NAD+ 500mg we yu go yuz

▎ NAD!Strɔkchɔ

Sos: PubChem

Sikyud: N/A Mɔlikul Fɔmula: C 21H 27N 7O 14P2 Molikul Weyt: 663,4 g/mol CAS Nɔmba: 53-84-9 PubChem CID: 5892. Di wan dɛn we de wok Sinonim: nadide;koɛnzym I;beta-NAD;Kɔdhaydrojɛnɛz I

▎ NAD + Risach

Wetin na NAD+?

NAD+ (Nicotinamide Adenine Dinucleotide) na imכtant kכεnzym we de bכku bכku wan insay liv כganism dεm. i de fכm bay di kכnεkshכn bitwin adenosin ribonuklyotid εn nikotinamid ribonuklyotid tru wan fכsfεt grup. as di kכr kכεnzym insay rεdכks riakshכn dεm, NAD+ de ple imכtant rol insay sεlyul mεtabolism. i kin kכnvכlt bitwin di כksidayz stet (NAD+) εn di rεdכks stet (NADH), we de tek pat pan enεji mεtabolism prכsεs dεm lεk glycolysis, di sitrik asid saykl, εn oksidativ fכsfכrayleshכn, we de εp di sεl dεm fכ kכnvכlt it to enεji (ATP). apat frכm dat, NAD+ de wok lεk nεsεsary kכfaktכ fכ difrεn εnzym dεm (lεk PARP εn Sirtuins), we de tek pat pan prכsεs dεm we riliyt to DNA ripa, sεl signal, εn anti-aging.

Wetin na di risach bakgrɔn fɔ NAD+?

Essential Cofactor in Multiple Riakshɔn dɛn: 

NAD+ na imכtant kכfaktכr insay mכltipכl rεdכks riakshכn dεm (Shats I, 2020). insay sεl dεm, i de involv insay plεnti sεl prכsεs dεm lεk εnεji mεtabolism, jεnomik stεbiliti, εn imyun rεspכns. fכ egzampl, insay enεji mεtabolism, NAD+ de akt lεk εlektrכn kεriכ insay prכsεs dεm lεk glycolysis εn di tricarboxylic acid saykl, i de tek pat pan rεdכks riakshכn dεm fכ kכnvכlt di kεmikכl enεji insay nyutriεnt dεm lεk glukכs to wan enεji fכm we sεl dεm kin yuz.

Intarakshכn wit mכltipכl εnzym dεm: 

NAD+ de intarakt bak wit mכltipכl εnzym dεm, lεk di DNA ripa εnzym poly-(adenosine diphosphate-ribose) polymerase (PARP), di protin dεacylase SIRTUINS, εn di saykli ADP ribose enzym CD38. dis εnzym dεm de rεgεl di sεlyul prכsεs dεm, lεk DNA ripa, jin εksprεshכn, εn sεl saykl rεgulεshכn, bay we dεn de it NAD+.

Wetin na di mεkanism fכ akshכn fכ NAD+?

As a Coenzyme in Rɛdɔks Riakshɔn dɛn

Mentεn Sεlyul Rεdכks Homכstasis: 

'NAD' kin tכk bכt di kεmikכl bakbכn fכ nikotinamid adenine dinucleotide, we 'NAD+' εn 'NADH' de tכk bכt in כksidayz εn rεdכks fכm dεm, rispεktivli. NAD+ de ple wan kכl rol fכ kכntro plεnti bayokεmik prכsεs dεm, εn di NAD+/NADH rεshכ na imכtant fכ mεnten sεlyul rεdכks homכstasis ^[1] . di intasεlulyar rεdכks bεlε implεnt fכ nכmal sεlyul fכnshכn dεm, inklud enεji mεtabolism, antioksidant difεns, εtk NAD+ de akt lεk εlektrכn aksepta כ dכna insay rεdכks riakshכn dεm, i de tek pat pan di intasεlulyar enεji prodakshכn prכsεs, lεk di trikarbכksilik asid saykl εn כksidεtiv fכsfכrayleshכn.

