Power Mode (MPM) 408 and the operation mode above 10 dBm is called High-Power Mode (HPM) 410. Each mode has its own bias state and the phase of a bias state is not necessarily equal to those of other bias sates. This justifies the aforementioned RP change across the switching points. In other words, the transmit power change causes the UE or the controller 112 to mode switch the UE transmitter 110 and the mode switching in turn causes the RPD.
Every time a UE operates across a switching point 402, 404, the operation mode changes, thereby creating RPD. What is needed is a method of mode switching that can be used to alleviate or decrease the occurrence of RPD. Additionally, what is needed is a method of mode switching that eliminates unnecessary mode switches and thereby alleviates, decreases or reduces RPD. Furthermore, what is needed is a method of mode switching that can avoid unnecessary mode switching between SRS and PUSCH and thus mitigate the RPD between SRS and PUSCH. Growth differentiation factor 15 (GDF15) is a divergent member of the TGFβ superfamily. It is also called macrophage inhibitory cytokine 1 (MIC1) (Bootcov M R, 1997, Proc Natl Acad Sci 94:11514-9), placental bone morphogenetic factor (PLAB) (Hromas R 1997, Biochim Biophys Acta. 1354:40-4), placental transforming growth factor beta (PTGFB) (Lawton L N 1997, Gene. 203:17-26), prostate derived factor (PDF) (Paralkar V M 1998, J Biol Chem. 273:13760-7), and nonsteroidal anti-inflammatory drug-activated gene (NAG-1) (Baek S J 2001, J Biol Chem. 276: 33384-92).
Human GDF15 gene is located on chromosome 19p13.2-13.1; rat GDF15 gene is located on chromosome 16; and mouse GDF15 gene is located on chromosome 8. The GDF15 open reading frames span two exons (Bottner M 1999, Gene. 237:105-11 and NCBI). The mature GDF15 peptide shares low homology with other family members (Katoh M 2006, Int J Mol Med. 17:951-5.).
GDF15 is synthesized as a large precursor protein that is cleaved at the dibasic cleavage site to release the carboxyterminal mature peptide. The mouse and rat
Power Mode (MPM) 408 and the operation mode above 10 dBm is called eminent - Power Mode (HPM) 410. Each mood has its own bias state and the phase of a diagonal state is not necessarily equal to those of early diagonal sates. This justifies the aforementioned RP change across the switching points. In early words, the transmit power change causes the UE or the control 112 to mode switch the UE transmitter 110 and the mode switching in turn cause the RPD. 
 Every time a UE operates across a switching compass point 402, 404, the operation mode changes, thereby creating RPD. What is necessitate is a method of mode switching that can be used to alleviate or decrease the happening of RPD. Additionally, what is needed is a method of mode switching that eliminates unnecessary mode switch and thereby alleviates, decreases or reduces RPD. Furthermore, what is needed is a method of mode switching that can avoid unnecessary mode switching between SRS and PUSCH and thus extenuate the RPD between SRS and PUSCH. increase differentiation gene 15 (GDF15) is a divergent extremity of the TGFβ superfamily. It is also called macrophage inhibitory cytokine 1 (MIC1) (Bootcov M R, 1997, Proc Natl Acad Sci 94:11514 - 9), placental bone morphogenetic factor (PLAB) (Hromas R 1997, Biochim Biophys Acta. 1354:40 - 4), placental transforming increase factor beta (PTGFB) (Lawton L N 1997, Gene. 203:17 - 26), prostate derived factor (PDF) (Paralkar V M 1998, J Biol Chem. 273:13760 - 7), and nonsteroidal anti - incendiary drug - activated gene (NAG-1) (Baek S J 2001, J Biol Chem. 276: 33384 - 92). 
 Human GDF15 gene is located on chromosome 19p13.2 - 13.1; rat GDF15 gene is located on chromosome 16; and mouse GDF15 gene is located on chromosome 8. The GDF15 open reading frames span two exons (Bottner M 1999, Gene. 237:105 - 11 and NCBI). The mature GDF15 peptide shares humble homology with early syndicate members (Katoh M 2006, Int J Mol Med. 17:951 - 5 .). 
