Bioentrepreneurial Idea

In Irvine researchers have discovered a dramatically improved method for genetically manipulating human embryonic stem cells, making it easier for easier for scientists to study and potentially treat thousands of disorders ranging from Huntington’s disease to muscular dystrophy and diabetes.
The technique for the first time blends two existing cell-handling methods to improve cell survival rates and increase the efficiency of inserting DNA into cells. The new approach is up to 100 times more efficient than current methods at producing human embryonic stem cells with desired genetic alterations.

“The ability to generate large quantities of cells with altered genes opens the door to new research into many devastating disorders,” said Peter Donovan, professor of biological chemistry and developmental and cell biology at UCI, and co-director of the UCI Sue and Bill Gross Stem Cell Research Center. “Not only will it allow us to study diseases more in-depth, it also could be a key step in the successful development of future stem cell therapies.”

This study appears online this week in the journal Stem Cells.

Donovan and Leslie Lock, assistant adjunct professor of biological chemistry and developmental and cell biology at UCI, previously identified proteins called growth factors that help keep cells alive. Growth factors are like switches that tell cells how to behave, for example to stay alive, divide or remain a stem cell. Without a signal to stay alive, the cells die.

The UCI scientists – Donovan, Lock and Kristi Hohenstein, a stem cell scientist in Donovan’s lab – used those growth factors in the current study to keep cells alive, then they used a technique called nucleofection to insert DNA into the cells. Nucleofection uses electrical pulses to punch tiny holes in the outer layer of a cell through which DNA can enter the cell.

With this technique, scientists can introduce into cells DNA that makes proteins that glow green under a special light. The green color allows them to track cell movement once the cells are transplanted into an animal model, making it easier for researchers to identify the cells during safety studies of potential stem cell therapies.

Scientists today primarily use chemicals to get DNA into cells, but that method inadvertently can kill the cells and is inefficient at transferring genetic information. For every one genetically altered cell generated using the chemical method, the new growth factor/nucleofection method produces between 10 and 100 successfully modified cells, UCI scientists estimate.

With the publication of this study, the new method now may be used by stem cell scientists worldwide to improve the efficiency of genetically modifying human embryonic stem cells.

“Before our technique, genetic modification of human embryonic stem cells largely was inefficient,” Hohenstein said. “This is a stepping stone for bigger things to come.”

Scientists can use the technique to develop populations of cells with abnormalities that lead to disease. They can then study those cells to learn more about the disorder and how it is caused. Scientists also possibly could use the technique to correct the disorder in stem cells, then use the healthy cells in a treatment.

The method potentially could help treat monogenic diseases, which result from modifications in a single gene occurring in all cells of the body. Though relatively rare, these diseases affect millions of people worldwide. Scientists currently estimate that more 10,000 human diseases are monogenic, according to the World Health Organization. Examples include Huntington’s disease, sickle cell anemia, cystic fibrosis and hemophilia.

UCI is at the forefront of stem cell research. The Sue and Bill Gross Stem Cell Research Center promotes basic and clinical research training in the field of stem cell biology. More than 60 UCI scientists use stem cells in their studies. These scientists study spinal cord injuries, brain injuries and central nervous system diseases such as multiple sclerosis, Alzheimer’s and Huntington’s. They also study muscular dystrophy, diabetes, cancer and other disorders.

UCI is raising money for a new building that would house its stem cell researchers, the core laboratory, training facilities and collaborative research space. It would accommodate evolving and expanding areas of stem cell study, serving as a university and regional hub for human embryonic stem cell research. UCI has applied to the California Institute for Regenerative Medicine for a facilities grant to build the structure.

April Pyle of UCLA and Jing Yi Chern of Johns Hopkins University also worked on the genetic modification study, which was funded by the National Institutes of Health.

http://stemcells.nih.gov/info/basics/basics1.asp/
http://stemcells.alphamedpress.org/
http://www.cnn.com/SPECIALS/2001/stemcell/
http://www.cellstemcell.com/
http://jwit.webinstituteforteachers.org/~hweiner/webquest/images/stem-cell-4.jpg/
Source : University of California - Irvine

biological breakthrough

CORVALLIS, Ore. – Researchers have made a fundamental advance in the understanding of cell biology that helps to explain how cells in higher organisms, including humans, send out signals that control cell division, cell death and other key functions.

The discovery should open new avenues to research on cancer, the scientists said.

The new study, to be published Friday in the journal Science by biochemists from Oregon State University and Wake Forest University, may also help resolve a significant debate in the science community about the role of hydrogen peroxide in cellular signaling and control of life processes.
This chemical would be recognized by most people as a common disinfectant found in the family medicine cabinet, used to cleanse wounds or a kitchen countertop.