Rigulεt εnεji Mεtabolism: 

NAD+ de involv insay mכltipכl kכl εnεji mεtabolism prכsεs dεm. fכ egzampl, insay glycolysis εn di tricarboxylic acid saykl, NAD+ de aksept haydrojen atכm dεm εn i de kכnvכlt to NADH. afta dat NADH de transfכm εlektrכn dεm to כksijεn tru di εlektrכn transpכt chen na di insay maytochכndrial mεmbran fכ prodyuz ATP. di rεgulεshכn fכ dis εnεji mεtabolism imכtant fכ di sεl dεm we de liv εn fכ wok, spεshal wan insay di tisu dεm we gεt hכy enεji dimand lεk di at εn di bren ^{[1] .}.

Patisipet in Enzymatic Riakshɔn

Di Rol wit Poli(ADP-ribose) Polimεrayz 1 (PARP1): 

NAD+ de akt lεk sεns כ kכnsכm εnzym fכ PARP1 εn i de involv insay mכltipכl kכl prכsεs dεm. PARP1 de ple imכtant rol fכ DNA damej ripa. we di sεl dεm de sכfa DNA dεm, PARP1 de aktibכt εn i de yuz NAD+ fכ sכntez poly ADP-ribose (PAR) chen dεm, we dεn de atak protin dεm, we de protεkt di DNA ripa prכsεs. כltu, we di PARP1 aktibכt pasmak go it bכku NAD+, we go mek di intasεlulyar NAD+ lεvεl dεm dכn, we in tכn de afekt di enεji mεtabolism εn di viabiliti fכ di sεl dεm ^{[1, 2].}.

Di Rol wit Sayklik ADP-riboz (cADPR) Sεntez dεm: 

saykli ADP-ribose sεntez dεm lεk CD38 εn CD157 na NAD+ kכnsum εnzym dεm bak. dis εnzym dεm de yuz NAD+ fכ sכntez cADPR. cADPR de akt lεk sεkכn mεsenja fכ tek pat pan kalsiכm signal, we de rεgεl di intasεlulyar kalsiכm ayכn kכnsantreshכn, εn so i de afekt difrεn sεlyul fכnshכn dεm, lεk mכsul kכntrikshכn εn nyurotransmitta rilis.

Di Rol wit Sirtuin Protein Deacetylases: 

Sirtuin protin deacetylases (SIRT) dεm de dip bak pan NAD+ fכ fכnshכn. SIRT dεm de rεgεl di jin εksprεshכn, sεlyul mεtabolism, εn strεs rεspכns dεm bay we dεn de katalayz di dεasetεlayshכn fכ di protin dεm. pan ay NAD+ lεvεl, di aktiviti fכ SIRT dεm de εnhans, we de protεkt di hεlth εn sכvayv fכ di sεl dεm. fכ egzampl, כnda kכndishכn dεm lεk kalori rεstrikshכn, di intasεlulyar NAD+ lεvεl de inkrεs, we de aktibכt SIRT dεm, we de mek i εksεnd layfspan εn impruv mεtabolik hεlth ^{[2] .}.

Di Rol we di Axonal Dijenereshɔn de ple

Di Intarakshɔn bitwin NMNAT2 ɛn SARM1: 

insay di prכsεs fכ aksכnal dεjεnεreshכn, di NAD+ sεntez NMNAT2 εn di pro-dijεnεreshכn fכktכ SARM1 de ple imכtant rol dεm. NMNAT2 na aksכnal sכvayv fכktכ, we SARM1 gεt NADase εn riletid aktiviti dεm εn na pro-dijεnεreshכn fכktכ. di intarakshכn bitwin di tu implεnt fכ mεnten di aksכnal integriti. plεnti kes dεm, di aksכnal dεjεnεreshכn de kכz fכ wan sεntri signal path, we na dεn tu kכl protin dεm ya de mεntal rεgεl wit opozit ifekt dεm. fכ egzampl, insay nyurodijεnεraytiv sik dεm lεk Alzaima sik εn Pakinsin sik, di aksכn dεm de dεjεnεret bifo di nyuronal sεl bכdi dεm day, εn dis aksכnal dεjεnεrayshכn de kכmכn bak pan aksכnal lεshכn dεm lεk hεridita spastik paraplejia. insay dεn sik dεm ya, di aktibכshכn fכ dis signal path kin mek di aksכnal patכlayz chenj dεm ^{[3, 4].}.

