Gorilla, the possible of the origin of human Malaria parasite P. falciparum

 

When the emergence of disease outbreak, first thing that in scientists or epidemiologists mind are the resources or disease reservoirs are from our phylogenetic closely related species, chimpanzees. But recently the scientists found the different story on the origin of human Malaria P.falciparum, which is from gorilla.

A research team led by virologist Beatrice Hahn of the University of Alabama, Birmingham, used the polymerase chain reaction to amplify Plasmodium DNA from a whopping 2739 fecal samples from chimpanzees,gorillas, and bonobos.

Using single-template amplification strategies and a much larger collection of ape specimens than previously analysed, the scientists show here that wild-living chimpanzees and western gorillas are naturally infected with at least nine plasmodium species. Among more than 1,100 SGA derived mitochondrial, apicoplast and nuclear gene sequences from 80 chimpanzee and 55 gorilla samples, they found a total of nine sequences that were related to P. malariae, P. ovale or P. vivax. All others grouped within one of six chimpanzee or gorilla-specific lineages representing distinct Plasmodium species,three of which had not previously been described. Significantly, all currently available human P. falciparum sequences constitute a single lineage nested within the G1 clade of gorilla parasites. This indicates that human P. falciparum is of gorilla origin, and not of chimpanzee , bonobo or ancient human origin, and that all known human strainsmay have resulted froma single cross-species transmission event.

From the finding, what is still unclear is when gorilla P. falciparum entered the human population and whether present-day ape populations represent a source for recurring human infection.(when date of the jump from gorillas to humans). Plasmodium does not mutate much, she explained, making it difficult to calibrate a so-called molecular clock that enables evolutionary biologists to back-calculate the timing of a pathogen moving from one species to another.

According to Ajit Varki, an evolutionary biologist at UC San Diego,  he believes a human gene mutation, CMAH, which arose about 2 million years ago, may provide a clue to how and when the jump occurred. The mutation changes sialic acid receptors on red blood cells, rendering them much less susceptible to P. reichenowi, and Varki suspects that the gorilla P. falciparum similarly would have great difficulty infecting human cells.

This is also support by Michael Worobey, an evolutionary biologist who has also focused on the origin of the AIDS epidemic, is similarly intrigued that gorilla P. falciparum has not repeatedly infected humans. The finding can help clarify the evolutionary history of P. falciparum.

(for more information please read the article on Natures magazines 23rd september 2010, "Origin of the human malaria parasite Plasmodium falciparum in gorillas")

Almost Indistinguishable, different in function.

If you see 2 amino acid sequence that just a 1-2% slightly different on the sequence, can we just ignore their differences and simply said the protein will be same with the same 3-D confirmation. Don’t simply make the easy conclusion like that because the slightly different can describes a lot.

One such of puzzle is related to the mammalian cytoskeletal protein β- and γ-actin, whose amino acid sequences are 98% identical.  The slightly difference of both protein make they differ in protein modification which β-actin is modified by addition of arginine (arginylation) and γ-actin is not modified, resulting the distinct role for each in the cell.

Scientists try to understand this phenomenon. This is unexpected example of the protein whose the properties are determined at the nucleotide rather than amino acid level, forcing a reassessment of what defines a synonymous change in the gene sequence.

Arginylation of certain protein occur after translation of their termini. Although discover in 40 year ago, the effect of the argynilation is fully understood than other posttranslational modifications. Proteins are arginylated during normal cell growth and in response to stress, and arginylation has been associated with protein degradation in the proteasome. One prominent group of substrates is actin group but not all actin groups are argynilated in posttranslation modification.

Selective modification of the actins is important for normal cell morphology and migration because the absence of arginylation  substantially decrease intracellular actin cellular level and changes its partial segregration.

In this case, the arginylation of β-actin on the posttranslation makes β-actin preferentially localizes at the protruding leading edge of a migrating cell, where rapid actin polymerization pushes the cell’s front forward. There, β-actin is present as a loose and branched arrangement of relatively short actin filaments. By contrast, γ-actin is found in the cell body in dense nonbranched networks and long contractile stress fibers that impart morphological stability and support cell adhesion.

Because of their slightly different of amino acid sequence they affect the rate of translation, and affect their polypeptide modification and also their stability.

What exactly the differences of their amino acid sequences that affect the translation rates.  As mentioned above to explain this is not in amino acids level but in nucleotide levels. The γ-actin contain high frequency of codon that slower the translation but the same region of codon, the alternate codon that coding same amino acid in β-actin is make the translation faster.

Fast translation allows only arginyation, thereby stabilizing the protein. In contrast slow translation allows both arginylation and ubiquitination occur that leading to fast degradation. In conclusions, the synonymous  mutation that encode same amino acid is again not exactly same in the protein comfirmation and modification.

Ada hikmah disebalik teguran PERKASA pasal isu masuk masjid Teo Nie

Politik Malaysia, isu-isu yang akan menjadi tumpuan adalah isu-isu agama dan isu perkauman. Kebelakangan ini Pribumi Perkasa Negara (PERKASA) ada menimbulkan isu tentang kebiadaban ahli parlimen Serdang, Teo Nie yang memasuki masjid tanpa menutup aurat dan ini seakan menghina Islam walaupun niat Teo Nie baik, untuk menyampaikan sumbangan kepada masjid.

Apabila isu ini dihebah-hebahkan. Jentera politik pembangkang membalasnya dengan mempersoalkan tentang kebiadaban beberapa wanita pemimpin negara yang tidak menutup aurat didalam masjid. Dengan pendedahan itu, pembangkang menggunakan modal agar pihak kerajaan tidak menggunakan isu ini untuk membedil pembangkang. Lihat photo dibawah:

Kalau dibandingkan dengan Teo Nie, ini lebih teruk. Kerana mereka dalam photo ini merupakan orang Islam, tahu buka aurat haram. Saya tak tahu la orang didalam photo ini pakai tudung ikut mazhab apa, tapi yang jelasnya sebagai penduduk di alam Melayu Nusantara, kita pengikut Mazhab Syafie, aurat perempuan harus ditutup seluruh badan kecuali muka dan tapak tangan.

