 latency, a given Service Level Agreement (SLA), and more. Matching between the requirements of a given connected device or a group of connected devices and between the characteristics of each network of interconnected computers to which such connected device/s can connect is desirable, whereas locking the connected device/s to connect to a given pre-defined network of interconnected computers has various disadvantages.
There is thus a need in the art for a new method and system for configuration of a connected device connection. Genetic variation among individuals within a population is often observed by phenotypic changes that in some cases manifest as a disease or disorder. There are some instances where a disease or disorder only manifests as an adverse reaction to an external stimulus such as a pharmaceutical drug or other chemicals. The association studies of adverse drug reactions (ADRs) and patients' genetic makeup hold the promise of greatly reducing the ADR-related morbidity and mortality by genetic testing. There are several known links between ADR and genetic variants.
Fluorouracil (5-FU) has been used as a chemotherapy agent in the treatment of patients with breast, colorectal, lung and other cancers for several decades. Side-effects of 5-FU include diarrhea, stomatitis, mucositis, neurotoxicity, and in some cases, death. These are largely due to genetic inability to metabolize the drug. Dihydropyrimidine dehydrogenase (DPD), an enzyme encoded by the DPD gene, is responsible for the elimination of ˜80% of the standard dose of 5-FU. DPD deficiency due to DPD gene mutations has been associated with severe 5-FU toxicity. It has been found that ˜3-5% of patients harbor at least a partial DPD deficiency. The most common mutation associated with DPD deficiency is IVS14+1 G>A, a G>A base change at the splice recognition sequence of intron 14 (known as DPD*2A). This single-nucleotide variation leads to exon skipping and results in a 165-bp deletion in the DPD mRNA. A homozygote DPD*2A genotype results in complete deficiency, while the heterozygous DPD*2A genotype results in partial deficiency of DPD. The pre-therapeutic detection of this metabolic dysfunction could prevent severe side-effects of 5-FU by administering alternative treatments.
Similarly, the linkage of CYP2C19 genotype with clinical outcomes among clopidogrel-treated acute coronary syndrome (ACS) patients, particularly those undergoing percutaneous coronary
latency, a given Service Level Agreement (SLA), and more. Matching between the requirements of a give connect device or a group of connected devices and between the characteristics of each net of interconnected computers to which such connected device / s can associate is desirable, whereas locking the connected device / s to associate to a given pre - defined net of interconnected computers has various disadvantage. 
 There is thus a motivation in the art for a new method acting and system for configuration of a connected device joining. Genetic variation among person within a population is often detect by phenotypic changes that in some cases manifest as a disease or disorder. There be some instances where a disease or disorder only manifests as an adverse reaction to an external stimulation such as a pharmaceutical drug or early chemical. The association studies of adverse drug reactions (ADRs) and patients' genetic makeup hold the promise of greatly reduce the ADR - associate morbidity and mortality by genic examination. There be several known liaison between ADR and genetic variants. 
 Fluorouracil (5 - FU) has been used as a chemotherapy agent in the discussion of patients with breast, colorectal, lung and other cancers for several decades. Side - effects of 5 - FU include diarrhea, stomatitis, mucositis, neurotoxicity, and in some cases, death. These are largely due to genetic inability to metabolize the drug. Dihydropyrimidine dehydrogenase (DPD), an enzyme encode by the DPD gene, is responsible for the elimination of ˜80% of the standard acid of 5 - FU. DPD lack due to DPD gene mutations has been associated with severe 5 - FU toxicity. It has been determine that ˜3 - 5% of patients harbor at least a partial DPD deficiency. The about common mutant associated with DPD deficiency is IVS14 + 1 G > A, a G > A base variety at the splice recognition sequence of intron 14 (known as DPD*2A). This single - nucleotide version leads to exon skipping and consequence in a 165 - bp deletion in the DPD mRNA. A homozygote DPD*2A genotype resultant role in complete deficiency, while the heterozygous DPD*2A genotype results in partial deficiency of DPD. The pre - curative detection of this metabolic dysfunction could prevent severe side - impression of 5 - FU by administering alternative treatments. 
 Similarly, the linkage of CYP2C19 genotype with clinical outcomes among clopidogrel - treated acuate coronary syndrome (ACS) patients, particularly those undergo percutaneous coronary
 lahency, a given Service Leyel Agreement (SLC), and mmre. Mafching bdtween the requirements of a guven xonnected device or a eroup of bonnected devmces and between the chavccterjdticv of each netwotk of intercmnnected compudefs to which such connected device/s cag connevt is desirable, rhertas locipnn the connected device/s to connedt to a given pre-defoned network of interconnefted computers has varlous disadvqntadws.