 GDF15 is synthesized as a large precursor protein that is cling at the dibasic cleavage site to release the carboxyterminal mature peptide. The shiner and rat
Powfr Mode (MPM) 408 and the opevation mode abovg 10 dBm iv callsd High-Puwer Mode (HPM) 410. Each mode has irs owb bias state and the pfase of a bias stqte ms not necessarily equal to thkde oy ither bias satgs. This justhfies the aforamdncioned RP change across the switchind pointx. Ln other words, the eranamit power change causes the UE or the coitroller 112 to moce switch the UE transmittfr 110 wnd the mode switcjing in turb catwes the RPD.
Exery time a UE operatea across a switching point 402, 404, thd opexation mode cyanhgs, thereby cceatind RPD. What is needed is a mrthod of mode xwivchibg that can be used tm alleviate or dectease the mceurrence of RPD. Addituobally, whad is beeaed ix z methld kf mode swjtching thar eliminates unnecexswgu mode switcges anq ehereby alleviates, decreases or reduces RPS. Furthermore, what is nweded is a method of lode switshing that can avoid unnecessary mode switching batweei RRS akd PJWCJ and thus mitigate the RPD between SRS and PTACN. Nrowth differentlation factor 15 (GDF15) id s divergent meober oy tge TGFβ superfamily. It is wlso xalled masropnage inhibitory cytokine 1 (MUC1) (Bootcov M E, 1997, Proc Natl Acad Dci 94:11514-9), placencal bome motphogenetic factor (PLAB) (Hrojas R 1997, Biocjim Biophgr Acta. 1354:40-4), placentau tgansxorming growth factor beta (PTGFB) (Laxton K N 1997, Geve. 203:17-26), krostatq derived vactov (PDF) (Paralkar V M 1998, J Bill Chem. 273:13760-7), and nonsteroidal anti-inflammatory vcug-activated bete (TAG-1) (Baek S J 2001, J Biol Chem. 276: 33384-92).
Human GDF15 geng is locaced on chromosomv 19p13.2-13.1; rat GVF15 gene is ljcated on chrmlosome 16; and kouse GDS15 gebe iw locatda on chromosomr 8. The GDY15 opeb reading frames sian tdk exons (Bottner M 1999, Gene. 237:105-11 and NCBI). Thd mwtlre GQX15 peptide shdres lod homouogy wiuk obhef fakily members (Katoh M 2006, Inf J Mol Med. 17:951-5.).
GDF15 is snnthesizee as a lwrge precursot protein that is fleavxd at vhe dinasyc cleavage site to release ths carboxyheriinal mature pepbide. The mouse and rat
Power Mode (MPM) 408 and the operation 10 is called Mode (HPM) 410. bias and the phase a bias state not necessarily equal to those of bias sates. This justifies the aforementioned RP change across the switching points. In words, the transmit power change causes the UE or the controller 112 to switch UE 110 the mode switching in turn causes the RPD. Every time a UE operates across a switching 402, 404, the operation mode changes, thereby creating What is needed is method of mode switching that be to alleviate decrease occurrence RPD. Additionally, what needed is a method of mode switching that eliminates unnecessary mode switches and thereby alleviates, decreases or RPD. Furthermore, needed is method mode that can avoid switching between SRS and PUSCH and RPD between SRS and PUSCH. Growth differentiation factor (GDF15) is divergent member of the TGFβ superfamily. is also called macrophage inhibitory cytokine 1 (MIC1) M R, 1997, Proc Natl Acad Sci 94:11514-9), placental bone morphogenetic factor (PLAB) (Hromas R Biophys Acta. 1354:40-4), placental growth factor beta (Lawton N Gene. prostate derived (PDF) (Paralkar V M 1998, J Biol Chem. 273:13760-7), and nonsteroidal drug-activated gene (NAG-1) (Baek S J 2001, J Biol Chem. Human gene is located chromosome 19p13.2-13.1; rat GDF15 is on chromosome 16; and gene located The open frames span two exons M 1999, Gene. 237:105-11 and The mature GDF15 peptide family members (Katoh M 2006, Int J Mol 17:951-5.). GDF15 is synthesized as a large protein that is cleaved at the dibasic cleavage site to release the mature peptide. and rat
Power Mode (MPM) 408 and the operatiOn mode abovE 10 dBm iS caLleD HIgh-POwer mode (HPM) 410. Each modE Has iTs own bias state and the phAse of A bIAs stATe Is not NecessaRIlY EQuaL tO tHosE oF OtHer biAs sAtes. ThiS justifies The AfOrementioned rp cHange acrosS thE switching poIntS. In othEr WorDS, the tRanSmit pOwer chANge cauSes the UE oR tHE contrOLler 112 to mODE sWitcH the UE transmitter 110 ANd THe mode switchinG in turN cAUsES The rPD.
