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n. 释放；松释动作；脱扣释放
v. 释放；排放（release的现在分词）
- 引用次数：164
Effects of long-term fertilization on accumulating and releasing of phosphorus in greenhouse soil was investigated.
研究了长期定位条件下不同施肥处理对保护地土壤磷素积累及释放的影响。
参考来源 -
- 引用次数：3
The achievements of domestication and manual releasing, demonstrated the feasibility to reproduce and put them into rivers under the existing condition.
人工驯养和放流的初步成功，论证了在鸭绿江上游支流目前的生态环境状况下进行细鳞鱼人工增殖放流的可行性。
参考来源 - 鸭绿江上游支流细鳞鱼（Brachymystax lenok）的生态环境调查及人工增殖研究
- 引用次数：1
参考来源 - 放归大熊猫Ailuropoda melanoleuca预选栖息地评估
- 引用次数：108
Both Elovich and two-constant equations could be used to fit the releasing kinetics quite well.
释放动力学过程可以用Elovich方程和双常数速率方程(Freundlich修正式)较好地描述。
参考来源 -
弃权；让渡；让渡证书
放弃；让予(财产、权利等)：
擒纵装置；排放装置；释放装置；(照相机等的)保险扣
释音；淡释
&2,447,543篇论文数据，部分数据来源于
re le a si n g
emotionally purging (of e.g. art)
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释放激素；释放因子
释放激素；释放因子
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感谢您的反馈，我们会尽快进行适当修改！1 1 th In te r n a tio n a l C o n fe r e n c e P R IM A R Y T H E R A P Y O F E A R L Y. A d ju v a n te S tr a h le n th e r a p ie - PDF
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1 1 1 th In te r n a tio n a l C o n fe r e n c e P R IM A R Y T H E R A P Y O F E A R L Y BREAST CANCER A d ju v a n te S tr a h le n th e r a p ie M & r z , S t.g a lle n L e o n o r e H a n d l-z e lle r2 3 4 5 6 7 RED DRESS AGAI NST PI NK RI BBON In a d & q u a te D o s e n a m H e r z e n e r h & h e n d e n s p & te n H e r z to d!8 Ex a m p l e - Br ea st D o s e w a s h (K o r r e m a n e t a l)9 MINIMIERUNG DER MORBIDIT&AT DER LOKALEN BEHANDLUNG BEI10 RADI ATI ON THERAPY: AFTER BCS R T fo r a ll p ts a fte r BCS? Y: 81 % N: 1 9% A: 0% 80% 1 5% 5% S h o u ld e ld e r ly w ith E R + a n d lo n g life e x p e c ta n c y r e c e iv e RT?11 RADI ATI ON THERAPY: AFTER BCS S h o u ld e n d o c r in e th e r a p y b e u s e d w ith o u t R T fo r E + T1 N 0 cancer? (p o s tm.) C o u ld e n d o c r in e th e r a p y b e u s e d in p la c e o f R T fo r E + T 1 N 0 c a n c e r? Y: 24% N: 73% A: 3% 51 % 46% 3%12 Ef f ek t d er LR- Red. Na c h 5 Ja h r en a u f d i e Mo r t a l i t & t n a c h 1 5J13 LR BEI I NVASI VEN UND NI CHTI NVASI VEN MA - TUMOREN14 RADI ATI ON THERAPY: DCI S S h o u ld R T b e c o n s id e r e d s ta n d a r t fo r e x c is e d D C IS? C a n R T b e a v o id e d in e ld e r ly? C a n R T b e a v o id e d in lo w g r a d e D C IS? J: 81 % N: 1 9% A: 0% 61 % 39% 0% 59% 32% 1 0%15 W o n g J S, K a e lin C H, T r o y a n S L, e t a l. P r o s p e c tiv e s tu d y o f w id e e x c is io n a lo n e fo r d u c ta l c a r c in o m a in s itu o f th e b r e a s t. J C lin O n c o l 2 4 : , P a t. (m e d ia n 5 1 J, ), m it k l. (&2,5 c m ), m a m m o g r a p h is c h d e d e k tie r te m, G 1 u. 2, D C IS, m it g r o & e n R R (&1 c m ), k e in e R T 1 3 L R im N a c h b. (0,6 5,2 J.) n a c h O P J & h r l.r e z.r a te : 2,4 % 5 -J.R e z.r a te :1 2 % A K Z E P T A B L E R G R E N Z W E R T E R R E IC H T S T U D IE N A B B R U C H!!16 THE EORTC AMAROS TRIAL17 PMRT EINFL.AUF L- Rez.+ &UBERL. (25 t r i a l s o f Ma st ec t + AC& RT) 8505 p t s N+18 PMRT EINFL.AUF L- Rez.