（至少2条主要标准）敏感性：93.5%
Cush标准
1、发热（≥39℃） 2、关节痛或关节炎 3、RF<1:80 4、ANA<1:100
a：WBC≥15×10 /L b：Still皮疹 c：胸膜炎或心包炎 d：肝肿大或脾肿大或全身淋巴结肿大
抗风湿药物：用激素后仍不能控制发热或激素减量即复
其他药物：如抗肿瘤坏死因子等。
预后
患者病情、病程呈多样性。少部分患者一次
发作缓解后不再发作，多数患者缓解后易反复发作。40%～50%患者有自限倾向，也有慢性持续活动的类型，无皮疹、HLA-B35阳性者病情较轻。20%发生慢性关节炎，出现软骨和骨质破坏。死亡原因多种多样，主要由于继发感染、糖皮质激素不良反应、肝功能衰竭等多脏器损害。幼年有Still病、持续类风湿因子、抗核抗体阳性、HLA-DR6阳性提示预后较差。
严重并发症
嗜血细胞综合征 DIC、呼吸窘迫、多脏器功能衰竭 AOSD患者出现2系或3系血细胞减少骨穿见嗜血细胞
急性肝衰竭
DIC-常见于出现严重肝损害的AOSD患者
多脏器功能衰竭
实验室检查

医学英语词汇复习

医学英语词汇复习一、单词homeostatic adj. 体内平衡的homeostasis n. 体内平衡geriatrics n. (做单数用)老人病学metabolism n. 新陈代谢extracellular adj （位于或发生于）细胞外的collagen n. 胶原质tendon n. [解]腱atheroma n. （pl. atheromas , atheromata）动脉粥样化atherosclerosis n. 动脉粥样硬化elastin n. 弹性蛋白glucose n. 葡萄糖mitosis n. (细胞的)有丝分裂radical adj [化]基（free radical 自由基，游离基）selenium n. 硒antioxidant n. 抗氧化剂superoxide n. 过氧化物bolster v. 支持enzyme n. 酶dismutase n. 歧化酶embryo n. 胚胎transcription n. [生物学]转录，信使核糖核酸的形成macromolecule n. 巨大分子，高分子intrinsically adv. 内在地（固有地，本征地，实质地）replicate v. 复制amino adj. 氨基的sickle-cell anemia 镰状细胞血症cystic adj. 包囊的，膀胱的，胆囊的fibrosis n. 纤维症hemophilia n. 血友病inhibitor n. 抑制剂immunodeficiency n. [生]免疫缺陷myocardial adj. [解]心肌的infarction n. 梗塞schizophrenia n. 精神分裂症outmoded adj 过时的，不时髦的milieu n. 周围ramification n. 交叉；分裂；衍生物morphology n. 形态学pathology n. 病理学histopathology n. 组织病理学cytopathology n. 细胞病理学haematology n. 血液学，血液病学toxicology n. 毒理学，毒物学cellular adj （生）细胞的，细胞质（状）的coagulable adj 可凝结的chromosome n. 染色体forensic adj 法医的，关于或应用法律程序的congenital adj（指疾病等）生来的，先天的inflammation n. （医）红肿，炎症tumor n. 肿块，肿瘤degeneration n. （生）退化appendicitis n. 阑尾炎systemic adj （生理）全身的，人体的systematic adj. 系统的carcinoma n. (carcinomas , carcinomata) 癌synonymous adj （后面与with连用）同义的be bereft of 丧失，剥夺allergy n. 变态反应，过敏反应antigen n. 抗原sequester vt. 使隔绝，使分离lymphatic n. 淋巴管effector n. 效应物sensitized adj. 致敏的precommitted adj. 前定向的polyclonal adj. 多细胞的precursor n. 先质，前体specificity n. 特异性mosaic n. 嵌合体，镶嵌体spectrum n. 系列，范围epitope n. 表位humoral adj, 体液的ensue vi. 接着发生，结果产生hapten n. 半抗原erythrocyte n. 红细胞distortion n. 扭转propensity n. 倾向，习性shaman n. 黄教的道士；僧人；巫师Hippocrates n. 希波拉底克（古希腊的名医）Jerusalem n. 耶路撒冷hospitaler n. 住院者distinguish v. 区别，辨别imbue v. 使感染，使蒙受，侵透massage n.v. 按摩peninsula n. 半岛logistical adj. 后勤的hygiene n. 卫生学，卫生barrack n. 简陋房舍overhaul n.v. 分解检查maternalistic adj 显示母性的superintendent n. 主管，负责人affordable adj. 支付得起二、构词法1.前缀prefixdys- , dis- 坏的；有病的；困难的dysfunction n. 机能不良，功能紊乱dysphonia n. 发生困难，言语障碍dysgraphia n. 书写困难anti- 相反；反对；抵抗antioxidant n. 抗氧化剂antibody n. 抗体antiallergic n. 抗变应性的homeo- , homo- 相同的homeostasis n. 体内平衡homeotherapy n. 同种疗法，顺势疗法homogeneity n. 同种，同质homosexual adj 同性恋tachy- 速，快速tachycardia n. 心悸，心动过速tachyphylaxis n. 快速免疫，快速脱敏，快速耐受tachypnea n. 呼吸急促geno- 基因genohormone n. 基因激素genome n. 基因组genospecies n, 基因型群fiber- 纤维fiberscope n. 纤维内窥镜fibrillation n. 纤维性震动fibrinolysis n. 纤维蛋白溶解myc(o)- 真菌mycetology n. 真菌学mycoplasma n. 支原体，衣原体mycotoxicology n. 真菌毒理学myo- 肌肉myoalbumin n. 肌清蛋白，肌白蛋白myoatrophy n. 肌萎缩myocardial adj. 心肌的path(o)- 病理，疾病pathography n. 病理学pathogenesis n. 发病机制pathomorphism n. 病理形态学chrom(o)- 色chromoblast n. 成色细胞chromosomal adj. 染色体突变chromophototherapy n. 色光疗法neur(o)- 神经neurobiology n. 神经生物学neurocirculatory adj. [解]神经与循环系统的neurodermatitis n. 神经性皮炎tox(o)- 毒，毒素toxoid n. 类毒素toxinemia n, 毒血症toxuria n. 尿毒症hyper- 过多，过度，超过hypreadrenia n, 肾上腺机能亢进hyperglycemia n. 高血糖，血糖过多hyperlipidemia n. 高血脂症，血脂过多hypertension n.高血压poly- 多，多数polyclonal adj. 多细胞株的，多克隆的polyase n. 多糖酶，多聚酶polycythemia n. 红细胞增多症erythr(o)- 红erythroblast n. 成红细胞erythromycin n. 红霉素erythropenia n. 红细胞减少brady- 缓，慢，迟钝bradyarrhythmia n. 听觉迟钝bradyarthria n. 言语过缓bradycardia n. 心动过慢lev(o)- 左，向左，左旋levocardia n. 左位心levodopa n. 左旋多巴levoduction n. 左旋眼pro- 前，以前，前体（酶或激素的）proaccelerin n. 前加速素，前加速因子proactivator n. 前激活剂，激活剂原proal adj. 向前运动的kine- 运动kinematics n. 运动学kineplastics n. 运动成形切断术kinesalgia n. 肌动痛，运动痛psych- 灵魂，精神，心智，呼吸psychedelic adj. 产生幻觉的psychiatry n. 精神病学psychopath n. 精神变态者psychotherapy n. 心理疗法xantho-xanthoma n. 黄色瘤xanthopathia n. 黄肤症xanthoprotein n, 黄色蛋白xanthopsy n. 黄市政hydr(o)- 水，积液，氢hydrogymnastic adj. 水中运动的hydroappendic adj. 阑尾积水hydrocholesterol adj. 氢化胆固醇opt(o)- 可见，视optometer n. 视力计，视力检查装置optometrist n, 验光师，视力测定者optophone n, 盲人电光阅读装置cyto- 细胞cytopathology n. 细胞病理学2.后缀suffix-therapy , -otherapy 疗法electrotherapy n. 电疗法physiotherapy n. 物理疗法chemotherapy n. 化学疗法-algia 痛neuralgia n. 神经痛odontalgia n. 牙痛rectalgia n. 直肠痛-asis 状态，情况（病的）cholelithiasis n. 胆石病nephrolithiasis n. 肾石病schistosomiasis n. 血吸虫病-cyte , 细胞acanthocyte n. 棘红细胞leucocyte n. 白细胞lymphocyte n. 淋巴细胞erythrocyte n. 红细胞-lith 石，结石broncholith n. 支气管结石cholelith n. 胆石urolith n. 尿结石-oma 瘤cerebroma n. 脑瘤epithelioma n. 上皮瘤，上皮癌hemangioma n. [医]血管瘤-ostomy 造口术cholecystoduodenostomy n. 胆囊十二指肠吻合术gastrostomy n. 胃造口术necystostomy n. 膀胱再造口术-penia 减少，缺少leucopenia n. 白细胞减少erythropenia n 红细胞减少.。

Stem Cell Biology and Regenerative Medicine

Stem Cell Biology and Regenerative Medicine Stem cell biology and regenerative medicine are fields that have gained significant attention in recent years. Stem cells are unique cells that have the ability to differentiate into various cell types and have the potential to regenerate damaged tissues. The field of regenerative medicine aims to use stem cells to replace or repair damaged tissues and organs in the body. While the potential benefits of stem cell research and regenerative medicine are vast, there are also ethical concerns and challenges that need to be addressed.One of the main ethical concerns surrounding stem cell research is the use of embryonic stem cells. Embryonic stem cells are derived from embryos that are typically discarded after in vitro fertilization. Some individuals argue that using these embryos for research purposes is unethical and violates the sanctity of human life. Others argue that the potential benefits of stem cell research outweigh these concerns and that the embryos used for research would have been discarded anyway.Another ethical concern is the potential for the commercialization of stem cells. As stem cell research continues to advance, there is a growing market for stem cell therapies. Some companies are already offering stem cell treatments for various conditions, despite the lack of sufficient clinical trials and regulatory oversight. This raises concerns about the safety and efficacy of these treatments, as well as the potential for exploitation of vulnerable patients.In addition to ethical concerns, there are also scientific and technical challenges that need to be addressed in the field of regenerative medicine. One major challenge is the ability to control the differentiation of stem cells into specific cell types. While stem cells have the potential to differentiate into any cell type, directing them to differentiate into a specific cell type can be difficult. This can limit the effectiveness of stem cell therapies and increase the risk of complications.Another challenge is the potential for immune rejection of transplanted stem cells. Since stem cells can differentiate into any cell type, they can potentially be used to replace damaged tissues and organs. However, the immune system may recognize thesetransplanted cells as foreign and mount an immune response, leading to rejection of the transplanted cells. This can limit the effectiveness of stem cell therapies and increase the risk of complications.Despite these challenges, the potential benefits of stem cell research and regenerative medicine are vast. Stem cells have the potential to revolutionize the treatment of a wide range of conditions, including cancer, heart disease, and neurological disorders. Stem cell therapies could also reduce the need for organ transplants and improve the quality of life for millions of people around the world.In conclusion, stem cell biology and regenerative medicine are fields that hold great promise for the future of medicine. While there are ethical concerns and scientific challenges that need to be addressed, the potential benefits of these fields are vast. As research in these areas continues to advance, it is important to ensure that ethical considerations are taken into account and that the safety and efficacy of stem cell therapies are rigorously tested. With careful consideration and continued research, stem cell biology and regenerative medicine could transform the way we treat a wide range of conditions and improve the lives of millions of people around the world.。

成人Still病54825

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糖化铁蛋白
J Rheumatol, 2001, 28 (2) : 322-329
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病理
无特异性，非诊断依据
－滑膜：非特异性滑膜炎－淋巴结：浆细胞、多形核白细胞浸润及反应性增生，
少数坏死性淋巴结炎－皮肤：皮肤胶原纤维水肿、血管周围有炎细胞浸润－肌肉：水肿－肝脏：肝细胞变性坏死，炎细胞浸润
Hyperimmunoglobulinaemia D syndrome (HIDS)1–3
Recurring episodes lasting several days Vaccination-induced Associated with elevated IgD and lymphadenopathy
脱发皮下结节急性肝衰竭心脏瓣膜病变弥漫性血管内凝血嗜血细胞综合征淀粉样变（炎性反应长期未能控制）
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心脏瓣膜损害
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临床表现 ——应有尽有
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严重并发症
嗜血细胞综合征 DIC、呼吸窘迫、多脏器功能衰竭 AOSD患者出现2系或3系血细胞减少骨穿见嗜血细胞
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铁蛋白（SF）
一种由24 个非共价键连接的亚单位组成的、分子量大约为 450 000 的大球形蛋白 • 强大的铁结合和储备能力。显示铁储备的标志 •SF 升高机制：尚不清楚:(1)肝脏损害时由肝细胞释放(2)由细胞因子诱导产生(3)铁蛋白受体下降 • 和CRP一样，可作为全身炎性反应中由肝脏产生的一种阳性反应蛋白 • AOSD 患者SF 水平显著高于其他炎症性疾病 • SF 大于1 500 μg/ L 时,有助于排除其他发热性炎性疾病

