CDC: New H1N1 Strain H3N2 Infected Two Children In Recent Months

The US Centers for Disease Control and Prevention (CDC) have made a startling announcement this week. Two children previously vaccinated for the H1N1 influenza virus have contracted a new strain named H3N2 in what is being...[read article]

Women Undergoing C-Sections Should Have Inflatable Compression Devices Fitted - ACOG Recommends

Women Undergoing C-Sections Should Have Inflatable Compression Devices Fitted - ACOG Recommends
Written by Christian NordqvistWomen undergoing a C-section (cesarean delivery) should have inflatable compression devices fitted to reduce the risk of blood clots, a leading cause of maternal mortality in the USA, says the American College of...[read article]

Medical Breakthrough For Heart Repair

In a medical breakthrough a man’s heart was saved through the use of a breakthrough medical technology. The man, John Christy, is the first person in the United States to undergo this procedure. The new procedure utilizes stem cells in helping repair the arteries all throughout a person’s body.Christy was suffering from coronary artery disease at a very advanced stage. What was done to him was to insert his own specific stem cells into his body during a CABG surgery. The stem cells are used to grow new blood vessels in the heart. This is a revolutionary procedure that can save millions of lives when it is further developed and become widely available.

Dengue fever
Causes, incidence, and risk factors
Dengue fever is caused by one of four different but related viruses. It is spread by the bite of mosquitoes, most commonly the mosquito Aedes aegypti, which is found in tropic and subtropic regions. This includes parts of:
Indonesian archipelago into northeastern Australia
South and Central America
Southeast Asia
Sub-Saharan Africa
Dengue fever is being seen more in world travelers.
Dengue fever should not be confused with Dengue hemorrhagic fever, which is a separate disease that is caused by the same type of virus but has much more severe symptoms.
Symptoms
Dengue fever begins with a sudden high fever, often as high as 104 - 105 degrees Fahrenheit.
A flat, red rash may appear over most of the body 2 - 5 days after the fever starts. A second rash, which looks like the measles, appears later in the disease. Infected people may have increased skin sensitivity and are very uncomfortable.
Other symptoms include:
Headache (especially behind the eyes)
Fatigue
Joint aches
Muscle aches
Nausea
Swollen lymph nodes
Vomiting
Signs and tests
Tests that may be done to diagnose this condition include:
Antibody titer for dengue virus types
Complete blood count (CBC)
Serology studies to look for antibodies to dengue viruses
Treatment
There is no specific treatment for dengue fever. You will need fluids if there are signs of dehydration. Acetaminophen (Tylenol) is used to treat a high fever. Avoid taking aspirin.
Expectations (prognosis)
The condition generally lasts a week or more. Although uncomfortable, dengue fever is not deadly. People with the condition should fully recover.
Complications
Febrile convulsions
Severe dehydration
Calling your health care provider
Call your health care provider if you have traveled in an area where dengue fever is known to occur and have developed symptoms of the disease.
Prevention
Clothing, mosquito repellent, and netting can help reduce exposure to mosquitoes. Traveling during periods of minimal mosquito activity can also be helpful.
Mosquito abatement programs may reduce the risk of infection.

Dilon Technologies, Inc., the leader in molecular breast imaging, announced today that they have formed an alliance with Terason Ultrasound to offer a

BSGI is a molecular breast imaging technique that can see lesions independent of tissue density and discover very early stage cancers, particularly for women with high risk factors or that present with questionable mammograms. With BSGI, metabolic activity is assessed and cancerous cells generally display as "hot spots."

Terason is the innovator and world leader in integrating patented microsystem technology with an Apple MacBook Pro PC. The Terason t3000(TM) Ultrasound System offers premium imaging performance with the portability and functionality of a laptop. When used as a complement to the Dilon 6800 Gamma Camera, physicians are able to move from BSGI to ultrasound without leaving the exam room.

Bob Moussa, President and CEO of Dilon Technologies said, "We are proud to partner with Terason to complement BSGI with ultrasound when appropriate. Through innovative products and partnerships such as this, Dilon continues to expand its offerings to be the best in patient care and cancer detection."

The Terason t3000 offers best-in-class image quality; ease of use with a dual user interface; and an integrated information management and communications protocol in one system. For quick on-the-spot, accurate scanning in a wide array of clinical applications, transducers quickly connect to the system allowing technicians to perform an ultrasound exam at the point of patient care. Terason's patented high-density, beam-forming architecture provides a superior performance cost-effective ultrasound solution.

