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.

Don't neglect the neglected tropical disease.

Most people in richer countries equate tropical disease with the big three—HIV/AIDS, tuberculosis and malaria—and funding agencies allocate aid accordingly. the big three diseases of course causing death.

But the situation is different in poor countries. The poorest people are not only poor. They are also chronically
sick, making it harder for them to escape poverty. A group of seven tropical diseases, mostly caused by parasitic worms, afflict a billion impoverished people worldwide. They seldom kill directly but cause lifelong misery that stunts children’s growth, leaves adults unable to function to their fullest, and heightens the risk of other diseases.


Fortunately, they can be easily treated, often with a single pill. Various agencies and foundations are collaborating to deliver these drugs, but they have reached only about 10 percent of the population so far. So many researcher, agencies too focus on the big three diseases and right now they more focus about the popular pandemic, H1N1 virus.

I don't blame them because of the researches, researches are good. But in the name of humanity, please increase some fund to help the poor. They deserve to live. Besides that, the neglected disease must be keep going on research to make sure the drugs used are still efficient, and is can prevent the reemergence

of disease.

Biased Vaccine

Manipulating the sites of synonymous mutations has allowed scientists to design genes that speed up protein manufacture, but the same technique can also be used to slow it down. Steffen Mueller and his colleagues at Stony Brook University recently took this approach to design a safer polio vaccine. Live viruses make the most potent vaccines because they provoke a strong immune response in the recipient, but live vaccines can reproduce and mutate, potentially causing disease. Mueller’s group took advantage of microbes’ preference for using certain codons to maximize the efficiency of protein production by designing a poliovirus that substituted rarer, less efficient codons in sequences encoding the viral shell. The resulting virus was able to copy itself, albeit more slowly. After the investigators administered the engineered virus to mice, the animals were protected from infection when they were later exposed to wild poliovirus. This technique for taking advantage of codon bias to create a live but weakened vaccine could be applied to other pathogens as well to produce potent but safer vaccines.

Synonymous but not the same- The new view of synonymous mutation

The classic view assumed that what are termed “silent” mutations were inconsequential to health, because such changes in DNA would not alter the composition of the proteins encoded by genes. Proteins function in
virtually every process carried out by cells, from catalyzing biochemical reactions to recognizing foreign invaders. Hence, the thinking went, if a protein’s makeup ends up being correct, any small glitches in the process leading to its construction could not do a body harm.

For example if one codon GGG is has point mutation to GGA, both still encode for acid amino glycine. So by classic view assumption, the silent or synonymous mutation is not cause any harm. By researches, scientists have proved that the assumption is totally wrong.

By researches, the evidences of the harmful silent mutation can be explained by 3 evidence, (may be have more), the evidence of bias, silent mutation that disrupt protein manufactured, and also some synonymously mutation affect pain sensitivity.

The evidence of bias: In the 1980s did scientists realize that silent mutations could also affect protein production—at least in bacteria and yeast. A key discovery at the time was that the genes of those organisms did not use synonymous codons in equal numbers. When the bacterium E-coli specifies the amino acid asparagine, for instance, the codon AAC appears in its DNA much more often than AAT. The reason for this biased usage of codons soon became apparent: cells were preferentially employing certain codons because those choices enhanced the rate or accuracy of protein synthesis.

It turned out that tRNAs corresponding to those synonymous codons typically are not equally abundant within the cell. Most important, then, a gene that contains more of the codons matching the relatively abundant tRNAs would be translated faster, because the higher concentration of those tRNAs would make them more likely to be present when needed. In other cases, a single tRNA variety matches more than one synonymous codon but binds more readily to one codon in particular, so the use of that codon maximizes the accuracy of translation. Consequently, a cell has good reasons not to use all codons equally. As expected, in bacteria and yeast the genes that encode especially abundant proteins exhibit the greatest codon bias, with the preferred codons matching the most common or better-binding tRNAs.

Later observations in other organisms—including plants, flies and worms—revealed similar biases. With such a diverse array of species employing this technique to improve the efficiency of protein production, it seemed likely that mammals would, too. Analyses of mammalian genes did indeed reveal tendencies toward favoring certain codons. The similarity between simple organisms and mammals, however, proved to be only superficial. For reasons not yet fully understood, mammalian genomes are organized into large blocks, each with a distinctively skewed nucleotide content: some regions are rich in G and C bases, whereas others are enriched for A and T. As a result, genes residing in a GC rich region of the genome tend to have many codons containing those bases. Our genes, then, do show a bias for using certain codons, but unlike simpler organisms, the mammalian pattern does not obviously suggest that the reason is to optimize protein synthesis.

