#UVA fertilization discovery may lead to male contraceptive Groundbreaking new reproductive research has identified key molecular events that could be playing a critical role as sperm
In rare instances, the internal chemical response of a cell can cause unregulated cell growth, leading to cancer.
or proteins that could be targeted by drugs, eventually leading to new medicines to fight cancer r
Indigo-Clean#was unveiled just before the annual meeting of theassociation for Professionals in Infection Control and Epidemiology (APIC) in Nashville."
"It bolsters current disinfection efforts by infection preventionists and environmental services professionals in the fight against HAIS."
it is lethal to pathogens but is safe for use in the presence of patients and staff."
"Breaking the chain of infection, from an infected patient, to the environment, to new patient, is vitally important,
and developing HINS-light technology for the purpose of reducing the environmental transmission of pathogens
We chose Kenall because of its extensive experience in providing lighting for the most challenging healthcare environments where infection prevention is a key consideration."
"The Centers for Disease Control and Prevention (CDC) reports around 1 in 25 hospital patients in the US have at least one infection contracted in the health care setting.
This technology has led to the identification for the first time of pathological mutations in the RNASEH1 gene in six subjects from three unrelated families.
These alterations cause impaired energy production in the cells and therefore, lead to the disease. The clinical manifestations of affected individuals are chronic progressive external ophthalmoplegia (CPEO), a slowly progressive paralysis of the extraocular muscles,
and exercise intolerance in early adulthood, followed by cerebellar and brain stem atrophy and a general weakness of the muscles affecting locomotion,
The identification of a new mitochondrial disease gene not only provides valuable basic information about the biological function
but also widens out knowledge on the mechanisms leading to disease and provide the basis for developing new and more effective therapies s
#Gel that can make drugs last longer A drug-delivering hydrogel has been developed to treat chronic diseases such as hepatitis C a liver disease that kills around 500,000 people worldwide every year.
Researchers at the Institute of Bioengineering and Nanotechnology (IBN) of A*STAR have developed a drug-delivering hydrogel to treat chronic diseases such as hepatitis C a liver disease that kills around 500,000 people worldwide every year."
and well-being of patients suffering from chronic diseases such as hepatitis C,"said IBN Executive director Professor Jackie Y. Ying.
The standard treatment for chronic hepatitis C infections includes a weekly injection of a protein drug called PEGYLATED interferon.
"Our hydrogels can significantly extend the half-life of hepatitis C drugs by up to 10 times longer than current treatment.
Up to 150 million people globally suffer from chronic hepatitis C infections according to the World health organization.""I believe that our method can pave the way for more effective and safe treatment of hepatitis C. We are also testing the microstructured gel for the treatment of other chronic diseases besides hepatitis C,"added Dr Kurisawa.
Story Source: The above post is reprinted from materials provided by The Agency for Science, Technology and Research (A*STAR.
and responds specifically to remove non-self pathogens invading our body. T cells play a central role in the immune response to non-self pathogens.
The T-cell repertoire is shaped by"education"that occurs in the thymus. A huge number of immature T cells, each of which can recognize a single antigen,
which keeps potentially useful cells able to detect non-self pathogens alive, and negative selection,
and may provide clues to the development of therapies for infectious diseases, cancers and immune diseases.,"
#Discovery could lead to personalized colon cancer treatment approach A UNC Lineberger Comprehensive Cancer Center discovery of just how a certain tumor suppressor molecule works to prevent tumor growth could lead to a personalized treatment
the researchers reported that the tumor-suppressing protein AIM2, or Absent in Melanoma 2, helps prevent colon cancer by restricting a signaling molecule called Akt.
With this finding, the researchers believe theye found a possible drug target for colon cancer patients who lack the tumor suppressor AIM2. everal studies
and clinical evidence suggest AIM2 functions as a tumor suppressor, but until now, wee had very little direct evidence to explains how this occurs,
said Justin E. Wilson, Phd, the study first author and a postdoctoral fellow at UNC Lineberger,
the UNC School of medicine Department of Microbiology and Immunology and the Department of Genetics. e found that AIM2 inhibits tumorigenesis in multiple animal models of colorectal cancer by restricting the pro-survival signaling molecule, Akt,
which is commonly hyperactive in many human cancers. The study builds on previous findings suggesting that AIM2 limits cancer cell growth in colon cancer cell lines,
Distinguished Professor in the UNC School of medicine Department of Genetics and a UNC Lineberger Comprehensive Cancer Center member.