The ultrasound system is built upon an industry respected combination of the Apple PC coupled with Windows Operating System to provide seamless networking capabilities, compatibility with various applications, standard connections, and software updates. The system includes DICOM, Wireless, Integrated CD/DVD, and USB capability. The ergonomically designed slide out dual-user interface is extremely easy to use. The Terason t3000(TM) Ultrasound System is a powerful ultrasound designed to work smarter, enhance workflow, and promote efficiency and diagnostic confidence.

"BSGI has proven to be an important adjunct to mammography and ultrasound in the diagnosis of breast cancer. We are excited to be in a partnership with Dilon as we both continue to offer important advances in care," said Alice Chiang, Ph.D., Terason's CEO.

A rich and unexpected payoff

"The nature of these new genes is not obvious and we wouldn't have guessed their relationship to cancer if we hadn't followed this approach," says Lowe. "They may now allow us to make headway into poorly understood areas of cancer."

The newly identified tumor suppressor genes affect a wide array of cellular activities, including maintenance of cell structure, cellular metabolism, cell proliferation and control of the levels of various tumor growth-enhancing proteins in the cell's nucleus. In one instance, the team's strategy also uncovered not genes in isolation but an entire network of genes that go awry in liver cancer. "Given that the cancer puzzle involves multiple genes in various combinations, we need to find all the hits that make the cell tip over the edge," says Lowe, explaining one advantage of his team's broad strategy.

Some of the genes identified might also lead to new strategies for cancer therapy. For example, some of the newly discovered tumor suppressor genes "code" for proteins that are secreted, which indicates that their ability to prevent cancer is dependent on their presence outside the cell. Reversing the loss of such proteins - by replenishing their levels via injections - is an easier fix than having to correct a defect in the genome via gene therapy.

In other words, the CSHL team's new strategy now makes it possible to rapidly filter from genomic information those genes that specifically impact cancer development in living animals, and thus focus follow-up studies on those that might be most clinically useful.

Pinpointing Tumor Suppressor Genes

Tumor suppressors are a crucial component of intracellular signaling networks that protect against uncontrolled cell proliferation. The benefits of such genes can be lost when DNA undergoes alterations, including mutations or deletions of entire stretches of chromosomes. A highly efficient genome-sequencing technique developed several years ago in the Wigler laboratory has made it possible to scan the genome of cancerous cells for, among other things, deleted portions of chromosomes where tumor suppressors are likely to reside.

Dr. Powers performed a genomic analysis of human liver cancer samples that provided a basis for the work of the combined teams. Powers' lab scanned the genomes of liver cancers from more than 100 patients to compile a list of deletions of chromosomal regions. These regions were hypothesized to be the location of most of the missing tumor suppressor genes. A comparison of this list with the genome sequence of a normal human cell revealed the identity of approximately 300 genes within the deleted chromosomal segments.

Chromosomal deletions aren't limited to cancer-related genes alone; any number of "passenger" or unrelated neighboring genes can inadvertently also be lost. The team therefore had to pinpoint the tumor suppressors among the 300 genes. "Genomic analysis of human tumors is important," Powers observed," but combining it with functional screening in mouse models is a notable step forward."

The usual route of characterizing a gene's function is to mutate it in mouse embryos and then create lines of mice that can then be examined for the mutation's effects. Lowe's group bypassed this step, which is time-consuming, by engineering mutations into the genome of adult mouse cells and then re-injecting these cells into adult mice. The team used a method honed by Dr. Hannon of introducing stable mutations into mouse cells via RNA interference, or RNAi, a technique in which small RNA molecules are introduced into cells to shut off specific genes.

RNA sequences that corresponded to all the 300 or so deleted genes were obtained from an RNAi "library" compiled by the Hannon lab. Lowe's team introduced these RNAi tools (known as "short-hairpin RNAs, or shRNAs) into progenitor cells that develop into mature liver cells, albeit ones engineered to over-produce a cancer gene product called Myc.

In cells with these Myc mutations, an additional "trigger" such as the shutting off of a tumor suppressor gene via RNAi would be sufficient to cause cancer. The engineered cells that carried a Myc mutation and an shRNA were injected into mice. Dramatically, those that received cells in which a tumor suppressor gene had been "silenced" by an shRNA developed tumors within a month.

The scientists homed in on the identity of the silenced tumor suppressors by simply isolating and analyzing the genetic material from the tumors. Their strategy identified 13 new tumor suppressor genes, most of which had not been linked to cancer before.