~The Songs From Awak~

~standing in the eyes of the world~



~waving flag~



~waka waka~

Sudah… maafkan aku… segala salahku
Dan bila kau tetap bisu ungkapkan salahmu

Dan aku… sifatku, dan aku khilafku…
Dan aku… cintaku, dan aku rinduku…

Sudah… lupakan semua… segala berubah
Dan kita terlupa… dan kita terluka

Dan aku… sifatku, dan aku khilafku…
Dan aku… cintaku, dan aku rinduku…

Reff :

Kutanya malam… dapatkah kau lihatnya
Perbedaan yang tak terungkapkan
Tapi mengapa kau tak berubah
Ada apa denganmu…

Oh hanya malam…
Dapat meleburkan segala rasa
Yang tak terungkapkan
Tapi mengapa kau tak berubah
Ada apa denganmu

~ada apa denganmu~

Oh Kekanda
Jangan iri hati, Dinda naik pangkat lagi
Oh Adinda
Kanda mana dengki, malah Kanda support bini

Jadi Dinda mahu mengambil masa
Tapi Kanda mahu segera
Dinda ingin berjaya dalam kerjaya
Tapi Kanda mahu cahaya mata

Dinda belum bersedia
Kanda dah beria ria
Jadi yang mana satu
Tak perlu bertengkar
Tak perlu bermasam muka

Oh Adinda, tolong jangan lekas curiga, lekas cemburu buta
Oh Kekanda, Dinda perlu berhati-hati, tak rela dikongsi

Kanda kerja overtime, terlebih masa
Itu yang Dinda harus berwaspada
Ini semua demi masa depan keluarga
Dengan Dinda atau sebaliknya

Kanda kerja malam
Dinda kerja siang
Jadi bila nak bertemu
Tak perlu bertengkar
Tak perlu bermasam muka

Oh adiwira, dewataku, mari ikut cara Dinda
Oh Tun Teja, intan permata, mari ikut cara Kanda
Oh bagaimana? Bagaimana kita nak selesaikannya?
Apa keputusannya?

Oh Kekanda mari nyawa, kita cuba komunikasi
Oh Adinda mari sayang, kita cuba toleransi

Walau kita janji sehidup semati, kita berlainan
Kanda polar kutub utara
Dinda kutub selatan
Komunikasi, sikap toleransi, itu yang kita perlu
Tak perlu bertengkar
Tak perlu bermasam muka

Walau kita sering dengan cara masing-masing
Kanda yang Perdana
Dinda yang Utama
Kanda segalanya
Dindalah nyawa
Kita tetap bahagia bila bersama sama
Bahagia bersama
Bersama selamanya
Bahagia selama-lamanya

~adinda kekanda~


Sayu terpisah
hikayat indah kini hanya tinggal sejarah
berhembus angin rindu
begitu nyamannya terhidu wangian kasihmu
hujan lebat mencurah kini
bagaikan tiada henti
kaulah laguku kau irama terindah
tak lagi kudengari
kau pergi.. pergi..
sepi tanpa kata
terdiam dan kaku tak daya kau kulupa
apa pun kata mereka
biarkan kenangan berbunga di ranting usia

~pergi~

Sudah… maafkan aku… segala salahku
Dan bila kau tetap bisu ungkapkan salahmu

Dan aku… sifatku, dan aku khilafku…
Dan aku… cintaku, dan aku rinduku…

Sudah… lupakan semua… segala berubah
Dan kita terlupa… dan kita terluka

Dan aku… sifatku, dan aku khilafku…
Dan aku… cintaku, dan aku rinduku…

Reff :

Kutanya malam… dapatkah kau lihatnya
Perbedaan yang tak terungkapkan
Tapi mengapa kau tak berubah
Ada apa denganmu…

Oh hanya malam…
Dapat meleburkan segala rasa
Yang tak terungkapkan
Tapi mengapa kau tak berubah
Ada apa denganmu

~ada apa denganmu~

Don’t want much, I just want everything
Thought that I could, do almost anything
One step in front of the other
Thought that I could do it alone

In the blink of an eye, it’s just another day
Telling me why, I’ll find another way
Got this feeling, got me reeling
I can almost start believing

Now there’s me and you
And we are not alone
You and me
We are together now
Through my window, I can see there’s
More than you and more than me
Me and you
And we are not alone
Different view
We are together now
Through my window, I can see
Our wildest dreams could be so real

I see a spark, it starts a fire
Get lyrics at http://liriksemualagu.blogspot.comIs this the one worth waiting for?
Thought that I could do it without you
Can’t exist like this anymore

Now there’s me and you
And we are not alone
You and me
We are together now
Through my window, I can see there’s
More than you and more than me

Now there’s me and you, you and me
We are not alone and we are together
Through my window I can see
Our wildest dreams could be so real


~through my window~



~the scientist~

Harus bagaimana lagi
Dan terus begini
Dengarkan aku
Lihat ke mataku

Cukup sudah kau menghukum
Salahku tetap salahku
Benarkan ku berbicara
Agar bisa pulih semua

Namun harus sampai bila
Kau kan diam seribu bahasa

Chorus
Maafkanlah ku tak bisa hidup tanpa kamu
Fahamilah ku tak mampu terus tanpa kamu
Bagaimana ku nanti
Bila tiada mengganti
Yang ku ada hanya kamu saja

Saat mata terpejam
Hanya kau ku terbayang
Menghapus semua segala rasa di jiwaku

Saat mata terbuka
Kamulah yang pertama
Tak mampu aku
Bayangkan
Hidup tanpa dirimu

