![kopimaya [dot] kom - Secangkir Kehangatan di Dunia Maya - Powered by vBulletin](images/misc/vbulletin4_logo.png){kind=logo}
Ya lu lihatnya misalnya ada kambing yg kakinya lima. Orang yg jari tangannya enam. Pohon pisang bercabang dua. Kan ada. Itu bukannya penambahan trait?Originally Posted by AsLan
Ya lu lihatnya misalnya ada kambing yg kakinya lima. Orang yg jari tangannya enam. Pohon pisang bercabang dua. Kan ada. Itu bukannya penambahan trait?
Kalau yang ditanya adalah orang awam tentunya akan menjawab bahwa penambahan kaki pada kambing adalah sebuah kemajuan genetis atau Evolusi.Ya lu lihatnya misalnya ada kambing yg kakinya lima. Orang yg jari tangannya enam. Pohon pisang bercabang dua. Kan ada. Itu bukannya penambahan trait?
Namun para ahli biologi molekular tidak akan menganggap hal ini sebagai suatu Mutasi positif karena kaki tambahan tersebut bukanlah sebuah sistim baru, bukan trait baru, melainkan hanya sistim lama yg salah diduplikasi.
Dr. Georgia Purdom :
are there such things as beneficial mutations? In short, no, but let me explain. While I have yet to see evidence of a truly beneficial mutation, I have seen evidence of mutations with beneficial outcomes in restricted environments. Mutations are context dependent, meaning their environment determines whether the outcome of the mutation is beneficial.
One well-known example is antibiotic resistance in bacteria.
In an environment where antibiotics are present, mutations in the bacterial DNA that alter the target of the antibiotic allow the bacteria to survive (the bacteria are faced with a “live or die” situation). However, these same mutations come at the cost of altering a protein or system that is important for the normal functioning of the bacteria (such as nutrient acquisition).
If the antibiotics are removed, typically the antibiotic resistant bacteria do not fare as well as the normal (or wild-type) bacteria whose proteins and systems are not affected by mutations (see also Is Bacterial Resistance to Antibiotics an Appropriate Example of Evolutionary Change?). There are numerous other examples as well.
Thus, the benefit of any given mutation is not an independent quality, but rather a dependent quality based on the environment.
Yang harus dicari oleh para penganut Evolusi adalah bukti bahwa sebuah sistim baru bisa terbentuk dalam sebuah organisme, inilah Engine yg dibutuhkan untuk perubahan dari amuba ke manusia.
Keep in mind that beneficial, information-gaining mutations are a necessary mechanism of molecules-to-man evolution, so focusing on any potential for this is essential for evolutionists. What doesn’t seem to be often addressed is the vast amount of data to the contrary.
But even if there were a clearly beneficial mutation, this would by no means “prove” the mechanism for evolution (for one thing, beneficial, information-gaining mutations would have to be a regularly occurring phenomenon and would have to “build” on previous mutations so as not to be “undone” and to keep the evolution going “uphill”)
---------- Post added at 10:03 AM ---------- Previous post was at 09:53 AM ----------
Biodata Dr Georgia Purdom
Spoiler for PhD:
Spoiler for Georgia:
Who is she?
http://www.answersingenesis.org/home...s/g_purdom.asp
Dr. Georgia Purdom is a compelling and dynamic lecturer and well qualified to speak on the relevance of Genesis to the issue of biblical authority. She is the only female Ph.D. scientist engaged in full-time speaking and research for a biblical creationist organization in North America. Dr. Purdom states,“A proper understanding of Genesis is very important because it is foundational to biblical authority and a Christian worldview. It’s about so much more than the creation/evolution controversy. It’s about the truthfulness and authority of God’s Word.”
AsLan, mendingan lu ngasih link langsung dari jurnal ilmiah, kayak gw ngasih link ke lu ttg pembentukan inti sel secara spontan, atau minimal link wiki deh. Jadi gak bias...