成人护理学重点英语词汇

成人护理学重点英语词汇总论1.休克：shock2.中心静脉压：central venous pressure，CVP4.心排血量：cardiac output，CO5.体重指数：body mass index，BMI6.营养支持：nutritional support，NS7肠内营养：enteral nutrition，EN8肠外营养：parenteral nutrition，PN9.自控镇痛PCA（patient controlled analgesia）11.肿瘤tumor12.烧伤burn13.麻醉：Anaesthesia14.病人自控镇痛：patient controlled analgesia ，PCA呼吸系统1 急性鼻炎acute rhinitis2.慢性鼻炎chronic rhinitis3.变应性鼻炎allergic rhinitis4.鼻息肉nasal polyps5.鼻内窥镜手术nose endoscopeic surgery6.喉阻塞laryngeal obstruction7.吸气期呼吸困难inspiration dyspnea8.气管支气管异物foreign bodies in the trachea and bronchi9.支气管哮喘bronchial asthma10.慢性阻塞性肺疾病chronic obstructive pulmonary disease (COPD)11.慢性肺源性心脏病chronic pulmonary heart disease12.肺动脉高压pulmonary arterial hypertension13.呼吸衰竭respiratory failure14.咳嗽：cough15.咳痰：expectoration16.呼吸困难：dyspnea17.咯血：hemoptysis循环系统1.二尖瓣狭窄mitral valve stenosis2.二尖瓣关闭不全mitral valve stenosis3.主动脉夹层分离aortic dissection4.肺癌lung Cancer5.下肢静脉曲张varicosity of lower extremity6.下肢深静脉血栓形成deep venous thrombosis ,DVT7.股青肿phlegmasia cerulean dolens8.血栓闭塞性脉管炎thromboangitis obliterans9.主动脉夹层分离aortic dissection10.冠状动脉粥样硬化性心脏病Coronary atherosclerotic heart disease11.冠心病Coronary heart disease12.缺血性心脏病ischemic heart disease13.稳定型心绞痛stable Angina pectoris14.不稳定型心绞痛unstable Angina pectoris，UAP15.心肌梗死myocardial infarction16.高血压hypertension17.原发性高血压Primary hypertension18.胰岛素抵抗insulin resistance，19. 心源性呼吸困难carcinogenic dyspnea20.心源性水肿carcinogenic edema21.心源性晕厥carcinogenic syncope22.心力衰竭heart failur e23.心功能不全cardiac dysfunction24.充血性心力衰竭congestive heart failure25.心脏再同步化治疗cardiac resynchronization therapy，CRT26.房颤atrial fibrillation Af27.室速ventricular tachycardia VT泌尿系统1.肾脏损伤injury of kidney2.膀胱破裂rupture of bladder3.尿道狭窄urethral stricture4.尿瘘urinary fistula5.尿外渗urinary extravasation6.肾盂肾炎pyelonephritis7.尿外渗urinary extravasation8.尿路结石urolithiasis9.输尿管结石ureteral calculi10.膀胱结石vesical calculi11.肾癌renal carcinoma12.膀胱癌carcinoma of bladder13.前列腺癌carcinoma of prostate14.前列腺增生hyperplasia of prostate15.肾积水hydronephrosis16.肾癌renal carcinoma17.膀胱癌carcinoma of bladder18.前列腺癌carcinoma of prostate19.前列腺增生hyperplasia of prostate20.肾积水hydronephrosis21.急性肾小球肾炎acute glomerulonephritis, AGN22.慢性肾小球肾炎chronic glomerulonephritis, CGN23.急进性肾小球肾炎rapidly progressive glomerulonephritis, RPGN24.尿路感染urinary tract infection25.急性肾衰竭acute renal failure, ARF26.慢性肾衰竭chronic renal failure, CRF27.血液透析haemodialysis, HD28.腹膜透析peritoneal dialysis, PD29.肾病综合征nephrotic syndrome, NS神经系统1.头痛headache2.神经系统nervous system3.感觉障碍sense disorders4.中枢神经系统central nervous system5.周围神经系统peripheral nervous system6.脑血管疾病Cerebral vascular disease7.卒中stroke8.脑血栓形成Cerebral thrombosis9.脑梗死Cerebral infarction10.脑出血intracerebral hemorrhage11.脑栓塞cerebral embolism12. 蛛网膜下腔出血Subarachnoid hemorrhage13.癫痫epilepsy14.癫痫持续状态Status epilepticus15.全面强直-阵挛发作generalized tonic-clonic seizure （GTCS）16.癫痫持续状态Status epilepticus17.全面强直-阵挛发作generalized tonic-clonic seizure （GTCS）18.帕金森病Parkinson disease, PD19.颅内压增高intracranial hypertension20.颅内压intracranial pressure，ICP21.脑疝brain herniation22. 脑损伤brain injury23.硬膜外血肿epidural hematoma24.硬膜下血肿subdural hematoma25.脑内血肿intracerebral hematoma26.颅内肿瘤intracranial tumor血液系统1.造血干细胞hematopoietic stem cell，HSC2.贫血anemia3.血红蛋白hemoglobin,Hb4.缺铁性贫血iron deficiency anemia，IDA5.再生障碍性贫血aplastic anemia，AA6.特发性血小板减少性紫癜idiopathic thrombocytopenic purpura，ITP7.白血病Leukemia8.急性白血病acute leukemia，AL9.慢性白血病chronic leukemia，CL10.急性淋巴细胞白血病acute lymphoblastic leukemia，ALL11.急性髓细胞白血病acute myelocytic leukemia，AML12.中枢神经系统白血病central nervous system leukemia ,CNSL13.造血干细胞移植hematopoietic stem cell transplantation，HSCT传染1.标准预防standard precaution2.稽留热sustained fever3.弛张热remittent fever4.间歇热intermittent fever5.回归热relapsing fever6.不规则热irregular fever7.疱疹vesicle8.艾滋病Acquired immunodeficiency syndrome9.人类免疫缺陷病毒human immunodeficiency virus，HIV免疫1.风湿性疾病rheumatic diseases2.类风湿关节炎rheumatoid arthritis，RA3.类风湿因子rheumatoid factor，RF4.晨僵morning stiffness5.系统性红斑狼疮systemic lupus erythematosus，SLE6.抗核抗体antinuclear antibody，ANA7.狼疮性肾炎lupus nephritis，LN消化系统1. 恶心nausea2. 呕吐vomiting3. 腹痛abdominal pain4. 腹泻 diarrhea5. 呕血与黑便 hematemesis and melena6. 便秘 constipation7. 龋病 Dental Caries ， Tooth Decay8. 牙周病 Periodontal Disease9. 全冠 Crown10.嵌体 Inlay11.固定桥 Fixed bridge12.可摘局部义齿 Removable partial denture13.全口义齿 Full denture14.牙拔除术 extraction of teeth15.牙拔除适应证 Indications for the extraction of teeth16.牙拔除禁忌证 Contraindications for the extraction of teeth17.智齿冠周炎 pericoronitis18.口底多间隙感染 cellulitis of the floor of the mouth19.颌骨骨髓炎 osteomyelitis of the jaws20.化脓性颌骨骨髓炎 pyogenic osteomyelitis of jaws21.擦伤 abrasion wound22.刺、割伤 punctured and incised wound23.颌骨骨折 fracture of jaws24.颌间牵引 Intermaxillary elastic traction 25.上颌骨骨折 fractures of maxilla26.撕裂或撕脱伤 lacerated wound27.下颌骨骨折 fractures of the mandible28.咬伤 bite wound29.挫伤 contused wound30.舌癌 carcinoma of tongue31.鳞状细胞癌 squamous cell carcinoma32.唇腭裂序列治疗 sequential treatment33.唇裂 cleft lip34.腭裂 cleft palate35.腭扁桃体炎 palatine tonsillitis36.扁桃体切除术 tonsillectomy37.腺样体 adenoid38.扁桃体肥大 tonsillar hypertrophic39.口咽部 oropharynx40.鼻咽癌 carcinoma of the nasophanx41.颈部包块 neck mass42.食管异物 foreign bodies of the esophagus43.消化性溃疡 Peptic ulcer44.胃溃疡 Gastric ulcer45.十二指肠溃疡 Duodenal ulcer Hematochezia,46.胃癌carcinoma of stomach47.上消化道出血Upper gastrointestinal hemorrhage48.呕血与黑便Hematemesis and melena49.便血50.炎症性肠病inflammatory bowel disease,IBD51.溃疡性结肠炎ulcerative colitis，UC52.克罗恩crohn s disease，CD53.肠梗阻：intestinal obstruction54.机械性肠梗阻：mechanical intestinal obstruction55.动力性肠梗阻：dynamic intestinal obstruction56.血运性肠梗阻：ischemic intestinal obstruction57.结肠癌：carcinoma of colon58.直肠癌：carcinoma of rectum59.阑尾炎：appendicitis60.急性阑尾炎：acute appendicitis61.慢性阑尾炎：chronic appendicitis62.腹外疝：abdominal external hernia63.易复性疝：reducible hernia64.难复性疝：irreducible hernia65.嵌顿性疝：incarcerated hernia66.较窄性疝：strangulated hernia67.急腹症：acute abdomen68.腹腔脓肿：abdominal abscess69.腹部损伤：abdominal injury70.急性腹膜炎：acute peritonitis71.原发性腹膜炎：primary peritonitis72.继发性腹膜炎：secondary peritonitis73.胆石症：cholelithiasis74.胆囊结石：cholecystolithiasis75.腹腔镜胆囊切除术:laparoscopic cholecystectomy,LC76.急性胆囊炎：acute cholecystits77.慢性胆囊炎：chrinic cholecystits78.急性梗阻性化脓性胆管炎：acute obstructive suppurative cholangitis AOSC79.急性胰腺炎Acute pancreatitis80.慢性胰腺炎Chronic pancreatitis81.乙型肝炎病毒hepatitis B virus，HBV82.急性黄疸型病毒性肝炎acute icteric viral hepatitis83.血清丙氨酸转氨酶alanine aminotransferase84.慢性肝炎chronic hepatitis85.肝硬化Cirrhosis of liver86.腹腔积液Ascites87.门静脉高压症Portal hapertension88.肝性脑病Hepatic encephalopathy89.肝昏迷Hepatic coma90.原发性肝癌：primary liver cancer91.肝细胞性肝癌：hepatocellular carcinoma ,HCC92.甲胎蛋白：alpha-fetoprotein,AFP93.肝脏移植：orthotopic liver transplantation ,OLT94.伤寒typhoid fever95.复发relapse96.再燃recrudescence内分泌系统1.促甲状腺激素释放激素thyrotropin hormone releasing hormone（TRH2.促性腺激素释放激素gonadotropin releasing hormone（GnRH）3.生长激素释放激素growth hormone releasing hormone（GHRH）4.促甲状腺激素thyroid stimulatingo horm ne （TSH）5.内分泌系统Endocrine system6.甲状腺功能亢进Hyperthyroidism7.甲状腺危象thyroid crisis8.糖尿病足Diabetic foot9.糖尿病肾病diabetic nephropathy10.糖尿病视网膜病变diabetic retinopathy11.胰岛素泵continuous subcutaneous insulin infusion（CSII）12.身体质量指数body mass density（BMI），13.口服葡萄糖耐量实验oral glucose tolerance test（OGTT）14.痛风gout15.非甾体类抗炎药non-steroidal an-ti-inflammatory drug，NSAID16.甲状腺癌thyroid carcinoma17.甲状腺癌thyroid carcinoma18.甲状腺功能亢进症hyperthyroidism19.急性乳腺炎：acute mastitis20.乳腺癌：breast cancer生殖系统外阴炎vulvitis滴虫阴道炎trichomonal vaginitis念珠菌阴道炎candidal vaginitis子宫颈炎cervicitis盆腔炎pelvic inflammatory disease滋养细胞疾病：(gestational trophoblastic disease, GTD):葡萄胎：（hydatidiform mole）妊娠滋养细胞肿瘤：（gestational trophoblastic tumor，GTT）侵蚀性葡萄胎：（invasive mole）绒毛膜癌：（choriocarcinoma）子宫肌瘤：myoma of uterus肌壁间肌瘤：intramural myoma浆膜下肌瘤：subserous myoma黏膜下肌瘤：submucous myoma子宫内膜癌：endometrial carcinoma分段诊刮：fractional curettage宫颈癌：carcinoma of cervix卵巢肿瘤：ovarian tumor功能失调性子宫出血：dysfunctional uterine bleeding闭经：amenorrhea子宫内膜异位症：endometriosis子宫腺肌病：adenomyosis不孕症：infertility感官系统眼球eye baii角膜cornea瞳孔iris睑腺炎hordeoiun睑板腺囊肿chalazion慢性泪囊炎chronic dacryocystitis慢性泪囊炎chronic dacryocystitis急性泪囊炎acute dacryocystitis结膜炎coniunctivitis急性细菌性结膜炎acute bacterial coniunctivitis沙眼trachoma角膜炎keratitis细菌性角膜炎bacterial keratitis单疱病毒性角膜炎herpes simplex keratitis HSK 真菌性角膜炎fungal keratitis角膜移植术keratoplasty白内障cataract年龄相关性白内障age-related cataract玻璃体积血vitreous hemorrhage视网膜脱离retinal dtachment糖尿病性视网膜病变diabetic retinopathy视网膜动脉阻塞retinalartery occlusion近视myopia远视hyperopia散光astigmatism老视presbyopia眼钝挫伤ocular blunt trauma眼球穿通伤perforating injury of eyeball眼内异物intraocular foreign bodies眼化学伤ocular chemical injury分泌性中耳炎：secretory otitis media咽鼓管：Eustachchian tube急性化脓性中耳炎：acute suppurative media慢性化脓性中耳炎：chronic suppurative media鼓膜穿孔：tympanic perforation胆脂瘤：cholesteatoma运动系统骨：bone关节：joint骨骼肌：muscle杜加征：Dugas sign托马斯征：Thomas sign牵引术：traction石膏固定术：plaster fixation肱骨干骨折：fracture of humeral shaft肱骨髁上骨折：supracondylar fracture of humerus 肱骨髁上骨折：supracondylar fracture of humerus 股骨颈骨折：transcervical fracture全髋关节置换术：total hiparthroplasty,THA全膝关节置换术：totalknee arthroplasty,TKA关节镜：arthroscope颈椎病：Cervical Spondylosis腰椎间盘突出症：lumbar disc herniation急性血源性骨髓炎：acutehematogenous osteomyelitis 骨与关节结核：Tuberculosis of Bone and Joint髋关节结核：Tuberculosis of hip膝关节结核：Tuberculosis of knee骨巨细胞瘤：giant cell tumor of bone，GCTB骨肉瘤：osteosarcoma尤文肉瘤：Ewing's sarcoma。

Adult Stem Cells, Homeostasis,and Regenerative Medicine分子与细胞PPT课件

Homeostasis
• The ability to regulate internal conditions, usually by a system of feedback controls
Stabilize health and functioning, regardless of the outside changing conditions.
• Responsible for covering the internal (i.e. intestinal lining) and external surfaces (i.e. skin) of the body, including the lining of vessels, glands, and other cavities.
• Epithelial stem cells are also found in the bulge region of the hair follicle
Retinal pigment epithelial cells © CIRM
Adult Stem Cell Therapies Bone Marrow Transplant

How Regeneration Works
• Adult stem cells normally remain quiescent (nondividing) for relatively long periods of time until they are activated by signals to maintain tissues
• They can self-renew and differentiate to become most or all of the specialized cell types within their specific tissue lineage.