Ulang Chorus

Aku memang bersalah
Selalu saja mengabaikan mu
Dan tapi dah ku sedari
Segala perit kau lalui
Ku terlupa kau terluka

Dan memang selalu
Aku bersalah
Selalu saja mengabaikan mu
Meninggalkan mu
Dan tetapi itulah aku sedari
Segala perit yang kau lalui
Kerna diriku yang terus hanyut

Maafkanlah ku tak bisa hidup tanpa kamu
Bagaimana ku nanti
Bila tiada mengganti
Yang ku ada hanya kamu saja

Bagaimana ku nanti
Bila kau tak di sisi
Yang ku ada hanya kamu saja

~hanyut~

You know I want to
You know I need to, yeah

(Make you forget him)
(Make you forget)

You know I want to
You know I need to, yeah

(Make you forget him)
(Make you forget)

Because I love you, yes
I love you, yes

Because I love you
Love you, yes

~love you yes~


[All]
When I get older
I will be stronger
They’ll call me freedom
Just like a wavin flag

[K'naan]
Born from a throne
Older than Rome
But violent prone
Poor people zone

[Nelly Furtado]
But it’s my home
All I have known

[Sam Roberts]
Where I got grown
but now its gone

[Avril Lavigne]
Out of the darkness
in came the carnage
threatening my very survival

[Pierre Bouvier of Simple Plan]
Fractured my streets
and broke all my dreams

[Tyler Connolly of Theory of a Deadman]
Feels like defeat to wretched retreat

[All]
So we strugglin’

[Kardinal Offishall]
Fighting to eat

[All]
And we wonderin’

[Kardinal Offishall]
If we’ll be free

[Jully Black]
We cannot wait for some faithful day
it’s too far away so right I’ll say

[All - Chorus]
When I get older
I will be stronger
They’ll call me freedom
Just like a waving flag
(And then it goes back x3)

Ahhho ahhho ahhho

[Lights]
So many wars, settling scores
[Deryck Whibley of Sum 41]
All that we’ve been through
and now there is more
[Serena Ryder]
I hear them say love is the way
[Jacob Hoggard of Hedley]
Love is the answer that’s what they say
[Emily Haines]
But were not just dreamers
of broken down grievers
[Hawksley Workman]
A hand will reach us
And will not forsake us
[Drake]
This can’t control us
no it can’t hold us down
[Chin Injeti]
We gon pick it up even though we still struggling
[Pierre Lapointe]
Au nom de la survie (In the name of survival)
[all]
and we wondering
[Pierre Lapointe]
Battant pour nos vie (Fighting for our lives)

[All]
We patiently wait
for some other day
[Fefe Dobson and Esthero]
thats too far away so right now we say

[All - Chorus]

[Drake - Rapping]
Uhh – well alright
How come when the media stops covering
and there’s a little help from the government
we forget about the people still struggling
and assume that its really all love again, nahh
see we don’t have to wait for things to break apart
if you weren’t involved before it’s never too late to start
you probably think that it’s too far to even have to care
well take a look at where you live what if it happened there?
you have to know the urge to make a change lies within
and we can be the reason that they see their flag rise again
lyrics courtesy of www.killerhiphop.com

[Nikki Yanofsky & Drake]
When I get older
I will be stronger
They’ll call me freedom
Just like a wavin’ flag

[Matt Mays]
and then it goes back
[Justin Nozuka]
and then it goes back
[Nikki Yanofsky]
Then it goes back

[Chorus - All]

[Justin Bieber]
When I get older
When I get older
I will be stronger
just like a waving flag.
[End]


~waving flag for haiti~

Yovie & Nuno lyrics

~menjaga hati~

so awak....sy masih ingt lg smua lagu2 tu...n maybe ada yg trcicir sy minx maaf ya...:)~

THE NEXT MAJJLIS TERTINGGI LITHIUM 0610....

ok...now it goes...as adli's wish...dy nk smbungn drpd mt form 5 bg tahun 2010...amboi adli...capab gila....hahahaha....lwk ja...at least muka aku pown ada kn...aiyo...so...ni da rest of the mt form la...~



*apa kata kita start dgn adli la kn...hahaha...dy presiden utk TRS...presiden MERBAU 2010...presiden apa lg xtaw la...hahahaha...jgn mrh adli...berwibawa...best bwat group trs kali ni...ikot suka nk plih sapa...kn sng tuh...*




*ni timbalan adli...so...amanina...sedap kn nma tuh...huhuhu...so...nina pown mmg sesuai sngt pegang jwtn neyh...dy ni dh la terer..thnx nina...hgpa bwat math mod km rsa sng...hehehehe*





*ha..ni plak yon...or farizul...dy ni presiden utk kebersihan dan keceriaan...hehehe...on da day jamuan merbau...aku tukar hadiah dgn ang kn yon...hehehe...nice gift dat i got from him...bwat aku brtmbh ceria..hahaha*






*ni plak timbalan yon...arina...my classmate..merangkap penolong ketua kelas 5Attentive...hehehe...meh nk cita psal bdk cantik lithium neyh...nk lwn dgn adli...vice president kebersihan dan keceriaan...vice president 5Attentive...vice president PRS...nsib x vice president cengal skali..kalau x kalah ar adli...hahaha..*






*waaa...ni kembaq aku...9/3/93...hehehe...hello my twins..ni pakya...or satria azhari...sedap nma..nk pangy azhari ar lpas ni...hehehe..pakya yg cute ni presiden utk rekreasi n kokurikulum...besa la...my twins ni kn rugger...hehehe...but...dy xdak timbalan..coz dh tarik diri awal2 lagi..iaitu melly...*





