I haven’t had a chance to write for a few years as I’ve been creating a truly groundbreaking company that preserves the sacred relationship between the physician and the patient. During these 2 years we’ve learned many lessons, none greater than the ones taught by my business partners. We are the first mobile company to facilitate housecall visits between patients and doctors utilizing technology. We are currently working with hospitals and healthcare systems to bring back the timeless housecall visit. Looking forward to continuing my journey with you!
June 25, 2015
June 24, 2013
Modern medicine is once again turning to nanotechnology to help our bodies help themselves. A new device comprised of nanoparticles monitors blood sugar levels and releases insulin when sugar levels get too high. It has already been shown to work in mice. If it does the same for humans, keeping people with type 1 diabetes healthy could be a simple matter of swallowing a pill.
It is comprised of a network of nanoparticles that releases insulin into the blood in response to changes in blood glucose levels. Each of the nanoparticles have a core of insulin, a charged molecular chain called dextran and the enzyme glucose oxidase. When blood glucose levels are high, glucose oxidase breaks the sugar down into gluconic acid, which then breaks down the dextran chains to release insulin. The gluconic acid and dextran are broken down by the body and the released insulin returns blood sugar levels back to normal. The degradable nano-network was shown to work in mice where a single injection kept blood glucose levels normal for a minimum of 10 days.
BY CHRISTOPHER VAUGHAN - Building on previous research showing that cancer cells send signals to the immune system to avoid being attacked, Stanford scientists have engineered new molecules that are highly proficient at neutralizing those signals.
The molecules dramatically increase the effectiveness of certain existingcancer therapies and may open up other avenues for treating cancerusing ' own immune systems.
School of Medicine researchers have previously shown that CD47, a molecule found on the surface of many , acts as a "don't eat me" signal that protects the cancer from roving immune cells called macrophages. The scientists found that when they used drugs to block this "don't eat me" signal, macrophages engulfed and destroyed the cancer cells.
More recently, Stanford scientists wondered if they could engineer molecules that block the signal more effectively. They began by modifying a protein called SIRP-alpha, which is found on macrophages and is the natural receptor for CD47. In a paper published online May 30 in Science, a team of scientists working with professors Christopher Garcia, PhD, and Irving Weissman, MD, report that they have engineered new versions of SIRP-alpha that bind much more strongly to CD47 than the natural version of the molecule, making them extremely potent blockers of the "don't eat me" signal.
Two MD/PhD students in the Stanford Medical Scientist Training Program — Kipp Weiskopf, MPhil, and Aaron Ring, MS — devised the strategy for engineering these new molecules and were lead authors of the Science paper.
"This is the best example of how science and medical can lead to discovery and medical translation," said Weissman, professor of pathology and of developmental biology. "Weiskopf and Ring fleshed out the ideas that led to this project, bringing the complementary expertise of our groups together."
The engineered SIRP-alpha variants bind approximately 50,000 times more strongly to CD47 than native SIRP-alpha, making them highly potent drugs, Weiskopf said. But the researchers found blocking the CD47 "don't eat me" signal is not, by itself, enough to stimulate macrophages to attackcancer cells. Instead, the group demonstrated that blocking CD47 boosts the activity of macrophages when a second "eat me" signal is provided. This signal can be provided by certain anti-cancer antibody therapeutics, many of which are already approved by the FDA and in use clinically.
These findings have tremendous therapeutic implications, Ring said, because the high-affinity SIRP-alpha molecules could selectively boost the destruction of cancer cells by these antibody therapies, without increasing toxic such as the destruction of healthy, non-cancerous cells.
The authors found that their engineered SIRP-alpha molecules would enhance a number of widely used antibody therapies such as rituximab (which targets certain lymphomas and leukemias), trastuzumab (which targets certain kinds of breastcancer) and cetuximab (which targets certain kinds of head and neck cancer and colon cancer).
When physicians used an anti-cancer antibody like these to fight cancer, the antibody's "eat me" signal to the macrophage is fighting against the cancer's "don't eat me" signal coming from the CD47, the researchers explain. When the high-affinity SIRP-alpha binds tightly to the CD47 molecules on the cancer, it takes the brakes off the macrophage attack on the cancercells.
"When physicians use an anti-cancer antibody like trastuzumab to fight breast cancer, the 'don't eat me signal' from CD47 on the cancer limits the effectiveness of the antibody," said Ring. "Potentially, any anti-cancer antibody that stimulates immune cells could benefit from this combination therapy."
In one experiment, when either rituximab or the high-affinity SIRP-alpha variants were used by themselves on mice with human lymphomas, they were only able to slow tumor growth. However, when the two therapies were combined, researchers found they were able to eliminate the tumors completely. "Antibodies are like guided missiles in terms of targeting cancercells," Weiskopf said. "By combining them with the high-affinity SIRP-alpha variants, you are adding high-explosive warheads to those missiles ."