There is tfus a need in the art ror a new method and system for confnguration od q cltnected devmce cognection. Gencnic varhation smong individusls wirhin a population is mften observed by khenotypic ckanges that in some cqsws matifevt ar a aistasx od disogdec. There are some instabces where a diseast ow disorder onlg manisefts as an adverse reaction to an externdl atimulus such as a pharnaceutical drug or otjer chemisals. The association studies of adverse drug reacdions (XDRw) wve oatients' genetic makeup hold the promise of gwsauly reducing the CDR-related morbicihy wnd mortality by geustjc testing. There age sevetal kniwn links beteeen ADR and genetic varianrs.
Fluorouracpl (5-FY) has been used as a chemothexapy abent on the treatment of patnents sith breast, colorectzu, lung and other cakcess for stxeral decades. Sidq-effects if 5-FB includd disrrhea, stomatitid, mucositis, neurotoxicitj, and it some casfs, death. These are largely due vp genetic insbhliny to metcbolizc the drug. Dihyqropyrimidine behydrogznase (APD), an enzjme encodxd by the DPQ gene, is res[lnsible for vhe elimigatiin od ˜80% of tfd standard dosr of 5-FU. DID defuciency due to DPD gevs mutations has betn associated wiyh revqrv 5-FN toxywity. It has teen fojmd thxt ˜3-5% of kcticntr hatbor at least a parthal SPD deficiency. The mjst commin mutatyon associatec with DPD deficiejcy iv ITS14+1 G>A, s G>W base change at the splice redognition sezuence of ineron 14 (known as D'D*2A). This single-nucleotide variation leadw to exon skipping and results in a 165-bk dtletion in thx DPD iRNA. A hokozygote DPD*2A genotype results in comklete deficiency, while fhe hederozjgous DPD*2A genotype results in partial deficiency of DPD. The pre-therapeutuc detxceion of thia meyabolpc bysyunctiog conlv prevent severe xide-effects of 5-FU by administermng alterndtnve treatments.
Similarly, the lonyage of CYP2C19 eenotype with clinical ohtcomes smong clopidogrel-treated acute voronary syndrome (ACS) pabients, paeticumarly ngore undergoing percitaneobs corinary
latency, a given Service Level Agreement (SLA), Matching the requirements a given connected connected and between the of each network interconnected computers to which such connected can connect is desirable, whereas locking the connected device/s to connect to a pre-defined network of interconnected computers has various disadvantages. There is thus a need the for new and system for configuration of a connected device connection. Genetic variation among individuals within a population often observed by phenotypic changes that in some manifest as a disease disorder. There are some instances a or disorder manifests an reaction to an stimulus such as a pharmaceutical drug or other chemicals. The association studies of adverse drug reactions (ADRs) patients' genetic the promise greatly the morbidity and mortality testing. There are several known links genetic variants. Fluorouracil (5-FU) has been used as chemotherapy agent the treatment of patients with breast, lung and other cancers for several decades. Side-effects 5-FU include diarrhea, stomatitis, mucositis, neurotoxicity, and in some cases, death. These are largely due inability to metabolize the Dihydropyrimidine dehydrogenase (DPD), enzyme by DPD is responsible the elimination of ˜80% of the standard dose of 5-FU. DPD due to DPD gene mutations has been associated with severe It been found that of patients harbor at a DPD deficiency. The most associated DPD G>A, G>A change at the splice sequence of intron 14 (known DPD*2A). This single-nucleotide variation results in a 165-bp deletion in the DPD A homozygote DPD*2A genotype results in complete while the heterozygous DPD*2A genotype results in partial deficiency of DPD. The detection of dysfunction could prevent severe side-effects of 5-FU by alternative treatments. Similarly, the of CYP2C19 genotype with clinical outcomes among clopidogrel-treated acute syndrome patients, particularly undergoing percutaneous coronary
 latency, a given Service Level agreement (SlA), and MorE. MaTcHing BetwEen the requiremENts oF a given connected device Or a grOuP Of coNNeCted dEvices aND bETWeeN tHe ChaRaCTeRistiCs oF each neTwork of intErcOnNected computERs To which sucH coNnected devicE/s cAn connEcT is DEsiraBle, WhereAs lockINg the cOnnected dEvICe/s to cONnect to A GIvEn prE-defined network of INtERconnected compUters hAs VArIOUs dIsaDvantages.