医学英语单词

homeostasis 体内平衡
homeotherapy 同种疗法，顺势疗法
homogeneity 同种，同质
swift 快速（英）
tachy-快速（希）
tachycardia 心动过速
tachyphylaxis 快速免疫、快速脱敏
tachypnea 呼吸急促
treatment 治疗（英）
glucose 葡萄糖
mitosis 有丝分裂
radical 基
selenium 硒
antioxidant 抗氧化剂
bolster 支持
enzyme 酶
superoxide 过氧化物
dismutase 歧化物
embryo 胚胎
bad 不良，坏（英）
dys-,dis-坏的，有病的，困难的(拉）
cell 细胞（英）
-cyte 细胞（希）
acanthocyte 棘红细胞
leucocyte 白细胞
lymphocyte 淋巴细胞
stone 石头（英）
-lith 石，结石（希）
broncholith 支气管石
cholelith 胆石
urolith 尿结石
Unite 8 Diagnosis 诊断
proactivator 激活剂原
proal 向前运动的
move 运动（英）
kine-运动（希）
kinematics 运动学
kineplastics 运动成形切断术
kinesalgia 肌动痛，运动痛
mass 肿块（英)
-oma 瘤（希)
cerebroma 脑瘤
epithelioma 上皮瘤

高级医学英语

高级医学英语The Role of Stem Cell Therapy in Regenerative Medicine IntroductionStem cell therapy is a promising approach for regenerative medicine. The foundation for stem cell therapy lies in the unique characteristics of stem cells, which have the ability to differentiate into various cell types. The regenerative potential of stem cells has shown great potential for disease treatments, tissue and organ repair, and the development of new therapies. This article will provide an overview of stem cell therapy, its types, and its applications in regenerative medicine.Types of Stem CellsStem cells can be classified into two broad categories: embryonic stem cells and adult stem cells.Embryonic stem cells are derived from the inner cell mass of the blastocyst, which is a stage of embryonic development. Embryonic stem cells have the ability to differentiate into all three germ layers – the ectoderm, mesoderm, and endoderm. Mesenchymal stem cells and hematopoietic stem cells are examples of adult stem cells. Adult stem cells are undifferentiated cells that reside in various tissues throughout the body. These cells have the ability to differentiate into various cell types within their origin tissue. Adult stem cells can be found in the bone marrow, adipose tissue, blood, brain, heart, liver, and other tissues.Applications of Stem Cell Therapy in Regenerative MedicineStem cell therapy has the potential to treat a variety of conditions, including degenerative diseases, injuries, and genetic disorders. Some of the major applications of stem cell therapy include:1. Tissue EngineeringStem cells are used to engineer tissues for replacement or repair of damaged or diseased tissues. For example, stem cells can be used to regenerate bone, cartilage, muscle, and skin tissue.2. Cellular TherapyStem cells can be used to treat diseases by transplantation of healthy cells. The transplantation of hematopoietic stem cells is an example of cellular therapy. It is used to treat conditions such as leukemia, lymphoma, and other blood-related disorders.3. Regeneration of OrgansStem cells are used to regenerate organs that have lost their function due to injury or disease. Researchers are exploring the use of pluripotent stem cells to regenerate the pancreas, liver, and heart.4. Drug DevelopmentStem cells can be used to develop new drugs. Stem cells can be manipulated to form specific cell types that are affected by certaindiseases. These cells can be used to test new therapies for the disease.Challenges and LimitationsThe success of stem cell therapy depends on the type of cells used and the patient’s immune response to the cells. Some of the challenges and limitations of stem cell therapy include:1. Transplant RejectionStem cells transplanted from a donor can be rejected by the patient’s immune system. This can result in various complications, including graft-versus-host disease.2. Tumor FormationThe use of pluripotent stem cells can result in the formation of tumors. These cells have the ability to differentiate into all cell types, which makes them more prone to produce tumors.3. Ethical and Legal IssuesThe use of embryonic stem cells is controversial due to ethical and legal issues. The destruction of human embryos is required to obtain embryonic stem cells.ConclusionStem cell therapy has immense potential for regenerative medicine.Stem cells can differentiate into multiple cell types and can regenerate tissues and organs. Stem cell therapy has been successful in treating various conditions, including blood-related disorders, injuries, and degenerative diseases. The success of stem cell therapy depends on the type of cells used and the patient’s immune response to the cells. Further research is required to fully explore the potential of stem cell therapy in regenerative medicine.Stem cell therapy is a fast-evolving field in regenerative medicine. The potential of stem cells to differentiate into various cell types and regenerate tissues and organs has opened up new avenues for the treatment of several degenerative diseases, injuries, and genetic disorders. The ability of stem cells to repair damaged tissues and organs has given hope to millions of patients who suffer from various ailments.One of the significant applications of stem cell therapy is tissue engineering, which involves the creation of various types of tissue for the replacement or repair of damaged or diseased tissues. Tissue engineering is becoming increasingly important as the need for transplantable organs continues to grow worldwide. For example, researchers are exploring the use of stem cells to regenerate bone tissue to replace damaged or fractured bones. Stem cells can differentiate into bone-forming cells, which can help repair bone fractures and defects. Similarly, the use of stem cells to regenerate cartilage is being researched for the repair of cartilage injuries and joint degeneration.Stem cells are also being used in cellular therapy, which involves the transplantation of healthy cells to treat diseases. Hematopoietic stem cell transplantation is one of the most successful cellulartherapies used for the treatment of several blood-related disorders, including leukemia, lymphoma, and multiple myeloma. Hematopoietic stem cells can differentiate into various blood cells, including red blood cells, white blood cells, and platelets. They are usually harvested from the bone marrow or peripheral blood of the donor before being transplanted into the patient.Regeneration of damaged or diseased organs is another potential application of stem cell therapy. Researchers are exploring the use of pluripotent stem cells to regenerate organs that have lost their function due to injury or disease. The pancreas, liver, and heart are some of the organs being studied for the regeneration potential of stem cells. Pluripotent stem cells are immortal cells that can differentiate into any cell type in the body. The use of pluripotent stem cells can provide a potential cure for several diseases that were once thought incurable.Stem cells are also being used for drug development. Stem cells can be manipulated to form specific cell types that are affected by certain diseases. These cells can be used to test new therapies for the disease. This approach can significantly reduce the cost and time required for drug development. The use of stem cells in drug development can also reduce the need for animal testing, which has ethical concerns and limitations.Despite the vast potential of stem cells, there are several challenges and limitations to their use in regenerative medicine. One of the significant challenges is transplant rejection. Stem cells transplanted from a donor can be rejected by the patient’s immune system, leading to various complications, including graft-versus-host disease. The immune response of the patient depends on several factors, including the type of stem cells used, the patient’s immune system, and the method of transplantation.Another limitation of stem cell therapy is tumor formation. The use of pluripotent stem cells can result in the formation of tumors. These cells have the ability to differentiate into any cell type in the body, which makes them more prone to producing tumors. The risk of tumor formation can be reduced by carefully monitoring the differentiation of pluripotent stem cells and ensuring that only fully differentiated cells are used for transplantation.The use of embryonic stem cells is controversial due to ethical and legal issues. The destruction of human embryos is required to obtain embryonic stem cells. This has led to ethical concerns regarding the use of embryos for research purposes. However, recent scientific discoveries have shown that stem cells can also be obtained from adult tissues. Adult stem cells are undifferentiated cells that reside in various tissues throughout the body and can be harvested without ethical concerns.In conclusion, stem cell therapy has tremendous potential for regenerative medicine. The ability of stem cells to regenerate tissues and organs has given hope to millions of patients suffering from various diseases and injuries. However, there are several challenges and limitations to the use of stem cells in regenerative medicine, including transplant rejection, tumor formation, and ethical concerns. Further research is required to address these challenges and fully explore the potential of stem cell therapy in regenerative medicine. With continued research and development,stem cell therapy has the potential to revolutionize the field of medicine and provide new treatments for many currently incurable diseases.。

Chapter_7 Stem Cell Research

当代医学英语综合教程—医学探索—主题阅读译文Chapter 7Stem Cells: the Hope and the HypeBy Nancy Gibbs干细胞：希望与炒作南希·吉布斯When there's nothing else to prescribe, hope works like a drug. A quadriplegic patient tells herself it's not a matter of if they find a cure but when. Who's to say whether salvation is still 10 or 15 years away? After all, researchers have been injecting stem cells into paralyzed rats and watching their spinal cords mend. "Stem cells have already cured paralysis in animals," declared Christopher Reeve in a commercial he filmed a week before he died.But what is the correct dose of hope when the diseases are dreadful and the prospects of cure distant? When President George W. Bush vetoed the bill that would have expanded funding for human embryonic-stem-cell (ESC) research, doctors got calls from patients with Parkinson's disease saying they weren't sure they could hang on for another year or two. The doctors could only reply that in the best-case scenario, cures are at least a decade away, that hope is no substitute for evidence, that stem-cell science is still in its infancy.It is the nature of science to mix hope with hedging. It is the nature of politics to overpromise and mop up later. But the politics of stem-cell science is different. Opponents of ESC research argue that you can't destroy life in order to save it; supporters argue that an eight-cell embryo doesn't count as a human life in the first place—not when compared with the life it could help save. Opponents say the promise当再没有别的药物可开时，希望就会起到药物的作用。

学术英语医学 Unit 6 Text A 翻译

Unit 6 Text A寻求临终护理数十年前，大多数人在自己家中去世，但是医疗方面的进步已经改变了这一情况。

如今，大多数美国人在医院或是疗养院中度过生命的最终时光。

他们中有些人是为了治疗疾病进了医院，有些可能是选择长期住在疗养院。

越来越多的人在生命的尽头开始选择临终关怀。

死亡没有一个称得上“合适”的地点。

何况，我们死亡的地方，大多数情况下也并非我们可以决定的。

但如果有选择的机会，每个人及其家属，都应该考虑究竟怎样的临终护理最为适合，在哪里可以享受到这样的关怀，家人和朋友能否提供帮助，以及他们应该如何支付相应的费用。

医院及疗养院64岁的George有充血性心力衰竭病史。

一天晚上，他因为胸痛被送入医院。

他与他最亲近的人事先便已决定，在任何情况下都要让医生使用最大努力来延续他的生命。

所以当他需要相应的治疗时，他选择了医院，因为那里有全天候工作的医生和护士。

医院提供一整套的治疗、检查及其他医疗照护。

一旦George的心脏出现持续衰竭，医院的重症监护病房（ICU）或冠心病重症监护病房（CCU）就可以提供及时的救护。

尽管医院有相关的规定，在有些情况下执行具有一定的弹性。

如果George的医生认为他的病情并没有因为治疗有所好转，并濒临死亡，他的家属可以要求更加宽松的探视时间。

如果他的家属想从家中给他带一些私人物品，可以向工作人员询问物品的尺寸限制或是是否需要消毒。

不论George住在ICU、CCU还是两病床的病房，其家属都可以要求更多的私人空间。

在医院环境中，对临终病人来说，身边永远会有知道该如何照料他的医务人员。

这一点令病人及其家属得以安心。

已有越来越多的人在生命尽头的时候选择疗养院，因为在这里，护理人员是随叫随到的。

疗养院有时也被称为专业护理所，在临终护理方面有利有弊。

与医院不同，疗养院里并不是全天候都有医生在场。

然而，由于临终护理可以事先安排，在病人濒临死亡时，不需要事先咨询医生而开展照护。

如果濒死病人已经在疗养院住了一段时间，家属很可能已经和护理人员建立了一定的关系，因而与医院相比，这里的护理工作更具个性化。

homeostasis名词解释

homeostasis名词解释Homeostasis is a term used to describe the internal balance or stability maintained by living organisms. It refers to the ability of an organism or a system to regulate its internal environment and keep it relatively constant, despite external changes or disturbances. The concept of homeostasis was first introduced by the French physiologist Claude Bernard in the 19th century and has since become an essential principle in the field of biology.The internal environment of an organism includes various factors such as temperature, pH, concentration of nutrients and waste products, fluid balance, and oxygen levels. These factors need to be regulated within a narrow range for the organism to function properly. Any deviation from this optimal range can have detrimental effects on the organism's health and well-being.To maintain homeostasis, organisms have various mechanisms and feedback loops in place that continuously monitor and adjust their internal conditions. These mechanisms can be broadly classified into two categories: negative feedback and positive feedback.Negative feedback is the most common mechanism in homeostasis. It works by detecting and counteracting any changes from the desired set point. For example, if the body temperature rises above the optimal range, skin blood vessels dilate and sweat glands produce sweat to cool down the body. This negative feedback loop restores the body temperature back to the normal range.Positive feedback, on the other hand, amplifies and reinforces a change, rather than restoring the system to its original state.Although less common, positive feedback loops play crucial roles in certain physiological processes such as blood clotting during injury or childbirth. In these cases, a small initial stimulus triggers a cascade of events that produces a larger and more pronounced response.The human body employs multiple systems and organs to maintain homeostasis. For example, the respiratory system regulates oxygen and carbon dioxide levels, the urinary system controls the balance of water and electrolytes, the endocrine system releases hormones to regulate various bodily functions, and the nervous system coordinates and monitors the overall homeostatic processes.Failure to maintain homeostasis can lead to various health problems. For example, diabetes mellitus occurs when the body cannot regulate blood glucose levels, and dehydration occurs when the body loses more water than it takes in. Both of these conditions can have serious consequences if left untreated.In summary, homeostasis describes the process by which living organisms maintain a stable internal environment despite external fluctuations. It is a fundamental concept in biology and is necessary for the survival and proper functioning of all living organisms. Through various feedback mechanisms and the coordination of different physiological systems, organisms continuously monitor and adjust their internal conditions to ensure their overall well-being.。

成人still’s病

子和抗核抗体可呈低滴度阳性。血补体水平正常或偏高。
• （5）血清铁蛋白（serum ferritin, SF）本病SF水平增高，
且其水平与病情活动呈正相关。SF显著增高提示本病可能性。
• （6）滑液和浆膜腔积液白细胞增高，呈炎性改变，其中
以中性粒细胞增高为主。
实验室检查 ESR（>50）白细胞增加12 ～40109/L 贫血中性粒细胞增加(≥ 80%) 低白蛋白血症肝酶升高血小板增多
诊断标准（美国Cush标准）
• 必备条件体温≥39℃ 关节痛或关节炎类风湿因子<1:80 抗核抗体<1:100
• 另具备下列任何两项白细胞≥ 15×109/L 皮疹胸膜炎或心包炎肝大或淋巴结肿大
诊断标准（日本1992年）
主要指标 1.发热≥39℃并持续一周以上 2.关节痛持续二周以上 3.典型皮疹 4.白细胞增高≥10×109/Ｌ包括中性粒细胞≥0.80
colony-stimulating factor，M-CSF)、细胞间黏附分子-1 (intracellular adhesion molecule-1，ICAM-1)、亚铁血红素加氧酶-1(heine oxygenase-1，HO-1)可能也参与了 AOSD的发病机制。
发病机制
（Th1/Th2比值与临床活动积分和血清IL18水平显著相关）
概述
成人发病即为成人Still's病（Bywaters,1971)，约12%由儿童期发病迁延而来。 • 曾经用过的名称： 1、变应性亚败血症；２、Wissler-Fanconi症候群或Wissler症候群；３、成人发病的幼年性类风湿性关节炎；４、成人急性发热性幼年风湿病性关节炎等。
定义