Kita pergi kepada tajuk tentang hikmah disebalik teguran PERKASA. Saya ada terbaca artikel dalam selangor kini tentang cadangan Hasan Ali untuk membuat peraturan yang lebih terperinci tentang masuk masjid.http://www.selangorkini.com.my/my/berita/16660

Kita lihat dari sudut positif, teguran PERKASA membuat semua pihak membuka mata tentang peraturan dan adab untuk masuk masjid yang selama ini tidak diendahkan. Dengan adanya teguran, barulah pemimpin-pemimpin politik yang selama ini asyik bertekak dengan isu-isu politik remeh mengambil inisiatif untuk meningkatkan pengurusan sistem masjid khususnya negeri Selangor.

Akan tetapi, teguran PERKASA bagi saya agak kasar dan terburu-buru sehinggakan boleh menimbulkan salah faham tentang Islam. Orang yang bukan Islam akan melihat Islam ini tidak terbuka kerana tidak membenarkan orang bukan Islam masuk masjid jika dibandingkan dengan gereja.

Saya ingin menegaskan disini, tidak salah orang bukan Islam masuk masjid asalkan mengikut peraturan yang digaris pandu oleh Islam. Isu Teo Nie saya rasa bukan salah dia, ini disebabkan sistem pengurusan  institusi masjid. Sepatutnya mereka lebih peka tentang ini contohnya memberikan Teo Nie jubah untuk menutup aurat seperti di masjid Putrajaya.

Saya harapkan kerajaan Negeri Selangor dan negeri-negeri lain dapat menaik taraf sistem pengurusan masjid agar orang bukan Islam boleh menyertai aktiviti-aktiviti masjid agar pemahaman mereka pada Islam lebih mendalam.

"ISLAM ITU SEJAHTERA"

The power of Mother’s Love

Love is something abstract.  We can’t measure love. Love is something did not have any unit. Some people relate love with Einstein’s relativity theory. But first what are relativity theory is? According to the theory, energy and matter are relative and light is constant.

Giving an example, the 2 cars, Car A moving in 60 km/h and Car B moving 80 km/h. Doesn’t care about the direction of the both cars, 2 of them are relatively moving in 20 km/h difference.  One spotlight from a building is focusing to both cars. The light moving to both cars is constant. Thus, same with love, love is constant. We love every one that we love constantly. No more or no less. That is how they relate the love with the physics.

It’s enough to elaborate love in scientific way.  Let’s discuss about the topic, the power of mother’s love. Some people believe, when some teenager’s suicide cases because of stress, failure, and many more reasons because of they did not have enough love from parent or the parental ignorance. But how this believe support by scientific evidence. I would like to say in the genetics’ point of view.

In 2004, Szyf and Meaney published a paper in Nature Neuroscience that helped launch the behavioral epigenetics revolution. It remains one of the most cited papers that journal has ever published. The paper built on more than a decade of research in Meaney’s  lab on rodent mothering styles.

Meaney had found that the type of mothering a rat receives as a pup calibrates how its brain responds to stress throughout its life. Rats raised by less-nurturing mothers are more sensitive to stress when they grow up. When confined to a Plexiglas tube that restricts their movement, for example, they exhibit a greater surge in corticosterone, a hormone pumped out by the adrenal glands in times of stress. The likely cause is reduced numbers of a receptor for steroid hormones in the brain. This so- called glucocorticoid receptor is part of a negative feedback loop that dials down the volume on communication between the brain and adrenal glands, thereby reducing reactivity to stress.

The Nature Neuroscience paper linked this reduction in glucocorticoid receptors to DNA methylation. Rats raised by less nurturing moms tended to have more methyl groups attached to the promoter region, the “on” switch, of the glucocorticoid receptor gene. These methyl groups block access by the transcription factors that turn the gene on. As a result, fewer receptors are produced. Subsequent experiments showed that enzymes that reverse DNA methylation of the glucocorticoid receptor gene also reverse the effects of unenthusiastic mothering on the offspring’s hormonal and behavioral responses to stress.

Several of Meaney’s students have carried on with this work and extended it in new directions. Frances Champagne, a co-author of the 2004 paper, went on to show that female rats raised by nurturing mothers are more nurturing mothers themselves. She also found that pups raised by less-nurturing moms exhibit greater methylation—and reduced expression—of the gene for a particular estrogen receptor in the hypothalamus, a brain region involved with reproductive behavior. This receptor amplifies signaling by oxytocin, a hormone that promotes mother-infant bonding.

Summarize from their finding, rat raised by less nurturing mother (not enough love) likely to sensitive to stress because of reduction the glucocorticoid gene activity that reducing reactivity of stress— more DNA methylation that repress the transcription of the gene.

The scientific evidence support that the important of mother’s love. But don’t blame to their mother if have suicide cases. A lot of factors that causing stress. The important point is the finding gives us a guidance to care more about our children and never ignore them. Happy families can build a happy society that lead to the peace.

The renaissance of DNA Drugs

“Rise and rise again, until lambs become lions”. The meaning of this phrase is never give up until we achieve our goals.

Why I write this post because I would like to show my appreciation to the scientists who are optimist in developing DNA drugs after the false start. DNA Drugs is the vaccine contains plasmid that carried DNA sequence of the pathogen, so that the immune system can produce antibody as preparation to fight the infection of the disease.