*last but not least is shahir tough!hahaha...knapa agknya org pngy dy tough ea??btw...dy mewakili mt form yg terakhir...president utk sahsiah dan kerohanian...hehehe..dy badri taw...jgn bwat maen2...hik3...ok2...kalau x silap aku...he's da one yg rapaaat sngt dgn imad...mcm dh kapel pown ada...ops..imad x baca rsanya blog aku neyh....huk3*





*ok...kalau smua nk taw...wajah di atas tu adalah timbalan shahir tough...huhuhu..its me..timbalan biro sahsiah dan kerohanian...hahaha...mcm mna ntah bleyh trplih xtaw la...coz nma2 ni dibuat pengumuman time prjumpaan form setiap khamis tu..*


p/s : tu ja utk tatapan kalian...wasalam~

~life without frens is like a dog without his owner...~

ok....yg ni nk tujukn kt kwn2 aku yg dh bnyk menolong aku.......erm....guys!sorry ter emo...smbil tulis blog ni rasanya mcm dh lma x nanges...brcucuran air mata ni....

Nurazandra Azyan.....




ntah la...bkn nk bwat cita sdeyh....but i miss u yan...eventhough kita bnyk gduh...i still owe u...u la yg jga i time i sakit...u ingt i lupa??x pnah azandra...sometimes i felt like...bngga sngt dpt kwn mcm u...knapa kita perlu gduh??ntah la...thnx for everything yan...mlm tu...sorry sngt2...sorry sngt2...i didnt mean anything for everything dat ive said...i sayang u azandra...hurmmm....hopefully u'll never forget our moment being together k...for every sec...u'll always in my mind...mmmuuuaahhhxx!!~

Nur Rafiqah....




tahun ni kita berenggang kn piqah....but lastly...i cried waktu pelukan terakhir kita...i miss u piqah...pelukan yg ketat..ntah bila blh dpt lg from kiosk ni...piqah...thnx tlg angkat km ari km sakit tu...hahahaha...lwknya...but dat's a memory rite...piqah..even kita laen2 dorm..but i'll never forget u...kenangan form 4 kita....kita KIOSK...hahaha...Kami.Ini.Orang.Setia.Kawan....bju pown dh x jd..adeyh...hahaha...forever kiosk~




*K.I.O.S.K tetap di hatiku...ingt lg our memory bila p outing kt pekan nat...kita beli kipas mainan yg dlm ada sweets...hahaha...malunya bila naik teksi kita bukak tingkap...kipas tu berpusing...hahaha..pastu pusing satu nat bbrpa kali..aduss...kenangan kita*


Nor Hatika...




so...hye hatika!!!nk peluk hgpa!!!hehehe...sukanya peluk hatika...but now xleyh dh...sdeyh2...ha...tik2...ayaq...doraemon...smua pnggilan utk dy...rindunya...xleyh dh tgk hatika time dy mengalir...hahaha...mrh org je taw...sombong bngt sih....hahahaha...tik2...thnx for everything hatiku...hgpa bnyk tlg km...bnyk dgr luahan km...thank you so much...kita x gduh2 kn...kalau gaduh pown...im sorry tik2!hehehe...love u forever tika...n i miss to hug u...mmuuaahhxx!!!~

Nurul Atiqah...



tqahmad!!!ermmmm...rindu sngt...ingt lg x kita jln2 dkt nat kuala nerang...kita beli gula-gula kapas...kita beli wafel...kita beli keychain kasut...aduss...lwk2...mcm2 nk beli....lastly beli kek utk mak hgpa...hahaha...pastu blik rumah hgpa...bwat mcm2...especially blik time musim durian...aduss...sedapnya durian...just hgpa x bwak km p dusun hgpa lg ja...sdeyh taw...sob3...tu smua skrg tinggal kenangan..dun u missed it??miss u our time tqahmad...kita nanges sma2...a very defensive fren...brapa bnyk thnx dh...kalau blh beribu2 thnx nk kata neyh...hgpa dh tlg km bnyk tqahmad...dgn time km sakit...suka berleter...aduss...haa..bnda yg xleyh lupa...K_ _ _ _ T...hahaha...isi tmpt kosong tuh...sayang hgpa!~



*walaupon hgpa nk hempuk km...tp km still sayang hgpa dua...;)~

~saya dan awak lagi~

haa..ni smbungan drpd ~saya dan awak~ aritu...hehehehe...aku nk brcerita...aritu aku kantoi dgn sapa2 ja...skrg ni aku dh nk bertros trang...aku mmg dgn si dia...dh2..stop2...jgn bnyk tnya...huk3...skrg ni dh xdak hide n seek...xdak dh bwat2 x kenal time jumpa...org tnya pown dh blh jwb ya ea awak...hahaha...so..aritu last day kt skolah...lpas ja abis exam bio paper 3..actually km dh planned nk jumpa kt kantin...tp...emmm...apa kn daya..aku p..tgk dy xdak...tgk2 selisih dgn aku time aku nk p bilik boss..selisih dgn dy yg nk ke kantin dr office...huh...aku pown dh abis dh berurusan dgn boss..aku cpt2 p kantin..lemah kaki aku time aku nk p kantin...tp..apa yg aku dpt...aku sdeyh sngt2...dy xdak??hurm....aku call ayah aku..."abah ada kt area pokok sena dh neyh.."...apa aku xkn dpt jumpa dy dh???air mata aku bercurah2 kluar bila smpai2 dorm...aku sdeyh sngt.......~