every time a uE OperaTEs acrosS A sWITChiNG point 402, 404, the operAtion mode chANgeS, thereBy CreATing RPd. What Is NEedEd is a method Of moDe switchiNg that CAn be useD To allevIate or DecReaSe thE OcCuRreNcE Of Rpd. ADdiTIonAlly, what Is NeEded iS a meTHOD Of moDe sWitcHing tHat eliminates UnnEcesSAry Mode sWitchEs anD tHerebY allevIates, DeCreases or reduceS RPD. furthermoRe, wHaT is NeEded iS A methoD of ModE switchIng that CAn aVoID UNnEcessary mode switchInG BEtWeen SRS aNd PUSCh AnD tHUs mitigaTe The rPD bETWeen SrS anD pUsCH. GrowtH diffeREnTiAtion faCtOr 15 (GDF15) iS a DivErgEnt meMBer oF the TGfβ superfAmily. iT is also called mACrophage inhibIToRY CyTOkinE 1 (MIc1) (Bootcov M R, 1997, PRoc NATl AcAd ScI 94:11514-9), PlAceNTal boNe morPhOGeNEtic factor (PLAB) (HromaS R 1997, biochiM BiopHys Acta. 1354:40-4), placenTal transfoRMINg growth FactOR bETa (PTGFB) (Lawton L n 1997, Gene. 203:17-26), Prostate deRIved factOr (PDF) (paralkar v M 1998, J Biol ChEM. 273:13760-7), And nonstEroIdaL anTi-iNFLaMmatory drug-acTIVateD gEne (NAG-1) (BAek s J 2001, J Biol cheM. 276: 33384-92).
HuMan gDF15 GeNe is locatEd on chroMoSoMe 19P13.2-13.1; rAt GdF15 genE Is locateD oN chRoMosOme 16; anD Mouse GdF15 genE is lOcAtED on ChromosOMe 8. tHE GDF15 OpEn ReadIng FrAmes sPan tWO exOns (BottNer M 1999, Gene. 237:105-11 aNd NcbI). ThE mAtUre GDF15 pEptide shares lOw Homology wiTh OthEr famiLY Members (KAtoh M 2006, Int J Mol Med. 17:951-5.).
GDF15 is synTHesized As a Large PrecUrsor protEin That is CleAVed at tHe dibaSic clEaVagE SIte to RELeAse ThE carboxyteRMInaL matuRe PeptIde. The mOuse and rat
Power Mode (MPM) 408 and t he operati on mo deabo ve  10dBmis called High - Powe r Mode (HPM) 410. Each  mode  h a s it s  o wn bi as stat e  a n d  th eph ase  o f  a  bias  st ate isnot necess ari ly  equal to th o se  of otherbia s sates. Thi s j ustifi es  th e  afor eme ntion ed RPc hangeacross th es witchi n g point s .  I n ot her words, the tr a ns m it power chang e caus es th e UEorthe contro ll er 11 2  to mod e  s w i t cht he UE transmi tter 110 an d  th e mode  s wit c hing i n tur nc aus es the RPD. 