Why I mean the “false start” is because the DNA Drugs has the head-to-head  competition with another potential vaccine that using adenovirus as carrier of DNA of pathogen seems not very effective with the latter vaccine. The competition is their compare the immune response of two vaccines. The DNA Drugs contains plasmids, each carrying a gene for one of five HIV proteins. Its goal was to get the recipient’s own cells to make the viral proteins in the hope they would provoke protective reactions by immune cells. The second vaccine used another virus called an adenovirus as a carrier for a single HIV gene encoding a viral protein.

The DNA recipients displayed only weak immune responses to the five HIV proteins or no response at all, whereas recipients of the adenovirus-based vaccine had robust reactions. To academic and pharmaceutical company researchers, adenoviruses clearly looked like the stronger candidates to take forward in developing HIV vaccines.

What I say they are optimistic, after the disappointing result of DNA drugs they did not just give up, they find what are the mistakes. The main reasons for those failures seemed to be that vaccine plasmids were not getting into enough cells and, where they did penetrate, the cells were not producing enough of the encoded proteins. As a result, the immune system was not being sufficiently stimulated.

The vaccines using adenovirus seems have a bigger problem. In 2007 pharmaceutical company Merck initiated a large trial of an HIV vaccine that used an adenovirus called AdHu5 to deliver HIV viral genes. In light of the potent immune responses seen in previous experiments with adenoviruses, great hope and excitement surrounded the beginning of this test, known as the STEP trial. In all, about 3,000 HIV-negative individuals received the vaccine or a placebo shot.

As the trial progressed, though, a disturbing difference between the two groups began to emerge: people who got the vaccine were no better protected than those who received the placebo, and eventually they appeared to be more vulnerable to being infected by HIV. As a result they found that 49 out of 914 men in the vaccine group became HIV-positive, whereas 33 out of 922 men in the placebo group did. With this realization, in the summer of 2009 the STEP trial was halted.

The STEP trial gives the scientists to look back on the DNA Drugs. To optimize the DNA Drugs effect, the scientist suggest the several steps as visualized on the figured below:

As conclusions, if we fail now is doesn’t means we fails forever. Keep trying and never give up.

Can we create clone of an extinct organism from a stretch of DNA?

If you hear from sci-fi (science fiction) story about when the villains get the superhero DNA sources like hair, blood and skins, so the villains clone it and make the world chaos? It seems like the very easy to clone organism, just get their DNA stretch. But in reality, is not just an easy step.

Another example,sci-fi  writers have been resurrecting Neandertals in novels for decades, imagining what it would be like to see and communicate with another species of human. So once the idea of sequencing the Neandertal genome became more than a glimmer in a paleogeneticist’s eye, some have asked, “Could we, should we, would we, bring this extinct human species back to life?” After all, biologists are trying to bring back the woolly mammoth by cloning. But for both technical and ethical reasons, experts say, bringing back a Neandertal is a pipe dream.

Could we do it? Robert Lanza laughed at the thought. Chief scientific officer for Advanced Cell Technology in Worcester, Massachusetts, he and his colleagues have cloned species from cows to goats to mice and extended their efforts to include endangered species and human embryos. But cloning Neandertals is fantasy, says Lanza. “You can’t clone from stone, and you can’t clone from DNA that has been destroyed from weather and the elements,” he points out.

From the statement above, to clone an organism is not simply get their DNA, a lot of factor must be considered.  We are specific in cloning Neandertals from their stretch of DNA.  Like Lanza says, we can’t cloned from from DNA that destroy by weather and element because of the DNA stretch that we get has a lot of missing gap in their genome.

Even we have their complete genome, it wouldn’t be enough. DNA itself doesn’t tell the whole story. Chemical modifications to the genome, the way chromosomes arrange in the nucleus, and maternal components in the egg all play a role in translating a genetic blueprint into a viable individual. “It’s not just the DNA; there’sa lot else going on,” says Lanza. None of that information is even available for Neandertals.

Then, too, cloning doesn’t typically start with a genome; it starts with two cells. One cell provides a nucleus (with DNA inside), and one is an egg cell, most often of the same species, whose DNA has been removed. The nucleus is then transferred to the egg, sometimes by fusing the two cells. “If you have just got DNA, you are asking an enormous amount of the oocyte that you are going to put the DNA into,” explains Ian Wilmut, who cloned Dolly the sheep and now works at the University of Edinburgh in the United Kingdom. “It has to reform the nucleus and reprogram [the DNA].”

That leads to the next problem: What species’ egg would play host to this DNA? The obvious candidate would be a modern human egg, but they are notoriously fickle and don’t take well to nuclear transfer, even of modern human DNA. “There’s something different about primates that we haven’t identified,” says Wilmut. “[Cloning] works very poorly.” And incompatibilities between Neandertal DNA and the human egg might further diminish the chances of a viable embryo.

Molecular geneticist George Church of Harvard University has proposed another approach: modify the DNA in a human cell line to resemble the Neandertal. “This is a daunting task,but with future technological developments and enough time and money, it may be possible,”says Adrian Briggs, who worked on the Neandertal genome sequence and is about to join Church’s lab. In theory, one could convert a human or chimp genome to a Neandertal genome—base by base—while it is still nicely nestled in a stem cell, then clone it. But there’s on the order of a million differences between the Neandertal and human genomes, and the more changes needed, the greater the risk of

introducing errors.

If, somehow, a viable embryo were produced, this developing chimera would need a surrogate mother. What species would that mother belong to? Again, the obvious choiceis a human, but no one knows whether a modern woman’s biochemistry would be compatible with that of a Neandertal fetus. And is it ethical for a human surrogate mother to birth a Neandertal baby? It’ll bring ethical issues. Once cloning works well in a variety of animals and stem cell–derived organs become commonplace, “I think the resistance to it will disappear,” he says.

I would like to share may be some other approach based on the research of J. Craig Venter, who for 15 years, J. Craig Venter has chased a dream: to build a genome from scratch and use it to make synthetic life. Now, he and his team at the J. Craig Venter Institute (JCVI) in Rockville, Maryland, and San Diego, California, say they have realized that dream.