The researchers hope that their work with high-affinity SIRP-alpha molecules will lead to more effective targeted-cancertherapies in the clinic. "This work further validates the strategy of targeting CD47 to enhance macrophage attack of cancer," according to Weissman. "This strategy must still be tested in humans to evaluate safety, but anti-CD47 antibodies are on schedule for the first trials in patients next year."
Other authors of the paper include graduate student Chia Chi M. Ho; instructor Jens-Peter Volkmer, MD; former postdoctoral scholar Aron Levin, PhD; postdoctoral scholars Anne Kathrin Volkmer, MD, Engin Özkan, PhD, and Nathaniel Fernhoff, PhD; and Matt van de Rijn, MD, PhD, professor of pathology.
This work was supported by the National Cancer Institute, theNational Institute of Diabetes and Digestive and Kidney Diseases, the Stanford Medical Scientist Training Program, the School of Medicine's SPARK program, the Deutsche Forschungsgemeinschaft, the Joseph & Laurie Lacob Gynecologic/Ovarian Cancer , the Virginia and D.K. Ludwig Fund for Cancer Research and the Howard Hughes Medical Institute.
SolarScan, a device to detect skin cancer, is demonstrated at its launch in Sydney May 7, 2002. The SolarScan works by capturing an image of a patient's skin spot and then an image analsis software compares the features against images of melanomas and non-melanomas in a database. Melanoma is the most common form of cancer in men and women aged 15-44 and is the most deadly form of skin cancer. Credit:Reuters
Responsible for more than 75 percent of skin cancer deaths, melanoma is a cancer of the skin, which affects the melanocytes (pigment carrying cells of the body). A new study now suggests that this dangerous cancer may be easily detectable - by odors from skin cells.
The study, carried out by a team of researchers from the Monell Center revealed two new ways to help early detection of skin cancer- by odors emitted by human skin, and by using a nanotechnology-based sensor that could differentiate between normal skin cells and melanoma skin cells.
"There is a potential wealth of information waiting to be extracted from examination of VOCs associated with various diseases, including cancers, genetic disorders, and viral or bacterial infections," senior author George Preti, PhD and an organic chemist at Monell, noted.The researchers took into consideration the fact that human skin produces a number of airborne chemical molecules, also known as volatile organic compounds (VOCs), many of which emit odor too, and put it to use as an early melanoma detection tool.
For this study, the researchers made use of sophisticated analytical and sampling techniques that helped detect VOCs emitted from melanoma skin cells at different levels of progression of the disease. They also sampled VOCs emitted from normal skin cells by using an absorbent device. Analysis of these VOCs was done using mass spectrometry and gas chromatography techniques.
To translate the results obtained from the VOC analysis into a diagnostic analysis, a reliable and portable sensor would be required, to which, the researchers used a nano-sensor.
The nano-sensor was made up of two nano-sized tubes that were coated with strands of DNA. The use of DNA as a sensor could be clarified by the fact that DNA tend to act as a wonderful sensor, which makes identification of the target easy. The results so obtained revealed a stunning fact- human skin cells emit odor different from that of melanoma skin cells; a new early diagnostic tool which may help cut down death rates due to melanoma considerably.
"This study demonstrates the usefulness of examining VOCs from diseases for rapid and noninvasive diagnostic purposes," Preti said. "The methodology should also allow us to differentiate stages of the disease process."
The study is now published in the Journal of Chromatography B.
(Nanowerk Spotlight) Despite significant advances in the medical/surgical management of severe thermal injury, wound infection and subsequent sepsis persist as frequent causes of morbidity and mortality for burn victims not only due to the extensive compromise of the protective barrier against microbial invasion, but also as a result of growing pathogen resistance to our therapeutic options.Burn wounds are further complicated by injury induced suppression of the immune system, further facilitating localized colonization and systemic entry of microbes from both endogenous and exogenous origins. Candida yeast species represent a prevalent threat to these patients, many variants demonstrating resistance to first line systemic antifungal treatments as these medications are not directly toxic, but instead inhibit yeast growth through a single mechanism of action.Therefore, innovative therapies are urgently needed that overcome mechanisms of pathogen resistance, and are easily administered without concerning systemic side effects.Nanoparticles represent a practical platform through which both established drugs and novel agents can be encapsulated and delivered more effectively or via new routes to target and reach pathogen cells/machinery with greater success then their macromolecular counterparts.In a paper published in the June 14, 2013 online edition of Nanomedicine: Nanotechnology, Biology and Medicine ("Amphotericin B releasing nanoparticle topical treatment of Candida spp. in the setting of a burn wound") we demonstrated that encapsulating Amphotericin B, a intravenously administered potent fungicidal polyene macrolide, in nanoparticles increased its killing impact against numerous candida species, was more effective at preventing candidal biofilm formation, and cleared a mouse burn model infected with candida more effectively than solubilized amphotericin.Images were taken on day 9 after infection. a) is topically applied solubilized Amphotericin B and b) Amphotericin B nanoparticle applied. (Images: Dr. Friedman, Montefiore - Albert Einstein College of Medicine)Materials at the nanoscale have a greater likelihood of interacting with their desired target, here, the cell wall, and therefore the payloads have greater efficacy. Furthermore, the nanoparticles themselves can physically damage pathogen structures and prevent cell-to-cell communication and sharing of resources, offering synergists but different antifungal properties.Encapsulating amphotericin in nanoparticles not only made it more effective, but also allowed for it to be directly and topically applied to a wound – an option not currently available. Systemic delivery, while very effective, comes at a great cost as amphotericin has multiple well established side effects and toxicities associated with its use.Our team here at Einstein represents a broad range of expertise calling from multiple departments including medicine (infectious diseases, dermatology), physiology and biophysics, and immunology and microbiology, highlighting the multidisciplinary nature of nanotechnology research. Other authors included David Sanchez; David Schairer; Chaim Tuckman-Vernon; Jason Chouake; Allison Kutner; Joy Makdisi; Joel Friedman; and Joshua d Nosanchuk.By Dr. Adam Friedman, Assistant Professor of Medicine (Dermatology)/ Physiology and Biophysics, and Director of Dermatologic Research at Montefiore Medical Center - Albert Einstein College of Medicine.
