External carotid artery branches

Sister Lucy's Powderd Face Attracts Silly Medicos

S :Superior thyriod
L :Lingual
P :post. auricular
F :Facial
O :Occipital
A :Ascendng pharyngeal
            ends as
S :Superior temporal
M :Maxillary

Not only humans,even bacteria gets addicted to caffeine

Caffeine-'Addicted' Bacteria: Finding May Lead to New Decontamination Methods, New Medicines

  — Some people may joke about living on caffeine, but scientists now have genetically engineered E. coli bacteria to do that -- literally. Their report in the journal ACS Synthetic Biology describes bacteria being "addicted" to caffeine in a way that promises practical uses ranging from decontamination of wastewater to bioproduction of medications for asthma.

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Genetically engineered bacteria are “addicted” to caffeine in a way that promises practical uses ranging from decontamination of wastewater to bioproduction of medications for asthma. (Credit: © volff / Fotolia)

Jeffrey E. Barrick and colleagues note that caffeine and related chemical compounds have become important water pollutants due to widespread use in coffee, soda pop, tea, energy drinks, chocolate and certain medications. These include prescription drugs for asthma and other lung diseases. The scientists knew that a natural soil bacterium, Pseudomonas putida CBB5, can actually live solely on caffeine and could be used to clean up such environmental contamination. So they set out to transfer genetic gear for metabolizing, or breaking down, caffeine from P. putida into that old workhorse of biotechnology, E. coli, which is easy to handle and grow.
The study reports their success in doing so, as well as use of the E. coli for decaffeination and measuring the caffeine content of beverages. It describes development of a synthetic packet of genes for breaking down caffeine and related compounds that can be moved easily to other microbes. When engineered into certain E. coli, the result was bacteria literally addicted to caffeine. The genetic packet could have applications beyond environmental remediation, the scientists say, citing potential use as a sensor to measure caffeine levels in beverages, in recovery of nutrient-rich byproducts of coffee processing and for the cost-effective bioproduction of medicines.
The author and co-authors acknowledge financial support from the University of Texas at Austin and the University of Iowa

PORPHYRIAS: ACUTE INTERMITTNT PORPHYRIA SYNDROME

5 P'S

P: Pain in abdomen
P:Polyneuropathy
P:Psychological abnormalities
P:Pink urine
P:precipitatd by drugs(eg.barbiturates, oc pills,sulpha drugs)

AXILLARY ARTERY BRANCHES                                            

Send The Lord to Say A Prayer

S-superior thoracic
T-thoracoacromial
S-subscapular
A-anterior circumflex humeral
P-posterior circumflex humeral
 

Artificial Spleen to Treat Bloodstream Infections: Sepsis Therapeutic Device Under Development

Mar. 30, 2013 — The Wyss Institute for Biologically Inspired Engineering at Harvard University announced today that it was awarded a $9.25 million contract from the Defense Advanced Research Projects Agency (DARPA) to further advance a blood-cleansing technology developed at the Institute with prior DARPA support, and help accelerate its translation to humans as a new type of sepsis therapy.

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The Spleen-on-a-chip, developed at the Wyss Institute, will be used to treat bloodstream infections that are the leading cause of death in critically ill patients and soldiers injured in combat. (Credit: Wyss Institute)

The device will be used to treat bloodstream infections that are the leading cause of death in critically ill patients and soldiers injured in combat.
To rapidly cleanse the blood of pathogens, the patient's blood is mixed with magnetic nanobeads coated with a genetically engineered version of a human blood 'opsonin' protein that binds to a wide variety of bacteria, fungi, viruses, parasites, and toxins. It is then flowed through microchannels in the device where magnetic forces pull out the bead-bound pathogens without removing human blood cells, proteins, fluids, or electrolytes -- much like a human spleen does. The cleansed blood then flows back to the patient.
"In just a few years we have been able to develop a suite of new technologies, and to integrate them to create a powerful new device that could potentially transform the way we treat sepsis," said Wyss founding director and project leader, Don Ingber, M.D., Ph.D. "The continued support from DARPA enables us to advance our device manufacturing capabilities and to obtain validation in large animal models, which is precisely what is required to enable this technology to be moved towards testing in humans."
The team will work to develop manufacturing and integration strategies for its core pathogen-binding opsonin and Spleen-on-a-Chip fluidic separation technologies, as well as a novel coating technology called "SLIPS," which is a super-hydrophobic coating inspired from the slippery surface of a pitcher plant that repels nearly any material it contacts. By coating the inner surface of the channels of the device with SLIPS, blood cleansing can be carried out without the need for anticoagulants to prevent blood clotting.
In addition to Ingber, the multidisciplinary team behind this effort includes Wyss core faculty and Harvard School of Engineering and Applied Science faculty member Joanna Aizenberg, Ph.D., who developed the SLIPS technology; Wyss senior staff member Michael Super, Ph.D., who engineered the human opsonin protein; and Mark Puder, M.D., Ph.D., Associate Professor of Pediatric Surgery at Boston Children's Hospital and Harvard Medical School who will be assisting with animal studies.                                                                                   courtesy:science daily