i love sketches....ntah la...hahaha...then..bila aku blik dorm...mmg aku xtaw nk bwat apa..dgn sdeyh nk blik....for the first time kimah comey blik dlu..kalau x dy yg last...hahaha...sdeyh brtmbh2....haih...nk nanges dh neyh...aduss...tp aku x putus asa...aku cri cik riang...ajak cik riang jmpa dy...aku sndiri xtaw cena nk jmpa dy neyh...tp kaki aku bwk aku jln...knapa agknya aku jln p kt blakang DM???sdgkn yg tu jln nk ke surau..then aku pusing ke arah aspura bila smpai blakang DM...awak di situ...cik riang gelak..."telepati ke hgpa dua neyh"....hahaha...instinct ni penting rupanya...we met at last...err...segan sngt...first time kn awak...walaupown x smpai 2 minit awak kata...ya la..ayah awak dh dtg...ayah sy pown dh dtg...xleyh la nk lma2....



sekarang dh xdak org nk bg chocolate kt sy...kita pown xleyh sma2 nk di boo kn oleh kwn2 kita bila chelsea kalah...adeyh...kenangan ni aku xkn lupa smpai bila2...hopefully 10 bulan kita brsma blh jd 10000 tahun...insyaAllah...~

p/s : sorry smua...aku trpksa brbohong sbb km dua sma2 nk kna jga reputasi km as km dua memegang jwtn yg pnting kt skolah...sekian~

SPM~

it's over now...shock rite??hahahaha....now the next posting....aku nk tulis pasal hari2 terakhir aku di bumi saina....sdeyhnya!!!!skrg bru aku nk tulis coz bru skrg aku rasa rindu dkt kwn2 aku....blob3....waaa...penangan smua org ni...aku rindu D01...aku rindu 5A...aku rindu MERBAU...aku rindu KD005A135....aku rindu 'awak'....last day is the sweetest memory that i will never let it out of my mind....nk taw apa?tunggu la bwh2 lg aku nk tulis.....:)


*last prep*


*tgk ni awak...saya walaupown time exam pown..sy riadah taw...bkn mcm awak...buncit je...gagagaga....haa...even mcm seminit je lg nk exam....km sempat jogging lg taw...bgn pg2...hahahaha...ksian kt diorng...sblm jogging mkn nasi goreng masin..yucks!*




so...the next day..km exam kot...eh eh..ni bila ntah...i guess jumaat...time ni rmai gk yg kluar jogging...hik3....ok..bkn sehari ja km jogging...but bnyk hari...rasa x puas kn menikmati keindahan alam saina ni...adussss....nk emo dh ni...waaaa....nk nanges...sob3~



*apa2 pown...tetap kna posing..*

btw....kenangan ni tetap in our memories...never forget this...~

*yeah?*
*stickhockey kechain vs cute bear?*
*is it?*
*aha*
*nvm*
*its the past*
*kuih raya+choc?*
*stiap blik*
*oh ok*
*dun wory*
*i keep it scret\*

di kala kakak aku kesedihan...
aku brtmbh sdeyh...
kak intan taw knapa atin sdeyh bila bca blog kak intan...
sbb kata2 ni kak intan...
kata2 kt ats tu bwat atin sdeyh..sakit..smua ada..
ntah ar...
u..thnx for saying all of this to me..
dats it..i'm too bad for everybody...*to u..a guy*

~saya dan awak~

ok..skrg aku nk crita....my heart has found someone like him...akhirnya aku jumpa jgk...awk...agknya kalau dh trkantoi tu apa mksudnya ea...:

*mcm ni ke??*



*ke mcm ni??*



*ini mcm ke??*





*mcm ni pown bkn*

x elok x elok...jd actually trkantoi mcm mana tu...??

~Majlis Tertinggi Lithium 0610~

uik2...aku tgh boring..so drpd aku dok merapu dgn adik2 aku kt bwh..better aku lyn update blog aku...so...skrg dh nk dkt kluaq skolah neyh...main storynya of coz berkaitan saina...hik3..aku bru tringat dkt organisasi aku..MT Form...bnyk bnda km lalui bersama..eceh...pemikiran..idea..bnyk yg dh km bincang dlm setiap meeting..grand skit ar sbut meeting...MT Form for da LITHIUM 0610 batch are starting with.....:



**haa..ni pak roy...ataupon ikhmal...dy ni KETUA FORM..berkaliber kn...**





**ni plak mama nida...hehehe...TIMBAlAN KETUA FORM...wahh...seorg yg berdedikasi dan berhati lembut...tingat dy settle mslh aku dgn my best fren..azandra azyan..**



**nie plak SETIAUSAHA km...pak yad..or hazayiad...dy ni mmg gud ar dlm bwat keja..hehehe**



**ni plak rosmi...ha..dy ni TIMBALAN SETIAUSAHA...tp sekerat jln...she quitted for more concentration on her studies...chill**



**hah..ni plak nasri...BENDAHARI form...dy ni dh la jujur..punctual plak...x slh plih ar km...n dy ni slh sorg top student kt saina...8A's trial kot..huhuhu**




**ni plak kak nora...haa..pndai pown pndai..trademark dy..~slow n steady wins da race~mmg sesuai ar..msuk bicycle lmbt dpt no.2 tu...hehehe...ni plak TIMBALAN BENDAHARI**

so..ni ja yg blh aku cita..nnti aku cita psai sub2 mt form..ada 8 org lg neyh..huhuhu...daaaaaaaaa~ p/s:strive for glory...history is rite now in my hand..~