Adult Stem Cells, Homeostasis,and Regenerative Med

• Myeloid (monocytes and macrophages, neutrophils, basophils, eosinophils, erythrocytes, megakaryocytes/platelets, dendritic cells)
• A progenitor cell, in contrast to stem cells, is already far more specific: they are pushed to differentiate into their "target" cell.
Asymmetric Cell Division
• Adult stem cells
– Maintain cell populations – Help you heal – Play a role in aging
Homeostasis
• The ability to regulate internal conditions, usually by a system of feedback controls
Adult Stem Cells, Homeostasis,and Regenerative Medicine分子与细胞
PPT课件
•
6、黄金时代是在我们的前面，而不在我们的后面。
•
7、心急吃不了热汤圆。
•
8、你可以很有个性，但某些时候请收敛。
•
9、只为成功找方法，不为失败找借口 (蹩脚的工人总是说工具不好)。
•
10、只要下定决心克服恐惧，便几乎能克服任何恐惧。因为，请记住，除了在脑海中，恐惧无处藏身。-- 戴尔．卡耐基。

造血综述-cell

Leading EdgeReviewHematopoiesis:An Evolving Paradigmfor Stem Cell BiologyStuart H.Orkin1,2,*and Leonard I.Zon1,21Division of Hematology/Oncology,Children’s Hospital Boston and the Dana Farber Cancer Institute,Harvard Stem Cell Institute,Harvard Medical School,Boston,MA02115,USA2Howard Hughes Medical Institute,Boston,MA02115,USA*Correspondence:stuart_orkin@DOI10.1016/j.cell.2008.01.025Establishment and maintenance of the blood system relies on self-renewing hematopoietic stem cells(HSCs)that normally reside in small numbers in the bone marrow niche of adult mammals. This Review describes the developmental origins of HSCs and the molecular mechanisms that reg-ulate lineage-speciﬁc differentiation.Studies of hematopoiesis provide critical insights of general relevance to other areas of stem cell biology including the role of cellular interactions in develop-ment and tissue homeostasis,lineage programming and reprogramming by transcription factors, and stage-and age-speciﬁc differences in cellular phenotypes.IntroductionThe blood system serves as a paradigm for understanding tissue stem cells,their biology,and involvement in aging,disease,and oncogenesis.Because mature blood cells are predominantly short lived,stem cells are required throughout life to replenish multilineage progenitors and the precursors committed to indi-vidual hematopoietic lineages.Hematopoietic stem cells (HSCs)reside as rare cells in the bone marrow in adult mammals and sit atop a hierarchy of progenitors that become progres-sively restricted to several or single lineages(Orkin,2000).These progenitors yield blood precursors devoted to unilineage differ-entiation and production of mature blood cells,including red blood cells,megakaryocytes,myeloid cells(monocyte/macro-phage and neutrophil),and lymphocytes.As with all other stem cells,HSCs are capable of self-renewal—the production of addi-tional HSCs—and differentiation,speciﬁcally to all blood cell lineages.HSCs are deﬁned operationally by their capacity to reconsti-tute the entire blood system of a recipient.In general,prepara-tion of patients for transplantation with donor bone marrow con-taining HSCs entails destruction of host bone marrow by irradiation or by treatment with high-dose cytotoxic drugs,in part to provide‘‘space’’for donor HSCs within the marrow mi-croenvironment(the niche)of the recipient.HSCs can be pro-spectively identiﬁed by monoclonal antibodies directed to sur-face markers,by dye efﬂux,or on the basis of their metabolic properties;HSCs can be separated from more-committed pro-genitors and other marrow cells byﬂuorescence-activated cell sorting(FACS).With contemporary methods,HSCs may be highly puriﬁed such that as few as one cell may provide long-term(>4months)hematopoietic reconstitution in a recipient. Technical considerations regarding the assays for quantitation of HSCs and evaluation of their function have recently been re-viewed(Purton and Scadden,2007).Because no ex vivo assays can replace in vivo transplantation for measuring biological activity of HSCs,characterizing cell populations based on the expression of cell-surface markers cannot be considered synonymous with determining their function.During stress or other manipulations(such as in mutant animals),the surface marker proﬁle of HSCs and their progenitors may be distorted. Here,we discuss the developmental origins of the hematopoi-etic system and the molecular control of self-renewal and lineage determination.The process of hematopoiesis is generally con-served throughout vertebrate evolution.Manipulation of animal models,such as the mouse and zebraﬁsh,has complemented and greatly extended studies of human hematopoiesis.Although not an entirely ideal experimental system,partial reconstitution of the blood system of immunodeﬁcient mice(such as NOD/SCID strains)has been commonly employed to study human hemato-poiesis.The remarkable regenerative properties of human HSCs are best illustrated by the success of marrow transplantation in hu-man patients,a current mainstay of therapy for a variety of genetic disorders,acquired states of bone marrow failure,and cancers. Emergence of HSCsIn vertebrates,the production of blood stem cells is accom-plished by the allocation and speciﬁcation of distinct embryonic cells in a variety of sites that change during development(Gallo-way and Zon,2003)(Figures1and2).In mammals,the sequen-tial sites of hematopoiesis include the yolk sac,an area surrounding the dorsal aorta termed the aorta-gonad meso-nephros(AGM)region,the fetal liver,andﬁnally the bone marrow (Figure1).Recently,the placenta has been recognized as an ad-ditional site that participates during the AGM to fetal liver period. The properties of HSCs in each site differ,presumably reﬂecting diverse niches that support HSC expansion and/or differentia-tion and intrinsic characteristics of HSCs at each stage.For in-stance,HSCs present in the fetal liver are in cycle,whereas adult bone marrow HSCs are largely quiescent.Although there is little dispute regarding where HSCs are found during development,few topics have polarized investiga-tors as much as the origin of HSCs.HSCs are derived from Cell132,631–644,February22,2008ª2008Elsevier Inc.631ventral mesoderm (see Review by C.E.Murry and G.Keller,page 661of this issue).The contribution of each hematopoietic site (such as the yolk sac and fetal liver)to circulating blood in the fe-tus or adult was seemingly answered more than 25years ago.Recent studies in mice and zebraﬁsh,however,challenge the ﬁeld with divergent views.Multiple Waves of Hematopoiesis during Development The initial wave of blood production in the mammalian yolk sac is termed ‘‘primitive.’’The primary function for primitive hemato-poiesis is production of red blood cells that facilitate tissue oxy-genation as the embryo undergoes rapid growth.The hallmark of primitive erythroid cells is expression of embryonic globin pro-teins.The primitive hematopoietic system is transient and rapidly replaced by adult-type hematopoiesis that is termed ‘‘deﬁni-tive.’’In mammals,the next site of hematopoietic potential is the AGM region.Hematopoietic cells were ﬁrst detected in the aorta of the developing pig more than 80years ago.Subsequently,studies of chick-quail chimeras and diploid-triploid Xenopus em-bryos demonstrated analogous AGM-like regions.Morphologi-cal examination revealed that a sheet of lateral mesoderm mi-grates medially,touches endoderm,and then forms a single aorta tube.Clusters of hematopoietic cells subsequently appear in the ventral wall.Similarly,an intraembryonic source of adult HSCs in mice capable of long-term reconstitution of irradiated hosts resides in the AGM region (Muller et al.,1994).At embry-onic day 10.5,little HSC activity is detectable,whereas by day 11engrafting activity ispresent.Figure 1.Developmental Regulation of Hematopoiesis in the Mouse(A)Hematopoiesis occurs ﬁrst in the yolk sac (YS)blood islands and later at the aorta-gonad meso-nephros (AGM)region,placenta,and fetal liver (FL).YS blood islands are visualized by LacZ stain-ing of transgenic embryo expression GATA-1-driven LacZ .AGM and FL are stained by LacZ in Runx1-LacZ knockin mice.(Photos courtesy of Y.Fujiwara and T.North.)(B)Hematopoiesis in each location favors the pro-duction of speciﬁc blood lineages.Abbreviations:ECs,endothelial cells;RBCs,red blood cells;LT-HSC,long-term hematopoietic stem cell;ST-HSC,short-term hematopoietic stem cell;CMP,common myeloid progenitor;CLP,common lymphoid pro-genitor;MEP,megakaryocyte/erythroid progenitor;GMP,granulocyte/macrophage progenitor.(C)Developmental time windows for shifting sites of hematopoiesis.Additional hematopoietic activity in the mouse embryo was detected subse-quently in other sites,including the umbil-ical arteries and the allantois in which hematopoietic and endothelial cells are colocalized (Inman and Downs,2007).Umbilical veins lack hematopoietic po-tential,suggesting that a hierarchy exists during deﬁnitive hematopoiesis in whichHSCs arise predominantly during artery speciﬁcation.In addi-tion,signiﬁcant numbers of HSCs are found in the mouse pla-centa (Gekas et al.,2005;Ottersbach and Dzierzak,2005),nearly coincident with the appearance of HSCs in the AGM region and for several days thereafter.Placental HSCs could arise through de novo generation or colonization upon circulation,or both.The relative contribution of each of the above sites to the ﬁnal pool of adult HSCs remains largely unknown.Subsequent deﬁnitive hematopoiesis involves the colonization of the fetal liver,thymus,spleen,and ultimately the bone marrow.It is believed that none of these sites is accompanied by de novo HSC generation.Rather,their niches support expansion of pop-ulations of HSCs that migrate to these new sites.However,until very recently (as discussed below),there has been no evidence by fate mapping or direct visualization that HSCs from one site colonize subsequent sites.Hemangioblasts and Hemogenic EndotheliumA common origin for blood and vascular cells,the ‘‘hemangio-blast,’’was hypothesized a century ago,based largely on the in-timate association of these lineages in the blood islands of the developing yolk sac.Sharing of markers between blood and blood vessel cells,and the impairment of both tissues in mu-tants,such as the mouse ﬂk1knockout (Shalaby et al.,1997)and zebraﬁsh cloche (Stainier et al.,1995),are consistent with a common origin.Clonal studies using in vitro differentiating mouse embryonic stem (ES)cells provide the strongest evi-dence in favor of the existence of hemangioblasts (Choi et al.,1998).Furthermore,hemangioblast activity has been detected632Cell 132,631–644,February 22,2008ª2008Elsevier Inc.at the mid-streak stage of gastrulation and during the neural plate stage but is extremely transient in vivo (Huber et al.,2004).Despite these ﬁndings,formal proof of the hemangioblast hypothesis requires direct demonstration that a single cell di-vides asymmetrically to form blood and vascular derivatives in vivo.Clonal analysis in mouse chimeras,however,presents contra-dictory evidence regarding the existence of the hemangioblast (Ueno and Weissman,2006).Three different,stably marked ES cells were mixed and coinjected into host blastocysts.Accord-ing to the hemangioblast hypothesis,each blood island of the yolk sac should be clonally derived.However,in these experi-ments more than a single ES cell often contributed to each blood island of the chimeric mice.The existence of the hemangioblast has also been addressed in zebraﬁsh.A primitive wave of hema-topoiesis occurs in a region called the intermediate cell mass that contains erythroid cells surrounded by venous endothelial cells (see Figure 2).Hematopoietic and endothelial markers seg-regate between the 3-to 10-somite period of development.By this time,there are few,if any,cells that might be considered he-mangioblasts based on overlapping blood and blood vessel gene expression.Alternatively,hemangioblasts could appear before the 3-somite stage and also exhibit wider developmental potential than solely blood and blood vessels.Ventral mesoder-mal cells are dedicated speciﬁcally to hematopoietic and endo-thelial fates.Fate-mapping studies have been performed in which a caged ﬂuorescent dye is injected into the zebraﬁsh em-bryo at the one-cell stage,and then at a later time the ﬂuorescent dye is uncaged in single cells using a laser.Individual cells ap-pear dedicated to hematopoietic and endothelial lineages at the 0-to 3-somite stage (Vogeli et al.,2006).However,other cell fates may also be present at this early time.Similarly,smooth muscle cells can be derived from populations of in vitro differen-tiated mouse ES cells exhibiting blood and blood vessel fates (Ema et al.,2003;Ema and Rossant,2003).These studies sup-port the existence of hemangioblasts,although it may beneces-Figure 2.Hematopoietic Development in the Zebraﬁsh(A)Hematopoiesis occurs ﬁrst in the intermediate cell mass (ICM)and subsequently in the aorta-go-nad mesonephros (AGM)region and caudal hema-topoietic tissue (CHT).Later hematopoietic cells are found in the kidney as well as in the thymus.In situ hybridization for GATA-1at 30hr (ICM),for c-myb at 36hr (AGM),for SCL/tal1at days 4and 6.5(CHT),and for c-myb at day 6(top view)to dem-onstrate expression in the kidney marrow and thy-mus.(Photos courtesy of X.Bai and T.Bowman.)(B)Developmental time windows for hematopoi-etic sites in the zebraﬁsh.sary to redeﬁne the potential of these cells to include additional lineages (such as smooth muscle).Principally based on morphology it has been proposed that as the AGM forms,‘‘hemogenic endothelial’’cells in the ven-tral wall of the aorta,rather than heman-gioblasts,bud off HSCs.The program of hemogenic endothelial cell development may be regulated differently from that of pre-sumptive hemangioblasts,given that the transcription factor re-quirements differ.For example,the transcription factor Runx1is necessary for blood formation from hemogenic endothelium but not from yolk sac hemangioblasts (North et al.,1999,2002).The potential to generate hematopoietic,endothelial,and smooth muscle cells has been attributed to another cell type,termed the mesoangioblast,present in the aorta (Cossu and Bianco,2003).Perhaps,the presumptive mesoangioblast might be a pre-cursor of the hemogenic endothelial cell.Other work has indicated that mesenchymal cell populations in the subaortic region poke through the aorta and bud off HSCs (Bertrand et al.,2005).As this occurs,mesenchymal cells express endothelial-speciﬁc genes and ultimately express HSC-associated markers.These observations suggest an alternative model in which subaortic mesenchymal cells,which may also have smooth muscle potential,rather than hemogenic endothe-lial cells,are the source of future deﬁnitive HSCs.Developmental Relationships between the Yolk Sac and the AGMAs with mesodermal derivatives,all blood cells in embryonic,fe-tal,and adult animals might arise from a small set of cells during development.Evidence for and against this notion is present in the literature.Fate mapping in the pre-gastrula Xenopus embryo with ﬂuorescent dye injected into individual blastomeres of the 32-cell embryo demonstrated that different blastomeres contrib-ute to primitive hematopoiesis and deﬁnitive HSC production (Ciau-Uitz et al.,2000).This ﬁnding contradicts the conclusion derived from diploid-triploid chimeric frogs that ventral meso-derm is the common origin of both primitive and deﬁnitive pop-ulations (Turpen et al.,1997).Technical aspects of fate mapping of the 32-cell embryo have been challenged (Lane and Sheets,2002).In situ hybridization and chimera studies in amphibians and birds suggest that the yolk sac and the AGM are derivedCell 132,631–644,February 22,2008ª2008Elsevier Inc.633independently and arise at different times in development (Turpen et al.,1997).With short-term culture and subsequent transplantation,mouse AGM tissue(isolated one day prior to the appearance of HSCs in vivo)generates cells with the capac-ity for long-term engraftment,whereas mouse yolk sac tissue does not(Cumano et al.,1996;Medvinsky and Dzierzak,1996). The origin of HSCs in the AGM can be traced by Runx1expres-sion in the embryonic day8.5(E8.5)mouse embryo,just before the onset of circulation.Because functional activity of stem cells as determined by transplantation into irradiated adults occurs much later(at day11),it is possible that cells of the yolk sac col-onize the AGM through the circulation.In fact,HSC-like activity of yolk sac cells(as deﬁned by a neonatal transplantation assay) (Palis et al.,2001)is detected as early as day9,although circu-lation has started by that time.Conclusive resolution of the de-velopmental relationship between cells of the yolk sac and AGM requires direct visualization of the migration event.Further-more,the speciﬁc assay used to determine stem cell activity for one population of cells(such as immune reconstitution following irradiation of adult animals)may not be appropriate for a different stem cell population.Distinct host requirements,such as the use of neonatal recipients for cells of the yolk sac,may be necessary. Some of the intrinsic differences between cell populations,such as developmental stage,ease of access,the local niche,and whether they are dividing,may preclude a host transplant assay from detecting engraftment and multilineage reconstitution. Such questions will plague studies of other tissue stem cells, as these stem cells are deﬁned by functional and biological read-outs.Does the Yolk Sac Contain HSCs?Based on cell fate mapping and transplantation experiments in avian and amphibian species,the AGM has been widely viewed as the principal site for HSC production during vertebrate devel-opment.Accordingly,the yolk sac has often been relegated to a subservient position,despite older experiments suggesting that the yolk sac might be the source of adult hematopoiesis. Metcalf and Moore cultured E7.5mouse embryos from which the yolk sac had been removed(Moore and Metcalf,1970).Given that no hematopoietic cells appeared in the fetal liver following several days in culture,they concluded that the yolk sac was the major site of adult blood formation for the embryo.Although hematopoiesis in the yolk sac is largely primitive in character, progenitors within the yolk sac do give rise to deﬁnitive type cells in hematopoietic colony assays,an observation consistent with a yolk sac origin for deﬁnitive cells.This view was supported by other experiments in which speciﬁc donor-derived T cell pop-ulations appeared following transplantation of cells of the yolk sac into fetuses(Weissman et al.,1978).In more recent work,Nishikawa and colleagues have also challenged the dogma that the yolk sac lacks deﬁnitive hemato-poietic stem cells(Samokhvalov et al.,2007).The fate of early embryonic tissues was traced in transgenic mice in which Runx1regulatory elements drive expression of hormonally acti-vated Cre recombinase.Administration of tamoxifen to pregnant female mice at a particular developmental window permits the fate of cells expressing Runx1(visualized by activation of a Flox-LacZ allele)to be assessed.Treatment of embryos at E7.5led to prominent marking of fetal liver cells and adult hema-topoietic cells.As the yolk sac is the only hematopoietic site at E7.5and the only tissue known to express Runx1at E7.5,these ﬁndings suggest that the yolk sac contains deﬁnitive HSCs(or cells that may give rise to HSCs).These experiments were inter-preted to support the yolk sac as a site of HSC formation prior to the AGM,although consensus in theﬁeld is far from unanimous (DeWitt,2007).Diploid-triploid transplants in frogs reveal that 20%of adult blood in some animals is derived from the ventral blood island(the equivalent to the yolk sac),providing indepen-dent evidence that adult hematopoiesis may arise from the yolk sac region.Despite thisﬁnding,it is also clear that the analogous AGM region in Xenopus is the predominant contributor to adult hematopoiesis.The precise origin of HSCs in the adult remains a topic for further debate and study.In Vivo Fate Mapping of Migrating CellsPresumptive HSCs in the zebraﬁsh express the transcription fac-tors c-myb and Runx1(see Figure2).Cagedﬂuorescein dye fate mapping of AGM cells has revealed a new hematopoietic region, the caudal hematopoietic ser uncaging is targeted to a region of cells in which transgenic expression of greenﬂuores-cent protein(GFP)driven by an HSC-speciﬁc promoter marks HSCs in the AGM(Ferkowicz et al.,2003).This approach ensures that laser uncaging occurs speciﬁcally within HSCs.Multiple cells are uncaged and their fate is followed(Jin et al.,2007;Mur-ayama et al.,2006).Uncaged cells of the AGM region that ex-press CD41(a surface marker of early HSCs)or c-myb appear later asﬂuorescent cell populations in the caudal hematopoietic tissue.The larval and adult site of hematopoiesis in the zebraﬁsh is the ter on in the fate map experiments,the larval kid-ney becomesﬂuorescent,demonstrating that cells of the caudal hematopoietic tissue colonize the kidney.In addition,ﬂuores-cence is detected in the thymus.Recent evidence suggests di-rect population of thymic primordia through tissue planes,aﬁnd-ing consistent with earlier experiments in birds showing migration of progenitors to the thymus along the thoracic duct.Thus,pop-ulation of the thymus may occur through circulation and direct migration through tissues.Alternatively,the caudal hematopoi-etic tissue may represent a site similar to the placenta or fetal liver prior to the onset of deﬁnitive hematopoiesis in the kidney.It is generally stated that HSCs of the fetal liver circulate to the adult bone marrow and,hence,are the source of adult hemato-poiesis in birds and mammals(see Review by ird et al., page612of this issue).In contrast,developmental studies reveal that the fetal liver and marrow are seeded at similar times during development(Delassus and Cumano,1996).Direct track-ing of cellular migration is required to distinguish these possibil-ities.Pathways Involved in the Emergence of HSCsThe AGM has been characterized largely by morphology and functional assays,but the pathways involved in HSC generation remain incompletely deﬁned.Studies of chick embryos demon-strate that endoderm has a prominent role and secretes inducing factors.Somitic mesoderm also contributes to the dorsal aspect of the aorta,and the addition of factors—such as VEGF,TGF-b, and FGF—to the somitic mesoderm leads to induction of hema-topoietic tissue.In contrast,TGF-a and EGF suppressed forma-tion of hematopoietic cells(Pardanaud and Dieterlen-Lievre, 1999).634Cell132,631–644,February22,2008ª2008Elsevier Inc.Signaling pathways that regulate the induction of the AGM have recently been uncovered in mouse and zebraﬁsh.Notch1 is required for artery identity and aortic HSC production(Kumano et al.,2003).In the zebraﬁsh mutant mindbomb that lacks Notch signaling,Runx1overexpression rescues HSC production (Burns et al.,2005).Similarly,a Notch1mutant is rescued by Runx1overexpression,suggesting that Runx1lies downstream or parallel to Notch signaling.Other pathways participate in the process including CoupTF-II(Pereira et al.,1999),as well as the CDX-HOX pathway(Davidson et al.,2003).The Wnt/b-catenin and Notch-Delta signaling pathways inﬂu-ence the function of adult HSCs.Treatment of puriﬁed HSCs with Wnt3a protein leads to a modest increase in engrafting cells (Reya et al.,2003).Whereas a pulse of Wnt signaling appears to induce HSCs,constitutive Wnt activation by stabilized b-cat-enin leads to anemia,possibly by stem cell exhaustion as a con-sequence of prolonged Wnt signaling(Kirstetter et al.,2006; Scheller et al.,2006).Wnt signaling may be dispensable for adult HSC homeostasis,given that conditional knockout of b-or g-catenin in hematopoietic cells fails to affect HSC number or engraftment potential(Cobas et al.,2004;Scheller et al.,2006). Stimulation of the Notch pathway also increases HSC activity and appears to be required for the increased self-renewal upon Wnt activation(Duncan et al.,2005).In addition to the Wnt and Notch pathways,new growth factors such as angio-poietin-like proteins appear capable of supporting ex vivo expansion of HSCs(Zhang et al.,2006).A chemical genetic screen has recently revealed a role for the prostaglandin pathway in the production of HSCs in the zebra-ﬁsh.Treatment of embryos with prostaglandin E2(PGE2)aug-ments stem cell production(North et al.,2007),most likely through the EP4receptor,a G-coupled receptor speciﬁcally ex-pressed in the aorta region and activated by PGE2(Villablanca et al.,2007).Prostaglandins also affect the homeostasis of deﬁn-itive adult hematopoiesis,as shown by irradiation recovery as-says,5-ﬂuorouracil stimulation assays,and long-term hemato-poietic reconstitution.Thus,the emergence of HSCs in the aorta involves the prostaglandin pathway and the Notch-Runx pathways,which appear to be independent based on genetic relationships.The hematopoietic system of the Drosophila embryo gener-ates myeloid-like cells critical for tissue remodeling and engulf-ment and phagocytosis of dead cells.The emergence of sites of hematopoiesis during embryogenesis is remarkably similar to that of vertebrates.Drosophila progenitors are also formed adjacent to the circulatory system.Hematopoietic progenitors bud off from head mesoderm.These myeloid cells are transient and ultimately replaced by cells that bud off near the heart re-gion and the great vessel.Vascular endothelial growth factor (VEGF)ligands are required for derivation of adult hematopoi-etic cells,as well as for attracting myeloid cells at speciﬁc sites (Cho et al.,2002).Genetic analysis demonstrates that speciﬁc signaling pathways,such as Notch,are required for the deriva-tion of the lymph gland and a hemangioblast-like cell population (Mandal et al.,2004).Recent studies demonstrate that the lymph gland of the third instar larva of the fruitﬂy is patterned and contains a signaling center that expresses Hedgehog li-gand(Krzemien et al.,2007;Mandal et al.,2007).Hedgehog co-operates with Notch ligands expressed in these regions to form a stem cell niche and regulates the cycling of hematopoietic progenitors.The search is underway for a similar signaling cen-ter in vertebrates.Hedgehog is also required for AGM hemato-poiesis in the zebraﬁsh(Gering and Patient,2005).More re-cently,studies of human embryonic stem cells have indicated that factors such as hedgehog and bone morphogenetic protein(BMP)promote blood production during in vitro differ-entiation.NichesStem cells depend on their microenvironment,the niche,for reg-ulation of self-renewal and differentiation.Studies of Drosophila testes and ovarian stem cells have led to formulation of concepts that may be applicable to the niche in other tissues(Decotto and Spradling,2005;see also the Review by S.J.Morrison and A.C. Spradling,page598of this issue).For instance,in the ovary, a hub cell directly binds to a stem cell and regulates its self-re-newal and differentiation,in part though BMP signaling(see Mini-review by R.M.Cinalli et al.,page559of this issue).In the testis, an apical hub cell expresses the ligand Upd,an activator of the JAK-STAT signaling pathway in adjacent germ cells to control their self-renewal.By analogy to the Drosophila reproductive or-gans,investigators have sought an equivalent of the hub cell for the HSC.As the site of hematopoiesis changes during vertebrate devel-opment,the nature of the stem cell niche must also change.The adult bone marrow niche(depicted in Figure3)has received most attention.Mutant mice in which the BMP pathway is dis-rupted have increased numbers of osteoblasts and HSCs(Calvi et al.,2003;Zhang et al.,2003).Theseﬁndings suggest that os-teoblasts may represent a critical component of the bone mar-row niche for HSCs.As assessed by intravital microscopy, HSCs appear to reside in the periosteal region of calverium mar-row(Sipkins et al.,2005).Transplanted GFP-marked or LacZ-marked HSCs appear to lodge adjacent to osteoblasts.Many factors,including ligands for Notch receptors and N-cadherin, are liberated by osteoblasts,although the contribution of these to adult hematopoiesis remains to be established.The role of N-cadherin as a mediator of interactions with osteoblasts(Zhang et al.,2003),as well as the prominence of osteoblasts for HSC adherence,have been challenged(Kiel et al.,2007).Recentﬁnd-ings suggest that HSCs are maintained in a quiescent state through interaction with thrombopoietin-producing osteoblasts (Yoshihara et al.,2007).The association of HSCs with osteo-blasts is countered by other studies that place HSCs adjacent to vascular cells.The chemokine CXCL12regulates the migra-tion of HSCs to the vascular cells(now called the vascular niche) (Kiel and Morrison,2006).Taken together,theseﬁndings sug-gest that HSCs reside in various sites within the marrow and that their function might depend on their precise localization. Much of the existing debate may be semantic,however,if the os-teoblastic and vascular niches are intertwined and not physically separate.Alternatively,HSCs may truly reside in distinct subre-gions,which may endow them with different activities.Cellular dynamics within the niche are relevant to clinical marrow trans-plantation.For example,recentﬁndings suggest that antibody-mediated clearance of host HSCs facilitates occupancy of the Cell132,631–644,February22,2008ª2008Elsevier Inc.635。