+ &UBERL. (25 t r i a l s o f Ma st,ac,& RT) p t s N-19 R. THERAPY: AFTER MASTECTOMY S h o u ld P M R T b e s ta n d a r t w ith 4 L N? S h o u ld a ll p ts. w ith N + (1-3 ) b e ir r a d.? E s p e c ia lly if y o u n g a n d w ith o th e r p o o r p r o g n o s tic fa c to r s? J: N: A: 93% 7% 0% 22% 70% 8% 72% 1 8% 1 0%20 1 5J LRR a s Fu n c t i o n o f Nu m b er o f + LN a n d PMRT21 22 23 APBI24 PHASE III MULTICENTER TRIAL Groupe Europ&en de Curietherapie European Society for Therapeutic Radiology and Oncology GEC-ESTRO APBI TRIAL25 RAD. THERAPY: ACCELERATED S h o u ld a c c e le r a te d W h o le B r e a s t R T (W B R T ) b e c o n s id e r e d a n a c c e p ta b le o p tio n? S h o u ld in tr a o p e r a tiv e p r im a r y b r e a s t R T b e c o n s id e r e d e x p e r im e n ta l? Y: N: A: 83% 1 0% 7% 84% 1 6% 0%26 27 28 29 30 1 5Y FREQUENCES OF LRR AND SURVIVAL AS A FUNCTION OF + LN AND PMRT31 Groupe Europ&en de Curietherapie European Society for Therapeutic Radiology and Oncology GEC-ESTRO APBI TRIAL32 EINFL.d.RT n a c h BET a u f L- Rez.u n d &UBERL. (1 0 t r i a l s o f BCS & RT) 6097 p t s N-33 EINFL.d.RT n a c h BET a u f L- Rez.u n d &UBERL. (1 0 t r i a l s o f BCS & RT) 6097 p t s N-34 35 Wa s b ed eu t et a d j u v a n t?& OP CHT S y s te m.t h e r a p ie n a c h O p e r a tio n CHT OP S y s te m.t h e r a p ie v o r O p e r a tio n M ETA CHT M e ta s ta s e n, k u r a tiv e r A n s a tz n ic h t m e h r m & g lic h, S y m p to m lin d e r u n g36 Regu l a t o r s o f a p o p t o t i c c el l d ea t h O n e m a s te r r e g u la to r is P 5 3 P53 bound to DNA Most of the p53 mutations that cause cancer are found in the DNAbinding domain37 Zi el d er n eo a d j u v a n t en Th er a p i e F r & h e T h e r a p ie v o n M ik r o m e ta s ta s e n T u m o r r e d u k tio n / b r u s te r h a lte n d e T h e r a p ie - E r h & h te R a te a n b r u s te r h a lte n d e n T h e r a p ie n P ie r g a e t a l ,1 % - 7 1,6 % Id e a l: p a th o lo g is c h e K o m p le ttr e m is s io n (P C R ) E in flu & a u f &U b e r le b e n s p a r a m e te r (O S ) In v iv o C h e m o s e n s itiv it& ts m e s s u n g - W ir k s a m k e it d e r B e h a n d lu n g k a n n a m A n s p r e c h e n d e s T u m o r s b e o b a c h te t w e r d e n!38 Neo a d j u v a n t e Th er a p i ebed i n gu n gen I P r & o p e r a tiv e C o r e B io p s ie G le ic h z e itig M a r k ie r u n g s c lip s H is to lo g ie m it R e z e p to r e n u n d H E R -2 -n e u39 Kl i ni s che Pr &s ent at i on40 Neo a d j u v a n t e Th er a p i ebed i n gu n gen II P a lp a tio n u n d In s p e k tio n d e r B r u s t u n d d e r A x illa v o r je d e m Z y k lu s M a m m o g r a p h ie u n d U ltr a s c h a ll z u B e g in n u n d b e i V e r d a c h t a u f P r o g r e s s io n MRI B ild g e b e n d e V e r fa h r e n n a c h 4 Z y k le n u n d u n m itte lb a r v o r d e r o p e r a tiv e n S a n ie r u n g P a th o lo g e n b e i O P in fo r m ie r e n41 Kl i n i sc h e Pr & sen t a t i o n H is to lo g ie d e r C o r e B io p s ie : In v a s iv e s M a m m a c a r c in o m, e h e r v o m d u c ta le n T y p, G 3 E R : s c h w a c h p o s, P g R : s c h w a c h p o s, H e r c e p Te s t: s ta r k p o s itiv,h e r -2 /n e u F IS H : a m p lifiz ie r t H o r m o n s ta tu s : F S H : 5 6 m U /m l, &O S tr a d io l: &1 0 p g /m l S ta g in g u n te r s u c h u n g e n : L u n g e n -R & : in tr a p u lm o n a le L & s io n e n n ic h t s ic h e r a u s s c h lie & b a r, d a r a u fh in C T d e r L u n g e : o B C T d e r L e b e r: o B S k e le tts z in tig r a p h ie : e r h & h te r K n o c h e n s to ffw