~ramadhan yg terakhir di saina~

waa...sdeyhnya rasa nk tinggai saina...alamak...ni yg menyeksa jiwa neyh...lwk plak..dulu msuk...rasa mcm nk kluar dr saina..tp makin dekat Allah bg masa nk kluar..makin dekat plak rasa dgn saina...aiyoyo...ramadhan kali x terasa langsung sbb time tu tgh trial...aduss...tp tu la..bz2 gk...tp ramadhan ni la pling enjoy...btol ark kwn2...huhuhu...mcm2 bnda km bwat...
**bersahur di awl pg...pling x lupa..ada satu mlm yg esknya nk trial fizik..satu side B x lena..trtumpu ke arah lampu tqahmad...stdy fizik...pastu sdar2 pkul 5 pg...km la org 1st jejak kaki ke dewan mkan asrama...hahaha**
**pastu km tadarus rmai2...aku sbg naqibah mengetuai anak2 buah aku..tqahmad...netty..n shazmira..haa..lupa plak..laili...sorry laili..time tu dy sakit...dok ats krusi roda...so..dy bca kt dorm...hari 1st tadarus...big applause to me..aku habiskn satu juzuk sorg2 sbbnya..tutt...aduyai...secreto de laveta...**
**hah...km msuk kelas...ops..ada hari2 trtntu km kna msuk kelas awl...ambik tmpt msing2...cikgu pass kertas..ha nah...ambik kertas..jwb!exam!!aduss...time posa ar gk..xpa2...dugaan2...**
**then...ptg km bca yasin ar plak..hehehe...utk kesejahteraan hidup dan ketenangan di bulan ramadhan serta utk kejayaan aku dan LITHIUM 0610 dlm SPM dengan kejayaan 9A++...Aminn...**
**haaa..ni yg bestnya...aku dgn kwn2 aku lpas ja habis baca yasin..tros blik..tidoq sat...dh hbis mandi apa smua..kluar pi ambik mknn nk brbuka..sblm brbuka tu km posing2 ar dlu...sakan redah saina neyh...sonok2...**





**dh brbuka...kna ar pi surau...kt surau lpas ja smyg maghrib...km tadarus lg...pastu smyg isyak...bru lah smyg teraweh..suka ja bwat 23 rakaat kt skolah**

kenangan ni yg pastinya mmg aku xkn lupa...sayang semuaaa!!! to tiqahmad...hatika...aina...hanim...siti...asma...kimah...syaza...i love you alll!!!~

i miss 'awak'...~

Di daun yang ikut mengalir lembut
terbawa sungai ke ujung mata
dan aku mulai takut terbawa cinta
menghirup rindu yang sesakkan dada

jalanku hampa dan kusentuh dia
terasa hangat oh didalam hati
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Human Genetics Web Tutorial




True/False

Indicate whether the sentence or statement is true or false.

TF 1. Hemophilia is a recessive, sex-linked disorder.

TF 2. An autosomal trait will occur with equal frequency in both males and females.

TF 3. Sex-linkd traits appear more often in females than in males.

TF 4. An individual who expresses a genetic disorder is called a carrier.

TF 5. A male can produce sperm that contains either an X or a Y chromosome.

TF 6. Mutations are always harmful.

TF 7. A pedigree is a family record that shows how a trait is inherited over several generations.



Multiple Choice

Identify the letter of the choice that best completes the statement or answers the question.

8. Hemophilia is a genetic disorder that is
a. sex-linked. c. fairly common.
b. sex-influenced. d. more common in women than in men.



9. Parents of a color blind female could have the genotypes
a. XCXc and XCY c. XCXc and XcY
b. XcXc and XCY d. XCXC and XcY



10. People who are heterozygous for sickle cell anemia are
a. partially resistant to the effect of ultraviolet radiation.
b. totally resistant to the effect of ultraviolet radiation.
c. partially resistant to malaria.
d. totally resistant to malaria.



11. Both sickle cell anemia and hemophilia
a. are caused by genes coding for defective proteins.
b. are seen in homozygous dominant individuals.
c. provide resistance to malaria infections.
d. are extremely common throughout the world.



12. This genetic disease occurs most frequently in the black population.
a. cystic fibrosis c. sickle-cell anemia
b. Tay-Sachs disease d. hemophilia



13. The trait for skin color in humans is cause by
a. crossing-over c. nondisjunction
b. multiple genes d. mutations



14. A hereditary disease in which the red blood cells have an abnormal shape is
a. galactosemia c. polydactyly
b. Tay-Sachs disease d. sickle-cell anemia



15. Sex-linked traits appear more often in males than in females because
a. males are produced in greater numbers
b. females with a sex-linked trait will die
c. males have only one X chromosome
d. sex-linked traits are carried on the Y chromosome


16. A diagram in which several generations of a family and the occurrence of certain genetic characteristics are shown is called a
a. Punnett square. c. pedigree.
b. monohybrid cross. d. family karyotype.



17. What is the percentage of chance that two people who carry a sickle-cell gene will have a child having the disease?
a. 0 c. 50
b. 25 d. 100



18. Which genetic trait is most influenced by the environment?
a. blood type c. baldness
b. eye color d. weight


19. Very dark-skinned people have alleles at all gene positions for skin color that code for
a. red-green colorblindness. c. the production of Rh antigens.
b. albinism. d. the production of melanin.