Di NAD+-Mεdiet Sεlf-Inhibishכn Mεkanism fכ SARM1: 

stכdi dεn fכnshכn se NAD+ na ligεnd we dεn nכ εkspεkt fכ di armadillo/hεt rεpεt mכtif (ARM) domεn fכ SARM1. di binding fכ NAD+ to di ARM domεn de inhεbit di NADase aktvכti fכ di Toll/interleukin-1 rεsεptכr (TIR) ​​domεn fכ SARM1 tru di domεn intafεys. disrupt di NAD+ binding sayt כ di ARM-TIR intarakshכn go lid to di kכnstityushכnal aktibכshכn fכ SARM1, we de rizulta in aksכnal dεjεnεreshכn. dis de sho se NAD+ de mεdiet di sεlf-inhibishכn fכ dis pro-nyurodijεnεraytiv protin ^{[5] .}.

Di Rol we di sik dɛn we de ambɔg di at ɛn di blɔd

Fɔ protɛkt di at ɛn di blɔd wɛlbɔdi biznɛs: 

NAD+ gɛt prɔtɛktiv ifɛkt pan di sik dɛn we de ambɔg di at ɛn di blɔd. fכ egzampl, NAD+ kin protεkt di at frכm sik dεm lεk mεtabolik sεndrכm, at fεil, ischemia-riperfyushכn injuri, aritmia, εn haypatεnshכn. di mεkanism we i de protεkt kin involv mכltipכl aspek dεm lεk fכ rεgεl di εnεji mεtabolism, fכ mεnten di rεdכks bεlε, εn fכ inhεbit di inflammatory rεspכns. we yu ol כ כnda strεs, di intasεlulyar NAD+ lεvεl de dכn, we de mek chenj dεm na di mεtabolik stet εn i de inkrεs di susεptibiliti fכ sik dεm. fכ dat, fכ mεnten di NAD+ lεvεl na di at כ fכ ridyus in lכs na implεnt fכ di kכdivaskyul hεlth ^{[1] .}.

Di Rol we Tubakulosis De Du

Di Impekt pan Maykobakteriɔm TB (Mtb): 

insay Mycobacterium tuberculosis (Mtb), di pathogen fכ tuberculosis, di tεminal εnzym fכ NAD sεntez, NAD synthetase (NadE), εn di tεminal εnzym fכ NADP bayosεntesis, NAD kinase (PpnK), gεt difrεn mεtabolik εn maykrobayolojikal ifekt dεm. di inaktivashכn fכ NadE de lid to wan paralel dεkrεshכn na di NAD εn NADP pul dεm εn wan dεklin in di viabiliti fכ Mtb, we di inaktivashכn fכ PpnK sεlektivli deplεt di NADP pul bכt כnli stכp di growth. di inaktivashכn fכ εvri εnzym de kכmכn wit mεtabolik chenj dεm we spεsifi k to di εnzym we afekt εn di riletid maykrobayolojikal fεnotayp. bakteriostatik lεvεl dεm fכ NAD dεplεshכn kin mek kכmpεnsatri rimodεlin fכ NAD-dipεndεnt mεtabolik path dεm we nכ de afekt di NADH/NAD rεshכ, we baktericidal lεvεl dεm fכ NAD dεplεshכn kin disrupt di NADH/NAD rεshכn εn inhεbit כksijεn rεspireshכn. dis fכnshכn dεm de sho di fysiolojikal spεsifisiti dεm we dεn nכ bin no bifo we riliyt to di nεsεsity fכ tu evolushכnal ubiquitous kכfaktכr dεm, we sho se NAD bayosεntesis inhibito dεm fכ prayoritεt insay di divεlכpmεnt fכ anti-tuberculosis drog dεm ^[6]..

Di Rol we pɔsin kin du we i ol ɛn sik dɛn

di dεkrεshכn pan di sεlyul NAD lεvεl dεm we de rilet to di ol we dεn de ol: 

wit ol ej, di intasεlulyar NAD+ lεvεl de dכn sכmtεm. dis dכn dכn na di NAD+ lεvεl de riliyt to di chenj na di mεtabolik stet fכ di ol sεl dεm εn i kin inkrεs di susεptibiliti fכ sik dεm. bכku patכlayz kכndishכn dεm, inklud kכdivaskyul sik dεm, fכ fat, nyurodijεnεraytiv sik dεm, kεnsar, εn ol, de riliyt to di dayrekt כ indayrekt impεryans fכ di intasεlulyar NAD+ lεvεl dεm ^{[2, 7].}.