They describe the stepwise creation of a bacterial chromosome and the successful transfer of it into a bacterium, where it replaced the native DNA. Powered by the synthetic genome, that microbial cell began replicating and making a new set of proteins. (You can read further at www.sciencemag.

org/cgi/content/abstract/science.1190719)

This is “a defining moment in the history of biology and biotechnology,” says Mark Bedau, a philosopher at Reed College in Portland, Oregon, and editor of the scientific journal Artificial Life. “It represents an important technical milestone in the new field of synthetic genomics,” says yeast biologist Jef Boeke of Johns Hopkins University School of Medicine in Baltimore, Maryland.

May be the finding can help in cloning the Neandertals but this is bring the ethical issues. “We do not—and

should not—create human beings just to satisfy our scientific curiosity,” says Pääbo, pointing out that Neandertals are a species of human.

Recombination hotspot?

Did you know what recombination hotspot is? In the meiosis the crossing over and homologous recombination produce the recombination chromosome. But not all segments in chromosome are crossing over equally in the entire genome. Is not the matter of position from centromere, but some place in chromosome are more frequent to crossing over than other segment. So the distribution of crossing over entire chromosome in the genome not equal.

So let us go to definition. Recombination hotspots are small regions in the genome of sexually reproducing organisms that exhibit highly elevated rates of meiotic recombination. What the significance of recombination hotspot?

The cause of hotspots is currently unknown, however all hotspots so far characterized share similar morphology and are approximately 1.5 to 2.0 kb in width, which suggests a common causal process. Furthermore, recent studies have used patterns in linkage disequilibrium to identify over 25,000 hotspots in the human genome, suggesting that hotspots are a ubiquitous feature of the genome.

Scientist try to compare the recombination hotspot in human and our closely relative chimpanzees, Despite 99% DNA similarity between humans and our nearest relative, chimpanzees, the locations of DNA swapping between chromosomes, known as recombination hotspots, are almost entirely different. Perhaps this is explanation about how human and chimpanzees are different eventhough their different in DNA just 1%.

Some study suggest a minimum number of required recombinations for proper meiosis; if so,what genes or pathways monitor this process? If this global monitoring system fails, aneuploidy may result? The questions can be answer by ongoing research.

Semiconservative model on new and old synthesize histone

The inheritance and maintenance new and old synthesize of DNA b can be explain by semiconservative model.  But how is the inheritance of epigenetic traits—modifications of chromatin proteins (histones) and DNA that do not alterthe sequence—affected by dynamic changes in chromatin organization during eukaryotic cell division?

Recently study (Xu et al.) explore how parental (old) and newly synthesized histones associate after replication. The basic unit of chromatin, the nucleosome, has a core particle of eight histones—two pairs of histone H3-H4 as a tetramer flanked by two dimers of histone H2A-H2B. Histones can be present in distinct forms or variants, and they may harbor specific posttranslational modifications that can define a given epigenome ( 1, 3). How do these particular markings sustain passage through replication? An attractive hypothesis has been a semiconservative mechanism in which parental histones are combined with newly synthesized histones within the same core nucleosome. The presence of parental information as a template to reproduce the same marks on new histones provides a convenient means to ensure accurate reproduction of the initial marking at the same place. But can parental and new histones mix?

Histones H2A-H2B readily exchange as dimers, but H3-H4 tetramers are thought not to split. However, newly synthesized H3 and H4 can exist as dimers when associated with histone chaperones. By their study that have 3 possibility of model of the Histone inheritance. First with H3-H4 only new tetramer,  second with mixed H3-H4 tetramer and third with only old tetramer.

Future work will investigate how the choice between histone splitting and nonsplitting is made within a cell and

whether this is regulated during cellular life or during development.

Naked for our brain???? (what make us human 1.8)

Did you notice that among mammal we are the fur-less. What are significantly this characteristic in human evolution. Recently studies, The evolution of hairlessness helped to set the stage for the emergence of large brains and symbolic thought.

Among primates, humans are unique in having nearly naked skin. Every other member of our extended family has a dense covering of fur—from the short, black pelage of the howler monkey to the flowing copper coat of the orangutan—as do most other mammals. Yes, we humans have hair on our heads and elsewhere, but compared with our relatives, even the hairiest person is basically bare.

Before explain further, lets discuss what important of hairy body to mammal and how human adaption differ from another animal.Hair provides insulation and protection against abrasion, moisture, damaging rays of sunlight, and potentially harmful parasites and microbes. It also works as camouflage to confuse predators, and its distinctive patterns allow members of the same species to recognize one another. Furthermore, mammals can use their fur in social displays to indicate aggression or agitation: when a dog “raises its hackles” by involuntarily elevating the hairs on its neck and back, it is sending a clear signal to challengers to stay away.


Another mammal that hairless because of  evolutionary adaptation. Such as the naked mole rat, hairlessness evolved as a response to living in large underground colonies, where the benefits of hair are superfluous because the animals cannot see one another in the dark and because their social structure is such that they simply huddle together for warmth. In marine mammals that never venture ashore, such as whales, naked skin facilitates long-distance swimming and diving by reducing drag on the skin’s surface.


Human hairlessness is not an evolutionary adaptation to living underground or in the water— the popular embrace of the so-called aquatic ape hypothesis notwithstanding.


Keeping cool is a big problem for many mammals, not just the giant ones, especially when they live in hot places and generate abundant heat from prolonged walking or running. These animals must carefully regulate their core body temperature because their tissues and organs, specifically the brain, can become damaged by overheating.