-------------------------------------------------------------------------------------------
Kembali ke masalah mutasi. Jadi apa contohnya (ilustrasi aja, gak perlu bukti ilmiah) information-gaining mutation?
Apakah manusia bertanduk? Gadis cantik bersayap? Kuda bertanduk dan bersayap? Atau apa?
Trus...
One well-known example is antibiotic resistance in bacteria.
In an environment where antibiotics are present, mutations in the bacterial DNA that alter the target of the antibiotic allow the bacteria to survive (the bacteria are faced with a “live or die” situation). However, these same mutations come at the cost of altering a protein or system that is important for the normal functioning of the bacteria (such as nutrient acquisition).
If the antibiotics are removed, typically the antibiotic resistant bacteria do not fare as well as the normal (or wild-type) bacteria whose proteins and systems are not affected by mutations .
Lihat yg ditebalkan. Itu maksudnya apa? Yg gw tau, bakteri yg resistan tsb tetap bisa hidup nyaman seperti sedia kala.
http://www.answersingenesis.org/home...s/g_purdom.asp
Dr. Georgia Purdom is a compelling and dynamic lecturer and well qualified to speak on the relevance of Genesis to the issue of biblical authority. She is the only female Ph.D. scientist engaged in full-time speaking and research for a biblical creationist organization in North America. Dr. Purdom states,“A proper understanding of Genesis is very important because it is foundational to biblical authority and a Christian worldview. It’s about so much more than the creation/evolution controversy. It’s about the truthfulness and authority of God’s Word.”
AsLan, mendingan lu ngasih link langsung dari jurnal ilmiah, kayak gw ngasih link ke lu ttg pembentukan inti sel secara spontan, atau minimal link wiki deh. Jadi gak bias...
-------------------------------------------------------------------------------------------
Kembali ke masalah mutasi. Jadi apa contohnya (ilustrasi aja, gak perlu bukti ilmiah) information-gaining mutation?
Apakah manusia bertanduk? Gadis cantik bersayap? Kuda bertanduk dan bersayap? Atau apa?
Trus...
One well-known example is antibiotic resistance in bacteria.
In an environment where antibiotics are present, mutations in the bacterial DNA that alter the target of the antibiotic allow the bacteria to survive (the bacteria are faced with a “live or die” situation). However, these same mutations come at the cost of altering a protein or system that is important for the normal functioning of the bacteria (such as nutrient acquisition).
If the antibiotics are removed, typically the antibiotic resistant bacteria do not fare as well as the normal (or wild-type) bacteria whose proteins and systems are not affected by mutations .
Lihat yg ditebalkan. Itu maksudnya apa? Yg gw tau, bakteri yg resistan tsb tetap bisa hidup nyaman seperti sedia kala.
Bakteri yg resistan terhadap Antibiotik itu sebenarnya sebuah variasi yg sudah ada dalam kelompok bakteri, namun memiliki kecacatan yg membuatnya tidak sensitif terhadap Antibiotik.
Contohnya seperti ikan buta.
Anggaplah manusia tidak suka dengan ikan dan membuat racun yg menyerang mata ikan, ikan2 yg matanya terkena racun pasti akan mati.
Namun ada ikan buta yg sejak menetas tidak memiliki bola mata, ikan2 ini tidak sensitif terhadap racun yg disebar oleh manusia sehingga kelompok ikan ini bisa hidup dan berkembang biak.
Namun dilingkungan yg tidak beracun, kelompok ikan buta ini kurang mampu bersaing dengan kelompok normal.
Pengamatan di laboratorium menemukan kerusakan genetis yg terjadi terus menerus.
Walaupun organisme sudah memiliki berbagai metoda untuk mengeliminir kerusakan gen, namun kerusakan terus terjadi, terutama karena dijaman2 terakhir ini semakin banyak bahan kimia yg mencemari lingkungan.