Di Rilayshɔn bitwin NAD+ Bayosintesis ɛn Kɔnsɔm Ɛnzaym ɛn Sik dɛn: 

NAD+ bayosεntesis εn kכnsכm εnzym dεm de involv insay sεvεra ki bayolojikal path dεm, we de afekt jin transkripshכn, sεl signal, εn sεl saykl rεguleshכn. So, bɔku sik dɛn gɛt fɔ du wit di abnɔmal wok we dɛn ɛnzaym ya de du. fכ egzampl, insay nyurodijεnεraytiv sik dεm, di mεkanism dεm we dipεnd pan NAD+ de involv protin dεm lεk WLD dεm, NMNAT2, εn SARM1, we de sho se nyurodijεnεraytiv sik dεm de inhεrentli rilayt to NAD+ εn εnεji mεtabolism ^[4].

Sos:PubMed ^{[7] we dɛn pul am.}

Wetin na di aplikeshɔn fil dɛm fɔ NAD+?

Aplikeshɔn dɛn na di sik dɛn we de ambɔg di at ɛn di blɔd

Ifɛkt we de protɛkt pɔsin: 

NAD+ de ple impɔtant pat pan di sik dɛm we de kam pan di at ɛn di blɔd, ɛn i kin protɛkt di at frɔm difrɛn sik dɛm. fכ egzampl, NAD+ kin protεkt di at frכm sik dεm lεk mεtabolik sεndrכm, at fεil, ischemia-riperfyushכn injuri, aritmia, εn haypatεnshכn ^[1] . dis na biכs NAD+ de akt lεk sεns כ kכnsכm εnzym fכ εnzym dεm lεk poly(ADP-ribose) polymerase 1 (PARP1), cyclic ADP-ribose (cADPR) synthases (CD38 εn CD157), εn sirtuin protein deacetylases (Sirtuins, SIRTs), εn i de involv insay sεvεra ki prכsεs dεm na kכdivaskyul sik dεm.

Mentɛn Rɛdɔks Balɛns: 

di NAD+/NADH rεshכ na imכtant fכ mεnten di rεdכks homכstasis fכ di sεl dεm εn fכ rεgεl εnεji mεtabolism ^[1] . fכ dat, fכ mεnten di NAD+ lεvεl na di at כ fכ ridyus in lכs na implεnt fכ di kכdivaskyul hεlth.

Aplikeshɔn dɛn na Anti-aging

Fɔ Ekstend Layf Spɛn: 

Di tin dɛm we de mek di mɔlikul ol ɛn di intavɛnshɔn fɔ lɔng layf dɔn witnɛs wan bɔku bɔku wan insay di pas tɛn ia. Nikotinamid adenine dinucleotide (NAD) εn in prεkursכr dεm, lεk nikotinamide riboside, nicotinamide mononucleotide, nicotinamide, εn nikotinic acid, dεn atrak intres as mכlikul dεm we kin intrestin fכ di aplikεshכn fכ sכm mכlikul dεm as pכtεnshal jεroprotεktכr εn/כ fכmakojεnomiks. dis kכmpawnd dεm dεn sho se dεn kin impruv di kכndyushכn dεm we de kכmכt frכm ol pipul dεm afta dεn dכn supliment εn kin mek mכdel כganism dεm n ^{כ day [8].}.

Influɛns Layfspan Rɛgyuleshɔn: 

insay mכdel כganism dεm lεk yist, stכdi dεn sho se NAD prεkursכr dεm de ple imכtant rol fכ ol εn lכng layf. tru di stכdi fכ di kronolojik layfspan (CLS) εn rεplikεtiv layfspan (RLS) fכ yist, wi kin bεtε כndastand di mεkanism fכ NAD mεtabolism εn in rεgεdyushכn rol fכ ol εn lכng layf ^[8]..

Pɔtɛnɛshɛl Aplikeshɔn fɔ Trit Tuberculosis

Di Target fɔ Drug: 

di inaktivashכn fכ di tεrminal εnzym fכ NAD sεntez, NAD sεntez (NadE), insay Mycobacterium tuberculosis (Mtb) de mek di NAD εn NADP pul dεm de dכn paralel εn di viability fכ Mtb de dכn, we di inaktivashכn fכ di tεrminal εnzym fכ NADP bayosεntesis, NAD kinase (PpnK), de sεlektivli dεplεt di NADP grכw pul bכt i nכmכ de stכp (Sharma R, 2023) ɛn di ɔda wan dɛn. dis sho se di NAD sεntesis inhibito dεm gεt prayoritεt fכ divεlכpmεnt fכ anti-tuberculosis drog dεm, biכs NAD dεfisiεns na baktericidal, we NADP dεfisiεns na bakteriostatik.