调制线粒体钙作为阿尔茨海默氏症的药物靶老龄化住宅

Ageing Research Reviews 9 (2010) 447–456Contents lists available at ScienceDirectAgeing ResearchReviewsj o u r n a l h o m e p a g e :w w w.e l s e v i e r.c o m /l o c a t e /a rrReviewModulation of mitochondrial calcium as a pharmacological target for Alzheimer’s diseaseClara Hiu-Ling Hung a ,Yuen-Shan Ho a ,Raymond Chuen-Chung Chang a ,b ,c ,∗aLaboratory of Neurodegenerative Diseases,Department of Anatomy,LKS Faculty of Medicine,The University of Hong Kong,Pokfulam,Hong Kong,China bResearch Centre of Heart,Brain,Hormone and Healthy Aging,LKS Faculty of Medicine,The University of Hong Kong,Pokfulam,Hong Kong,China cState Key Laboratory of Brain and Cognitive Sciences,The University of Hong Kong,Pokfulam,Hong Kong,Chinaa r t i c l e i n f o Article history:Received 8February 2010Received in revised form 14May 2010Accepted 19May 2010Keywords:Mitochondria CalciumAlzheimer’s diseaseVoltage dependent anion channel Mitochondrial membrane potentiala b s t r a c tPerturbed neuronal calcium homeostasis is a prominent feature in Alzheimer’s disease (AD).Mito-chondria accumulate calcium ions (Ca 2+)for cellular bioenergetic metabolism and suppression of mitochondrial motility within the cell.Excessive Ca 2+uptake into mitochondria often leads to mitochon-drial membrane permeabilization and induction of apoptosis.Ca 2+is an interesting second messenger which can initiate both cellular life and death pathways in mitochondria.This review critically discusses the potential of manipulating mitochondrial Ca 2+concentrations as a novel therapeutic opportunity for treating AD.This review also highlights the neuroprotective role of a number of currently available agents that modulate different mitochondrial Ca 2+transport pathways.It is reasoned that these mitochondrial Ca 2+modulators are most effective in combination with agents that increase the Ca 2+buffering capacity of mitochondria.Modulation of mitochondrial Ca 2+handling is a potential pharmacological target for future development of AD treatments.© 2010 Elsevier B.V. All rights reserved.1.IntroductionAs the average life span of human population gradually increases,the prevalence of age-related diseases has signiﬁcantly increased.Alzheimer’s disease (AD)is a fatal neurodegenerative disorder,affecting approximately 35.6million people worldwide (Prince and Jackson,2009).AD is the most common form of dementia.The disease is characterized by progressive synaptic dys-function and neuronal loss in various brain regions,especially in the cortex and hippocampus.Severe neurodegeneration in these brain regions results in cognitive,emotion,social and motor impair-ments.With more than a 100years of research,the underlying mechanism of this incurable disease still remains elusive.Per-turbed neuronal calcium (Ca 2+)homeostasis is a common feature in many neurodegenerative diseases including AD,amyotrophic lat-eral sclerosis (ALS),ischemic stroke and Parkinson’s disease (PD)(Mattson and Chan,2003).Increasing lines of evidence support the idea that Ca 2+dysregulation plays a key role in AD pathogenesis∗Corresponding author at:Rm.L1-49,Laboratory Block,Faculty of Medicine Building,Department of Anatomy,LKS Faculty of Medicine,21Sassoon Road,Pok-fulam,Hong Kong SAR,China.Tel.:+852********;fax:+852********.E-mail address:rccchang@hku.hk (R.C.-C.Chang).(Bezprozvanny,2009;Bojarski et al.,2008;LaFerla,2002;Mattson and Chan,2003;Yu et al.,2009).2.Neuronal Ca 2+dysregulation and Alzheimer’s disease Ca 2+signaling is essential for life and death processes includ-ing neuronal excitability,synaptic plasticity,gene transcription and apoptosis (Berridge,1998;Berridge et al.,1998).The Ca 2+dysregulation hypothesis postulates that sustained increase in cytosolic Ca 2+concentrations can lead to neurodegeneration in AD (Khachaturian,1994;Toescu and Verkhratsky,2007).Disturbances in Ca 2+signaling have been found in both sporadic and familial cases of AD (LaFerla,2002).Several age-related perturbations in pathways regulating Ca 2+homeostasis have been reported,sug-gesting a possible linkage between aging and the development of sporadic AD (Bezprozvanny,2009).A small proportion of AD patients (∼5%)suffer from an early-onset familial form that occurs under age of 65(Hardy,2006).The genes involved in familial AD include presenilins (presenilin 1and 2)and amyloid precursor pro-tein (APP)(Hardy and Gwinn-Hardy,1998).Both have been shown to play important roles in Ca 2+signaling (LaFerla,2002).The mech-anisms of how Ca 2+homeostasis is disrupted in AD have been extensively reviewed (Bezprozvanny,2009;Bojarski et al.,2008;LaFerla,2002;Mattson and Chan,2003;Yu et al.,2009).In the fol-1568-1637/$–see front matter © 2010 Elsevier B.V. All rights reserved.doi:10.1016/j.arr.2010.05.003448 C.H.-L.Hung et al./Ageing Research Reviews9 (2010) 447–456lowing sections,we will brieﬂy discuss this issue for readers to understand how Ca2+dyshomeostasis is linked with AD.2.1.APP mutation induces Ca2+inﬂux and elevates cytosolic Ca2+ concentrationsAccumulation of senile plaques and neuroﬁbrillary tangles are two important pathological hallmarks in AD brains.Senile plaques are made of beta-amyloid(A␤)peptides which are derived from APP.Mutations associated with familial AD result in increased pro-duction of the amyloidogenic A␤fragments(Mattson,1997).APP derivatives such as secreted forms of APP(sAPP),A␤-containing fragments,and APP intracellular domain(AICD)have been shown to modulate cellular Ca2+signaling(Leissring et al.,2002;Mattson et al.,1993,1992).A␤aggregates have been found to form cation-selective ion channels in the plasma membrane,resulting in increased cytosolic Ca2+concentrations(Arispe et al.,1993a,b; Kagan et al.,2002).Nevertheless,how A␤-induced membrane pores are related to human AD is still unclear.Oxidative dam-age is another mechanism by which A␤causes disruption in Ca2+ homeostasis and neurotoxicity(Hensley et al.,1994;LaFerla,2002). Accumulation of A␤leads to formation of reactive oxygen species (ROS),which promotes DNA damage,lipid peroxidation,protein carbonylation and nitrosylation.Lipid peroxidation modiﬁes func-tions of membrane transporters and ion channels(Mark et al., 1995),which in turn further elevates basal cytosolic Ca2+concen-trations,forming a vicious cycle(LaFerla,2002;Mattson and Chan, 2003).2.2.Presenilins modulate ER Ca2+signaling and enhance ER Ca2+ releasePresenilins(PS1and PS2)are components of the␥-secretase complex which are involved in the proteolytic cleavage of APP.PS1 and PS2are located in various intracellular compartments such as the endoplasmic reticulum(ER)(Annaert et al.,1999),Golgi apparatus(Annaert et al.,1999),and mitochondria(Ankarcrona and Hultenby,2002).Notably,presenilins are highly enriched in a speciﬁc region where the ER membranes are in close contact with mitochondria namely the ER-mitochondrial-associated mem-branes(MAM)(Area-Gomez et al.,2009).FAD-linked presenilin mutations are believed to alter the activ-ity of␥-secretase such that more A␤are produced,especially the ﬁbrillogenic A␤1–42peptides(Xia et al.,1997).FAD-related mutant presenilins can also affect ER Ca2+handling independent of A␤by exaggerating Ca2+release from the ER in response to agonist stim-ulation.FAD mutant PS1and PS2have been shown to interact with the inositol1,4,5-triphosphate receptor(InsP3R)Ca2+-releasing channels and enhance their gating activity by a gain-of-function effect(Cheung et al.,2010,2008).InsP3Rs are more likely to be in a high-probability burst mode,resulting in enhanced ER Ca2+release (Cheung et al.,2010).However the molecular mechanism of this modulation remains elusive.Depletion of ER Ca2+store triggers Ca2+inﬂux from extracellu-lar space via store-operated Ca2+channels(Putney,1986).This is known as capacitive Ca2+entry(CCE or store-operated Ca2+entry). Stromal interacting molecule1(STIM1)protein acts as Ca2+-sensors on the ER which interacts with Orai1/TRPC channels in the plasma membrane and activates store-operated channels for Ca2+entry (Ong et al.,2007;Zhang et al.,2005).CCE has been shown to be attenuated by presenilin mutants,possibly due to increased Ca2+ in the ER store(Herms et al.,2003;Leissring et al.,2000;Yoo et al.,2000).Moreover,increased levels of STIM1have been found in mouse embryonicﬁbroblasts lacking presenilins,implicating that expression of STIM1may be presenilin-dependent(Bojarski et al., 2009).2.3.Ca2+-dependent tau phosphorylation and dephosphorylationNeuroﬁbrillary tangles formed by hyperphosphorylation of the microtubule-associated protein tau are another hallmark in AD.The phosphorylation state of tau is highly Ca2+-dependent. Tau phosphorylation is regulated by Ca2+-dependent calmodulin-dependent protein kinase II(CaMKII)and calpain(Litersky et al., 1996;Maccioni et al.,2001).Activation of cyclin-dependent pro-tein kinase5(Cdk5)by calpain via p25has been suggested to play a role in tau hyperphosphorylation(Maccioni et al.,2001). On the other hand,calcineurin,a Ca2+/calmodulin-dependent pro-tein phosphatase is involved in tau dephosphorylation(Fleming and Johnson,1995).Tau dephosphorylation was completely atten-uated in rat cerebral-cortical slice pre-treated with the calcineurin inhibitor Cyclosporin A(Fleming and Johnson,1995).Injection of FK506(a calcineurin inhibitor)has been reported to enhance tau phosphorylation at various phosphorylation sites in mouse brain (Luo et al.,2008).On the other hand,calcineurin inhibitors have also been shown to increase phosphorylation of glycogen synthase kinase-3beta(GSK-3␤)at serine-9(Kim et al.,2009).Phosphoryla-tion of GSK-3␤at serine-9inhibits tau phosphorylation by GSK-3␤(Hughes et al.,1993).Hence,both increase and decrease cytosolic Ca2+concentrations contribute to tau phosphorylation,therefore perturbed Ca2+homeostasis may associate with the tau pathology in AD.2.4.Sporadic AD:ApoE4and CALHM1Apolipoprotein E is involved in transporting cholesterol from the blood to the cells.Individuals with the allele for the E4isoform of apolipoprotein E(ApoE4)have an increased risk of sporadic AD (Mahley et al.,2006).ApoE4was found to disrupt Ca2+homeosta-sis by triggering extracellular Ca2+inﬂux and amplifying neuronal Ca2+responses(Hartmann et al.,1994;Tolar et al.,1999).Recent research has identiﬁed polymorphism of a gene called calcium homeostasis modulator1(CALHM1)that may link with sporadic AD.CALHM1encodes for a protein which forms a Ca2+channel on the plasma membrane and controls A␤levels(Dreses-Werringloer et al.,2008).Since then several studies have shown that the P86L polymorphism of CALHM1is associated with AD(Boada et al.,2010; Cui et al.,2010),whilst other studies failed toﬁnd a link between CALHM1and risk of AD(Bertram et al.,2008;Minster et al.,2009; Nacmias et al.,2010;Sleegers et al.,2009).The relevance of CALHM1 in AD remains unclear.2.5.Current“Ca2+-targeted”drugsAs illustrated above,it is clear that Ca2+signaling pathways are highly involved in AD pathogenesis.Several FAD-approved drugs and drugs tested in clinical trials therefore aim to tar-get different Ca2+signaling pathways in order to re-establish the cytosolic Ca2+homeostasis.Memantine(Namenda)is the most common drug for moderate to severe AD.Memantine is a non-competitive N-methyl D-aspartate(NMDA)antagonist.It inhibits Ca2+entry into neurons through the NMDA receptors and therefore reduces excitotoxicity(Bezprozvanny,2009).How-ever,currently it only provides limited beneﬁts for AD patients. Hu et al.(2009)found that speciﬁc antagonists targeting at NMDA receptors containing the GluN2B subunit e.g.ifenprodil and Ro25–6981,might be effective in protecting neurons from A␤-induced inhibition of synaptic plasticity in vivo.EVT-101 (Evotec AG,Hamburg,Germany;/)is a newly developed NMDA receptor subunit2B speciﬁc antagonist. Phase I trial of EVT-101is completed and cognitive performance of patients was improved(NCT00526968).This speciﬁc NMDA receptor antagonist is believed to greatly reduce the chance ofC.H.-L.Hung et al./Ageing Research Reviews9 (2010) 447–456449Fig.1.Life and death pathways of mitochondrial Ca2+accumulation.Left:Under normal conditions,Ca2+inﬂux from extracellular matrix or Ca2+release from the ER causes increase in cytosolic Ca2+concentration([Ca2+]i).Mitochondria rapidly take up cytosolic Ca2+,which is crucial for life processes such as mitochondrial movement,Ca2+ homeostasis and bioenergetic metabolism.Right:When mitochondria are overloaded with Ca2+,mitochondrial permeability transition pores will be triggered to open. Several pro-apoptotic factors will be released to the cytosol,thereby inducing apoptosis.side effects caused by the unspeciﬁc NMDAR antagonist meman-tine.Nimodipine is an isopropyl Ca2+channel blocker which has been shown to improve cognitive performance of dementia patients including AD(Lopez-Arrieta and Birks,2002).MEM-1003(Memory Pharmaceuticals,Montvale,New Jersey,USA; /)is a nimodipine-related neu-ronal L-type Ca2+channel antagonist.Phase IIa clinical trial has recently been completed(NCT00257673),but failed to show sig-niﬁcant improvements in patients(Hareyan,2007).Evidence from NMDA receptor antagonists and Ca2+channel blockers indicates that decreased Ca2+ﬂux into neurons may beneﬁt AD patients.Indeed,classic therapies which aim to compensate the level of acetylcholine in AD patients also cause alteration in Ca2+home-ostasis.FAD-approved acetylcholinesterase(AChE)inhibitors e.g. Donepezil,Galatamine,and Rivastigmine inhibit degradation of acetylcholine and therefore increase acetylcholine concentrations in the brain which is believed to associate with improvement in cognitive functions.In fact,the AChE inhibitors will cause an increase opening of acetylcholine receptors,which are receptor-activated Ca2+channels themselves.The two major classes of FAD-approved AD drugs(NMDA receptor antagonists and AChE inhibitors)apparently will have opposite effects on cytosolic Ca2+ concentration,implying that there is evidence for both increased and decreased cytosolic Ca2+in AD.Dimebon(Latrepirdine)(Medivation Inc.,San Francisco,CA)is an antihistamine drug used in Russia(Bachurin et al.,2001).Recent studies have discovered the novel role of Dimebon as a neuropro-tective agent as well as a cognition-enhancing agent(Bachurin et al.,2001).As an antagonist of NMDAR and Ca2+channels,Dimebon protects neurons by preventing NMDA and Ca2+-induced neurotox-icity(Bachurin et al.,2001).On the other hand,it also increases the level of acetylcholine by inhibiting the AChE(Bachurin et al.,2001). Phase II clinical trial reported that Dimebon is well tolerated and exhibit signiﬁcant improvements in patients with mild to moder-ate AD(Doody et al.,2008).However,a recent Phase III clinical trial failed to show the same promising results(Neale,2010).Additional Phase III clinical trials of Dimebon are still on-going at the moment; therefore the effectiveness of Dimebon in AD remains debatable.Most of the current AD treatments such as AChE inhibitors can provide a one-time elevation of cognitive performance.How-ever,the decline of cognitive ability from this elevated level will occur with the same speed as in non-treated patients.This urges researchers to seek for disease-modifying drugs.3.Mitochondrial Ca2+governs neuronal life and death pathwaysMitochondria are important in maintaining neuronal Ca2+ homeostasis.Normal mitochondrial functions are extremely important for neurons,as neuronal activities such as synaptic transmission and axonal transport require high level of energy. In particular,mitochondrial Ca2+levels are crucial for maintaining cellular functions including bioenergetic metabolism.On the other hand,excessive Ca2+uptake into mitochondria results in rupture of the outer mitochondria membrane,which may then lead to ini-tiation of apoptosis.However,this phenomenon is likely to occur only in vitro.The regulatory systems maintaining the mitochondrial Ca2+homeostasis thus provide an attractive therapeutic target in treating AD.In the following sections we will explain how mito-chondrial Ca2+is involved in life and death pathways in the cell (Fig.1),and how mitochondrial Ca2+is linked to AD.3.1.The cell life pathway:physiological roles of mitochondrialCa2+uptakeCa2+uptake into mitochondria plays a key role in cellular ATP production and mitochondrial motility.Bioenergetic metabolism in mitochondria highly relies upon Ca2+.In the mitochondrial matrix,activity of the metabolic enzymes involved in the Krebs450 C.H.