20. Sex-linked traits such as color blindness
a. are never carried by females c. occur more frequently in males
b. occur more frequently in females d. never occur in males



21. What would be the blood type of a person who inherited an A allele from one parent and an O allele from the other?
a. type A c. type AB
b. type B d. type O.



22. Genetic counseling is a process that
a. helps identify parents at risk for having children with genetic defects.
b. assists parents in deciding whether or not to have children.
c. uses a family pedigree.
d. All of the above


23. If both parents carry the recessive allele that causes cystic fibrosis, the chance that their child will develop the disease is
a. one in two. c. two in five.
b. one in four. d. 100 percent.



24. People with Down syndrome have
a. 45 chromosomes. c. 47 chromosomes.
b. 46 chromosomes. d. no X chromosomes.



25. If nondisjunction occurs,
a. there will be too many gametes produced.
b. no gametes will be produced.
c. a gamete will receive too many or too few homologues of a chromosome.
d. mitosis cannot take place.



26. A human female inherits
a. one copy of every gene located on each of the X chromosomes.
b. twice as many sex chromosomes as a human male inherits.
c. one copy of every gene located on the Y chromosome.
d. all of the same genes that a human male inherits.



27. A pedigree CANNOT be used to
a. determine whether a trait is inherited.
b. show how a trait is passed from one generation to the next.
c. determine whether an allele is dominant or recessive.
d. none of the above


28. If a man with blood type A and a woman with blood type B produce an offspring, what might be the offspring’s blood type?
a. AB or O
b. A, B, or O
c. A, B, AB, or O
d. AB only



29. Sickle cell disease is caused by a
a. change in one DNA base.
b. change in the size of a chromosome.
c. change in two genes.
d. change in the number of chromosomes in a cell.

30. Many sex-linked genes are located on
a. the autosomes.
b. the X chromosome only.
c. the Y chromosome only.
d. both the X chromosome and the Y chromosome.

3.1 Mendel & Genetics.

Human genetics, or more specifically the inheritance of biological characteristics from previous generations, follows the laws established by Gregor Mendel in the 19th century. Most people know a little about Mendel's work, that his research studies involved the breeding of pea plants, and that he was a monk. But the real science behind Mendel's work was that he established that the inheritance of certain characteristics can be predicted mathematically when sexual reproduction is involved. These patterns apply equally to peas and people.

Mendel's genetics or Mendelian genetics as it is commonly called, involves a set of principles.

1. Inherited characteristics are determined by units of biological information (genes).Each gene may have different forms called alleles.

2. Each individual has a pair of alleles for each gene (one from mum, one from dad).

3. When eggs and sperm are made using meiotic division, each pair of alleles separates so that each egg or sperm has only one allele. When reproduction occurs (fertilization of egg by sperm) the pair of alleles is restored.

4. It is different genes which control the different biological characteristics of an organism and the alleles of these genes will re assort into new combinations independently of each other.

So, when a new human is formed from the fertilization of an egg, the characteristics it inherits are determined by which alleles have been passed from its parents. We must also understand that any biological characteristic (called the phenotype) is dependent on the combination of alleles passed from each parent (the genotype).

Children may inherit identical alleles from their parent and these children are then said to be homozygous for that allele. Or, they may inherit different alleles from their parents in which case they are said to be heterozygous. Knowing whether a person is homozygous or heterozygous for a certain allele will give big clues to the way in which the biological characteristic will manifest itself.

To give a clinical example, a person will inherit cystic fibrosis from its parents only if they are homozygous for a mutated allele of the CFTR gene. However they will not inherit cystic fibrosis if they have a heterozygous genotype.

But what dictates which allele is actually chosen by the body to produce the CFTR protein? Well that is decided by another property of alleles, namely their dominance or recessivity. A dominant allele is one which is always chosen when in a pair with other alleles, whilst a recessive allele is one which is only chosen if the other allele in the pair is identical (i.e. the person is homozygous for the recessive allele). In the cystic fibrosis example above, the mutated and abnormal form of the CFTR gene is a recessive allele.

The consequence of understanding homozygous and heterozygous alleles and the concept of dominance, is that we can make very good predictions about the biological characteristics of a person according to the alleles they have inherited. This is the basis for attributing risk of inheriting certain genetic diseases as well as the rationale of genetic screening to determine which alleles a certain individual possesses.

The fourth principle highlighted above, basically means that we will inherit a range of characteristics from our parents, but not necessarily in the proportions dictated by sexual reproduction (50% from mum, 50% from dad). It actually means that we could inherit a large proportion from one side of the family, because the alleles of genes assort themselves independently.This is the explanation for the differences in characteristics that may occur even in brothers and sisters from the same parents.


Mendels laws

Basic Principles of Genetics

3.2 Chromosomal Changes.

The pairs of human chromosomes from number 1 to number 23 each carry a proportion of the total number of genes required to build and maintain a human body. All this information, the entire repertoire of genes is referred to as the genome. It is estimated that the human genome contains in the region of 25,000 individual genes.

Therefore any changes to either the number or structure of a human chromosome is likely to involve many hundreds of genes. A little known fact is that approximately 80% of all human conceptions fail to go to full term. The majority of losses are thought to be due to conceptions that result in the collection of faults in chromosome structure or number which are incompatible with successful development or life maintenance.

3.2.1 Changes to Chromosomal Structure.

The first type of structural change is seen when a translocation event occurs. A translocation is where parts of chromosomes are exchanged between two or more chromosomes during cell division. Two major types of translocation are recognized, namely reciprocal and Robertsonian translocations. Both types of abnormality have the potential to produce humans with essentially normal characteristics, but the likelihood is that the offspring of affected individuals may have a chromosomal imbalance.