Mεtabolik Chenj dεm εn Maykrobial Fεnotayp dεm: 

di inaktivashכn fכ εvri εnzym de kכmכn wit mεtabolik chenj dεm we spεsifi k to di εnzym we afekt εn di riletid maykrobial fεnotayp. di bakteriostatik lεvεl dεm fכ NAD dεplεshכn de mek kכmpεnsatri rimכdelin fכ NAD-dipεndεnt mεtabolik path dεm we nכ de afekt di NADH/NAD rεshכn, we baktericidal lεvεl dεm fכ NAD dεplεshכn de lid to di disrupshכn fכ di NADH/NAD rεshכn εn di inhibishכn fכ כksijεn rεspireshכn ^[6]..

Di Rol we Sεlyul Mεtabolism De Ple

Bɔku Impɔtant Fɔnkshɔn dɛn: 

NAD(H) εn NADP(H) dεn bin tradishכnal fכ tek am as kכfaktכ dεm we de involv insay kכntlεs rεdכks riakshכn dεm, inklud εlektrכn tכnfכs insay maytochכndria. כltu, NAD path mεtabolit dεm gεt bכku כda imכtant fכnshכn dεm, inklud rol dεm fכ signal path, post-transleshכnal modifyushכn, epijenεtik chenj dεm, εn rεgεl RNA stεbiliti εn fכnshכn tru NAD kכp fכ RNA ^[9]..

Dynamik Mεtabolik Pכsεs: 

nכn-oksidativ riakshכn dεm kin lid to di nεt katabolism fכ dεn nyukliotayd dεm ya, we de sho se NAD mεtabolism na εkstrim dinamik prכsεs. infakt, stכdi dεm we dεn jכs du sho klia wan se insay sכm tisu dεm, di haf-layf fכ NAD na lεk fכ minit ^[9]..

Di Rol we Sɛl Bayoloji de Du

Ekstrasεlyul NAD Mεtabolism: 

εkstrasεlula NAD na di kכl signal mכlikul כnda difrεn fysiolojikal εn patכlayz kכndishכn dεm. i de akt dayrekt bay we i de aktibכt spεsifi k purinerjik rεsεpכta dεm כ indaykt wan as sabstεrayt fכ εksonukliεz dεm (lεk CD73, nyukliotayd payrofosfataz/fכsfodiεstεrayz 1, CD38 εn in paralog CD157, εn εkto-ADP-ribosyltransfεras dεm). dis εnzym dεm de ditarεmin di avεlayblεti fכ εkstrasεlyul NAD bay we dεn de haydrolayz NAD, so dat de rεgεl in dayrεkt signal ifekt (Gasparrini M, 2021). pan tap dat, dεn kin jεnarεt sכm sכm signal mכlikul dεm frכm NAD, lεk di immunomodulator adenosine, כ yus NAD fכ ADP-ribosylate difrεn εkstrasεlula protin dεm εn mεmbran rεsεpכta dεm, we gεt bכku impak pan imyun kכntrכl, inflammatory rεspכns, tumorigenesis, εn כda sik dεm. di εkstrasεlula envayroment gεt bak nikotinamid fכsfכribosiltransfεrayz εn nikotinik asid fכsfכribosiltransfεrayz, we de katalayz ki riakshכn dεm na di NAD sכlvεj path intasεlula. di εkstrasεlula fכm dεm fכ dεn εnzym dεm ya de akt lεk saytokεn dεm wit pro-inflammatory fכnshכn dεm ^{[10] .}.

fכ kכnklud, NAD+ dכn bi wan kכl mכlikul we de kכnekt hεlth εn sik bay we i de rεgεl di εnεji mεtabolism, delay fכ ol, rεgεl imyuniti, εn de gi protεkshכn fכ mכltipכl sistεm dεm. fכ supliment in prεkursכr dεm kin impruv di maytochכndrial fכnshכn εn slo dכn di prכgreshכn fכ mεtabolik εn nyurodijεnεraytiv sik dεm. I de sho pɔtnɛshɛl pan di fild dɛm fɔ protɛkshɔn fɔ di at ɛn di blɔd, anti-infɛkshɔn, ɛn anti-aging, we de gi nyu tritmɛnt target fɔ sik dɛm we gɛt fɔ du wit ol ej.