Mammals employ a variety of tactics to avoid burning up: dogs pant, many cat species are most active during the cooler evening hours, and many antelopes can off-load heat from the blood in their arteries to blood in small veins that has been cooled by breathing through the nose. But for primates, including humans, sweating is the primary strategy. Sweating cools the body through the production of liquid on the skin’s surface that then evaporates, drawing heat energy away from the skin in the process. This whole body cooling mechanism operates according to the same principle as an evaporative cooler (also known as a swamp cooler), and it is highly effective in preventing the dangerous overheating  of the brain, as well as of other body parts.


Not all sweat is the same, however. Mammalian skin contains three types of glands—sebaceous, apocrine and eccrine—that together produce sweat. In most species, sebaceous and apocrine glands are the dominant sweat glands and are located near the base of hair follicles. Their secretions combine to coat hairs with an oily, sometimes foamy, mixture (think of the lather a racehorse generates when it runs). This type of sweat helps to cool the animal. But its ability to dissipate heat is limited. G. Edgar Folk, Jr., of the University of Iowa and his colleagues showed nearly two decades ago that the effectiveness of cooling diminishes as an animal’s coat becomes wet and matted with this thick, oily sweat. The loss of efficiency arises because evaporation occurs at the surface of the fur, not at the surface of the skin itself, thus impeding the transfer of heat. Under conditions of duress, heat transfer is inefficient, requiring that the animal drink large amounts of water, which may not be readily available. Fur-covered mammals forced to exercise energetically or for prolonged periods in the heat of day will collapse from heat exhaustion.


The human not sweat like other primates. Humans, in addition to lacking fur, possess an extraordinary number of eccrine glands—between two million and five million—that can produce up to 12 liters of thin, watery sweat a day. Eccrine glands do not cluster near hair follicles; instead they reside relatively close to the surface of the skin and discharge sweat through tiny pores. This combination of naked skin and watery sweat that sits directly atop it rather than collecting in the fur allows humans to eliminate excess heat very efficiently.


What are significant of the different adaption of human for heat regulation in the body The loss of most of our body hair and the gain of the ability to dissipate excess body heat through eccrine sweating helped to make possible the dramatic enlargement of our most temperature-sensitive organ, the brain. Whereas the australopithecines had a brain that was, on average, 400 cubic centimeters— roughly the size of a chimp’s brain—H.ergaster had a brain twice that large. And within a million years the human brain swelled another 400 cubic centimeters, reaching its modern size. No doubt other factors influenced the expansion of our gray matter—the adoption of a sufficiently caloric diet to fuel this energetically demanding tissue, for example. But shedding our body hair was surely a critical step in becoming brainy.

Again the naked adaptation of human just for increase brain ability, perhaps the explanation about the evolution of minds. Perhaps some evidence.

Ancient Siberian finger leads to new possible human lineage

The scientist has found that the DNA from ancient Siberian finger did not match any of modern human DNA or a Neadratal.  To be more specific this is the mitochondrial DNA (mtDNA). When ancient-DNA expert Svante Pääbo gave his colleague Johannes Krause a sample of a 40,000-year-old human finger bone from a Siberian cave, he had only one question: Was its mitochondrial DNA (mtDNA) that of

a Neandertal or a modern human?

It was neither. Evolutionary geneticists Pääbo and Krause, of the Max Planck Institutefor Evolutionary Anthropology in Leipzig, Germany, have apparently identified a new lineage of ancient human, the first time that this has been done using ancient DNA and not fossil bones.

“I couldn’t believe it,” Pääbo says. “I thought Johannes was pulling my leg.” The

complete sequence of mtDNA from the finger bone, reported online this week in Nature, suggests that Central Asia was occupied at that time not only by Neandertals and Homo sapiens but also by a third, previously

unknown hominin lineage. “This is the most exciting discovery to come from the ancient DNA field so far,” says Chris Tyler-Smith, a geneticist at the Sanger Institute in Hinxton, United Kingdom. “A stunning piece of

work,” says Terence Brown of the University of Manchester in the U.K.

The work complicates the human story, much as the discovery of the controversial H. floresiensis—a.k.a. the hobbit—has upset earlier and simpler views of early human migrations around the globe. If four hominins including the hobbit were alive about 40,000 years ago, “the amount of human biodiversity … was pretty remarkable,” says geneticist Sarah Tishkoff of the University of Pennsylvania. For now, Pääbo’s

team is not naming the new lineage.

"Mind make human difference from animal"

 

And Allâh has brought you out from the wombs of your mothers while you know nothing. And He gave you hearing, sight, and hearts( minds)  that you might give thanks (to Allâh). (al-Nahl , 16:78)

 “Dan Allah mengeluarkan kamu dari perut ibu kamu dengan keadaan tidak mengetahui sesuatu pun; dan Ia mengurniakan kepada kamu pendengaran dan penglihatan serta hati (akal fikiran); supaya kamu bersyukur.” (Surah al-Nahl, ayat 78)


From the surah above, is very clear that Allah give us minds or inteligence besides hearing and sight for us. Minds make us very different from any intelligence creatures in the planet of the earth. From the post of story about 3 alien is clear that human very distinguish from another because of their intelligence.


Scientist not fully understanding what the relationship of genetic with minds ability, perhaps not all about genetic. May be something else. Wallahualam.(only Allah Know). let us pray to Allah to borrow His knowledge to us in understanding genetic.

The heart disease: the genes responsible still elusive

The researcher try one approach in understanding disease by find what are genes are responsible in the particular disease (the common genes express in patients). The type of study begin 5 year ago when a study of 146 Caucasian volunteers turned up a common gene variant among those with the eye disease macular degeneration.

Researchers had used a new strategy: They scanned large stretches of the genomes of the sick and the healthy and found a single DNA base that was much more likely to be present in those whose eyes were failing.

The finding was remarkable: Relatively few people participated in the study, yet those with two copies of the suspect gene variant had 10 times the risk of macular degeneration, a huge increase. Furthermore, the method the group used, called genome-wide association (GWA), had some big advantages: It was unbiased, testing thousands of gene-disease associations at once, not just a researcher’s favorites. And it pointed to common variants, found in at least 5% of individuals studied. GWA studies offered hope of identifying people at risk for diseases, uncovering new disease mechanisms, and finding new targets for therapy.