But the new study provides strong evidence for how hydrogen peroxide is able to signal cells to divide, differentiate, or even commit suicide. These biochemical functions are essential to human life, and if they are dysfunctional may lead to cancer – which, from a simple perspective, is uncontrolled cell division.

“Hydrogen peroxide, like some other oxidative molecules, is usually a toxin we’re trying to get rid of,” said Andrew Karplus, a professor of biochemistry at OSU. “In most cases it’s an unnecessary byproduct that results from our processing of oxygen, which we need to live. And there is a considerable community of scientists who believe that’s about all it is, a toxin that needs to be eliminated.”

But another group of researchers, Karplus said, point to a wide range of evidence that hydrogen peroxide plays a key role in cellular signaling and communication – a switch, in a way, that’s only flipped on rare occasion but is critical to such cellular processes as division and programmed cell death. It’s never been clear, however, exactly how the same chemical can be both an unwanted toxin and a chemical that’s literally essential to the survival of higher life forms.

The newest findings, Karplus said, appear to answer that question.

In this research, the scientists were studying the function of peroxiredoxin, an enzyme whose primary task in a wide range of plant, animal and even bacterial life forms appears to be the detoxification of hydrogen peroxide.

The new discovery started out as purely basic research, Karplus said – the OSU and Wake Forest researchers were trying to model the atomic structure of peroxiredoxin from salmonella bacteria, as part of their programs in protein crystallography and understanding the basic biochemical processes of life.

They found that the peroxiredoxin from bacteria does a great job of detoxifying hydrogen peroxide, keeping it from killing cells. But when the scientists then compared the peroxiredoxin from bacteria with that from humans, they found that the enzyme from humans was larger and, for some reason, appeared only to be able to detoxify low levels of hydrogen peroxide – larger amounts of hydrogen peroxide would overwhelm the peroxiredoxin and kill it. What they discovered was that the extra size of peroxiredoxin molecule in humans causes it to work a little more slowly, and that makes in vulnerable to being killed.

“This was really pretty strange,” Karplus said. “There’s not a lot of biological precedent for an enzyme that exists primarily to get rid of another molecule, but when too much of that molecule exists, the enzyme itself becomes the victim. In humans, depending on the levels of these two compounds, this is a little dance of death in which sometimes the hydrogen peroxide is the winner.”

But the fact that hydrogen peroxide can actually survive, and even overwhelm the compound that exists to detoxify it must have evolutionary value, the researchers believed. They hypothesized that this adaptation allows the peroxiredoxin to act much like a floodgate would, keeping resting levels of hydrogen peroxide low, while permitting higher levels to flow throughout the cell to perform their signaling function.

“What we now understand, in other words, is how hydrogen peroxide could function in mammals and other higher life forms both as a toxin and a signal,” Karplus said. “In our bodies, hydrogen peroxide appears to be part of the mechanism that induces cell death at appropriate times – for instance, in cancer cells when they are attacked by our immune system.”

Some anti-cancer drugs, such as cisplatin, actually function by causing more hydrogen peroxide to be made in cells, Karplus said. And some cancer cells that are resistant to cisplatin or other forms of cancer therapy such as radiation appear to be making larger amounts of peroxiredoxin. The findings that emerged from this basic research program could have immediate value to suggest new types of cancer research, Karplus said, and eventually therapies.

http://www.cancer-info.com/cancer.gif/
http://www.jongonews.com/articles/07/0330/10850/MTA4NTAMpPAxkaK.html
http://www.drrathresearch.org/lab_research/cancer.html

Bio Entrepreneur: Genentech :)

Genentech Inc. was founded in 1976 by Robert A. Swanson and Doctor Herbert W. Boyer. Boyer with a fellow researcher, in 1973, invented recombinant genetic engineering, by realizing that restriction enzymes could be cut DNA fragments. As of 2006, Genentech employs more than 10,000. Products of Genentech are Activase/Cathflo, Nutropin, Pulmozyme, Rituxan, Herceptin, TNKase, Xolair, Raptiva, Avastin, Tarceva, and Lucentis. Taken from Wikipedia:

"