Bɔt di pɔsin we rayt di buk

Di tin dɛn we wi dɔn tɔk bɔt ɔp, na ɔl di tin dɛn we Cocer Peptides dɔn du risach, ɛdit ɛn kɔmpilayt.

Sayɛns Jɔnal Author

Jiang YF na risachman we gɛt fɔ du wit sɔm big big institiushɔn dɛn, lɛk Peking Yunivasiti, Lanzhou Jiaotong Yunivasiti, di Nashɔnal ɛn Lokal Jɔyn Ɛnjinia Risach Sɛnta fɔ Tɛknɔlɔji ɛn Aplikeshɔn, di Beijing Ɛnjinia ɛn Tɛknɔlɔji Risach Sɛnta fɔ Fɔd Aditiv, di Chaynish Akademi fɔ Sayns, di Yunivasiti fɔ Sayns ɛn Tɛknɔlɔji fɔ (CAS), Beijing Tɛknɔlɔji ɛn Biznɛs Yunivasiti, ɛn Mɛdikal Yunivasiti. In risach de pan bɔku difrɛn difrɛn tin dɛn, lɛk kemistri, patɔlɔji, injinɛri, ɔnkɔlɔji, ɛn akostik. In wok de sho wan mɔltidisiplinari we, we de intagret sayɛns ɛn tɛknɔlɔjik advansmɛnt dɛn akɔdin to dɛn fild ya. Jiang YF de list in di rεfrεns כf saytεshכn [5].

▎ Saytayshɔn dɛn we gɛt fɔ du wit dis

[1] Lin Q, Zuo W, Liu Y, ɛn ɔda pipul dɛn. NAD ɛn di sik dɛn we de ambɔg di at ɛn di blɔd[J]. Klinika Chimika Akta, 2021,515:104-110.DOI:10.1016/j.cca.2021.01.012.

[2] Shats I, Li X. Baktri dεm de bכst di hכst NAD mεtabolism[J]. Aging-Us, 2020, 12 (23): 23425-23426.DOI: 10.18632/ɛj.104219.

[3] Hopkins E. L., Gu W, Kobe B, ɛn ɔda pipul dɛn. wan nכvel NAD Sayn mεkanism in Akson Dijεnεreshכn εn in Rilεshכn to Innat Imyuniti[J]. Frɔntiers in Mɔlikul Bayosayns, 2021,8.DOI:10.3389/fmolb.2021.703532.

[4] Cao Y, Wang Y, Yang J. NAD+-dipεndεnt mεkanism fכ patכlayz aksכn dεjεnεreshכn.[J]. Sεl Insayt, 2022,1(2):100019.DOI:10.1016/j.sεlin.2022.100019.

[5] Jiang Y F, Liu T. T., Li C, ɛn ɔda pipul dɛn. di NAD ⁺ -mεdiet sεlf-inhibishכn mεkanism fכ pro-nyurodijεnεraytiv SARM1[J]. Nature, 2020,588(7839):658.DOI:10.1038/s41586-020-2862-z.

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ƆL DI ATIKUL ƐN PRODƆKT INFƆMƐSHƆN WE DƐN GI NA DIS WƐBSAYT NA FƆ ƆL FƆ DI INFƆMƐSHƆN ƐN FƆ EDYUKESHƆN.  

Di prɔdak dɛn we dɛn gi na dis wɛbsayt na fɔ in vitro risach nɔmɔ. in vitro risach (Latin: *in glas*, we min insay glas) dεn de du am ausayd mכtalman bכdi. Dɛn prɔdak ya nɔto mɛrɛsin, dɛn nɔ gɛt di aprɔval frɔm di US Food and Drug Administration (FDA), ɛn dɛn nɔ fɔ yuz dɛn fɔ protɛkt, trit, ɔ mɛn ɛni mɛrɛsin, sik, ɔ sik. Di lɔ nɔ gri fɔ mek dɛn put dɛn tin ya insay mɔtalman ɔ animal bɔdi ɛni we.