The researcher also used the GWA studies in the heart disease. But the results are not like expexced. “People did studies with 300 or 500 people and didn’t find anything, then did 1000 and didn’t find anything,” says Deepak Srivastava, who directs the Gladstone Institute of Cardiovascular Disease at the University of California (UC), San Francisco. It quickly became clear that macular degeneration was an exception.

The results from one group of GWA studies, for heart disease, are typical, with a mixed record and an uncertain legacy. The technique has identified dozens of variants, but all have weak effects; so far, almost none has led to DNA changes that actually cause disease. Researchers have had more success finding variants that link to tightly defined conditions like high cholesterol than to heart failure, a catch-all disease.

For me I suggest that the GWA studies must be more specific to what causes of heart disease so may be we can know what genes cause particular heart disease.

The story about 3 alien? (what make us human version 1.50)

Not too long ago three aliens descended to Earth to evaluate the status of intelligent life. One specialized in engineering, one in chemistry and one in computation. Turning to his colleagues, the engineer reported (translation follows): “All of the creatures here are solid, some segmented, with capacities to move on the
ground, through the water or air. All extremely slow. Unimpressive.” The chemist then commented: “All quite similar, derived from different sequences of four chemical ingredients.” Next the computational
expert opined: “Limited computing abilities. But one, the hairless biped, is unlike the others. It exchanges information in a manner that is primitive and inefficient but remarkably different from the others. It creates many odd objects, including ones that are consumable, others that produce symbols, and yet others that destroy members of its tribe.”


“But how can this be?” the engineer mused. “Given the similarity in form and chemistry, how can their computing capacity differ?” “I am not certain,” confessed the computational alien. “But they appear to have  a system for creating new expressions that is infinitely more powerful than those of all the other living kinds. I propose that we place the hairless biped in a different group from the other animals, with a separate origin, and from a different galaxy.” The other two aliens nodded, and then all three zipped home to present their report.


What so special about human? Again, because of our brain. From the post "what make us human", the 1% or 2% difference, they differ genes in brain developments. But scientist not fully understanding the role of genes differences in human can give significantly give the brain has ability that only human race have. The gene encoded for protein no longer the answer, may be non coding DNA, perhaps RNAs.

In Islamic perspectives, Human are the very special creatures that create as Khalif (leader) and the give the very special "nikmat" which is the intelligence. In Al-quran, always repeat this phrases أفلا تعقلون reads "Affala Ta'kiluun" which means Don't you think?. So Islam teach people always to use their intelligence.

 Key ingredient of human mind

 The four traits below distinguish the human mind from those ofanimals. Uncovering the origin of the human mind will require explaining how these unique properties came about.

Generative computation enables humans to create a virtually limitless variety of words, concepts and things. The characteristic encompasses two types of operation: recursive and combinatorial. Recursion is the repeated use of a rule to create new expressions. The combinatorial operation is the mixing of discrete elements to engender new ideas.

Promiscuous combination of ideas allows the mingling of different domains of knowledge—such as art, sex, space, causality and friendship—thereby generating new laws, social relationships and technologies. Mental symbols encode sensory experiences both real and imagined, forming the basis of a rich and complex system of communication. Such symbols can be kept to oneself or expressed to others as words or pictures.

Abstract thought permits contemplation of things beyond what we can see, hear, touch, taste or smell.

Hobbit from Indonesia- human evolution need revision

In 2004 a team of Australian and Indonesian scientists who had been excavating a cave called Liang Bua on the Indonesian island of Flores announced that they had unearthed something extraordinary: a partial skeleton of an adult human female who would have stood just over a meter tall and who had a brain a third as large as our own. The specimen, known to scientists as LB1, quickly received a fanciful nickname—the hobbit,like a race in Lord of the Ring. The team proposed that LB1 and the other fragmentary remains they recovered represent a previously unknown human species, Homo floresiensis. Their best guess was that H. floresiensis was a descendant of H. erectus—the first species known to have colonized outside of Africa. The creature evolved its small size, they surmised, as a response to the limited resources available on its island home—a phenomenon that had previously been documented in other mammals, but never humans.


Scientists initially postulated that H. floresiensis descended from H. erectus, a human ancestor with body proportions similar to our own.New investigations show that the hobbits were more primitive than researchers thought, however—a finding that could overturn key assumptions about human evolution.

H1N1 is not new virus?

H1N1 swine influenza gives great threats to human races nowadays. Its don’t have any cure yet. Believe me or not the H1N1 is not a new virus. How come?

Let have closer look on its structure. Its surface protein, hemagglutinin (HA) — which spikes cells and starts an infection— closely matches the HA in the H1N1 virus responsible for the 1918 pandemic. Separated by 91 years, the two strains of the highly mutable virus ought to be vastly different. This newfound similarity answers many mysteries about the 2009 pandemic, including why it largely spared the elderly.

The 1918’s virus evolved quickly in order to survive to different form of virus and lastly to be H1N1 virus that cause human pandemic.

Figure 1:  Descendants of the 1918 virus dodged antibodies by mutating (red) the tips of the HA to change shape and hold glycans, but the 2009 pandemic strain (far right) turned back the clock

This finding give scientist new way in curbing the next pandemic, so to make sure this not happen again, research on how the possibility of the virus mutate, and how they cause disease and how to cure it must be done. But I have bad feeling about these researches,   which will be underground research to build lethal bio-weapon, if human understanding the behavoiur of virus and how to create a new disease.