-L.Hung et al./Ageing Research Reviews9 (2010) 447–456cycle(pyruvate,␣-ketoglutarate,and isocitrate dehydrogenases) is all Ca2+-dependent(Rizzuto et al.,2000).Ca2+directly regulates ␣-ketoglutarate and isocitrate dehydrogenases,whilst pyruvate dehydrogenases are activated by Ca2+-dependent phosphatases (Rizzuto et al.,2000).Ca2+concentration in mitochondria therefore determines the rate of ATP synthesis for the cell.Mitochondria are mobile organelles which travel along the axons to regions of increased energy need in the cell,such as synapses(Chang et al.,2006;Hollenbeck and Saxton,2005). Microtubules-dependent mitochondrial motility is regulated by the kinesin1/Miro/Milton complex(Glater et al.,2006;Guo et al., 2005;Stowers et al.,2002).Miro(mitochondrial Rho GTPase)is a mitochondrial outer membrane protein.The activity of Miro is Ca2+-dependent due to the presence of a pair of Ca2+-binding EF hand motifs(Frederick et al.,2004).Milton is a cytoplasmic protein which binds with Miro to form a protein complex that links kinesin-1to mitochondria for anterograde transport(Glater et al.,2006;Guo et al.,2005;Stowers et al.,2002).The Ca2+-binding EF-hand domain of Miro is essential for Ca2+-dependent mitochondrial movement. Elevated Ca2+causes kinesin heavy chain to dissociate with micro-tubules,suppressing mitochondrial motility(Wang and Schwarz, 2009).Ca2+-dependent mitochondrial motility is crucial for dis-tribution of mitochondria in neurons.It recruits mitochondria to cellular regions with the need of ATP supply and Ca2+buffering e.g. activated synapses(Macaskill et al.,2009).In addition,Miro is essential for regulation of mitochondrial morphology.At resting low cytosolic Ca2+levels,Miro facil-itates the formation of elongated mitochondria by inhibiting dynamin-related protein1(Drp-1or dynamin-like protein1,DLP-1)-mediatedﬁssion(Saotome et al.,2008).On the other hand, high cytosolic Ca2+triggers fragmentation and shortening of mito-chondria(Saotome et al.,2008).Miro-mediated redistribution of mitochondria has also been shown to increase their ability to accumulate Ca2+(Saotome et al.,2008).Evidence from the above studies demonstrates that Miro acts as a cytosolic Ca2+-dependent regulator of mitochondrial dynamics.Meanwhile,calcineurin,a Ca2+-dependent phosphatases,has been shown to regulate the translocation of cytosolic Drp-1via dephosphorylation duringﬁs-sion(Cereghetti et al.,2008).Clearly,Ca2+regulates motility,distribution,morphology and functions of mitochondria in physiological conditions.It is there-fore crucial to maintain mitochondrial Ca2+homeostasis for normal cellular functioning.If this homeostasis is disrupted,a death signal can be resulted.3.2.The cell death pathway:mitochondrial Ca2+overload triggers intrinsic apoptosisThe physiological Ca2+signal can switch to a death signal when the Ca2+level is beyond the threshold.Hence,excessive Ca2+ uptake into mitochondria can be lethal to neurons.The intrinsic (mitochondrial)pathway of apoptosis is triggered by intracellu-lar stress,such as Ca2+overload and oxidative stress(Galluzzi et al.,2009).Mitochondria integrate pro-and anti-apoptotic signals and determine the fate of the cell.If death signals predomi-nate,mitochondrial-membrane-permeabilization(MMP)occurs, and large conductance permeability-transition-pores(PTP)opens (Galluzzi et al.,2009).PTP opening allows uncontrolled entry of solutes and water into the mitochondrial matrix by osmotic forces (Galluzzi et al.,2009).This causes mitochondria to swell and leads to rupture of the outer mitochondria membrane,releasing proteins from the intramembrane space e.g.cytochrome c into the cytosol (Galluzzi et al.,2009).MMP results in mitochondrial depolariza-tion,uncoupling of oxidative phosphorylation,overproduction of ROS and release of pro-apoptotic proteins to the cytosol,eventually leading to cell death.When MMP is permanent and numerous mito-chondria are continuously affected,neurons can no longer cope with the stress and apoptosis is initiated(Galluzzi et al.,2009). Physiological mitochondrial Ca2+concentrations do not induce PTP opening,but will work in synergy with pro-apoptotic stim-uli(Rizzuto et al.,2009).The“double hit”hypothesis proposes that apoptotic stimuli have dual targets(Pinton et al.,2008).On one hand,it causes Ca2+release from the ER and subsequent Ca2+uptake by mitochondria.On the other hand,it makes mitochondria more sensitive to potential Ca2+damaging effects(Pinton et al.,2008).The above pathways are summarized in Fig.1.Given the dual roles of mitochondria Ca2+in neurons,we will critically discuss the possibility of modulating Ca2+in mitochondria as a potential pharmacological target for AD in this review.4.Mitochondrial Ca2+handling and ADMitochondrial dysfunction is a prominent feature in AD.A␤has been found in mitochondria of AD brain and transgenic mouse model of AD overexpressing A␤.A␤peptides accumulate in mito-chondria and are associated with oxidative stress,disrupted Ca2+ homeostasis,impaired energy metabolism and induction of apop-tosis(Mattson et al.,2008).Mitochondria from aged cerebellar granular neurons are depolarized and less efﬁcient in handling Ca2+ load(Toescu and Verkhratsky,2007).Cortical mitochondria from 12-month-old mice also show a reduced capacity for Ca2+uptake when challenged with CaCl2pulses,compared to that of6-month-old mice(Du et al.,2008).Mitochondria isolated fromﬁbroblasts of AD patients exhibit reduced Ca2+uptake compared to age-matched control,suggesting that Ca2+buffering ability may be impaired in the mitochondria of ADﬁbroblasts(Kumar et al.,1994).Follow-ing oxidative stress,the increase in Ca2+uptake in mitochondria of ADﬁbroblasts is much greater than that in control,implicat-ing that mitochondria from ADﬁbroblasts have a higher sensitivity towards oxidative stress(Kumar et al.,1994).Mitochondria with over-expression of human APP also show a lower Ca2+capacity compared to non-transgenic mitochondria(Du et al.,2008).A␤1–42 oligomer induces Ca2+overload in mitochondria in both cortical and cerebellar granular neurons(Sanz-Blasco et al.,2008).The increase is limited to a pool of mitochondria close to the sites of Ca2+entry and release(Sanz-Blasco et al.,2008).Ca2+overload in mitochondria causes increased ROS production and impairment of bioenergetic metabolism which eventually leads to cell death. Mutations in presenilins may promote mitochondrial dysfunction by perturbing ER Ca2+handling,which promotes synaptic mito-chondrial Ca2+overload and in turn triggers apoptosis.A recent study has also shown that mutated CALHM1may cause slower kinetics of mitochondrial Ca2+uptake and release,increasing the risk of mitochondrial Ca2+overload(Moreno-Ortega et al.,2010).The importance of mitochondrial Ca2+in apoptosis has been emphasized in neuronal death in AD.However,mitochondrial Ca2+ is also important in earlier stages of the disease.The rupture of mitochondrial membrane caused by Ca2+overload reduces the number of“healthy”mitochondria,and this will affect crucial neu-ronal functions including synaptic transmission and axonal trans-port.This could perhaps account for some of the early symptoms of the disease e.g.memory impairment.In this notion,the main-tenance of mitochondrial Ca2+homeostasis is important for both early and later stages of the disease.In the following paragraphs, we will illustrate different inﬂux and efﬂux pathways regulating the mitochondrial Ca2+homeostasis,and how different agents tar-geting these pathways can provide neuroprotection in AD.5.Mitochondria in neuronal Ca2+signalingCa2+signaling causes transient changes in cytosolic Ca2+con-centration.Mitochondria rapidly take up Ca2+when a physiologicalC.H.-L.Hung et al./Ageing Research Reviews 9 (2010) 447–456451Table 1Current agents showing neuroprotective effect via modulation of mitochondrial Ca 2+concentrations. «(mitochondrial membrane potential);Ca 2+(calcium ions);FCCP [carbonyl cyanide-p-(triﬂuoromethoxy)phenylhydrazone];mAPP (mutant amyloid precursor protein);mPTP (mitochondrial permeability transition pore);NMDA (N-methyl D-aspartate);NSAIDs (non-steroid anti-inﬂammatory drugs),TAB (Tournefolic acid B);VDAC (voltage-dependent anion channel).Agent/Drug Site of action EffectModelNeurotoxicity model ReferenceFCCP DepolarizationReduce Ca 2+uptake Rat cerebellar granule neurons Rat cortical neuronsA ␤1–42oligomer Sanz-Blasco et al.(2008)NSAIDS DepolarizationReduce Ca 2+uptake Rat cerebellar granule neurons A ␤1–42oligomer Sanz-Blasco et al.(2008)Minocycline VDACDepolarizationReduce Ca 2+uptake Rat cerebellar granule neurons NMDAGarcia-Martinez et al.(2010)KB-R7943Na +/Ca 2+exchanger Reduce Ca 2+uptake Rat cerebellar granule neurons Glutamate Storozhevykh et al.(2009)TABUnknown Reduce Ca 2+uptake Rat cortical neurons A ␤25–35Chi et al.(2008)DimebonmPTPInhibit mPTP opening Rat liver mitochondriaA ␤25–35Bachurin et al.(2003)Cyclosporin ACyclophilin DInhibit mPTP opening Increase Ca 2+buffering capacityMouse cortical mitochondriamAPPTrangenic miceDu et al.(2008)stimulus elicits an increase in cytosolic Ca 2+concentrations.This uptake machinery allows mitochondria to act as “Ca 2+buffers”to maintain the normal homeostasis.At the same time,it also provides Ca 2+for various mitochondrial functions.Mitochondrial Ca 2+sig-naling therefore plays an important role in determining the fate of neurons.Mitochondria possess various Ca 2+inﬂux and efﬂux path-ways (Fig.2),which provide attractive targets for manipulation of Ca 2+concentrations within the organelle (Table 1).5.1.Pathways for Ca 2+uptake5.1.1.Voltage-gated anion channel regulates Ca 2+uptake in theouter mitochondrial membraneThe outer mitochondrial membrane (OMM)is relatively per-meable to Ca 2+due to the high conductance voltage dependent anion channel (VDAC)located in this membrane.Over-expression of VDAC has been shown to promote Ca 2+uptake into mitochon-dria (Rapizzi et al.,2002).Closure of VDAC enhances Ca 2+inﬂux into mitochondria,thereby promoting mitochondrial permeabil-ity transition and subsequent cell death (Rizzuto et al.,2009;Rostovtseva et al.,2005;Tan and Colombini,2007).5.1.2.Mitochondrial membrane potential regulates Ca 2+entry via the uniporter in the inner mitochondrial membraneIn the inner mitochondrial membrane (IMM),the mitochon-drial Ca 2+uniporter regulates Ca 2+entry into mitochondria.The uniporter is a highly selective divalent cation channel (Kirichok et al.,2004).The electron transport chain (ETC)in the IMM con-Fig.2.Mitochondrial Ca 2+signaling pathways. «m (mitochondrial membrane potential);[Ca 2+]m (mitochondrial Ca 2+concentration);[Ca 2+]c ,(cytosolic Ca 2+con-centration);H +(hydrogen ions);PTP (mitochondria permeability transition pore);Na +(sodium ions),VDAC (voltage-dependent anion channel);CypD (cyclophilin D);ANT (adenine nucleotide translocase).sists of ﬁve protein complexes for the production of ATP.The ETC maintains an electrochemical gradient of −180mV across the IMM,and is known as the mitochondrial membrane potential ( «m ). «m provides a driving force for Ca 2+to enter the mitochondria via the uniporter.Given that mitochondrial Ca 2+overload can lead to cell death,depolarization of «m (hence reduced driving force for Ca 2+entry)can be a drug target for stopping excessive Ca 2+from entering mitochondria.5.2.Pathways for calcium efﬂux5.2.1.Antiporters and permeability transition pores for mitochondrial calcium sequestrationBesides various Ca 2+uptake systems mentioned,there are also a few pathways for Ca 2+efﬂux.The Na +/Ca 2+and H +/Ca 2+antiporters are two main routes for Ca 2+release from mitochondria.Generally,3Na +and 3H +enter mitochondria via the respective antiporters when a Ca 2+is extruded (Fig.2).Hence,concentrations of Na +and H +can affect Ca 2+concentration in the mitochondria.These efﬂux pathways can become saturated when there is high Ca 2+concentration in the matrix,which can lead to mitochondrial Ca 2+overload (Rizzuto et al.,2009).As mentioned earlier,mitochon-drial Ca 2+overload triggers opening of PTP which locates across the OMM and IMM.The molecular identity of PTP is still uncer-tain,but it is suggested to be a multimeric complex composed of the VDAC,an integral protein called adenine nucleotide translo-case (ANT)on the IMM,and a matrix protein called cyclophilin D (CypD).However,mitochondria lacking VDAC (Szalai et al.,2000)and ANT (Kokoszka et al.,2004)have been shown to undergo Ca 2+-induced PTP opening,implying that the two components may not be prerequisite for MPT (Rizzuto et al.,2009).PTP is a non-selective channel of which operation is dependent on the mitochondrial matrix Ca 2+.High Ca 2+levels in the mitochondrial matrix activate translocation of CypD to the IMM.CypD binds to ANT and inhibits ATP/ADP binding,thereby inducing opening of PTP (Rizzuto et al.,2009).5.3.ER/mitochondria calcium crosstalk is important for efﬁcient mitochondrial calcium signalingMitochondria rapidly take up Ca 2+released from the ER.The proximate juxtaposition between these two organelles ensures efﬁcient Ca 2+transfer (Rizzuto et al.,1993,1998).In fact,the contact between the ER and mitochondria is estimated to be 5–20%of the total mitochondrial surface (Rizzuto et al.,1998).MAM is a region between the ER and mitochondria enriched with enzymes and proteins involved in lipid biosythesis and Ca 2+sig-naling between the organelles (Vance,1990).Indeed,VDAC on the OMM is located in the interface between the ER and mitochon-。