And in mouse models lacking AIM2, the researchers found that they had smaller tumors and precancerous colon polyps when blocked Akt.
Wilson said the researchers believe their findings mean that drugs used to inhibit Akt could be used as a personalized therapy for people who don have AIM2. ur research paves the way for future clinical trials that screen for AIM2 expression in colon cancer
and possibly other cancers to identify patients who may potentially benefit from personalized anti-Akt therapy,
#Stretchy mesh heater for sore muscles If you suffer from chronic muscle pain a doctor will likely recommend for you to apply heat to the injury.
while deformed and under stress on knee and wrist joints. It is lightweight, breathable and generates heat over the entire surface area of the material.
and the most common end-stage disease is when an atherosclerotic plaque ruptures. If this occurs in one of your large coronary arteries,
This is what causes most heart attacks. The clot can also dislodge and cause a stroke if it lodges in a blood vessel in the brain.
"Eighty-two percent of the smooth muscle cells within advanced atherosclerotic lesions cannot be identified using the typical methodology
since the lesion cells down-regulate smooth muscle cell markers. As such, we have underestimated grossly how many smooth muscle cells are in the lesion."
"Suddenly, the role of smooth muscle cells is much more complex, much less black-and-white. Are they good or bad?
which cell is which within the lesion."("The research also shows other subsets of smooth muscle cells were transitioning to cells resembling stem cells and myofibroblasts.
in order to see where those cells were later in disease.""Further, Shankman identified a key gene, Klf4,
and exhibited features indicating they were more stable--the ideal therapeutic goal for treating the disease in people.
Of major interest, loss of Klf4 in smooth muscle cells did not reduce the number of these cells in lesions
but resulted in them undergoing transitions in their functional properties that appear to be beneficial in disease pathogenesis. That is,
Shankman's findings raise many critical questions about previous studies built on techniques that failed to assess the composition of the lesions accurately.
Moreover, her studies are the first to indicate that therapies targeted at controlling the properties of smooth muscle cells within lesions may be highly effective in treating a disease that is the leading cause of death worldwide.
#Researchers develop world's most sensitive test to detect infectious disease, superbugs Researchers at Mcmaster University have developed a new way to detect the smallest traces of metabolites, proteins or fragments of DNA.
In essence, the new method can pick up any compound that might signal the presence of infectious disease,
researchers developed a molecular device made of DNA that can be switched'on'by a specific molecule of their choice--such as a certain type of disease indicator
"This invention will allow us to detect anything we might be interested in, bacterial contamination or perhaps a protein molecule that is a cancer marker.
simple answers that appear on test paper indicating the presence of infection or contamination in people, food or the environment t
#Two biomarkers linked to severe heart disease found Arrayarrayinterestingly, Nichols and his colleagues did not set out to pinpoint the two key biomarkers.
They wanted to create an insulin resistant animal model that mimicked human heart disease. They chose pigs,
But only about half of the pigs developed the most severe form of the disease.
Sure enough, all the pigs with severe heart disease had elevated levels of fructosamine and oxidized LDL.""Also, this correlation was more common in females,
"Clemmons found a study from Finland published in 2005 showing that elevated glycated protein levels were associated strongly with advanced heart disease and increased mortality in women but not in men."
"A next step could be to study the affected heart tissue to find abnormal biochemical reactions in the cellular pathways involved in glycated proteins and severe coronary disease.
Clemmons added,"We could also study what's different about these female pigs that make them much more susceptible to severe heart disease,
a discovery that could pave the way to new treatments for the disease. The researchers at the Medical Research Council's (MRC) Toxicology Unit based at the University of Leicester
that if targeted stops the disease. The study is published in Nature Communications. Malaria is caused by a parasite that lives inside an infected mosquito
and is transferred into the human through a bite. Once inside the body parasites use a complex process to enter red blood cells
The discovery could be the first step in developing a new drug to treat malaria. The scientists--funded by the Medical Research Council (MRC)
"This is a real breakthrough in our understanding of how malaria survives in the blood stream
and if it can be targeted by drugs we could see something that stops malaria in its tracks without causing toxic side-effects."
and also helps to avoid drug resistance which is a major problem in the control of malaria worldwide."