In principle, any mutation that does not affect an organism is invisible to the force of natural selection,
which preserves variations that are beneficial.According to the thinking at the time, regions invisible to selection would include sites of silent mutations within genes as well as the 98 percent of the genome that does not specify protein—the noncoding DNA. Yet when scientists began looking at whether silent sites in genes evolved at the same rate as noncoding regions, they unexpectedly found differences—a sign that silent mutations could affect physiology after all.

Initially researchers had no idea how such mutations could disturb protein manufacture in mammals. Lately, however, studies of human disease have provided not just one mechanism but many. Silent disease-causing mutations interfere with several stages of the protein-making process, from DNA transcription all the way through to the translation of mRNA into proteins.

One example involves silent mutations changing how a gene transcript is edited. Shortly after a gene is transcribed into RNA form, that transcript is trimmed to remove noncoding regions known as introns. Like a movie editor who cuts out unwanted film, cellular splicing machinery needs to find the good bits that encode amino acids, known as exons, and then splice them together to produce the final mRNA version of the gene. Human genes are especially rich in introns, with each gene having an average of eight long intronic stretches, so the splicing machinery needs a way to tell where each exon starts and ends.

Research over the past few years has revealed that exons not only specify amino acids, they also contain within their sequences cues necessary for intron removal. Chief among these are exonic splicing enhancer (ESE) motifs—short sequences of about three to eight nucleotides that sit near the ends of the exons and define the exon for the cellular splicing machinery. The need for such motifs can in fact explain a preference
for certain nucleotides in human genes. Although the codons GGA and GGG, which encode glycine, can both occur in splicing enhancers, the former codon acts as a more potent enhancer, leading to more efficient splicing.GGA is also correspondingly more common close to the ends of exons.


In support of the view that preserving codon sequence in splicing enhancers matters, research of  University of Bath  J. V. Chamary , Laurence D. Hurst and Joanna L. Parmley has shown that exonic motifs that apparently function as splicing enhancers show slower evolution in their synonymous codons than do neighboring sequences uninvolved in splicing. This slow evolution indicates that natural selection has kept enhancer motifs relatively unchanged because their specific sequences are so significant. Silent alteration to codons containing these enhancers,although they do not change an amino acid, can nonetheless have a major effect on a protein simply because they disrupt the proper removal of introns.


The long explanation can be visualized in the figure below:

Another evidence is synonymously mutation that affect pain sensitivity A synonymous mutation was found to affect pain sensitivity by changing the amount of an important enzyme that cells produced. The difference results from alterations in the shape of mRNA that can influence how easily ribosomes are able to unpackage and read the strand. The folded shape is caused by base-pairing of the mRNA’s nucleotides; therefore,
a synonymous mutation can alter the way nucleotides match up.

To date, some 50 genetic disorders have been linked to silent mutations, many of which also appear to interfere with intron removal. Splicing enhancers can overlap with a considerable length of a gene’s protein-coding sequence, imposing significant limitations on where a silent mutation would be tolerated. A striking example of the damage a mutation in a splicing enhancer can do was recently documented by Francisco Baralle of the International Center for Genetic Engineering and Biotechnology in Trieste, Italy. The investigators found that 25 percent of the silent mutations they induced in one exon of the cystic fibrosis transmembraneconductance regulator (CFTR) gene disrupted splicing and presumably would thus contribute to cystic fibrosis or related disorders.

As a conclusion, this post mainly about to expose to reader to recent view about silent mutations. Silent mutation doesn't means we just ignored it, silent does not mean nothing, thanks to researches. From researches they give us data, from data after interpretation and process they give us knowledge. Knowledge is power.

Copy number variation (CNV) in understanding the complexity of disease

Recently geneticists have taken a closer look at a genetic aberration previously considered rare: copy number variation (CNV). CNV  is a segment of DNA in which copy-number differences have been found by comparison of two or more genomes.

Copy number variation could help explain why complex diseases are often inherited but not always linked to the same genes: they may affect risk in a probabilistic manner, explains Steven McCarroll, a population geneticist at the Massachusetts Institute of Technology and a co-author of the Crohn’s disease study.

To explain furthermore, lets us review some assumption about CNV and disease. American geneticist Calvin Bridges discovered copy number variation in 1936, when he noticed that flies that inherit a duplicate copy of a gene called Bar develop very small eyes. Two decades later a French researcher studying human chromosomes under a microscope identified CNV as the cause of Down syndrome: sufferers inherit an extra copy of chromosome 21. By all appearances,CNV was rare and always a direct cause of disease.

