By Absolute truth
This topic is for miscellaneous darwinism-related information in sha Allah..
Don't you understand how microbes turned to humans ???!!!!
You need to educate yourself on biology...
Philip Ball’s opinion piece in this week’s Nature, the most popular science magazine in the world, is news not because he stated that we don’t fully understand how evolution works at the molecular level, but because he urged his fellow evolutionists to admit it. On this 60th anniversary of the discovery of the DNA double helix, Ball reviews a few of the recent findings that have rebuked the evolution narrative that random mutations created the biological world.
But it’s a Fact Anyway ?!
By Tia Ghose, LiveScience Staff Writer | LiveScience.com
Neanderthals Doomed by Vision-Centered Brains
Neanderthals' keen vision may explain why they couldn't cope with environmental change and died out, despite having the same sized brains as modern humans, new research suggests.
The findings, published today (March 12) in the journal Proceedings of the Royal Society B, suggest that Neanderthals developed massive visual regions in their brains to compensate for Europe's low light levels. That, however, reduced the brain space available for social cognition.
"We have a social brain, whereas Neanderthals appear to have a visual brain," said Clive Gamble, an archaeologist at the University of Southampton, who was not involved in the study.
As a result, the extinct hominids had smaller social and trading networks to rely on when conditions got tough. That may have caused Neanderthals to die off around 35,000 years ago.
Brain size riddle
Just how smart Neanderthals were has been a long-standing debate.
"Either they get regarded as lumbering brutes, or the other side says, 'No, they weren't that stupid. They had enormous brains, so they must have been as smart as we are,'" said study co-author Robin Dunbar, an evolutionary psychologist at the University of Oxford.
To help solve the riddle, Dunbar and his colleagues looked at 13 Neanderthal skull fossils dating from 25,000 to 75,000 years ago and compared them with 32 anatomically modern human skeletons. The researchers noticed that some of the Neanderthal fossils had much larger eye sockets, and thus eyes, than do modern humans. [10 Odd Facts About the Brain]
The team concluded that Neanderthals used their oversized eyes to survive in the lower-light levels in Europe, where the northern latitude means fewer of the sun's rays hit the Earth. (Modern humans also tend to have slightly bigger eyes and visual systems at higher latitudes than those living in lower latitudes, where light levels are higher.) The researchers hypothesized that Neanderthals must, therefore, also have had large brain regions devoted to visual processing.
And in fact, Neanderthal skulls suggest that the extinct hominids had elongated regions in the back of their brains, called the "Neanderthal bun," where the visual cortex lies.
"It looks like a Victorian lady's head," Dunbar told LiveScience.
Anatomically modern humans, meanwhile, evolved in Africa, where the bright light required no extra visual processing, leaving humans free to evolve larger frontal lobes.
By calculating how much brain space was needed for other tasks, the team concluded that Neanderthals had relatively less space for the frontal lobe, a brain region that controls social thinkingand cultural transmission.
Isolated and dying
The findings explain why Neanderthals didn't ornament themselves or make art, Gamble told LiveScience.
These results may also help explain the Neanderthals' extinction, Dunbar said.
Smaller social brain regions meant smaller social networks. In fact, artifacts from Neanderthal sites suggest they had just a 30-mile (48.3 kilometers) trading radius, while human trade networks at the time could span 200 miles (321.9 km), Dunbar said.
With competition from humans, a bitter ice age and tiny trading networks, the Neanderthals probably couldn't access resources from better climates, which they needed in order survive, he said.
By Absolute truth
According to darwinism, human has a microbe-like grandfather, It kept reproducing till we found an imaginary common ancestor for human and chimp.
This tale was confronted by the fact that human has 46 chromosomes while apes have 48 !
Looks more or less similar ?!
Let's have a look at creatures that have the same number of chromosomes-just like human !
- Black rat (Rattus rattus) , but not all of them have 46
- Merriam’s ground squirrel (Spermophilus canus)
- Southern short-tailed shrew (Blarina carolinensis)
- Grevy’s zebra (Equus grevyi)
- Mountain beaver (Aplodontia rufa)
- Muntjacs (Muntiacus reevesi)
- Beach vole (Microtus breweri)
- Nilgai (Boselaphus tragocamelus)
- Kirk’s dik-dik (Rhynchotragus/Madoqua kirkii )
- Grey/common vole (Microtus arvalis)
- Large bentwing bat (miniopterus schreibersi)
- Bolivian Tuco-tuco (Ctenomys boliviensis)
- Crowned Lemur (Lemur mongoz coronatus)
- Red Titi (Callicebus cupreus)
Sable antelope (Kafue, Zambia)
On the other hand these species also have 48 chromosomes, just like chimpanzee.
- European hare/jackrabbit (Lepus europeus)
It's obvious that none is a supposed relative neither for human nor chimpanzee !
In fact, the number of chromosomes doesn't hold much importance. What really counts is the genetic information itself.
By Absolute truth
One of the most popular alleged evidences for evolution on the internet is Endogenous RetroViral sequences (ERVs). Evolutionists think that a type of virus called a 'retrovirus', once inserted genetic information into one of our ape ancestors' genome. So how is this evidence for evolution?