mnemonic

ABDOMINAL MUSCLES: TIRE
    T : Transversus abdominis
    I : Internal abdominal oblique
    R : Rectus abdominis
    E : External abdominal oblique

Fat stem cells to treat brain cancer.......

Using Fat to Fight Brain Cancer: Stem Cells from Human Adipose Tissue Used to Chase Migrating Cancer Cells

Mar. 12, 2013 — In laboratory studies, Johns Hopkins researchers say they have found that stem cells from a patient's own fat may have the potential to deliver new treatments directly into the brain after the surgical removal of a glioblastoma, the most common and aggressive form of brain tumor.

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The investigators say so-called mesenchymal stem cells (MSCs) have an unexplained ability to seek out damaged cells, such as those involved in cancer, and may provide clinicians a new tool for accessing difficult-to-reach parts of the brain where cancer cells can hide and proliferate anew. The researchers say harvesting MSCs from fat is less invasive and less expensive than getting them from bone marrow, a more commonly studied method.

Results of the Johns Hopkins proof-of-principle study are described online in the journal PLOS ONE.

"The biggest challenge in brain cancer is the migration of cancer cells. Even when we remove the tumor, some of the cells have already slipped away and are causing damage somewhere else," says study leader Alfredo Quinones-Hinojosa, M.D., a professor of neurosurgery, oncology and neuroscience at the Johns Hopkins University School of Medicine. "Building off our findings, we may be able to find a way to arm a patient's own healthy cells with the treatment needed to chase down those cancer cells and destroy them. It's truly personalized medicine."

For their test-tube experiments, Quinones-Hinojosa and his colleagues bought human MSCs derived from both fat and bone marrow, and also isolated and grew their own stem cell lines from fat removed from two patients. Comparing the three cell lines, they discovered that all proliferated, migrated, stayed alive and kept their potential as stem cells equally well.

This was an important finding, Quinones-Hinojosa says, because it suggests that a patient's own fat cells might work as well as any to create cancer-fighting cells. The MSCs, with their ability to home in on cancer cells, might be able to act as a delivery mechanism, bringing drugs, nanoparticles or some other treatment directly to the cells. Quinones-Hinojosa cautions that while further studies are under way, it will be years before human trials of MSC delivery systems can begin.

Ideally, he says, if MSCs work, a patient with a glioblastoma would have some adipose tissue (fat) removed -- from any number of locations in the body -- a short time before surgery. The MSCs in the fat would be drawn out and manipulated in the lab to carry drugs or other treatments. Then, after surgeons removed the brain tumor, they could deposit these treatment-armed cells into the brain in the hopes that they would seek out and destroy the cancer cells.

Currently, standard treatments for glioblastoma are chemotherapy, radiation and surgery, but even a combination of all three rarely leads to more than 18 months of survival after diagnosis. Glioblastoma tumor cells are particularly nimble, migrating across the entire brain and establishing new tumors. This migratory capability is thought to be a key reason for the low cure rate of this tumor type.

"Essentially these MSCs are like a 'smart' device that can track cancer cells," Quinones-Hinojosa says.

Quinones-Hinojosa says it's unclear why MSCs are attracted to glioblastoma cells, but they appear to have a natural affinity for sites of damage in the body, such as a wound. MSCs, whether derived from bone marrow or fat, have been studied in animal models to treat trauma, Parkinson's disease, ALS and other diseases.
                                      courtesy:science daily
                            

A NEW WINDOW TO APPROACH RHEUMATOID ARTHRITIS

Rheumatoid Arthritis Prevented in Mice: Infusions of Regulatory T Cells Turn Off Autoimmune Attack On Joints

Feb. 8, 2013 — Dana-Farber Cancer Institute scientists have demonstrated a new strategy for treating autoimmune disease that successfully blocked the development of rheumatoid arthritis in a mouse model. They say it holds promise for improved treatment of arthritis and other autoimmune disorders in people.