In 2004, however, things changed. Two groups of researchers published the first genome-wide CNV maps, which illustrated that variation in gene quantity is actually quite common: each group found about 12 copy number imbalances per person.“When these papers came out, they really turned everything on its head,” says Stephen Scherer, a geneticist at the Hospital for Sick Children in Toronto and a co-author of one of the papers. “People always thought, as did we, that these large changes in DNA were always associated with disease.

Scherer and his colleagues, who included population geneticist Matthew Hurles of the Wellcome Trust Sanger Institute in Cambridge, England, followed up with a higher-resolution CNV study in 2006, which analyzed DNA from 270 individuals and identified an average of 47 copy number variations per person. And in 2007 researchers sequenced the genome of genetic pioneer J. Craig Venter and found 62 copy number variations. Evidently, Hurles says, “it’s not normal to be walking around with the perfect genome.”

Scientists are still trying to decipher exactly how these variations— most of them which are inherited—affect the body. Typically if a genome has three copies of a gene instead of the normal two (one from each parent), a cell will make proteins from all three, producing more than it probably needs. But such gene expression is “not always the case—there are exceptions exceptions,” Scherer says. Sometimes cells make the correct amount anyway;other times CNVs affect DNA regions that regulate the expression of stillother genes, making the problem more

complicated.

Even so, scientists have been able to link CNVs to a handful of complex diseases. A September 2008 study in Nature confirmed earlier findings suggesting that 30 percent of people who have a deleted length of three million base pairs in a region of chromosome 22 suffer from psychiatric conditions such as autism and schizophrenia. A Nature Genetics study from August 2008 found a link between Crohn’s disease and a 20,000 base-pair deletion in a region upstream of a genecalled IRGM, which is involved in fighting invasive bacteria.

And in January 2009 another Nature Genetics paper found an association between high body mass index and a 45,000 base-pair deletion in a gene called NEGR1, which affects neuronal growth in the hypothalamus, a brain region that regulates hunger and metabolism. “We’re coming up with so much data, and new kinds of data, that it’s hard to keep up,” remarks Edwin Cook, Jr., a psychiatrist at the University of Illinois at Chicago.

As researchers hunt for more links between known CNVs and disease, Scherer and Hurles are scouting out new variants to add to the mix. Their 2006 map identified CNVs only down to 20,000 base pairs; now they are finishing a revised map that includes variants as short as 500 base pairs. The analysis suggests that about 1,000 copy number variations exist in each person, spanning at least 1 percent of the genome.

All above information explain about researches on the relationship of CNV with disease. By observing the CNV map in smaller bases, this is a new sense in understanding how variable numbers of genes cause disease.

Dilema Bulan Merdeka Bulan Ramadhan

 Kebelakangan ini ada sambutan kemerdekaan di kolej-kolej kediaman. Memang meriah suasananya dan diisi dengan pelbagai aktiviti bagi meningkat semangat patriotik.

Saya ada mendengar ada ucapan-ucapan dari pihak penganjur yang mengatakan bahawa "walaupun bulan kemerdekaan jatuh pada bulan Ramadhan, kami cuba untuk membuat sambutan kemerdekaan". ucapan itu seolah menganggap bulan ramadhan merupakan satu penghalang.

"terlajak perahu boleh berundur, terlajak kata buruk padahnya" ucapan diatas seolah-olah mempersendakan agama Islam... sangat berbahaya.

bagaimana untuk menyambut kemerdekaan dibulan ramadhan? jawapanya mudah, buatkan aktiviti yang boleh membuat pengisian kedua-duanya dalam satu aktiviti,

Misalnya majlis solat hajat sempena kemerdekaan. Boleh dibuat seiiring dengan solat isyak, solat terawikh.

Ada menimbulkan bantahan, aktiviti tu macam perlibatan sesetengah pihak saje, kita kan 1Malaysia, kena penglibatan semua kaum dan agama....

jawapanya adalah solat hajat,terawikh kan habis dalam pukul 10 lebih mlm, sementara menunggu detik12 malam (di malam 30 august, countdown kemerdekaan) buatlah aktiviti serta hiburan sederhana yang melibatkan semua kaum serta berunsur patriotik,... Dingatkan hiburan yang ada kena mengena dengan kemerdekaan la... jangan sebab nak ramai orang datang, buat aktiviti yang tidak ada kena mengena semata-mata nak tarik ramai orang.

itu lari dari tujuan asal. jadinya bukan sambutan kemerdekaan, jadi sambutan Maksiat di bulan ramadhan. MashaAllah..