Kerusakan Genetis tidak bisa membangun mahluk hidup, bayangkan sebuah mobil toyota yg terus menerus dipakai dan mengalami kerusakan, tidak akan berubah menjadi Jet F22.
Untuk membentuk sebuah Jet F22 dibutuhkan suatu perancang cerdas yg bisa membentuk berbagai mesin yg berfungsi baik, hal ini tidak bisa diharapkan terjadi dari mobil Toyota yg mengalami kerusakan.
Teori Perancang Cerdas tidak memaksa orang untuk menjadi Theis.
Karena Science tidak bisa membuktikan apakah dia itu Allah, Yesus, Brahma, Alien atau Manusia Kripton.
Yang bisa dibuktikan oleh Science hanyalah kehidupan ini merupakan hasil rancangan, atau sebaliknya bahwa kehidupan ini tidak bisa muncul tanpa rancangan.
Sorry tulisan lu yg lain gw buang. Gw ambil yg ini aja:
Lha itu namanya lu pake kacamata pesimis (pinjam istilahnya rumus).
Gw udah eksplor apa yg lu maksud dgn istilah mutasi negatif, sampe gw dapetin istilah information-gaining mutation. Kemudian pernyataan Ms. Purdom gw timpalin dgn hasil eksperimen Lederberg yg menunjukkan bahwa bakteri yg resisten tetap bisa hidup dgn nyaman meski tidak ada penisilin lagi. Juga ada eksperimen ecoli oleh Lenski yg menunjukkan adanya information-gaining mutation pada bakteri ecoli. Tapi buntutnya tetap aja lu bilang itu adalah kerusakan. Jadi, kesimpulannya apapun minumannya eh mutasinya, tetep aja lu bilang kerusakan. Itu lagi2 bukan sains coy.. tapi iman pokoknya....
bakteri yg resisten tetap bisa hidup dgn nyaman meski tidak ada penisilin lagi.Sorry tulisan lu yg lain gw buang. Gw ambil yg ini aja:
Lha itu namanya lu pake kacamata pesimis (pinjam istilahnya rumus).
Gw udah eksplor apa yg lu maksud dgn istilah mutasi negatif, sampe gw dapetin istilah information-gaining mutation. Kemudian pernyataan Ms. Purdom gw timpalin dgn hasil eksperimen Lederberg yg menunjukkan bahwa bakteri yg resisten tetap bisa hidup dgn nyaman meski tidak ada penisilin lagi. Juga ada eksperimen ecoli oleh Lenski yg menunjukkan adanya information-gaining mutation pada bakteri ecoli. Tapi buntutnya tetap aja lu bilang itu adalah kerusakan. Jadi, kesimpulannya apapun minumannya eh mutasinya, tetep aja lu bilang kerusakan. Itu lagi2 bukan sains coy.. tapi iman pokoknya....
ya ikan buta juga tetap hidup nyaman, yang bilang gak nyaman siapa ?
cuma intinya ada loncatan logika dari Mutasi menjadi Evolusi.
Apalagi jaman sekarang Biologi Molekular sudah menemukan bahwa mahluk hidup bisa memperbaiki kerusakan genetis dan cenderung membuang gen cacad. Dari Mekanisme ini sudah kelihatan bahwa parubahan genetis sebenarnya bukan sesuatu yg diinginkan oleh sistim.
Maka Mutasi bukan sistim dasar bawaan dari mahluk hidup, mutasi terjadi karena intervensi faktor luar, dari link yg lu kasi sudah ada daftar faktor2 pemicu mutasi, misalnya UV dan pencemaran bahan Kimia.
Dimasa lalu, sebelum Ozon berlubang dan sebelum banyak pabrik2 Kimia, Mutasi adalah peristiwa yg sangat langka.
Peneliti sudah mencoba menghitung perkiraan matematis dari kejadian Mutasi dan hasilnya sangat tidak masuk akal kalau mahluk hidup yg sekarang berasal dari Virus atau Protozoa yg mengalami mutasi berulang2.