雅思阅读中关于生物生理的高频词汇

雅思阅读中关于生物生理的高频词汇下面是我搜集的雅思阅读中关于生物生理的高频词汇：molecule 分子protein 蛋白质enzyme 酶catalyst 催化剂chlorophyll 叶绿素photosynthesis 光合作用botany 植物学flora 植物群fauna 动物群bacterium bacteria 细菌carnation 康乃馨fade 凋谢，褪色organism 机体，组织arthropod 节肢动物reptile 爬行动物amphibian 两栖动物mammal 哺乳动物primate 灵长目动物evolution 进化anthropoid 类人猿gene 基因genetics 遗传学helix 螺旋，螺旋壮物identical 同一的mutation 突变predator 捕食者embryo 胚胎roe 鱼子tadpole 蝌蚪caterpillar 毛毛虫grasshopper 蚱蜢，蝗虫cricket 蟋蟀 (另)板球pollen 花粉传粉hive 蜂房pupa 蛹penguin 企鹅raccoon 浣熊hibernate 冬眠torpid 麻木的，蛰伏的cerebral (大)脑的hemisphere 半球cortex 脑皮层migraine 偏头疼somatic 躯体的limb 四肢anatomy 解剖，剖析paralyze 使瘫痪artery 动脉gland 腺体pancreas 胰hormone 荷尔蒙，激素cholesterol 胆固醇efficacy 功效。