e c h s e l in L W K 4, R & n tg e n z ie la u fn a h m e L W K 4 : o B42 43 44 &OR + PR In T u m o r e n w e r d e n W a c h s u m s fa k to r e n & s tr o g e n a b h & n g ig p r o d u z ie r t. M it d ie s e n k & n n e n s ic h d ie T u m o r z e lle n s e lb s t s tim u lie r e n St a r k e Ex p r essi o n d er &OR St a r k e Ex p r essi o n d er PR45 Her - 2- Rez ep t o r Hu m a n ep i d er m a l gr o wt r ec ep t o r 2 &Ub er ex p r essi o n : ~20% Agr essi ver er Ver l K& r z er e &Ub er l eb en sz ei t46 Zei t i c h er Ab l a u f d er Th er a p i e Sentinel-OP d Tumorvermessung Quadrantenresektion 7 Strahlentherapie 8 Trastuzumab 3 w f&r 1 a 12 Wochen Epirubicin + Cyclophosphamid 12 Wochen Taxan + Trastuzumab47 Chi r ur gi s che Ther api e Core Biopsie 1. Sentinel node biopsy Systemische Therapie 1. BET/Mastektomie48 Neo a d j u v a n t e Th er a p i e: CHT A n th r a z y k lin e Z y to s ta tis c h e s A n tib io tik u m S ta n d a r d Ta x a n e P fla n z e n a lk a lo id /M ito s e h e m m e r s e h r p o te n t P C R 20% P a c lita x e l (Ta x o l ) D o c e ta x e l (Ta x o te r e ) P a z ifis c h e n E ib e /Ta x u s b r e v iv o lia D e u ts c h e n E ib e /Ta x u s b a c c a ta M o n o k lo n a le r A n tik & r p e r b in d e t H E R -2 -R e z e p to r E p ir u b ic in (E p ir u b ic in ) T r a s tu z u m a b (H e r c e p tin ) 67% P C R!49 Chi r ur gi s che Ther api e 1. S e n tin e l n o d e b io p s y In v a s iv e T u m o r z e lle n b r e ite n s ic h & b e r L y m p h g e f& & e a u s L y m p h k n o te n = F ilte r s ta tio n e n 1.F ilte r = W & c h te r ly m p h k n o te n /S e n tin e l Id e n tifik a tio n m itte ls M e th y le n b la u u./o d. R a d io k o llo id Veronesi U et al, N Engl J Med 349: , 2003 Morton DL et al, Ann Surg 230: , 199950 51 Un t er sc h i ed l i c h e Th er a p i eo p t i o n en SN 2. N e o a d ju v.s y s t.t h e r a p ie 3. Q R (fa lls S N + ) + A x illa d is s52 Un t er sc h i ed l.th er a p i eo p t i o n en 1. QR + S N / A x illa d is s S y s te m.t h e r a p ie53 Un t er sc h i ed l.th er a p i eo p t i o n en 1. A b la tio + 2. S y s t.t h e r a p ie A x illa d is s.54 Un t er sc h i ed l.th er a p i eo p t i o n en 1. Neo a d j u v.sy st.th er a p i e 2. QR + Ax i l l a d i ss. 3.55 Un t er sc h i ed l.th er a p i eo p t i o n en Core Biopsie Syst. Therapie =56 Vor ber ei ung P a tie n tin M.E.: V e r k le in e r u n g d e s T u m o r s v o n 2 c m a u f 8 m m P r & o p e r a tiv e D r a h tm a r k ie r u n g d e s T u /C lip57 Ver m ei d u n g ei n es LR V e r m e id u n g e in e s L R v o n s u b s ta n tie lle r B e d e u tu n g V e r m e id u n g v o n 4 L R b e d e u te t V e r m e id u n g e in e s d u r c h B r u s tk r e b s b e d in g te n To d e s n a c h 1 5 J a h r e n58 Technique lateral and medial tangential opposed radiation fields Cobalt-60: small breast A/B CUP linear accelerator ( 6 MeV) large breast E/D CUP59 Simulation film Verification film (LINAC)60 Ver m ei d u n g ei n es LRs V e r m e id u n g e in e s L R v o n s u b s ta n tie lle r B e d e u tu n g V e r m e id u n g v o n 4 L R b e d e u te t V e r m e id u n g e in e s d u r c h B r u s tk r e b s b e d in g te n To d e s n a c h 1 5 J a h r e n61 WH - Ch i u r gi e Operative Therapie Q R + B e s tr a h lu n g s o s ic h e r w ie A b la tio B e i g r o s s e n T u m o r e n k a n n P S T e in e A b la tio o ft v e r h in d e r n S N -K onzept A x illa d is s e k tio n z u m L y m p h k n o te n s ta g in g62 WH Sy st em i sc h e Th er a p i e S ys temis che Therapie C h e m o th e r a p ie m it A n th r a c y c lin e n (u n d Ta x a n e n ) E n d o k r in e T h e r a p ie m it A r o m a ta s e h e m m e r n / Ta m o x ife n A n tik & r p e r th e r a p ie m it T r a s tu z u m a b (H e r c e p tin )63 WH Neo a d j u v a n t e Th er a p i e Neoadjuvante Therapie (PS T) In v iv o C h e m o s e n s itiv it& ts a s s a y T u m o r u n d L K N D o w n s ta g in g e r m & g lic h t V e r b e s s e r te K o s m e s is E r h & h te R a te v o n B r u s te r h a lt S o fo r tig e T h e r a p ie v o n M ik r o m e ta s ta s e n64 CUMULATIVE DOSE OF ERT AND BRACHYTHERAPY N. + ST R 100 gy 88,25 gy 75,5 gy 70,5gy 62,75 gy 57,75 gy 52,75 gy 50 gy 45 gy 40 gy 37,75 gy 25 gy LUNG R MEDIASTINUM LUNG R N.= Reference point65 66 67 68 69 70 71 72 Th e p 53 Net wo r k Stalled UV radiation replication forks & radiation p53 DNA damage repair Oncogenes Ribosomal Stress Mdm2 Apoptosis Cell cycle arrest Senescence73 P53- d ep en d en t a p o p t o si s a n d m a l i gn a n c y Defects in processes such as DNA double-strand break (DSB) repair, DNAdamage checkpoint function, and telomere maintenance, result in DSBs or exposed chromosomal ends WT p53 cells with DSBs or uncapped telomeres are predisposed to apoptosis, which limits tumorigenesis In contrast, cells with missing wt p53 can survive inappropriately, creating a permissive environment for the generation of genomic instability that can drive carcinogenesis NHEJ, non-ho HR, homologous recombination Brown & Attardi Nature Reviews Cancer 5, , 200574 PCD i m p o r t a n t a sp ec t s Programmed cell death (PCD = apoptosis) originally referred to specifically instances in which an irreversible sequence of events led to cell death Requirement for protein synthesis to initiate cell death Apoptosis is associated with a particular morphology in which the chromatin condenses and cells shrink and become denser and often fragment into several pieces Apoptotic morphology is now considered to derive from the activation of caspases, and is common to many (but not all!) cell deaths These processes are directly or indirectly genetically regulated, as opposed to necrosis or oncosis, in which the cell has no active role. Necrotic cells most typically lyse, provoking a substantial inflammatory response75 Qu a n t i t a t i ve a sp ec t s o f a p o p t o si s & Rel eva n c e f o r r esp o n se t o r a d i o t h er a p y ex a m p l es76 Di f f er en c es i n r a d i o sen si t i vi t y b et ween t wo c el l l i n es wi t h d i f f er i n g a b i l i t y t o u n d er go a p o p t o si s Kodym R et al, JBC, 200077 Ap o p t o si s q u a n t i t a t i ve ef f ec t s LY-as LY-ar Apoptosis ( 5Gy, 4h ) ~70% ~20% Survival ( 3Gy ) ~0.5% ~10% Survival 16 Gy ( 8 * 2 Gy) 6.6* *10-6 Tumor weight controlled 1.5 kg 0.4 mg Fractionated RT:78 Det er m i n a t i o n o f r a d i a t i o n c el l k i l l i n g In vivo, p r e d o m in a n t fo r m o f c e ll d e a th fo llo w in g ir r a d ia tio n o c c u r s d u r in g m ito s is a t d o s e s o f ~ 1-2 Gy A d d a k n o w n n u m b e r o f c e lls to a n e w fla s k a n d in c u b a te fo r 1-2 w e e k s E a c h s in g le c e ll w ill d iv id e s e v e r a l tim e s to fo r m c o lo n ie s th a t a r e fix e d, s ta in e d a n d c o u n te d C o u n t c o lo n ie