Di Hari Malaysia Ini, Marilah kita mengenang peristiwa Sabra dan Syatila

Tangal 16 september 2010, sudah 47 tahun penubuhan gagasan Malaysia. Pahit getir, suka duka dalam penubuhan negara bangsa Malaysia ini. Tarikh ini harus diingat sebagai tarikh keramat bagi setiap warga Malaysia, sama pentingya dengan 31 ogos.

Tetapi jangan dilupa, sebagai negara Islam, tarikh ini merupakan tarikh yang tragis, lagi menyedihkan iaitu pada tanggal 16-18 September 1982, berlaku peristiwa yang menyayat hati, iaitu penyembelihan beramai-ramai umat Islam di kem Sabra dan Syatila.

Dua peristiwa yang amat bersejarah ini, marilah kita menyambutnya dengan doa dan solat hajat agar negara Malaysia kekal aman dan rakyatnya bersatu atas nama Islam serta kita memohon agar Allah memberikan bantuan pada para mujahiddin seluruh dunia dalam menegakkan syiar Islam.

Islam akan bangkit di negeri-negeri timur dibawah naugan panji-panji hitam. Duhai bangsa seagama ku, hidup ini adalah perjuangan, jangan lah kalian lena dan alpa dengan keseronokan dunia yang penuh tipu daya. Berjihadlah di jalan-Nya.

The new construction of coral family tree and shows the ocean's evolutionary potential

The deep sea may not seem like a crucible of evolution. For me, according to Darwin, evolution is correlate to natural selection. Compare with the organism living in land and shallow seas, they may have more competition to survive especially when human take control in the world — cause many pollution and destruction. So evolution rates are increase in the name of survival.


But, to the surprise of biologists, a new construction of the coral family tree suggests that evolution proceeds at full bore in waters well below where sunlight penetrates. Moreover, some coral diversity may have bloomed there first, before spreading coastward—the reverse of what has long been thought. “As people look in the deep sea, they are finding much more diversity than they expected,” says Clifford Cunningham, an evolutionary biologist at Duke University in Durham, North Carolina. “We’re just at the very beginning of understanding deep-sea evolution.”

Besides that, the evolution potential not only seem in coral, but in other deep sea organism too. Marymegan Daly, a systematist at Ohio State University, Columbus, and co-coordinator of the Cnidarian Tree of Life project, has found a similar pattern among the sea anemones she’s analyzed. “We see lots of radiations of deep-deep sea forms,” she reported. In short, concludes France, “we can’t say that the deep sea is a boring
environment in terms of evolution.”

I think this are the beginning of the new saga in evolutionary study to understand the evolution pattern in deep sea.

Debates about how eukaryotes get the mitochondria.

 I would like to share with you the debates about eukaryotic evolution. The evolution of eukaryotes is something very hard to understand the process of evolution. One of them that always debate, how they acquired the membranebound organelle, mitochondria. Mitochondria produce energy in nearly all eukaryotic cells and regulate cell metabolism by controlling the flow of factors such as ions, amino acids, and carbohydrates between themselves and the cytoplasm. Mitochondria evolved from a bacterial endosymbiont (an α-proteobacterium), and this process depended on the establishment of new pathways that facilitated the import of proteins into and across the double membrane (inner and outer) of the ancestral endosymbiont. Herein lies a debate: How did the process of protein import in mitochondria—which facilitated the evolution of this organelle, and thus, eukaryotic cell evolution— arise? Was the process driven by the ancestral host cell or by the prokaryotic endosymbiont, or by both?


Recently, Gross and Bhattacharya discussed the possibility that evolution of protein import into mitochondria was driven by the host cell (see the fi gure).In this paradigm, to capitalize on energy production by the ancestral endosymbiont, a protein sorting and importing mechanism was necessary to relocate host cell proteins to the endosymbiont. Thus, in the earliest evolutionary stages of mitochondria, host proteins were “imposed” on the ancestral endosymbiont.


It was argued that because the endosymbiont’s outer membrane had greatest access to host factors in the cytoplasm, evolution of mitochondrial protein import began at the outer membrane. Once established there, host proteins could then gain access to the intermembrane space and the inner membrane in an “outsideto- inside” trajectory of evolution.

Two views of mitochondrial evolution. The “Inside” view of the transition from intracellular bacterium to mitochondrion acknowledges that the ancestral endosymbiont’s genome encoded protein complexes (SecYEG and YidC) that facilitated the assembly of bacterial proteins into its inner membrane (e.g., metabolite carriers) and outer membrane (the bacterial β-barrel protein BAM). An early outer-membrane protein of the TOM complex (Tom40) may have arisen from a bacterial β-barrel protein with affinity for basic, amphipathic amino acid sequences on host cell proteins. Progenitors of modern protein import components (TIM) were also encoded by the endosymbiont’s genome. The “Outside” view proposes that proteins of the ancestral host cell were imported into the endosymbiont. It assumes that the endosymbiont’s genome is reduced (and unable to encode progenitor proteins of the import machinery). In this case, some host cell β-barrel protein is imposed into the endosymbiont’s outer membrane. It then facilitates the import of other protein import machinery components from the host cell.

To read further please refer this article on Science Magazine 5 february 2010 titled "Tinkering Inside the Organelle".

Understanding nanobacteria, understanding disease, perhaps more understanding genetic

Scientists debate about what are classification of nanobacteria, is that a new class of life or just a particle from bacteria or another life form. Finish researcher Olavi Kajander and Turkish researcher Neva Citcioglu, Universiy of Kuopio, Findland  confirm that the nanobacteria is a living entity.The scientists assigned their discovery, which they named Nanobacterium sanguineum, to a subgroup of bacteria that includes Brucella and Bartonella, both of which have been shown to cause disease. The Finnish group also noted unusual features of the nanobacteria, including their ability to change shapes in culture, a property known as pleomorphism, which is a rare trait in living organisms. The nanobacteria were seen to change from small spherical bodies to films and clumps of mineralized material. The mineral in question turned out to be hydroxyapatite (apatite), a crystalline complex of calcium and phosphate found everywhere in nature, including mammalian bones as well as the shells of some invertebrates.