Reciprocal translocation means that there is a reciprocal exchange of material between chromosomes, whilst Robertsonian translocations are known as centric fusions as they involve the fusion of chromosomes near the centromere. Robertsonian translocations, normally affecting 14,15,21 and 22 actually involve a loss of genetic material, but are termed "balanced" because the genes lost have little bearing on the new individual. All the affected chromosomes have extremely short arms and the material lost is largely confined to genes for ribosomal RNA.

Chromosomes may also suffer deletions during division and development. Deletions are a loss of material from the generation of two breaks in the chromosome followed by a fault in the repair mechanisms employed by the cell. Obviously the effect of the deletion is dependent on the amount of genetic information lost and the significance (dominance or recessivity) of the missing genes.

When a chromosome breaks in two places, there is always a chance of the two broken ends fusing together, this is known as ring chromosome formation. A chromosome may also break and the resulting fragment may then fuse to a similar region on another chromosome of the same structure. This fusion results in what is called a duplication event.

3.2.2 Changes to Chromosomal Number (aneuploidy).

The term aneuploidy refers to any change to the normal number of 46 chromosomes. Another term is also used when their are multiples of the normal number, this term is polyploidy. Aneuploidies can involve both autosomes and sex chromosomes.In cases of where an individual has inherited only one of a chromosome pair, this is known as monosomy, whilst the inheritance of three copies of a chromosome is termed a trisomy. It has been estimated that at least a quarter of conceptions may involve a chromosomal disorder, but loss occurring mainly in the first trimester of pregnancy reduces the proportion at birth to below 1%.The loss or gain of a chromosome means that there can be a significant accompanying loss or gain of genetic information. However there are a number of conditions that result in live births as well as conditions for which their may be a normal life span.

The most well known aneuploidy is probably a trisomy of chromosome 21, which accounts for 96% of those individuals with the condition Down syndrome. The karyotype of these individuals is written as 47,XX,+21 or 47,XY,+21 (the 47 indicates an extra chromosome, XX or XY indicates male or female and +21 indicates the number of the extra chromosome).

Other trisomies include Edward syndrome, trisomy 18 and Patau syndrome, Trisomy 13.

Aneuploidy with regard to the sex chromosomes involves both X and Y forms.

Individuals with Klinefelter syndrome are males who have a karyotype which indicates the inheritance of extra X chromosomes (47, XXY; 48 XXXY; 49, XXXY etc). Whilst those with Turner syndrome are females with a missing X chromosome (45, X).

Males with an extra Y chromosome have XYY syndrome (47,XYY) whilst females with an extra X chromosome have Triple X syndrome.

Aneuploidies are all thought to be the result of the failure of chromosome conjugation in the first division of meiosis or non-dysjuntion, premature disjunction or delayed separation in the second meiotic division. Non dysjunction of chromosomes can also occur in mitotic division and results in individuals with two different cell lines from the same fertilised egg. These persons are known as mosaic individuals.




3.3 Autosomal Dominant Inheritance.

Autosomal dominant inheritance is the term used to describe the inheritance of a characteristic imparted by an allele which dominates over the normally occurring allele. The term autosomal refers to genes carried on the non sex chromosomes (everything except X and Y).

A number of genetic diseases are caused by the inheritance of a dominant allele from a parent. Huntington disease, neurofibromatosis, FAP (familial adenomatous polyposis) and familial hypercholesterolaemia all follow a pattern of autosomal dominant inheritance. These diseases may be apparent at birth, but many only manifest themselves in later life. The pathology is determined by the dominating effect of a faulty gene over the normal genetic background.For some conditions, the inheritance of the dominant allele may predispose the person to a particular future disease.

A parent affected or predisposed to a condition arising from the inheritance of a dominant faulty allele, will pass on either the faulty or normal allele during sexual reproduction, and therefore there are a number of possible outcomes from the resulting pregnancy. These possible outcomes can be seen in figure 3.3, below.

In this figure we see a mother whose chromosome pairs contain the normal allele "d", she will provide the eggs for the next generation and these will contain the normal allele. However, the father carries a faulty dominant gene "D" and the probability that he will pass this on to the next generation in his sperm is 1 in 2 or 50%. As a result of sexual reproduction between these parents, there are four possible outcomes. Two of the four outcomes will produce babies who inherit two copies of the normal allele "d", whilst the other two possible outcomes are babies who have inherited a copy of the dominant faulty gene "D" from their father. Therefore there is a 2 in 4 or 50% chance that children of these parents will be unaffected by the faulty allele and a 2 in 4 or 50% chance that children of these parents will be affected by the faulty allele. In reality, we are saying that for every pregnancy that arises from these two parents, there is a 50% chance of a baby with the inherited faulty allele.

Figure 3.3 Autosomal Dominant Inheritance : The faulty dominant allele is shown as "D", the normal allele is shown as "d".




Although this example shows a father affected by the disorder, the mother could also be affected whilst the father is normal. Autosomal dominant conditions usually affect both sexes equally.

So what happens if both parents carry the faulty dominant allele. Well, in this case both parents can contribute a faulty allele to the next generation.


Where both parents carry the faulty dominant allele, the chance of passing on any associated genetic condition is 75% in each possible pregnancy. This 75% chance is the same for all autosomal dominant disorders where both parents are heterozygous (carrying different forms of the gene).

