the aim work analys prolifer tumour cell treatment gapdur radiotherapi head neck cancermateri method the clinic materi base record head neck patient treat radiotherapyalon our institut the effect radiotherapi assum describ linearquadrat model the patient data were fit direct radiobiolog model theparamet were estim use maximumlikelihood proceduresresult accord our model result treatment were signific correl normalis total dose radiat tumour progress accord tnm overal treatment time gap durat the laryng cancer had better prognosi cancer oroand nasopharynx when treatment time prolong without treatment interrupt 036 gylday lost due repopul tumour cell dure treatment gap prolifer faster 067 gylday lostconclus prolifer tumour cell faster dure treatment gap dure day irradi

Rafal Tarnawski

Krzysztof Skladowski

Andrzej Swienrniak

Andrzej Wygoda

Anna Mucha

Repopulation of Tumour Cells during Radiotherapy Is Doubled during Treatment Gaps

nonlinear model develop epidem contact trace it dynam studi linear version model present both determinist stochast version present data cuban hiv aids epidem fit linear model data obtain estim size cuban hiv epidem

H. De Arazoza

R. Lounes

T. Hoang

Y. Interian

Modeling HIV Epidemic under Contact Tracing — The Cuban Case

the problern regul proliferationdifferenti process analys framework model unipotenti cell clone dynam assum two altern way scenario everi newborn cell develop which long run defin correspond prolifer differenti cell status the scenario choic suppos random event influenc both inher mitot activ cell differenti factor special messeng synthes differenti cell differenti factor be accept everynew born cell can chang way cell develop take account clonal heterogen shown mechan regul proliferationdifferenti process can result select activ prolifer insensit respect differenti factor action cell say cell cancer phenotyp framework investig cell cancer phenotyp which herit within variabl motherdaught correl appear through seri perman nonmut chang prolifer cell autoselect mechan retain divis generat progeni onli activ prolifer cell which less sensit respect action differenti factor the progress normal cell clone toward appear increas number cell cancer phenotyp can consid possibl mechan carcinogenesi which altern clonal select theori cancer origin

Galina I. Solyanik

Alexander A. Serikov

Autoselection Phenomenon in the Normal Cell Clone Undergoing Differentiation: From Cell Population Heterogeneity to Cancer Phenotype via Nonmutational Changes

sever aids cohort studi observ incub period between hiv infect aids onset can shorter than 3 year about 10 seroposit individu longer than 10 year about 1015 individu other hand mani individu remain seroneg even after multipl exposur hiv these distinct outcom have recent been correl some mutant gene hiv coreceptor ccr5 ccr2 cxcr4 for instanc mutant allel 32 m303 ccr5 may provid full protect against hiv infect homozygot partial protect heterozygot moreov infect heterozygot may progress more slowli than individu who have mutant allel frequenc mutant allel veri low caucasian popul therefor effect may insignific base avail data propos onesex model suscept classifi have partial full natur resist hiv infect infect classifi rapid normal slow progressor our goal investig impact heterogen spread hiv identifi key paramet the basic reproduct number 0 deriv from simplifi model the relat contribut 0 from three group infect investig present rough estim procedur make use limit data estim some new paramet specif our model final rough estim procedur appli exampl focus ccr5 32 san francisco gay men the relat contribut 0 among three infect group compar use two differ classifi criteria infect under given assumpt conclud without ani intervent hiv infect continu spread popul epidem main driven normal progressor the transmiss rate from infect identifi key paramet

Shu-Fang Hsu Schmtiz

A Mathematical Model of HIV Transmission in Homosexuals with Genetic Heterogeneity

new logic statist method use analysi relationship between surviv immunolog variabl these method base search regular syndrom multidimension space the syndrom element partit allow area variabl estim statist valid found regular new techniqu base montecarlo comput simul usedw present some result from immunolog research illustr method logist regular search two task describ the broad panel monoclon antibodi differenti lymphocyt antigen were use lymphocyt subpopul analysi the purpos first task evalu signific immunolog paramet predict 1year metastasisfre surviv nonmetastat osteosarcoma extrem the second task construct predict alghorithm prognosi 2year surviv patient stomach cancer the optim set paramet predict surviv found both task found out high forecast inform hladr cell percentag 1 task percentag adhes cell cd50 lymphocyt 2 task multivari forecast alghorithm develop

A. V. Kunznetsova

O. V. Sen'ko

G. N. Matchak

V. V. Vakhotsky

T. N. Zabotina

O. V. Korotkova

The Prognosis of Survivance in Solid Tumor Patients Based on Optimal Partitions of Immunological Parameters Ranges

develop molecular biolog have result veri signific increas volum data avail scientist handl model data requir electron tool which worldwid access via internet essenti this paper summaris contribut area summer school organis magdel septemb 1999

Ralf Hofestädt

Summer School Bioinformatics &#8212; Information Systems and Network Analysis of Gene Regulation and Metabolism

B. D. Sleeman

Editorial

model hiv pathogenesi hivinfect individu under veri general condit model have consid five differ type cd4 cell two differ type hiv mtropic versus ttropic well infect uninfect macrophag this 9dimension stochast process for process have develop stochast differenti equat differ type cell use stochast equat have generat some mont carlo data studi stochast behavior hiv pathogenesi hiv progressionthrough mont carlo studi have reveal acut infect stage earli stage hiv infect have confirm basic role play lymph node some longliv cell macrophag serv reservoir hiv escap elimin immun system dure long asymptomat stage hiv infect the mont carlo result have shown hiv heterogen divers may major factor determin time period sinc infect uninfect cell drop below 200 3 blood the numer result have also confirm our previous find see 1 which conclud probabl distribut cell free hiv can classifi three period over time the latent period transit period pseudosteadi period

Wai-Yuan Tan

Zhengzheng Ye

Assessing Effects of HIV Heterogeneity and Macrophage on the HIV Pathogenesis in HIV-Infected Individuals

the gompertz function formul repres actuari curv yet often fit growth organ organ tumor despit numer attempt consensus has been forg about biolog foundat broad applic model here revisit gompertzian notion power grow equat growth fraction aside from confer biolog interpret model approach allow lead possibl explor behavior gompertzian growth fractal kinet signific found empir model logist model von bertalanffi model von bertalanffi richard model togeth origin gompertz model special case gampertzian growth fractal space this find permit analysi growth kinet tumor which might affect model base design chemotherapi protocol

Željko Bajzer

Stanimir Vuk-Pavlovic

New Dimensions in Gompertzian Growth

the prolifer eukaryot cell driven process call cell cycl proper regul process lead order execut sequenti step within cycl ensur normal develop homeostasi organ other hand perturb cell cycl frequent attribut cancer cell mechan ensur order fidel event cell cycl call checkpoint the checkpoint induc damag dna delay cell cycl progress provid more time repair lesion befor dna replic segreg the dna damageinduc checkpoint can recogn signal transduct pathway communic inform between dna lesion compon cell cycl protein involv cell cycl well compon signal transduct pathway communic cell cycl frequent product oncogen tumor suppressor gene malfunct gene play critic role develop human cancer the key compon checkpoint machineri tumor suppressor gene p53 involv either regul cell cycl progress arrest cell treat dna damag factor activ program cell death apoptosi postul p53 protein activ dna damag detector one candid role dnadepend protein kinas dnapk which recogn dna strand break phosphoryl p53 protein

Piotr Widlak

The DNA Damage-Induced Cell Cycle Checkpoints

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