"According to the World health organization malaria currently infects more than 200 million people world wide and accounts for more than 500,000 deaths per year.
Most deaths occur among children living in Africa where a child dies every minute of malaria and the disease accounts for approximately 20%of all childhood deaths.
"Tackling malaria is a global challenge, with the parasite continually working to find ways to survive our drug treatments.
and exploit the disease's weak spots but with limited side-effects for patients
#Cancer drug 49 times more potent than Cisplatin Based on a compound of the rare precious metal osmium and developed by researchers at the University of Warwick's Department of chemistry and the Warwick Cancer Research Unit,
FY26 is able to shut down a cancer cell by exploiting weaknesses inherent in their energy generation. The researchers argue that the drug could be cheaper to produce,
Similar results were obtained by the National Cancer Institute USA in tests conducted on 60 cell lines.
This can lead to a wide-range of side-effects from renal failure to neurotoxicity, ototoxicity, nausea and vomiting.""
""Existing platinum-based cancer treatments often become less effective after the first course, as cancer cells learn how they are being attacked,
"The research could also lead to substantial improvements in cancer survival rates, suggests co-researcher Dr Isolda Romero-Canelon:"
"Current statistics indicate that one in every two people will develop some kind of cancer during their life time, with approximately one woman dying of ovarian cancer every two hours in the UK according to Cancer Research UK
and two deaths every hour from bowel cancer.""It is clear that a new generation of drugs is necessary to save more lives
In its absence, mice reproduce Seckel syndrome. The scientists rescued the microcephaly during mouse embryonic development by removing a protein that caused the loss of stem cells.
This defect in brain growth is present in several neurodevelopmental diseases, including Seckel syndrome.""There are diagnostic tests for some of these kinds of pathologies that can be performed during pregnancy,
but other than early detection, the expectant parents are limited to two choices, either to abort or to continue with the pregnancy,
being fully aware of the outcome, "explains the North american scientist Travis Stracker.""Our research paves the way to explore therapeutic approaches for microcephaly involving the inhibition of the protein p53,
"says the head of the Genomic Instability and Cancer Lab at IRB Barcelona. The scientists describe that this protein triggers the death of brain stem cells.
The discovery could eventually benefit millions of patients with chronic pain from trauma, diabetes, shingles, multiple sclerosis or other conditions that cause nerve damage."
"said co-author Bruce Hammock, distinguished professor at the UC Davis Department of Entomology and Nematology and the UC Davis Comprehensive Cancer Center."
"We can now specifically search for agents to control ER stress and its downstream pathways,
"This search is already underway in a number of laboratories working on cancer and other diseases."
"Working with Professor Fawaz Haj of the UC Davis nutrition department, Bettaieb found that key molecular signatures associated with diabetes
and diabetic pain were linked to ER stress. Neuropathic pain is a common consequence of both Type 1
and Type 2 diabetes, affecting up to 70 percent of patients. Inceoglu, working in Hammock's laboratory,
The team was able to show that blocking soluble epoxide hydrolase blocks ER stress and associated neuropathic pain.
#Activated T cell therapy for advanced melanoma developed Published in the July/August issue of Journal of Immunotherapy,
these new findings demonstrate that T cells derived from lymph nodes of patients with melanoma can be expanded in number
Led by Julian Kim, MD, Chief Medical officer at UH Seidman Cancer Center, the research team has developed a novel technique to generate large numbers of activated T cells
which can be transferred back into the same patient to stimulate the immune system to attack the cancer."
which is the natural site of the immune response against pathogens as well as cancer, "says Dr. Kim who is also Professor of Surgery at Case Western Reserve University School of medicine and the Charles Hubay Chair at UH Case Medical center."
which have been exposed to growing melanoma in the patient's body. Rather than trying to activate the T cells while in the body,
This novel approach to cancer treatment, termed adoptive immunotherapy, is offered only at a few institutions worldwide.
These promising findings have led to the recent launch of a new Phase I human clinical trial at UH Seidman Cancer Center in patients with advanced melanoma.
The research leading to the clinical trial was funded by the National institutes of health and the Case Comprehensive Cancer Center.
and is an area of great potential for the treatment of patients with cancer, "said Dr. Kim."