The small, round nanobacteria were not only covered by apatite walls but were often found hiding within large “igloo-shaped castles” or “dwelling places,” the researchers wrote.

Attempting to identify the source of nanobacteria, the Finnish team was surprised to find the creatures in most animal and human body fluids they examined—blood, saliva and urine, among others—and concluded that the tiny bugs posed a risk for diseases involving abnormal mineral agglomerations, such as kidney stones. Eventually conditions linked by various researchers with nanobacteria would expand to include many types of cancer, atherosclerosis, degenerative diseases such as arthritis, scleroderma, multiple sclerosis, peripheral neuropathy, Alzheimer’s disease, and even viral infections such as HIV. Initial studies by the Finnish team had shown that 14 percent of healthy Scandinavian adults tested positive for antibodies against nanobacteria. Other scientists, such as Andrei P. Sommer of the University of Ulm in Germany, would later promote the idea that nanobacteria behave as transmissible pathogens, incriminating nanobacteria as a global health hazard.

Despite all these frightening implications, in many ways nanobacteria fulfilled the wildest dream of every scientist. Their very primitive nature, unusual characteristics and ubiquitous distribution suggested that nanobacteria might help explain the origins of life—not only on Earth but elsewhere in the cosmos.

Nanobacteria is just a new field to decipher the DNA code and could reveal the secret of life.

A Star Is Born—With Difficulty

"Physics is hard to understand but always amaze me, sometimes its explain anything. for me by understanding physics and genetic, perhaps we can get the theory of everything. The section of "amazing physics" is the section for me to share with readers what are the mystery of physics, that very complicated like the mystery of DNA code."

Is very hard to be a superstar right? Same with formation of the universe star. They have a long process and the astronomy not fully understand overall of the process.In the simplest terms, the process represents
the victory of gravity over pressure. It starts with a vast cloud of gas and dust floating in interstellar space. If the cloud—or, more often, a dense part of such a cloud called a core—is cool and dense enough, the inward pull of its gravity overpowers the outward push of gaseous pressure, and it begins to collapse under its own weight. The cloud or core becomes ever denser and hotter, eventually sparking nuclear fusion. The heat generated by fusion increases the internal pressure and halts the collapse. The newborn star settles into a dynamic equilibrium that can last millions to trillions of years.

The theory is self-consistent and matches a growing body of observations. Yet it is far from complete. Every sentence of the above paragraph cries out for explanation. Four questions, in particular, trouble astronomers. First, if the dense cores are the eggs of stars, where are the cosmic chickens? The clouds must themselves come from somewhere, and their formation is not well understood. Second, what causes the core to begin collapsing? Whatever the initiation mechanism is, it determines the rate of star formation and the final masses of stars.

Third, how do embryonic stars affect one another? The standard theory describes individual stars in isolation; it does not say what happens when they form in close proximity, as most stars do. Recent findings suggest that our own sun was born in a cluster, which has since dispersed. How does growing up in a crowded nursery differ from being an only child?

Fourth, how do very massive stars manage to form at all? The standard theory works well for building up stars of as much as 20 times the mass of the sun but breaks down for bigger ones, whose tremendous luminosity should blow away the cloud before the nascent star can accumulate the requisite mass. What is more,massive stars blast their surroundings with ultraviolet radiation, high-velocity outflows and supersonic shock waves. This energy feedback disrupts the cloud, yet the standard theory does not take it into account.

The 4 questions arise too fill the gaps of how a star is form. A lot of mystery to solved it.

What make us human version 1.2

What make us human version 1.2? Why?? This post is the additional information of the post "what make us human". That post distinguish us from chimpanzees significantly from only 1% of DNA difference. From 1% difference involve genes that involve in brain development, opposing thumb and  facilitates formation of words by the mouth, enabling modern human speech.


This post I would to share with you the information that make us differ from chimpanzees in scientific evidence. Adult humans share features associated with immature chimpanzees,
such as small jaws and flat faces. The retention of juvenile features, called neoteny, may
explain why humans are so different from chimps despite a mostly similar genome.



In animals, neoteny comes about because of delays in development, points out molecular biologist Philipp Khaitovich of the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany. For instance, humans sexually mature roughly five years after chimps do, and our teeth erupt later. “Changes in the timing of development are some of the most powerful mechanisms evolution can use to remodel organisms, with very few molecular events required,” he explains.

To look for genetic evidence that neoteny played a role in the evolution of Homo sapiens, Khaitovich and his colleagues compared the expression of 7,958 genes in the brains of 39 humans, 14 chimpanzees and nine rhesus monkeys. They collected samples from the dorsolateral prefrontal cortex—a region linked with memory that is relatively easy to identify in the primate brain. These tissues came from deceased individuals at several stages of life, from infancy to middle age, enabling the researchers to see how genetic activity changed over time in each species.

In both humans and chimps, about the same percentage of genes changed in activity over time. But roughly half these age-linked genes in humans differed from chimps in terms of when they were active during development. Analysis of the 299 genes whose timings had shifted in all three species revealed that almost 40 percent were expressed later in life in humans, with some genetic activity delayed well into adolescence.


Actually proving that neoteny helped to drive human evolution and brain size is difficult. Khaitovich suggests analyzing genetic activity in cases of faster-than normal development in people, “which past research already shows can lead to a reduction in cognitive abilities,” he says.

Other experts certainly think that neoteny’s role is reasonable. The ability of the brain to learn is apparently greatest before full maturity sets in, “and since neoteny means an extended childhood, you have this greater chance for the brain to develop,”says molecular phylogeneticist Morris Goodman of Wayne State University,who did not participate in this study. In other words, human evolution might have been advanced by the possibilities
brimming in youth.