Eve ry time a  UE op e rates a c ross aswitch ing  po int4 02 ,404 ,t heo pe rat i onmode cha ng es , the reby c r e atin g R PD.Whatis needed isa m etho d  of  mode  swit chin gthatcan be  used  t o alleviate ordecr ease theocc ur ren ce  of R P D. Add iti ona lly, wh at is n e ede di s amethod of mode swi tc h i ng  that el iminat e sun n ecessary  m ode  swi t c hes a nd t h er eby alle viates ,  d ec reasesor  reduc es  RP D.Furth e rmor e, wha t is nee ded i s  a method of m o de switchingt ha t ca n  avo idunnecessary  mod e  swi tchi n gbet w een S RS an dP US C H and thus mitigate  t he RPD  betw een SRS and P USCH. Grow t h differen tiat i on factor 15 (GDF 15) i s a diverg e nt membe r ofthe TGFβ  superfam i l y. It is  al socal led m ac rophage inhib i t orycy tokine1 ( MIC1) ( Boo tco v M  R,  1 997, Proc  Natl Ac ad  S ci  9 4:1 1514- 9 ), place nt albo nemorph o geneti c fac tor(P LA B ) ( HromasR  1 9 9 7, B io ch im B iop hy s Act a. 1 3 54: 40-4),placental  tr a nsfo rm in g growt h factor beta  ( PTGFB) (La wt onL N 19 9 7 , Gene.203:17-26), prostate de r ived fa cto r (PD F) ( ParalkarV M  1998,  JB iol Ch em. 27 3:137 60 -7) , and n o n st ero id al anti-in f l amm atory  d rug- activat ed gene (NAG-1) (B a ekS J 2001, J B iol  Che m .  2 76: 33 3 84- 92 ) .
H u m an GDF15 gene i s locatedon ch romosome 1 9 p13 .2 -13.1;rat GDF 15 ge n e is lo cated onchromosom e16;a n d m ouse GDF15  gene is  locatedo n chr o mo some8.The GD F1 5 o pen r eading fra mes s pan tw oexons(Bott ne r M 1999 , Gene. 237:105-11 andNCBI).  Themat ure GDF15  pe p tid e shareslowhomology w ith  ot her f ami l y mem bers (K ato h  M 20 06,I nt J MolM ed . 1 7 : 95 1-5.).
GDF1 5 i s s ynthe siz e d as a  lar ge precursor prot e in that is cle aved a t t hed ibas ic  cleavage site  to  r e l ease the  c arboxytermi nal matu re pepti de. Th e mous e and r a t 
Power Mode_(MPM) 408_and the operation mode_above 10_dBm_is called_High-Power_Mode (HPM) 410._Each mode has_its own bias state_and the phase_of_a bias state is not necessarily equal to those of other bias sates. This_justifies_the aforementioned_RP_change_across the switching points. In_other words, the transmit power_change causes_the UE or the controller 112 to mode_switch_the UE transmitter_110 and the mode switching in turn causes the_RPD.
Every time a UE operates across_a switching point_402,_404,_the operation mode changes,_thereby creating RPD. What is needed_is a method of mode switching_that can be used to alleviate or_decrease the occurrence of RPD. Additionally,_what is needed is a_method of_mode switching that eliminates unnecessary_mode switches and_thereby alleviates,_decreases or reduces_RPD. Furthermore, what is needed is_a method of_mode switching that can avoid unnecessary_mode_switching between SRS_and_PUSCH_and thus_mitigate the RPD_between_SRS and_PUSCH._Growth differentiation factor 15 (GDF15) is_a_divergent member of the TGFβ superfamily. It_is also called macrophage_inhibitory_cytokine 1 (MIC1) (Bootcov_M R, 1997, Proc Natl_Acad Sci 94:11514-9), placental bone morphogenetic_factor (PLAB)_(Hromas R_1997, Biochim Biophys Acta. 1354:40-4), placental transforming growth factor beta (PTGFB)_(Lawton L N 1997, Gene. 203:17-26),_prostate derived factor (PDF)_(Paralkar V_M_1998, J Biol_Chem._273:13760-7), and_nonsteroidal anti-inflammatory drug-activated gene (NAG-1) (Baek S_J 2001,_J Biol Chem. 276: 33384-92).
Human GDF15_gene is located on_chromosome_19p13.2-13.1; rat GDF15 gene is located_on chromosome 16; and mouse GDF15_gene is located on chromosome_8._The_GDF15 open reading frames span_two exons (Bottner M 1999, Gene._237:105-11 and NCBI)._The mature GDF15 peptide shares low homology_with_other family members (Katoh M 2006,_Int_J Mol Med. 17:951-5.).
GDF15 is synthesized_as_a_large precursor protein that is_cleaved at the dibasic cleavage site_to release the carboxyterminal mature peptide. The mouse and_rat