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Friday, July 31, 2009

How to Post and View Comments?

I have received few queries about how to post/viww comments.

To view / post comments, click on the comments link on the right hand top corner of the post under which you want to comment.

You will see various comments posted under the title..

Below the comments you will see the following:
Drop down the menu Comment as: by clicking on the button shown below

Select the Name/Url from the drop down menu
Then you will see the following
Enter your Name and click Continue. Type your comment in the comment box.
Preview your comment by clicking on the Preview button
Click on Post Comment. If yow want to make any changes click the 'x' at the top right of preview box. It will take you back to the comments box.
Click "Post Comment" to post the comment.
It will be sent to me and will appear under the post after I publish it (in a day or few)
I will reply If you ask any question in your comment

Wednesday, July 29, 2009

What are Foragers?

Foragers are those who wander in search of food or provisions.
Forage (fôr'ĭj)
noun: Food for domestic animals; fodder.
verb: To wander in search of food or provisions.

Why is sucrase called invertase?

Sucrase (systematic name: beta-fructofuranosidase) is an intestinal enzyme that hydrolyzes sucrose.
C12H22O11   +   H2O   →   C6H12O6    +   C6H12O6
 (sucrose)        (water)         (glucose)          (fructose) 
Sucrase Secretion 
It is not present in newborn animals so that they are unable to digest sucrose and feeding of the sugar will cause severe, osmotic diarrhea. Sucrase activity in the intestine increases as the need for, and secretion of, lactase decreases with age.
Why is it called invertase? 
Sucrase is also known as invertase or saccharase. It catalyzes the hydrolysis (breakdown) of sucrose (table sugar) to fructose and glucose, usually in the form of inverted sugar syrup. Invert sugar is the mixture of glucose and fructose produced by hydrolysis of sucrose, 1.3 times sweeter than sucrose. It is called invert sugar because the optical activity is reversed in the process.
The method of measuring the concentration of sugar syrup 
The concentration of sugar syrup is measured using a polarimeter. Plane-polarized light, when passed through a sample of pure sucrose solution, is rotated to the right (optical rotation). As the solution is converted to a mixture of sucrose, fructose and glucose, the amount of rotation is reduced until (in a fully converted solution) the direction of rotation has changed (inverted) from right to left.

Saturday, July 4, 2009

Claude Bernard - Homeostasis

The tendency toward internal stabilization of the animal body was first recognized by Claude Bernard. He was a great French physiologist of the nineteenth century. Through his studies of blood glucose and liver glycogen, he first discovered internal secretions. From a lifetime of study and experimentation he propounded the principle of constancy of the internal environment. 
Walter B. Cannon coined the name homeostasis.He was an American physiologist at Harvard University. He reshaped and restated Bernard's idea. From his studies of the nervous system and reactions to stress, he described the ceaseless balancing and rebalancing of physiological processes that maintain stability and restore the normal state when it has been disturbed.

Wednesday, July 1, 2009

Silent mutations can also be harmful

Single-letter changes to the DNA, known as point mutations, can therefore change a codon to one that specifies the wrong amino acid (known as a missense mutation) or to a stop signal (nonsense mutation), causing the final protein to be truncated. A single-base change can also alter a stop codon so that it then encodes an amino acid (sense mutation), resulting in a lengthened protein. And a final change is possible: a mutation that alters a nucleotide but yields a synonymous codon. These mutations are the ones termed “silent.”
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.
Only 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 Escherichia 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.
Lately, studies of human disease have indicated that 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 (introns) and then splice the coding regions (exons) together to produce the final mRNA version of the gene. 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.

Michael Jackson Dies of Cardiac arrest

Michael Jackson, the moon-walking pop star who once patented "anti-gravity" shoes to enhance his stage performances, died of cardiac arrest on 25th June, 2009 at age 50.
What is the difference between cardiac arrest and heart attack?
Christie Ballantyne, interim chief of cardiology at Baylor College of Medicine in Houston, Tex., tells Scientific American that cardiac arrest just means that someone has lost their blood pressure and their pulse. "Usually, this means there has been a collapse of the circulatory systems and many times, it is due to an [accelerated] heartbeat," he says. When the heart is contracting so quickly, blood can no longer be squeezed from the pumping chamber and circulate to the brain, leading to death within minutes.
This accelerated heartbeat, or arrhythmia, can be a sign of a heart attack, which stems from buildup of plaque in the arteries. But not all heart attacks lead to cardiac arrest, and they are not the only cause of cardiac arrests, Ballantyne says. Cardiac arrest can occur from a major blood clot in the lung or a heart enlarged from infection or other damage. Previous heart attacks can also leave scars that injure the heart's pacemaking electrical system.

Birds of a feather

The size of flighted birds is limited by the demands of feather maintenance.

Sievert Rohwer at the University of Washington in Seattle and his colleagues studied 43 species of bird, assessing size, the length of flight feathers and timing of moulting cycles.

Flight-feather length is proportional, they say, to body mass raised to the one-third power, so that feather length roughly doubles with a tenfold increase in a bird's weight. But feather growth rate is proportional to body mass raised only to the one-sixth power. The trade-offs in time and energy required to replace long feathers therefore limit maximum bird size.