s c o n ta in in g 5 0 c e lls (5-6 g e n e r a tio n s o f p r o life r a tio n ) to e x c lu d e c e lls th a t h a v e lim ite d g r o w th a s a r e s u lt o f s ta r tin g to d iffe r e n tia te o r b e in g s u b -le th a lly d a m a g e d79 Cl o n o gen i c c el l d ea t h T h e clonogenic cell survival assay d e te r m in e s th e a b ility o f a c e ll to p r o life r a te in d e fin ite ly, th e r e b y r e ta in in g its r e p r o d u c tiv e a b ility to fo r m a la r g e c o lo n y o r a c lo n e T h is c e ll is th e n s a id to b e clonogenic A c e ll s u r v iv a l c u r v e is th e r e fo r e d e fin e d a s a r e la tio n s h ip b e tw e e n th e d o s e o f th e a g e n t u s e d to p r o d u c e a n in s u lt a n d th e fr a c tio n o f c e lls r e ta in in g th e ir a b ility to re p ro d u c e80 Co l o n y f o r m a t i o n (c l o n o gen i c ) i n v i t r o a ssa y From: Hall - Radiobiology for the Radiologist Colony = &50 cells Small colonies?81 Ox y gen ef f ec t H y p o x ia T P 53 C hem o-& RT M a lig n a n c y82 Ox y gen ef f ec t i n Ra d i o b i o l o gy On e o f t h e m o st si gn i f i c a n t f a c t o r s a f f ec t i n g o u t c o m e83 Ox y gen t en si o n a n d r a d i o sen si t i vi t y84 eo x y gen a t i o n & f r a c t i o n a t i o n F r a c tio n a tio n S id e e ff e c ts E ffic a c y M u ltip le s m a lle r fr a c tio n s a r e b e tt e r to le r a te d th a n s in g le la r g e fr a c tio n s!85 i o l o gy o f r eo x y gen a t i o n a) In hypoxic regions, stress granules form containing HIF1mediated transcripts, sequestering the transcripts from being translated into protein. a) After radiation treatment, better oxygenated cells die and there is an increase in perfusion, leading to reoxygenation of the previously hypoxic cells. a) Macrophages are attracted to the dying tumour cells, become activated and release nitric oxide (NO), which also stabilizes HIF1. a) The increase in HIF1 activity increases vascular endothelial growth factor (VEGF) levels, promoting endothelial cell survival, angiogenesis and tumour cell survival and proliferation. Mark W. Dewhirst, Yiting Cao & Benjamin Moeller. Nature Reviews Cancer 8, , 200886 Gen es/p r o t ei n s a f f ec t i n g r a d i o sen si t i vi t y T P 53 B c l-2 fa m ily m e m b e r s D N A -r e p a ir g e n e s EGFR R O S r e la te d p r o te in s, s u c h a s S O D, c a ta la s e,... C y to k in e s : T N F -a lp h a C e ll s u r v iv a l a n d c e ll c y c le r e g u la tin g e n z y m e s : A k t, P T E N, M a p K in a s e, a n d o th e r s...87 Candi dat e genes i nvol ved i n t he pat hogenes i s of r adi at i on t oxi ci t y88 TP53, t h e m a st er r egu l a t o r o f c el l su r vi va l TP53 modulates (amongst others) Radio- and chemoresponse Cellular resistance against hypoxia Metastasis TP53 mutations in ~ 50 % of all tumors - abrogation of function of the tumor-suppressor protein p53 is one of the most common genetic alterations in cancer cells.89 Ov er v i ew c el l u l a r ef f ec t s o f i o n i z i n g r a d i a t i o n a n d c el l u l a r t a r get s n ex t sl i d e90 Membrane DNA Cellular response Genetic Instability Repair Apoptosis G1 / G2 DELAY91 Cl i n i c a l a sp ec t s o f Ra d i o b i o l o gy92 Ra d i a t i o n r esp o n se st r u c t u r a l l y u n d ef i n ed FSUs C lo n o g e n ic c e lls in th e s e s y s te m s n o t c o n fin e d to o n e p a r tic u la