• 1982 - Synthetic "human" insulin approved by the U.S. Food and Drug Administration (FDA), thanks largely to its partnership with insulin manufacturer Eli Lilly and Company, who shepherded the product through the FDA approval process. The product (Humulin) was licensed to and manufactured by Lilly, and was the first-ever approved genetically engineered human therapeutic.
• 1985 - Protropin (somatrem) - Supplementary growth hormone for children with growth hormone deficiency (ceased manufacturing December 2002).
• 1987 - Activase (recombinant tissue plasminogen activator)- To dissolve blood clots in patients with acute myocardial infarction. Also used to treat non-hemorrhagic stroke.
• 1990 - Actimmune (interferon gamma 1b) - Treatment of chronic granulomatous disease (licensed to Intermune).
• 1993 - Nutropin (recombinant somatropin) - Growth hormone for children and adults for treatment before kidney transplant due to chronic renal insufficiency.
• 1994 - Pulmozyme (dornase alfa) - Inhalation treatment for children and young adults with cystic fibrosis - recombinant DNAse.
• 1997 - Rituxan (rituximab)- Treatment for specific kinds of non-Hodgkins lymphomas.
• 1998 - Herceptin (trastuzumab) - Treatment for metastatic breast cancer patients with tumors that overexpress the HER2 gene. Recently approved for adjuvant therapy for breast cancer.
• 2000 - TNKase (tenecteplase) - "Clot-busting" drug to treat acute myocardial infarction.
• 2003 - Xolair (omalizumab) - Subcutaneous injection for moderate to severe persistent asthma.
• 2003 - Raptiva (efalizumab) - Antibody designed to block the activation and reactivation of T cells that lead to the development of psoriasis. Developed in partnership with XOMA
• 2004 - Avastin (bevacizumab) - Anti-VEGF monoclonal antibody for the treatment of metastatic cancer of the colon or rectum.
• 2004 - Tarceva (erlotinib) - Treatment for patients with locally advanced or metastatic non-small cell lung cancer, and pancreatic cancer.
• 2006 - Lucentis (ranibizumab injection) - The U.S. Food and Drug Administration (FDA) has approved LUCENTIS(TM) (ranibizumab injection) for the treatment of neovascular (wet) age-related macular degeneration (AMD). The FDA approved LUCENTIS after a Priority Review (six-month). Genentech started shipping product on June 30, 2006, the day the product was approved.

"

"Genentech markets itself as a research-driven corporation that follows the science to make new innovations. They employ more than 700 scientists and cover a wide range of scientific activity - from molecular biology to protein chemistry to bioinformatics and physiology. Genentech scientists in these various areas of expertise currently focus their efforts on three disease categories: Oncology, Immunology, and Tissue Growth and Repair. Genentech recent hiring and acquisitions indicate an intent to expand into Microbiology and Neuroscience divisions. Genentech research facilities are located only on the South San Francisco campus" - Wikipedia.

I think Genentech's research and projects will continue to make very nice progress. Genentech is OBVIOUSLY recognized by many researchers and scientists. Genentech was named Top Employer by Science Magazine on October 15, 2007. Also in October 2007, Genentech was named Most Admired Biotech Company as well as most admired Pharmaceutical company in Fortune in 2008.

Genentech seems like a very interesting business, but personally, I wouldn't enter a profession that works in the area of sciences. Science is bearable for me, but it is very hard for me to understandand to pickup... therefore frustrating for myself.
http://www.gene.com/gene/index.jsp?p=genentech&fr=fptb-&toggle=1&cop=mss&ei=UTF-8
http://topics.nytimes.com/top/news/business/companies/genentech_inc/index.html?inline=nyt-org