Nih kalo mau baca kemungkinan Matematis dari Evolusi berdasarkan Mutasi:
Mathematical challenges.
Problem number one is the mathematical. I won’t dwell on this one, because it’s written up in many books and widely acknowledged by evolutionists themselves as a serious problem for their theory.
Fortunately, mutations are very rare.
They occur on an average of perhaps once in every ten million duplications of a DNA molecule (10'7, a one followed by seven zeroes).
That’s fairly rare. On the other hand, it’s not that rare.
Our bodies contain nearly 100 trillion cells (10'14).
So the odds are quite good that we have a couple of cells with a mutated form of almost any gene.
A test tube can hold millions of bacteria, so, again, the odds are quite good that there will be mutant forms among them.
The mathematical problem for evolution comes when you want a series of related mutations.
The odds of getting two mutations that are related to one another is the product of the separate probabilities: one in 10'7 x 10'7, or 10'14.
That’s a one followed by 14 zeroes, a hundred trillion!
Any two mutations might produce no more than a fly with a wavy edge on a bent wing.
That’s a long way from producing a truly new structure, and certainly a long way from changing a fly into some new kind of organism.
You need more mutations for that. So, what are the odds of getting three mutations in a row? That’s one in a billion trillion (10'21). Suddenly, the ocean isn’t big enough to hold enough bacteria to make it likely for you to find a bacterium with three simultaneous or sequential related mutations.
What about trying for four related mutations? One in 10'28. Suddenly, the earth isn’t big enough to hold enough organisms to make that very likely.
And we’re talking about only four mutations. It would take many more than that to change a fish into a philosopher, or even a fish into a frog. Four mutations don’t even make a start toward any real evolution. But already at this point some evolutionists have given up the classic idea of evolution, because it just plainly doesn’t work.
It was at this level (just four related mutations) that microbiologists gave up on the idea that mutations could explain why some bacteria are resistant to four different antibiotics at the same time.
The odds against the mutation explanation were simply too great, so they began to look for another mechanism—and they found it. First of all, using cultures that are routinely kept for long periods of time, they found out that bacteria were resistant to antibiotics, even before commercial antibiotics were “invented.” Genetic variability was “built right into” the bacteria.
Did the nonresistant varieties get resistant by mutation? No. Resistant forms were already present. Furthermore, certain bacteria have little rings of DNA, called plasmids, that they trade around among themselves, and they passed on their resistance to antibiotics in that way. It wasn’t mutation and asexual reproduction at all, just ordinary recombination and variation within kind.
Bacteria can be made antibiotic resistant by mutation, but biologist Novick9 calls such forms “evolutionary cripples.” The mutation typically damages a growth factor, so that the mutationally crippled bacteria can scarcely survive outside the lab. The antibiotic resistance carried by plasmids results from enzymes produced to break down the antibiotic. Such bacteria do not have their growth crippled by mutation.
Their resistance is by design.
Contrary to popular opinion, drug resistance in bacteria does not demonstrate evolution. It doesn’t even demonstrate the production of favorable mutations.
It does demonstrate natural selection (or a sort of artificial selection, in this case), but only selection among already existing variations within a kind.
It also demonstrates that when the odds that a particular process will produce a given effect get too low, good scientists normally look for a better explanation, such as the plasmid explanation for resistance to multiple antibiotics.
At this point, evolutionists often say that “Time is the hero of the plot.” That’s what I used to say to my students. “Sure, the odds are low, but there’s all that time, nearly 5 billion years!” But 5 billion years is only about 10'17 seconds, and the whole universe contains fewer than 10'80 atoms.
So even by the wildest “guesstimates,” the universe isn’t old enough or big enough to reach odds like the 1 in 103,000,000 that Huxley, an evolutionist, estimated as the odds against the evolution of the horse.
Way back in 1967, a prestigious group of internationally known biologists and mathematicians gathered at the Wistar Institute to consider Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution.