r F S U C e lls c a n m ig r a te fr o m o n e F S U to a n o th e r A llo w s r e p o p u la tio n o f a d e p le te d F S U E x a m p le r e -e p ith e lia liz a tio n o f a d e n u d e d a r e a o f s k in c a n o c c u r e ith e r fr o m s u r v iv in g c lo n o g e n s w ith in d e n u d e d a r e a o r b y m ig r a tio n fr o m a d ja c e n t a r e a s FSU.functional subunit93 Ti ssu e Resc u e Un i t C o n c e p t p r o p o s e d to lin k s u r v iv a l o f c lo n o g e n ic c e lls a n d fu n c tio n a l s u r v iv a l D e fin e d a s m in im u m n u m b e r o f F S U s r e q u ir e d to m a in ta in tis s u e fu n c tio n A ssum es N u m b e r o f T S U s is p r o p o r tio n a l to n u m b e r o f c lo n o g e n ic c e lls F S U s c o n ta in c o n s ta n t n u m b e r o f c lo n o g e n s F S U s c a n b e r e p o p u la te d fr o m s in g le c lo n o g e n94 Issu es wi t h FSUs S o m e tis s u e s d e fy c la s s ific a tio n C r y p ts o f je ju n u m (s tr u c tu r a lly w e ll d e fin e d b u t s u r v iv in g c r y p ts c a n /d o m ig r a te fr o m o n e c r y p t to a n o th e r to r e p o p u la te d e p le te d n e ig h b o r s95 Vo l u m e Ef f ec t i n Ra d i o t h er a p y : Ti ssu e Ar c h i t ec t u r e To ta l d o s e th a t c a n b e to le r a te d d e p e n d s o n v o lu m e ir r a d ia te d Tolerance dose is d e fin e d a s th e d o s e th a t p r o d u c e s a n a c c e p ta b le p r o b a b ility o f a tr e a tm e n t c o m p lic a tio n. In c lu d e s o b je c tiv e c r itie r a a n d s u b je c tiv e fa c to r s96 Do se vs Co m p l i c a t i o n s S p a tia l a r r a n g e m e n t o f F S U s in tis s u e is c r itic a l S e r ia lly a r r a n g e d F S U s E x a m p le : s p in a l c o r d in te g r ity o f e a c h F S U is c r itic a l to o r g a n fu n c tio n E lim in a tio n o f a n y F S U in th is s y s te m c a n r e s u lt in m e a s u r a b le p r o b a b ility o f c o m p lic a tio n R a d ia tio n d a m a g e s h o w s b in a r y r e s p o n s e th r e s h o ld b e lo w w h ic h is n o r m a l fu n c tio n, a b o v e w h ic h th e r e is lo s s o f fu n c tio n97 Do se vs. Co m p l i c a t i o n s Ex a m p l es f o r d i f f er en t t i ssu es 100 % Probability of Complications C B A Dose, (Gy) 7698 The t oxi ci t y of r adi ot her apy99 Dos e r es pons e cur ves f or r adi ot her apy100 Ea r l y (Ac u t e) a n d La t e Ef f ec t s R a d ia tio n e ffe c ts c o m m o n ly d iv id e d in to e a r ly a n d la te S h o w s d iffe r e n t p a tte r n s o f r e s p o n s e to d o s e fr a c tio n a tio n D o s e -r e s p o n s e r e la tio n s h ip s c h a r a c te r iz e d b y &/& r a tio s (m o r e o n th is la te r ) L a te e ffe c ts m o r e s e n s itiv e to c h a n g e s in fr a c tio n a tio n th a n e a r ly e ffe c ts E a r ly (a c u te ) e ffe c ts r e s u lt fr o m d e a th o f la r g e n u m b e r o f c e lls a n d o c c u r w ith in w e e k s to d a y s o f ir r a d ia tio n in tis s u e s w ith r a p id r a te o f tu r n o v e r101 Ex a m p l es o f ea r l y ef f ec t ed t i ssu es E x a m p le s : E p id e r m a l la y e r o f s k in G a s tr o in te s tin a l e p ith e liu m H e m a to p o ie tic s y s te m R e s p o n s e is d e te r m in e d b y h ie r a r c h ic a l c e ll lin e a g e c o m p o s e d o f s te m c e lls a n d d iffe r e n tia tin g o ffs p r in g. 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