Scientists have noticed that chimps and humans have ERV genetic sequences at very similar points in our DNA. And so the story goes: our common ancestor acquired these ERVs and since humans and chimps are closely related, we should have them in similar spots in our genomes. We do. If we and chimps didn't evolve from a common ancestor (which first acquired the ERVs), how is it possible that we and chimps have ERVs in almost precisely the same locations? The only plausible explanation, evolutionists say, is evolution.
But this is far from the truth. If we can show that ERVs are not the product of retroviruses, this evidence for evolution would fall flat.
ERVS are simply more or less similar to retrovirus genome:
The first problem with this argument is that it’s hard to tell what an ERV is when you meet one. It doesn’t come with a tag attached saying: ” This is an ERV “. It could be that these genes something completely different. That is because if a virus is embedded in it’s complete form, its almost impossible to pass it down to further generations.
ERVS are Functional
If ERVs are found to have function, it would be highly likely that they didn't originate from retroviruses. It would be inconceivable that viral non-functional ERVs somehow became functional. Evidence has surfaced that they do have function.
"We report the existence of 51,197 ERV-derived promoter sequences that initiate transcription within the human genome, including 1,743 cases where transcription is initiated from ERV sequences that are located in gene proximal promoter or 5' untranslated regions (UTRs)."(Conley, A.B., Piriyapongsa, J. and Jordan, I.K., "Retroviral promoters in the human genome," Bioinformatics 24(14):1563, 2008)
The previous quote is very telling. There are many thousands of ERV sequences in our genome and in that of chimps. Does this mean that all are beneficial?
"Our analysis revealed that retroviral sequences in the human genome encode tens-of-thousands of active promoters; transcribed ERV sequences correspond to 1.16% of the human genome sequence ... and PET tags that capture transcripts initiated from ERVs cover 22.4% of the genome."("Ancient Retroviruses Spurred Evolution Of Gene Regulatory Networks In Humans And Other Primates," ScienceDaily, University of California - Santa Cruz, Nov. 15, 2007.)
As we can see, it has been discovered that ERVs aid transcription in one fifth of the human genome!
"We report that human ERVs actively shape the p53 transcriptional network in a species-specific manner ... At least one ERV insertion likely reshaped the transcriptional landscape of its surrounding genomic area and was instrumental in creating a new gene that became part of the human-specific p53 regulatory network ... We discovered a unique distribution pattern of p53 sites within repetitive sequences of the human genome, and several ERV families emerged as being substantially enriched for p53 sites in their LTRs."("Retroviral promoters in the human genome,2008"
By Absolute truth
Introduction BACTERIAL VARIATION
Any change in the genotype of a bacterium or its phenotype is known as variation. Genotypic variation can occur as a result of changes in the genes by way of mutation, loss or acquisition of new genetic elements.
These variations are heritable. Phenotypic variations are seen temporarily when bacteria are grown under certain environmental conditions. These variations are not heritable.
A gene will mutate spontaneously, about once in a hundred million cell divisions. Such bacteria are called mutants. Most of these mutants die, but a when a mutant can adapt itself to the environment more readily; it may emerge as a new variant. Chromosomal mutations may lead to Emergence of drug resistance in bacteria. Examples include methicillin resistance in Staphylococcus aureus, Multi-drug resistance in Mycobacterium tuberculosis.
Mechanisms of horizontal gene transfer (HGT) in bacteria
Some bacteria have ability to uptake naked DNA fragment from the surrounding environment. When such a DNA confers new property to the bacterium, it is termed transformation. Change from R form of Streptococcus pneumoniae to S form as demonstrated by Griffith is due to transformation.
Transfer of genetic material (usually plasmids) from one bacterium to another through the mediation of sex pili. Any property that is coded on a transmissible plasmid can be transferred to a recipient bacterium. Properties such drug resistance mediated by beta-lactamases, bacteriocin production etc can be transferred by conjugation.
Transfer of genetic material through mediation of bacteriophage is known as transduction. Only those strains of Corynebacterium diphtheriae that are infected by a beta phage are toxigenic. Change in O antigen in Salmonella (S. anatum->S. newington-> S.minneapolis) is because of lysogenic phage.
Variations in the flagellar antigens in Salmonella are due to transposons. Similar gene rearrangements may result in antigenic variations, as in Neisseria gonorrhoeae and Borrelia recurrentis.
A variation in the phenotype of a microorganism, where the genetic constitution remains unchanged is a non-heritable variation. Such variations are seen due to a change in environmental conditions and such variations are neither permanent nor heritable. They may revert back to normal state when the conditions are restored.
Some examples are:
Loss of flagella in S.typhi when grown in phenol agar (H-O variation) Pleomorphism (variation in shape) in old cultures Lack of pigment production by S.aureus in anaerobic conditions Formation of spheroplasts and protoplasts V-W variation in Salmonella typhi that is characterized by loss of Vi antigen S-R variation in Salmonella typhi that is characterized by loss of O antigen and change in colony morphology to rough type. Production of flagella in Listeria monocytogenes occurs at temperature less than 20oC Last edited in June 2006 http://www.microrao.com/micronotes/variation.htm