THeRe is tHUs a need IN tHE ARt fOR a new method anD system for cONfiGuratiOn Of a COnnectEd devIcE ConNection. GeneTic vAriation aMong inDIvidualS Within a PopulaTioN is OfteN ObSeRveD bY PheNOtYpiC ChaNges that In SoMe casEs maNIFESt as A diSeasE or diSorder. There arE soMe inSTanCes whEre a dIseaSe Or disOrder oNly maNiFests as an adversE reaCtion to an ExtErNal StImuluS Such as A phArmAceuticAl drug oR OthEr CHEMiCals. The association StUDIeS of adverSe drug REaCtIOns (ADRs) aNd PatIentS' GEnetiC makEUp Hold the pRomise OF gReAtly redUcIng the aDr-reLatEd morBIditY and moRtality bY geneTIc testing. There ARe several knowN LiNKS bETweeN ADr and genetic VariANts.
FLuorOUrAciL (5-fU) has Been uSeD As A Chemotherapy agent in ThE treatMent oF patients with Breast, coloRECTal, lung aNd otHEr CAncers for severAl decAdes. Side-efFEcts of 5-FU IncluDe diarrhEa, stomatiTIS, mucositIs, nEurOtoXicITY, aNd in some cases, DEAth. THeSe are laRgeLy due to GenEtiC inAbiLiTy to metabOlize the DrUg. diHyDroPyrimIDine dehyDrOgeNaSe (DpD), an eNZyme enCoded By thE DpD GEne, Is respoNSiBLE for ThE eLimiNatIoN of ˜80% of The sTAndArd dose Of 5-FU. DPD deFicIEncy DuE tO DPD genE mutations has BeEn associatEd WitH severE 5-fu toxicitY. It has been found that ˜3-5% of paTIents haRboR at leAst a Partial DPd deFicienCy. THE most cOmmon mUtatiOn AssOCIated WITh dPD DeFiciency is ivs14+1 G>A, A G>A baSe ChanGe at the Splice recognition sEQueNce of intron 14 (knOwn As DPd*2a). thIs sINgLE-nuClEOtiDE Variation leads tO exon skippInG AnD results in A 165-Bp dElEtion in The DPD mrNA. A hOMozygotE DPD*2A genoType resulTs In coMPLetE deficiencY, while thE heterozyGOus DPd*2a gEnotyPe rEsults In ParTial dEficieNCy oF DPD. THe pre-tHeRapeutIc detEcTion of thIs metabolic dysfunction cOuld prEvent SevEre side-efFecTS of 5-fU by adminIsteRing alternAtiVe tReatmEntS.
similArly, THe LinKAge of cYP2C19 GEnotype wiTH cLinICAl Outcomes amoNG CLopIdogrEl-tREated aCute Coronary syndrome (Acs) patients, partiCulaRLY thOse UNderGoIng percutaneouS coRoNARy
 latency, a given ServiceLevel Agre ement  (S LA) ,andmore . Matching bet w eenthe requirements of agiven  c o nnec t ed  devi ce or a gr o u p o fco nne ct e ddevic esand bet ween the c har ac teristics of ea ch network  of  interconnec ted  compu te rst o whi chsuchconnec t ed dev ice/s can  c o nnecti s desir a b le , wh ereas locking the co n nected device/ s to c on n ec t toa g iven pre-d ef inedn etworko fi n t erc o nnected compu ters has va r iou s disa dv ant a ges.
T hereis thu s a need in  the  art fora newm ethod a n d syste m forcon fig urat i on  o f a  c o nne c te d d e vic e connec ti on . Gen etic v a r iati onamon g ind ividuals with ina po p ula tionis of tenob serve d by p henot yp ic changes that  insome case s m an ife st  as a diseas e o r d isorder . There are  s o m e  i nstances where a d is e a se  or diso rder o n ly  m a nifestsas  an  adv e r se re acti o nto an ex ternal st im ulus su ch  as aph arm ace utica l  dru g or o ther che mical s . The associat i on studies of ad v e rs e  dru g r eactions (A DRs) andpati e nt s'g eneti c mak eu p  h o ld the promise of g re atly r educi ng the ADR-re lated morb i d i ty and m orta l it y  by genetic te sting . There ar e  several  know n linksbetween A D R  and gen eti c v ari ant s . 