These types of clinical trials place the UH Seidman Cancer Center at the forefront of immune therapy of cancer."
and eventually study other tumor types including lung, colorectal and breast cancers s
#Omnidirectional free space wireless charging of multiple wireless devices Scientists have made great strides in wireless-power transfer development.
University of Valencia and IGENOMIX have discovered that chromosomal abnormalities in human embryos created for in vitro fertilization,
because chromosomal abnormalities may not be identified until day five or six.""Many couples are choosing to have children later in life,
and make the connections needed for our collaborators to identify the genes that cause diseases
#Gene therapy restores hearing in deaf mice Using gene therapy, researchers at Boston Children's Hospital and Harvard Medical school have restored hearing in mice with a genetic form of deafness.
Their work, published online July 8 by the journal Science Translational Medicine, could pave the way for gene therapy in people with hearing loss caused by genetic mutations."
"Our gene therapy protocol is not yet ready for clinical trials--we need to tweak it a bit more
More than 70 different genes are known to cause deafness when mutated. Holt, with first author Charles Askew and colleagues at École Polytechnique Fédérale de Lausanne in Switzerland
because it is a common cause of genetic deafness, accounting for 4 to 8 percent of cases,
Children with two mutant copies of TMC1 have profound hearing loss from a very young age, usually by around 2 years.
--and is a good model for the dominant form of TMC1-related deafness. In this form, less common than the recessive form, a single copy of the mutation causes children to gradually go deaf beginning around the age of 10 to 15 years.
To deliver the healthy gene, the team inserted it into an engineered virus called adeno-associated virus 1,
In the recessive deafness model, gene therapy with TMC1 restored the ability of sensory hair cells to respond to sound--producing a measurable electrical current--and also restored activity in the auditory portion of the brainstem.
Most importantly, the deaf mice regained their ability to hear. To test hearing, the researchers placed the mice in a"startle box
In the dominant deafness model, gene therapy with a related gene, TMC2, was successful at the cellular and brain level,
and is already in use in human gene therapy trials for blindness, heart disease, muscular dystrophy and other conditions.
"Current therapies for profound hearing loss like that caused by the recessive form of TMC1 are hearing aids,
a specialist in genetic hearing loss at Boston Children's Hospital who is familiar with the work."
"Holt believes that other forms of genetic deafness may also be amenable to the same gene therapy strategy.
Overall, severe to profound hearing loss in both ears affects 1 to 3 per 1, 000 live births.""I can envision patients with deafness having their genome sequenced and a tailored,
precision medicine treatment injected into their ears to restore hearing, "Holt says. Sound transducers: How TMC works Holt's team showed in 2013 that TMC1
a mutation in the TMC1 gene is sufficient to cause deafness. However, Holt's study also showed that gene therapy with TMC2 could compensate for loss of a functional TMC1 gene,
restoring hearing in the recessive deafness model and partial hearing in the dominant deafness model."
and can ultimately challenge, the burden of deafness in humans. The results are testament to the immense dedication of the research team
in order to specifically knock out the growth factors required by individual cancer types s
#Cell structure discovery advances understanding of cancer development A cell structure has been discovered that could help scientists understand why some cancers develop.
For the first time, a structure called'the mesh'has been identified which helps to hold together cells. This discovery changes our understanding of the cell's internal scaffolding.
which is found to change in certain cancers, such as those of the breast and bladder.
associate professor and senior Cancer Research UK Fellow at the division of biomedical cell biology at Warwick Medical school.
and support from Cancer Research UK and North West Cancer Research. Dr Royle said:""We had been looking in 2d
TACC3, is overproduced in certain cancers. When this situation was mimicked in the lab, the mesh and microtubules were altered
Dr Emma Smith, senior science communications officer at Cancer Research UK, said:""Problems in cell division are common in cancer-cells frequently end up with the wrong number of chromosomes.
and it might be a crucial insight into why this process becomes faulty in cancer
"North West Cancer Research (NWCR) has funded the research as part of a collaborative project between the University of Warwick and the University of Liverpool,
which could potentially better inform future cancer therapies.""As a charity we fund only the highest standard of research,
#Gene therapy advance thwarts brain cancer in rats Researchers funded by the National Institute of Biomedical Imaging
and Bioengineering have designed a nanoparticle transport system for gene delivery that destroys deadly brain gliomas in a rat model,
The nanoparticles are filled with genes for an enzyme that converts a prodrug called ganciclovir into a potent destroyer of the glioma cells.