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The scientists report in the Journal of Clinical Investigation that infusing a highly specific type of cell that regulates immune responses into arthritis-prone mice shuts down the cascade of inflammation that damages tissues and joints.

The method worked best when the infusions of CD8⁺ Treg cells were given at the same time that the animals were injected with a protein that triggered the arthritis-causing autoimmune reaction. "We found we could almost completely inhibit the disease in this setting," said Harvey Cantor, MD, chair of the Department of Cancer Immunology and AIDS at Dana-Farber and the study's senior author.

Even when administered weeks after the disease was initiated, CD8⁺ Treg infusions combined with low doses of methotrexate -- a commonly used drug for rheumatoid arthritis -- were able to significantly slow the arthritis process, the scientists reported.

The new strategy also blocked disease progression when the scientists injected peptide antigens to expand the rodents' own pool of CD8⁺ Tregs, rather than infusing them from outside. Overall, the results "suggest that [these] strategies represent a promising therapeutic approach to autoimmune disorders," the researchers wrote.

The human immune system is a network of cells, tissues, and organs that, when functioning normally, attacks and destroys infections, viruses, parasites, and other foreign "invaders."

In autoimmune disorders, however, parts of the immune system attack the individual's own healthy cells and tissues -- the result of the immune forces failing to recognize "self" identifying tags on the body's cells.

An estimated 50 million Americans suffer from autoimmune disorders, which include rheumatoid arthritis, lupus, type 1 diabetes, multiple sclerosis, and celiac disease. At least 100 different autoimmune diseases have been identified, and are more common among women. The incidence of these diseases is rising in the United States for unknown reasons.

Rheumatoid arthritis is caused by inflammation throughout the body, attacking many tissues, especially the joints, frequently causing painful and deformed fingers and hands. About 1.5 million Americans are afflicted with rheumatoid arthritis. Drugs of several types, including corticosteroids, are given to reduce inflammation and slow the disease. The newest treatments are biologic agents, which block secreted chemicals called cytokines that carry out the misguided attacks. However, even with these agents -- which can have serious side effects -- rheumatoid arthritis treatment is often not optimal, said Cantor.

In contrast to these "downstream" players in the complex autoimmune cascade, the strategy described in the new report is aimed "upstream," where the attacks begin with overactive immune fighters, called T follicular helper cells, that mistakenly respond to "self" markers on healthy cells. These T cells can become chronically overactivated, spurring a continuous attack by antibodies on the body's tissues.

"Current treatment strategies that inhibit cytokines, such as TNF or IL-1 production, spare the upstream initiating events that continuously induce new effector T cells and cytokine secretion," noted Cantor. "We believe that targeting the CD4 T cells that initiate this cascade may be a more effective approach to rheumatoid arthritis therapy."

T regulatory cells, or Tregs, play an important role in turning off an immune response when it's no longer needed, such as after the body has repelled viral or bacterial invaders. Cantor previously found that certain Tregs, known as CD8⁺ Tregs, can recognize and eliminate overactive CD4 T helper cells that display a marker called Qa-1 in mice; the human equivalent is HLA-E.

In the new experiments, Cantor's team showed that these Qa-1-recognizing CD8⁺ Tregs could be recruited to kill off the subset of the harmful T helper cells causing arthritis "and exert strong inhibitory effects on disease progression." They found that CD8⁺ Tregs that recognized an Hsp60 molecule on the Qa-1 T helper cells were the most effective in eliminating the overreacting T cells. The researchers showed that administering the Hsp60 antigen to the mice triggered expansion of the CD8⁺ Tregs already present in the animals and slowed or stopped disease development.

Moving closer to clinical relevance, the researchers will test this approach in mice carrying human immune cells that provoke an autoimmune response.

Cantor said they are also studying the possibility of using nanoparticles coated with Qa-1/Hsp60 molecules to expand CD8⁺ Tregs as a more practical method that might be used someday for human therapeutic tests.

First author of the paper is Jianmei W. Leavenworth, PhD, of the Cantor laboratory.