Dominant faulty alleles may arise in an individual due to mutation in an egg cell or sperm cell or during the fertilization process. This type of mutation is known as a spontaneous mutation.



3.4 Autosomal Recessive Inheritance.

As you are now probably aware, there are two copies of each of every autosomal gene. People may carry autosomal recessive mutations that are capable of causing disease, but because their effects are masked by the presence of dominating "normal" genes, they cause no symptoms. These people may pass the mutated allele to their children, and are therefore known as "carriers" of the disease.

However if a person inherits two copies of the mutated recessive allele, they will become affected by the deleterious effects of the mutation, usually the consequences of a mutated allele is the loss of a biological function. One of the commonest conditions resulting from autosomal recessive inheritance is cystic fibrosis. In this conditions symptoms arise from the failure to move water across cell membranes in sufficient quantities.

Because symptoms are associated with the inheritance of two copies of the mutated allele, both parents have to be heterozygous carriers of the mutation.

Other autosomal recessive disorders include the nervous system disorder Tay-Sachs disease, Spinal muscular atrophy and Phenylketonuria.




3.5 Sex-Related Inheritance.

Men and women differ in the types of gametes they produce (eggs or sperm) and their physiology. These differences can influence inheritance. However, the majority of disorders that are called "sex linked" are caused by X chromosome linked recessivity in males. In these conditions the incidence is much higher in men than women, the mutant allele is never passed from father to son, the mutated allele is passed to all of a father's daughters (but they never express it) and a heterozygous carrier woman passes the allele to half of her sons, who express it, and half her sons who don't.

The best example of this type of disorder is Haemophilia A, a deficiency in blood clotting factor VIII which causes prolonged bleeding in untreated individuals. A single copy of the recessive allele will not affect any heterozygous individual who inherits it. Heterozygous females are normal. As a man receives his Y chromosome from his father and passes a copy to every son, he also receives an X chromosome from his mother and passes a copy to every daughter.

Dominant X-linked disorders are rare, but include conditions such as Hyperphosphataemia. In these conditions the condition occurs twice as frequently in females, an affected man passes the condition to every daughter, but never to a son. An affected woman passes the condition to every son and half her daughters.





3.6 Congenital Abnormalities.

The process of human development is an impressive biological feat. The transformation of a single cell at conception to a living organism consisting of trillions of cells arranged into tissues, organs and organ systems is almost miraculous. The process is made possible by a highly coordinated series of genetic events that lead to the construction of the human body.The process is nowhere near foolproof however, and it is estimated that over 75% of human conceptions fail to result in live birth. The term congenital means existing at birth and includes all birth defects regardless of how they are caused.

Only approximately 15% of congenital abnormalities have a recognized genetic basis, whilst approximately 10% have recognized environmental triggers such as the exposure to toxic chemicals and infections. An additional 25% of these abnormalities are thought to have a multifactorial basis. Up to 60% of birth defects are of unknown origin.

Birth defects can be classified into six main groups:

1. Syndromes - groups of abnormalities found together.

2. Malformations - resulting from errors in the initial formation of structures.

3. Disruptions - occurring as a result of destructive processes after an organ or tissue has formed.

4. Deformations - caused by mechanical forces out of the normal range.

5. Dysplasias - failure of cells to organize properly into tissues.

6. Sequence effects - result from the effect of an earlier abnormal event.



The genetic disorders described elsewhere on this site, all fit into the category of congenital abnormality. The other types are explained and analysed in other places.



3.7 Multifactorial & Polygenic Disorders.

3.8 Genetics of Common Diseases.

INHERITENCE....

Gregor Mendel-



Gregor Mendel was a monk who lived in Austria, he was born in 1822 and lived until 1884. He was often called the father of genetics. Mendel was born to a peasant family but went on to study at St. Thomas Monastery of Augustnitian Order and proudly in 1847 he became a priest. For a few years Mendel enjoyed this occupation but he realized that was not his life goal. Mendel strived to become a teacher and later attended the University of Vienna to study math and biology. Mendel studied hard but it was not enough his dream of becoming a teacher was shattered. Even though Mendel did not become a teacher he did not give up and he began to study genetics.



Mendel was very curious and decided to investigate the inheritance of traits amoung pea plants, he studied their height, flower and pod position, seed shape, seed color, pod shape, and pod color. This was indeed very interesting to Mendel and because of him we have been able to experiment alot more today. Mendel created an experiment in which he crossed a true-breeding for plants of regular height and a true-breeding for plants of short height. The first generation plants were all of regular height although the second generation had three regular height and one dwarf. Through this experiment Mendel decided that an organism has two factors one from each parent and the second factor could be hidden by the first. These were later called dominant and reccesive traits. Using his discoveries Mendel uncovered three laws. The first law says that the sex cells of a plant can have two different traits both not the same. The second law read that characteristics are inherited independently from another. And the last law states that each inherited trait is determined by a gene from each parent. Gregor Mendel was extremly important and his amazing discovery has been greatly benefited today.

what a life...

People often asked me, “How can you be so carefree?”. I often laughed at this. Because being me, there is no such thing as ignoring things the way it should be. Can you be carefree when people talked about you behind your back? Can you be carefree when nobody wants to talk to you because you made one mistake? To me, I’m not being carefree, I’m simply living life like the way it should be. I’ve always told myself, “life can be hard as it wants to, but you can make it sweet and simple as you like”. Of course, putting it in mere words is easy, but we are just human, so it’s normal for us to be questioning: “how can we achieve a sweet, simple life?”