Glioma is one of the most lethal human cancers, with a five year survival rate of just 12,
Advances in the understanding of the molecular processes that cause these tumors has resulted in therapies aimed at delivering specific genes into tumors--genes that make proteins to kill
or suppress the growth of the tumor. Currently this approach relies heavily on using viruses to deliver the anti-tumor genes into the target cancer cells.
Unfortunately, viral delivery poses significant safety risks including toxicity, activation of the patient's immune system against the virus,
and the possibility of the virus itself encouraging tumors to develop.""Efforts to treat glioma with traditional drug
and radiation therapies have not been very successful, "says Jessica Tucker, Ph d.,NIBIB Director for the Program in Gene and Drug Delivery Systems and Devices."
rather than potentially harmful viruses, is a significant step that reinvigorates the potential for gene therapy to treat deadly gliomas as well as other cancers."
and Pathology, as well as Tang Du Hospital in China, University of the Negevin, Israel, and the Instituto Neurologico C. Besta in Italy.
A number of polymer structures were tested for their ability to deliver DNA into two rat glioma cell lines.
Among the many polymers tried, the one known as PBAE 447 was found to be the most efficient in delivering the HSVTK gene into the cultured rat glioma cells.
the HSVTK-encoding nanoparticles were 100%effective in killing both of the glioma cell lines grown in the laboratory.
Next, the gene therapy system was tested in live rats with brain gliomas. Because it is important that the nanoparticles spread throughout the entire tumor,
they were infused into the rat gliomas using convection-enhanced delivery (CED). The method involves injection into the tumor and the application of a pressure gradient,
which efficiently disperses the nanoparticles throughout the tumors. To test the tumor-killing ability of the system,
the tumor-bearing rats were given systemic administration of ganciclovir for two days, then CED was used to infuse the HSVTK-encoding nanoparticles into the rat gliomas,
and systemic ganciclovir treatment continued for eight more days. The treatment resulted in shrinkage of the tumors
and a significant increase in survival when compared with control glioma-bearing animals that did not receive the combination treatment."
"The results provide the first demonstration of a successful non-viral nanomedicine method for HSVTK/ganciclovir treatment of brain cancer,"stated Green."
"Next steps will include enhancing the efficiency of this nanoparticle delivery system and evaluating the technology in additional brain cancer animal models."
"In the future, the investigators envision that doctors would administer this therapy during the surgery commonly used to treat glioma in humans.
They are interested also in testing the ability to deliver other cancer-killing genes and whether the nanoparticles could be administered successfully systemically
--which could broaden the use of the therapy for a wide range of solid tumors and systemic cancers s
#Ultrasound accelerates skin healing, especially for diabetics and the elderly Researchers from the University of Sheffield's Department of Biomedical science discovered the ultrasound transmits a vibration through the skin
and wakes up cells in wounds helping to stimulate and accelerate the healing process. More than 200,000 patients in the UK suffer with chronic wounds every year at a cost of over £3. 1 billion to the NHS.
The ultrasound treatment, which also reduces the chance of wounds getting infected, is particularly effective
when treating diabetics and the elderly. There are 11 million over-65s three million diabetics, and 10 million smokers in the UK--all of whom are likely to suffer problems with healing wounds.
A quarter of diabetics suffer from skin ulcers, particularly foot ulcers, due to the loss of sensation and circulation in the legs.
Lead author of the study Dr Mark Bass, from the University's Centre for Membrane Interactions and Dynamics (CMIAD), said:"
"Skin ulcers are excruciatingly painful for patients and in many cases can only be resolved by amputation of the limb."
"Using ultrasound wakes up the cells and stimulates a normal healing process. Because it is just speeding up the normal processes,
the treatment doesn't carry the risk of side effects that are associated often with drug treatments."
"Arraydr Bass added:""Now that we have proven the effectiveness of ultrasound we need to explore the signal further.
We have found that the ultrasound signal we currently use is effective, but it is possible that by refining the treatment we could improve the effects even further."