亚专科医学英语

亚专科医学英语亚专科医学英语是指涉及亚专科医学（subspecialty medicine）的英语表达和专业术语。

亚专科医学是指在一定的医学领域内专注于某个特定疾病、器官系统或治疗方法的医学专业。

以下是一些常见的亚专科医学英语词汇和表达：1. 亚专科医生(Subspecialist)：专注于某个亚专科领域的医生。

2. 亚专科领域(Subspecialty field)：医生专注研究和治疗的亚专科医学领域。

3. 临床症状(Clinical symptoms)：指患者表现出的身体上的异常状况，如疼痛、呕吐等。

4. 诊断(Diagnosis)：通过病史、体格检查、实验室检查等手段确定疾病或病因。

5. 治疗方案(Treatment plan)：根据诊断结果制定的治疗计划，包括药物治疗、手术等。

6. 手术(Surgery)：外科医生通过切除、修复、置入植物等方法治疗疾病或损伤的操作。

7. 药物治疗(Medical treatment)：使用药物来预防、缓解、治疗疾病的方法。

8. 康复(Rehabilitation)：通过物理疗法、运动疗法等手段帮助患者康复和恢复功能。

9. 研究报告(Research report)：描述亚专科领域研究成果或临床试验结果的专业报告。

10. 学术会议(Academic conference)：汇集亚专科医生和研究人员展示和讨论研究成果的会议。

以上只是一些常见的亚专科医学英语词汇，具体内容还有很多。

在学习亚专科医学英语时，除了掌握专业词汇，还要了解相关的医学知识和研究进展，以便更好地理解和运用这些专业术语。

医学英语分类词汇常见疾病名称

医学英语分类词汇常见疾病名称医学英语分类词汇常见疾病名称医学英语是一门大学专业，学制是四年(北京大学医学部为五年制)授予学位是文学学士学位或教育学学士学位或理学学士(如北大)。

下面是yjbys店铺为大家带来的医学英语分类词汇常见疾病名称的知识，欢迎阅读。

常见疾病名称Internal Medicine 内科Acidosis 酸中毒Adams-Stokes syndrome 亚-斯氏综合症alcoholism, alcoholic intoxication 酒精中毒alkalosis 碱中毒anaphylaxis 过敏症anemia 贫血iron deficiency anemia 缺铁性贫血megaloblastic anemia 巨幼红细胞性贫血aplastic anemia 再生障碍性贫血angiitis 脉管炎angina pectoris 心绞痛arteriosclerosis 动脉硬化apoplexy 中风auricular fibrillation 心房纤颤auriculo-ventricular block 房室传导阻滞bronchial asthma 支气管哮喘bronchitis 支气管炎bronchiectasis 支气管扩张bronchopneumonia 支气管肺炎carcinoma 癌cardiac arrhythmia 心律紊乱cardiac failure 心力衰竭cardiomyopathy 心肌病cirrhosis 肝硬化coronary arteriosclerotic heart disease 冠状动脉硬化性心脏病Crohn disease 克罗恩病Cushing's syndrome 库欣综合症diabetes 糖尿病diffuse intravascular coagulation 弥散性血管凝血dysentery 痢疾enteritis 肠炎gastric ulcer 胃溃疡gastritis 胃炎gout 痛风hepatitis 肝炎Hodgkin's disease 霍奇金病hyperlipemia 高脂血症，血脂过多hyperparathyroidism 甲状旁腺功能亢进hypersplenism 脾功能亢进hypertension 高血压hyperthyroidism 甲状腺功能亢进hypoglycemia 低血糖hypothyroidism 甲状腺功能减退infective endocarditis 感染性心内膜炎influenza 流感leukemia 白血病lobar pneumonia 大叶性肺炎lymphadenitis 淋巴结炎lymphoma 淋巴瘤malaria 疟疾malnutrition 营养不良measles 麻疹myeloma 骨髓瘤myocardial infarction 心肌梗死myocarditis 心肌炎nephritis 肾炎nephritic syndrome 肾综合症obstructive pulmonary emphysema 阻塞性肺气肿pancreatitis 胰腺炎peptic ulcer 消化性溃疡peritonitis 腹膜炎pleuritis 胸膜炎pneumonia 肺炎pneumothorax 气胸purpura 紫癜allergic purpura 过敏性紫癜thrombocytolytic purpura 血小板减少性紫癜pyelonephritis 肾盂肾炎renal failure 肾功能衰竭rheumatic fever 风湿病rheumatoid arthritis 类风湿性关节炎scarlet fever 猩红热septicemia 败血症syphilis 梅毒tachycardia 心动过速tumour 肿瘤typhoid 伤寒ulcerative colitis 溃疡性结肠炎upper gastrointestinal hemorrhage 上消化道血Neurology 神经科brain abscess 脑脓肿cerebral embolism 脑栓塞cerebral infarction 脑梗死cerebral thrombosis 脑血栓cerebral hemorrhage 脑出血concussion of brain 脑震荡craniocerebral injury 颅脑损伤epilepsy 癫痫intracranial tumour 颅内肿瘤intracranial hematoma 颅内血肿meningitis 脑膜炎migraine 偏头痛neurasthenia 神经衰弱neurosis 神经官能症paranoid psychosis 偏执性精神病Parkinson's disease 帕金森综合症psychosis 精神病schizophrenia 精神分裂症Surgery 外科abdominal external hernia 腹外疝acute diffuse peritonitis 急性弥漫性腹膜炎acute mastitis 急性乳腺炎acute pancreatitis 急性胰腺炎acute perforation of gastro-duodenal ulcer急性胃十二指肠溃疡穿孔acute pyelonephritis 急性肾盂肾炎anal fissure 肛裂anal fistula 肛瘘anesthesia 麻醉angioma 血管瘤appendicitis 阑尾炎bleeding of gastro-duodenal ulcer 胃十二指肠溃疡出血bone tumour 骨肿瘤breast adenoma 乳房腺瘤burn 烧伤cancer of breast 乳腺癌carbuncle 痈carcinoma of colon 结肠炎carcinoma of esophagus 食管癌carcinoma of gallbladder 胆囊癌carcinoma of rectum 直肠癌carcinoma of stomach 胃癌cholecystitis 胆囊炎cervical spondylosis 颈椎病choledochitis 胆管炎cholelithiasis 胆石症chondroma 软骨瘤dislocation of joint 关节脱位erysipelas 丹毒fracture 骨折furuncle 疖hemorrhoid 痔hemothorax 血胸hypertrophy of prostate 前列腺肥大intestinal obstruction 肠梗阻intestinal tuberculosis 肠结核lipoma 脂肪瘤lithangiuria 尿路结石liver abscess 肝脓肿melanoma 黑色素瘤osseous tuberculosis 骨结核osteoclastoma 骨巨细胞瘤osteoporosis 骨质疏松症osteosarcoma 骨质疏松症osteosarcoma 骨肉瘤Paget's disease 佩吉特病perianorecrtal abscess 肛管直肠周围脓肿phlegmon 蜂窝织炎portal hypertension 门静脉高压prostatitis 前列腺炎protrusion of intervertebral disc 椎间盘突出purulent arthritis 化脓性关节炎pyogenic ostcomyclitis 化脓性骨髓炎pyothorax 脓胸rectal polyp 直肠息肉rheumatoid arthritis 类风湿性关节炎rupture of spleen 脾破裂scapulohumeral periarthritis 肩周炎tenosynovitis 腱鞘炎tetanus 破伤风thromboangiitis 血栓性脉管炎thyroid adenocarcinoma 甲状腺腺癌thyroid adenoma 甲状腺腺瘤trauma 创伤urinary infection 泌尿系感染varicose vein of lower limb 下肢静脉曲张Paediatrics 儿科acute military tuberculosis of the lung 急性粟粒性肺结核acute necrotic enteritis 急性坏死性结肠炎anaphylactic purpura 过敏性紫癜ancylostomiasis 钩虫病ascariasis 蛔虫病asphyxia of the newborn 新生儿窒息atrial septal defect 房间隔缺损birth injury 产伤cephalhematoma 头颅血肿cerebral palsy 脑性瘫痪congenital torticollis 先天性斜颈convulsion 惊厥Down's syndrome 唐氏综合症glomerulonephritis 肾小球肾炎hemophilia 血友病infantile diarrhea 婴儿腹泻intracranial hemorrhage of the newborn 新生儿颅内出血intussusception 肠套叠necrotic enterocolitis of newborn 新生儿坏死性小肠结膜炎neonatal jaundice 新生儿黄疸nutritional iron deficiency anemia 营养性缺铁性贫血nutritional megaloblastic anemia 营养性巨幼细胞性贫血patent ductus arteriosis 动脉导管未闭poliomyelitis 骨髓灰质炎premature infant 早产儿primary tuberculosis 原发性肺结核progressive muscular dystrophy 进行性肌肉营养不良pulmonary stenosis 肺动脉狭窄purulent meningitis 化脓性脑膜炎rickets 佝偻病sepsis of the newborn 新生儿败血症tetanus of the newborn 新生儿破伤风tetralogy of Fallot 法洛四联症thrush 鹅口疮，真菌性口炎varicella 水痘ventricular septal defect 室间隔缺损viral encephalitis 病毒性脑炎viral myocarditis 病毒性心肌炎Gynecology and Obstetrics 妇产科abortion 流产adenomyosis 子宫内膜异位症amniotic fluid embolism 羊水栓塞Bartholin's cyst 巴氏腺囊肿carcinoma of cervix 子宫颈癌carcinoma of endometrium 子宫内膜癌carcinoma of ovary 卵巢癌cervicitis 宫颈炎chorio-epithelioma 绒毛膜上皮癌corpora luteum cyst 黄体囊肿dystocia 难产eclampsia 子痫edema-proteinuria-hypertension syndrome 水肿蛋白尿高血压综合征(妊娠高血压综合征) endometriosis 子宫内膜异位症extrauterine pregnancy 子宫外孕hydatidiform mole 葡萄胎hyperemesis gravidarum 妊娠剧吐infertility 不育症irregular menstruation 月经失调lochia 恶露monilial vaginitis 念珠菌性阴道炎multiple pregnancy 多胎妊娠myoma of uterus 子宫肿瘤oligohydramnios 羊水过少ovarian tumour 卵巢肿瘤pelvic inflammatory disease 盆腔炎placenta previa 前置胎盘placental abruption 胎盘早期剥离pregnancy-hypertension syndrome 妊娠高血压综合症premature birth 早产premature rupture of membrane 胎膜早破postpartum hemorrhage 产后出血puerperal infection 产褥感染rupture of uterus 子宫破裂trichomonas vaginitis 滴虫性阴道炎uteroplacental apoplexy 子宫胎盘卒中vulvitis 外阴炎Ophthalmology and Otorhinolaryngology 五官科amblyopia 弱视amygdalitis, tonsillitis 扁桃体炎astigmatism 散光carcinoma of nasopharynx鼻咽癌carcinoma of larynx 喉癌cataract 白内障tinnitus 耳鸣chalazion 霰粒肿，脸板腺囊肿colour blindness 色盲deflection of nasal septum 鼻中隔偏曲deafness 聋furuncle of nasalvestibule 鼻前庭疖glaucoma 青光眼heterotropia 斜视hyperopia 远视injury of cornea 角膜损伤ceruminal impaction 耵聍嵌塞iritis 虹膜炎keratitis 角膜炎labyrinthitis 迷路炎，内耳炎laryngitis 喉炎mastoiditis 乳突炎myopia 近视nasal sinusitis 鼻窦炎otitis media 中耳炎obstruction of larynx 喉梗阻peritonsillar abscess 扁桃体中脓肿pharyngitis 咽炎rhinitis 鼻炎Dermatoloty 皮肤科acne 痤疮carcinoma of skin 皮肤癌bed sore 褥疮decubitus ulcer 褥疮性溃疡drug eruption 药皮疹eczema 湿疹herpes simplex 单纯疱疹herpes zoster 带状疱疹lupus erythematosis 红斑狼疮psoriasis 牛皮癣urticaria 荨麻疹wart 疣【医学英语分类词汇常见疾病名称】。

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Types of Adult Stem Cells
Hematopoietic stem cells: blood and immune system Mesenchymal stem cells: bone, cartilage, fat, muscle, tendon/ligament Neural stem cells: neurons, glial cells Epithelial stem cells: skin, linings
Asymmetric Cell Division
1. Proliferates 2. Maintains pop. 3. Creates Progenitor Cell
Progenitor cell
Stem cell
Stem cell
Location of Adult Stem Cells
• Adult stem cells and progenitor cells reside through out your body • These stem cells reside in a specific area of each tissue called the “stem cell niche” • This niche is a particular microenvironment that fosters the growth of resident stem cells • Mutations in cells, signals they receive, and changes in the microenvironment can activate a stem cell
Adult Stem Cells, Homeostasis, and Regenerative Medicine
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What arem cell is an undifferentiated (or partially-differentiated) cell found in tissues and organs • They can self-renew and differentiate to become most or all of the specialized cell types within their specific tissue lineage. • Adult stem cells
How Regeneration Works
• Adult stem cells normally remain quiescent (nondividing) for relatively long periods of time until they are activated by signals to maintain tissues • When activated they divide through a process called asymmetric cell division • Through this process they are able to maintain their populations and differentiate into the desired cell types by the creation of a progenitor cell • A progenitor cell, in contrast to stem cells, is already far more specific: they are pushed to differentiate into their "target" cell.
Stabilize health and functioning, regardless of the outside changing conditions.
• One piece of homeostasis is the constant or periodic generation of new cells to replace old, damaged, and dying cells • Adult stem cells fulfill this role through the process of regeneration
Found in the bone marrow from very early on in development, as well as in umbilical cord blood and placental tissue
Mesenchymal stem cells
• These stem cells will differentiate into:
– Maintain cell populations – Help you heal – Play a role in aging
Homeostasis
• The ability to regulate internal conditions, usually by a system of feedback controls
Hematopoietic stem cells
Give rise to all the blood cell types:
• Myeloid (monocytes and macrophages, neutrophils, basophils, eosinophils, erythrocytes, megakaryocytes/platelets, dendritic cells) • Lymphoid (T-cells, B-cells, NK-cells)