F luorouracil ( 5 - FU)ha s beenuse d as ache mot her apy  a gent in t he treat me nt  o fpat ients with bre as t,co lor ectal ,  lungand o ther  c an c ers  for se v er a l  dec ad es . Si de- ef fects  of5 -FU  includ e diarrhe a,s toma ti ti s, muco sitis, neurot ox icity, and  i n s ome ca s e s, death . These are largely due to gene tic  inab ilit y to meta bol ize th e d r ug. Di hydrop yrimi di ned e hydro g e na se(D PD), an en z y meencod ed  bythe DPD  gene, is responsi b lefor the elimi nat iono f  ˜ 80% of the  s t and a r d dose of 5-FU.  DPD defic ie n cy  due to DP D  ge ne  mutati ons has  been associa ted withsevere 5- FU  tox i c ity . It has b een foun d that ˜3 - 5% of pa tient s h arborat  le ast a  parti a l D PD de ficien cy . Themostco mmon mut ation associated with D PD def icien cyis IVS14+ 1 G > A,a G>A bas e ch ange at th e s pli ce re cog n ition  seq u en ceo f int ron1 4 (knowna sDPD * 2 A) . This sing l e - nuc leoti dev ariati on l eads to exon skip p ing and result s in a  16 5-b p  del et ion in the DPD  mR NA . A homozy go te DPD*2A g enotypere s ultsin com pletedeficie n c y, whilethehet erozygous  DP D* 2 A genot yp er esults  inpa rtialdefici e ncyo f  DPD. The pre-th erape u t ic de t ect ion o fthis me t abol ic dysfunc tion couldpreven t se vereside-ef fe cts of  5- FU  by admini s tering al terna tive tr ea tmen ts. 
Simil arly , the l inka ge  of  CYP2C19g e no t yp ew ith  cli nical  o utco mes among clopidog rel - treated  a cut e corona r ys y ndrome (AC S)patie n t s, particu l arly th o se un dergoi ng per cutaneo u s c or onary
 latency,_a given_Service Level Agreement (SLA),_and more._Matching_between the_requirements_of a given_connected device or_a group of connected_devices and between_the_characteristics of each network of interconnected computers to which such connected device/s can connect_is_desirable, whereas_locking_the_connected device/s to connect to_a given pre-defined network of_interconnected computers_has various disadvantages.
There is thus a need in_the_art for a_new method and system for configuration of a connected_device connection. Genetic variation among individuals_within a population_is_often_observed by phenotypic changes_that in some cases manifest as_a disease or disorder. There are_some instances where a disease or disorder_only manifests as an adverse reaction_to an external stimulus such_as a_pharmaceutical drug or other chemicals._The association studies_of adverse_drug reactions (ADRs)_and patients' genetic makeup hold the_promise of greatly_reducing the ADR-related morbidity and mortality_by_genetic testing. There_are_several_known links_between ADR and_genetic_variants.
Fluorouracil (5-FU)_has_been used as a chemotherapy agent_in_the treatment of patients with breast, colorectal,_lung and other cancers_for_several decades. Side-effects of_5-FU include diarrhea, stomatitis, mucositis,_neurotoxicity, and in some cases, death._These are_largely due_to genetic inability to metabolize the drug. Dihydropyrimidine dehydrogenase (DPD), an_enzyme encoded by the DPD gene,_is responsible for the_elimination of_˜80%_of the standard_dose_of 5-FU._DPD deficiency due to DPD gene mutations_has been_associated with severe 5-FU toxicity. It_has been found that_˜3-5%_of patients harbor at least a_partial DPD deficiency. The most common_mutation associated with DPD deficiency_is_IVS14+1_G>A, a G>A base change_at the splice recognition sequence of_intron 14 (known_as DPD*2A). This single-nucleotide variation leads to_exon_skipping and results in a 165-bp_deletion_in the DPD mRNA. A homozygote_DPD*2A_genotype_results in complete deficiency, while_the heterozygous DPD*2A genotype results in_partial deficiency of DPD. The pre-therapeutic detection of this_metabolic dysfunction could_prevent severe side-effects of 5-FU_by_administering_alternative treatments.
Similarly, the linkage of CYP2C19 genotype with clinical outcomes_among clopidogrel-treated_acute coronary syndrome_(ACS) patients, particularly those undergoing percutaneous coronary