"Because ultrasound is relatively risk free we could expect to see it in broad clinical use within three or four years. s
#New cell division mechanism discovered Canadian and British researchers have discovered that chromosomes play an active role in animal cell division.
It was observed by a team of researchers including Gilles Hickson, an assistant professor at the University of Montreal's Department of Pathology and Cell biology and researcher at the CHU Sainte-Justine Research Centre, his assistant Silvana Jananji, in collaboration with Nelio
it can be a source for triggering cancer, for example,"said Hickson. It is well known that microscopic cable-like structures,
and to certain diseases,"said Hickson, who has devoted the last 15 years of his research life to cell biology.
In fact, all cancers are unchecked characterised by cell division, and the underpinning processes are potential targets for therapeutic interventions that prevent cancer onset and spread."
"But before we get there, we must continue to expand our knowledge about the basic processes
#Lynchpin molecule for the spread of cancer found Cancer is a disease of cell growth,
but most tumors only become lethal once they metastasize or spread from their first location to sites throughout the body.
For the first time, researchers at Thomas Jefferson University in Philadelphia report a single molecule that appears to be the central regulator driving metastasis in prostate cancer.
The study, published online July 13th in Cancer cell, offers a target for the development of a drug that could prevent metastasis in prostate cancer,
and possibly other cancers as well.""Finding a way to halt or prevent cancer metastasis has proven elusive.
We discovered that a molecule called DNA-PKCS could give us a means of knocking out major pathways that control metastasis before it begins,
"says Karen Knudsen, Ph d.,Director of the Sidney Kimmel Cancer Center at Thomas Jefferson University, the Hilary Koprowski Professor and Chair of Cancer Biology, Professor of Urology, Radiation Oncology,
Metastasis is thought of as the last stage of cancer. The tumor undergoes a number of changes to its DNA--mutations--that make the cells more mobile
able to enter the bloodstream, and then also sticky enough to anchor down in a new location,
such as the bone, the lungs, the liver or other organs, where new tumors start to grow.
Now, Dr. Knudsen and colleagues have shown that one molecule appears to be central to many of the processes required for a cancer to spread.
In fact, previous studies had shown that DNA-PKCS was linked to treatment resistance in prostate cancer, in part because it would repair the usually lethal damage to tumors caused by radiation therapy and other treatments.
Importantly, Dr. Knudsen's work showed that DNA-PKCS has other, far-reaching roles in cancer.
The researchers showed that DNA-PKCS also appears act as a master regulator of signaling networks that turn on the entire program of metastatic processes.
In addition to experiments in prostate cancer cell lines, Dr. Knudsen and colleagues also showed that in mice carrying human models of prostate cancer,
And in mice with aggressive human tumors, an inhibitor of DNA-PKCS reduced overall tumor burden in metastatic sites.
In a final analysis that demonstrated the importance of DNA-PKCS in human disease the researchers analyzed 232 samples from prostate cancer patients for the amount of DNA-PKCS those cells contained
and compared those levels to the patients'medical records. They saw that a spike in the kinase levels was a strong predictor of developing metastases and poor outcomes in prostate cancer.
They also showed that DNA-PKCS was much more active in human samples of castrate-resistant prostate cancer, an aggressive and treatment-resistant form of the disease."
"These results strongly suggest that DNA-PKCS is a master regulator of the pathways and signals that lead to the development of metastases in prostate cancer,
and that high levels of DNA-PKCS could predict which early stage tumors may go on to metastasize,
"says Dr. Knudsen.""The finding that DNA-PKCS is a likely driver of lethal disease states was unexpected,
and the discovery was made possible by key collaborations across academia and industry,"explains Dr. Knudsen.
in addition to leaders of the Sidney Kimmel Cancer Center's Prostate Program, included the laboratories of Felix Feng (University of Michigan), Scott Tomlins (University of Michigan), Owen Witte (UCLA),
and will be available at multiple centers connected through the Prostate Cancer Clinical Trials Consortium, of which we are explained a member
this new trial will provide some insight into the effect of DNAP-PKCS inhibitors as anti-tumor agents.
In parallel, using this kinase as a marker of severe disease may also help identify patients whose tumors will develop into aggressive metastatic disease,
"Given the role of DNA-PKCS in DNA repair as well as control of tumor metastasis, there will be challenges in clinical implementation,
or treating advanced disease
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