10 All present were evolutionists, and they agreed, as the preface clearly states, that no one would be questioning evolution itself. The only question was, could mutations serve as the basis—with natural selection—as a mechanism for evolutionary change? The answer of the mathematicians: no. Just plain no!
Emotions ran high. After a particularly telling paper by Marcel Schutzenberger of the University of Paris, the chairman of the gathering, C. H. Waddington, said, “Your argument is simply that life must have come about by special creation!” The stenographer records, “Schutzenberger: No! Voices: No!” Anything but creation; it wasn’t even fair (in spite of the evidence!) to bring up the word.
Dr. Waddington later called himself, impressively, a “post-neo-Darwinist,” someone who believes in evolution, but who also believes that mutation-selection cannot explain how evolution can occur. Many research evolutionists (but not many textbook writers or teachers) recognize the need for a new generation of evolutionists to forge the “post-neo-Darwinian synthesis.”
In his chapter “Beyond the Reach of Chance,” Denton11 discusses attempts to simulate evolutionary processes on computers. He concludes with these strong words:
If complex computer programs cannot be changed by random mechanisms, then surely the same must apply to the genetic programs of living organisms. The fact that systems in every way analogous to living organisms cannot undergo evolution by pure trial and error [i.e., by mutation and selection] and that their functional distribution invariably conforms to an improbable discontinuum comes, in my opinion, very close to a formal disproof of the whole Darwinian paradigm of nature.
By what strange capacity do living organisms defy the laws of chance which are apparently obeyed by all analogous complex systems? (Emphasis added).
---------- Post added at 10:36 PM ---------- Previous post was at 10:23 PM ----------
Ini ada lagi penelitian bakteri resistant yg dimuat di daily science
3. ScienceDaily: “Resistance to Antibiotics Can Be Drawback for Bacteria”
Microbial resistance to antibiotics is commonly provided as an example of “evolution in action.” But when it comes to Neisseria meningitidis, scientists haven’t observed such “evolution” in years.
N. meningitidis is already well known to medical researchers, for it can cause meningitis; and as a target for antibiotics, some have worried the bacterium may evolve increased antibiotic resistance.
However, a new study from Sweden’s Örebro University indicates that the rate of resistant bacterium has not increased in more than a decade. That is, while resistant N. meningitidis individuals do exist, they are not spreading—at least, not in Sweden.
Biomedical researcher Sara Thulin Hedberg conducted the study for her doctoral dissertation. She concluded that the reason resistant strains are not spreading is that resistance is not particularly advantageous for the bacteria. Resistant bacteria cannot multiply as rapidly as other strains and do not infect hosts well. They are easily out-competed for resources by other strains in antibiotic-free environments.
That conclusion is notable for creationists, who point out that nearly all common examples of “evolution in action” do not demonstrate the increase in genetic information that true molecules-to-man evolution would require. The fact that the antibiotic-resistant N. meningitidis are less fit than their susceptible siblings suggests that their resistance probably involves a loss of genetic information or else no change in information.
Last edited by AsLan; 03-05-2012 at 11:32 PM.
Jadi ketika dahulunya ikan gua punya mata lengkap, lalu mutasi negatif membuat matanya tidak memiliki kemampuan melihat, maka dia menjadi nyaman. begitu?
sejak awal saya sudah menyarankan untuk membaca buku evolusinya yang bener dan lengkap. jelas situh (sengaja) melupakan mekanisme evolusi lain: variasi, seleksi, adaptasi.
dan mengenai loncatan logika, mengapa di zaman dinosaurus tidak pernah ditemukan fosil mamalia bahkan burung? tanpa evolusi, bisa dijelaskan mengapa terjadi hal ini tanpa loncatan logika?
mutasi tidak sama dengan kanker, jika itu yang situh maksud. lagian, zaman sekarang juga ditemukan varian yang lebih beragam virus dan bakteri darpada masa lampau.
you can also find me here
Posting Permissions
Reply With Quote