Read more: http://www.nanowerk.com/spotlight/spotid=30997.php#ixzz2X9QjwHzd
Read more: http://www.nanowerk.com/spotlight/spotid=30997.php#ixzz2X9QjwHzd
April 12, 2013
April 10, 2013
A single drug can shrink or cure human breast, ovary, colon, bladder, brain, liver, and prostate tumors that have been transplanted into mice, researchers have found. The treatment, an antibody that blocks a "do not eat" signal normally displayed on tumor cells, coaxes the immune system to destroy the cancer cells.
A decade ago, biologist Irving Weissman of the Stanford University School of Medicine in Palo Alto, California, discovered that leukemia cells produce higher levels of a protein called CD47 than do healthy cells. CD47, he and other scientists found, is also displayed on healthy blood cells; it's a marker that blocks the immune system from destroying them as they circulate. Cancers take advantage of this flag to trick the immune system into ignoring them. In the past few years, Weissman's lab showed that blocking CD47 with an antibody cured some cases of lymphomas and leukemias in mice by stimulating the immune system to recognize the cancer cells as invaders. Now, he and colleagues have shown that the CD47-blocking antibody may have a far wider impact than just blood cancers.
"What we've shown is that CD47 isn't just important on leukemias and lymphomas," says Weissman. "It's on every single human primary tumor that we tested." Moreover, Weissman's lab found that cancer cells always had higher levels of CD47 than did healthy cells. How much CD47 a tumor made could predict the survival odds of a patient.
To determine whether blocking CD47 was beneficial, the scientists exposed tumor cells to macrophages, a type of immune cell, and anti-CD47 molecules in petri dishes. Without the drug, the macrophages ignored the cancerous cells. But when the anti-CD47 was present, the macrophages engulfed and destroyed cancer cells from all tumor types.
Next, the team transplanted human tumors into the feet of mice, where tumors can be easily monitored. When they treated the rodents with anti-CD47, the tumors shrank and did not spread to the rest of the body. In mice given human bladder cancer tumors, for example, 10 of 10 untreated mice had cancer that spread to their lymph nodes. Only one of 10 mice treated with anti-CD47 had a lymph node with signs of cancer. Moreover, the implanted tumor often got smaller after treatment—colon cancers transplanted into the mice shrank to less than one-third of their original size, on average. And in five mice with breast cancer tumors, anti-CD47 eliminated all signs of the cancer cells, and the animals remained cancer-free 4 months after the treatment stopped.
"We showed that even after the tumor has taken hold, the antibody can either cure the tumor or slow its growth and prevent metastasis," says Weissman.
Although macrophages also attacked blood cells expressing CD47 when mice were given the antibody, the researchers found that the decrease in blood cells was short-lived; the animals turned up production of new blood cells to replace those they lost from the treatment, the team reports online today in the Proceedings of the National Academy of Sciences.
Cancer researcher Tyler Jacks of the Massachusetts Institute of Technology in Cambridge says that although the new study is promising, more research is needed to see whether the results hold true in humans. "The microenvironment of a real tumor is quite a bit more complicated than the microenvironment of a transplanted tumor," he notes, "and it's possible that a real tumor has additional immune suppressing effects."
Another important question, Jacks says, is how CD47 antibodies would complement existing treatments. "In what ways might they work together and in what ways might they be antagonistic?" Using anti-CD47 in addition to chemotherapy, for example, could be counterproductive if the stress from chemotherapy causes normal cells to produce more CD47 than usual.
Weissman's team has received a $20 million grant from the California Institute for Regenerative Medicine to move the findings from mouse studies to human safety tests. "We have enough data already," says Weissman, "that I can say I'm confident that this will move to phase I human trials."
*Correction, 2 April 2013: One reference to the compound used to treat mice was previously named as CD47, but in all cases was the antibody to that protein, anti-CD47.