Sheep Eye Dissection

I learned from sheep eye dissection was the stump of the optic nerve to the left, and the cornea to the right . The sclera is the tough, outer coat of the eyeball, which helps keep the shape of the eye,and protect it from injury.The pinkish parts around the sclera are the remnants of extrinsic muscles, which have been cut off. These muscles move the eyeball in its socket from left to right, up and down , and a little bit of rotation. The back of the eyeball, seen from inside, shows the retina as a translucent greenish membrane, with wrinkles in it. Although some of the wrinkles formed from taking the eye apart, many of them are the remains of blood vessels, which supply the retina with nutrients and oxygen.
The point where all these blood vessels, and also all the nerves of the retina, gather together to leave the eye and become the optic nerve, is the blind spot. There is no room for any light receptors in the blind spot, because of all the nerves and blood vessels here.
A tiny bit of black choroid is exposed at the bottom of the eyeball. The rest of the choroid can only be seen through the veil of the retina.
The black part of the choroid blocks and absorbs light, preventing light from bouncing around in the eye, and washing out the image. It also prevents bright light from coming through the sclera from outside.
Because sheep have to watch out for predators, such as wolves, which might attack when it is getting dark, they have a band of very reflective choroid, called the tapetum lucidum, across the middle of the eyeball, from left to right. The tapetum makes the retina in front of it twice is sensitive to light, by bouncing back light rays which may have missed a light-sensitive cell, and giving them a second chance to be picked up. Behind the retina here, the tape tum lucidum may be silvery, pearly white, or a beautiful iridescent blue when exposed.
The blind spot is not visible, but its approximate position can be guessed at by following the direction of the optic nerve.
The blind spot is never located over the tape tum, as this is the zone where sensitive vision is needed for sheep to see danger coming. Humans do not have a tape tum. Instead, in the human eye, a small central area in each eye, called the fovea, is packed with colour-sensitive cells called cones. This gives us sharp, full-colour vision in the centre of our visual field. Sheep do not see colour, and do not have a fovea.
Sheep do not have a round pupil like humans. Instead of varying from a small circular opening in bright light, to a large circular opening in dim light, the sheep's pupil remains wide, and only varies in height. In bright light, the pupil may have a peanut-like shape. As the light becomes dimmer, the sheep's pupil will chance to an oval shape, then finally to a full circle. This gives the sheep wide-angle vision, to scan the horizon for predators without moving its head.
The iris is made of muscles, which change the size (and shape, in sheep) of the pupil. Pigment such as melanin in the iris prevents light from entering the eye, except through the pupil.The ciliary muscle (or ciliary body) surrounds the edge of the lens, and causes the lens to change in thickness, to focus on near or far-away objects.The lens is clear and transparent as crystal in a living eye, but the preservative changes it to a cloudy orange color, almost opaque to light. In life, it is flexible, and able to change shape to focus. In preserved eyes, it becomes hard and rigid.

en.wikipedia.org/wiki/Eye/
http://retina.anatomy.upenn.edu/~lance/eye/eye.html
http://www.macula.org/anatomy/eyeframe.html

Lagomorpha

Domain: eukaryote
Kingdom: Animalia
Phylum: Chordata
Kingdom: Animalia
Phylum: Chordata
Subphylum: Vertebrata
Class: Mammalia
order: Lagomorpha

habitat: rabbit are ground dwellers that live in environments ranging from desert to tropical forest and wetland. Their natural geographic range encompasses the middle latitude of the Western hemisphere.In the eastern hemisphere rabbits are found in Europe, portions of Central and southern Africa, the Indian subcontinent, Sumatra, and Japan.

predators : foxs , humans, and bears


prey:Rabbit are herbivores who feed by grazing on grass, and leafy weeds.In addition , their diet contains large amounts of cellulose, which is hard to digest. Rabbits solve this problem by passing two distinctive types of feces;hard dropping and soft black viscous pellets, the latter of which are immendicately eaten.

Anatomy: The long ears of rabbits are most likely an adaptation for detecting predators. In addition to their prominent ears, which can measure up to 6 cm ( more than 2 inches) long, rabbit have long, powerful hind legs and a short tail.

other information: they soon spread to both countries and multiplied so rapidly that rabbit control became a serious problem. In Australia a virus deadly only to true rabbits was developed, and in 1951 decimation of the rabbit population began through the artificial promotion of this virus infection , known as myxomatosis.

evolution

Later week a lady from National Center for science education came to speak on evidence of evolution. She told everybody about evolution,and what is evolution ? She said'' evolution is a change in the inherited traits of a population from one generation to the next.''Then she talk about
domestication of plants and animals. Then she talk about genetic engineering,and selectable such as antibiotic genes being used to manipulate DNA in molecular biology.
Another thing she talk about was genetic drift arises from the role chance

scientists discover new role for miRNA in ieukemia

The article about scientists here have found that mini- molecules called micro RNA may play a critical role in the progression of chronic myelitis leukemia from its more treatable chronic phase to a life-threatening phase, called blast crisis. They discovered an entirely new function for these molecules. The researchers show that micro RNAs can sometimes directly control a protein's function -not just whether or not the protein is made by the cell , as has been believed.Another thing study using cells from (CML) patients in blast crisis, suggest that certain progenitor white blood cells are kept from maturing when levels of one micro RNA, called miR-328. the finding are presented at 2007 annual meeting of the American society of hematology." say Principal investigator Danilo Perrotti, assistant professor of molecular virology, immunology and medical genetics and a researcher with the Ohio state university comprehensive cancer center.In case , a micro RNA called MIR-328 binds with a protein that, in phase CML, prevent imature blood cells from maturing. The MIR- 328 acts as a decoy molecule that normally ties up the protein.My feelling would be excellent aout scientists discover new role for miRNA in ieukemia