Publisher Health

Federal health officials have directed airlines to provide the Centers for Disease Control and Prevention with the names and contact information of all passengers who boarded flights bound for the United States since Nov. 29 and who had been in southern Africa during the prior two weeks.The directive, issued Wednesday, applies to passengers who spent time in Botswana, the Kingdoms of Eswatini and Lesotho, Malawi, Mozambique, Namibia and South Africa in the two weeks before flying to the United States. The airlines were directed to provide their names, addresses while in the United States, phone numbers, email addresses, dates of birth and flight information, including seat numbers.“C.D.C. is issuing this directive to prevent the importation and spread of a communicable disease of public health importance,” a statement from the agency said, an apparent reference to the new Omicron variant of the virus that causes Covid.Last week, the White House announced a ban on travel from eight countries in southern Africa. And late Tuesday night, the C.D.C. said it planned to toughen virus testing and screening of people flying to the United States by requiring all international passengers to provide a negative result from a test taken within 24 hours of departure.The new directive was issued under an Oct. 25 order that instructed airlines and aircraft operators to collect specific information from all passengers before boarding, retain the information for 30 days, and transmit it to C.D.C. within 24 hours if requested to do so.The C.D.C. can share the information with state and local health departments at passengers’ destinations, enabling local health authorities to monitor travelers for Covid, identify symptomatic individuals, notify their contacts, and direct those who are infected to isolate and their contacts to quarantine to avoid further disease spread. They can also use the information to ensure infected individuals get appropriate care.The order applies to flights that have departed for the United States since Monday morning. Two flights left Johannesburg for the United States that day: a Delta Air Lines flight with more than 300 seats that was headed for Atlanta, and a United Airlines flight with more than 250 seats that was headed for Newark, N.J. Both flights landed in the United States on Tuesday morning, according to schedules from Cirium, an aviation data provider. Two more United flights are scheduled to leave South Africa for Newark on Wednesday, one from Cape Town and one from Johannesburg.Delta and United are currently the only two carriers that offer direct or single-layover flights between the countries covered by the C.D.C. order and the United States, according to Cirium schedule data. Delta operates three weekly flights between Johannesburg and Atlanta. United operates five flights a week between Johannesburg and Newark. It also plans to restart seasonal flights between Cape Town and Newark on Wednesday.Both airlines have said that they are not planning to adjust their flight schedules in response to the administration’s ban on travelers from the region, which took effect on Monday and does not apply to American citizens or lawful permanent residents. The airlines also said that they plan to comply with the C.D.C. order.Sixty-one people who arrived in the Netherlands on Friday aboard two flights that departed from South Africa tested positive for the virus that causes Covid, including over a dozen who were carrying the new Omicron variant. The number of overall positive cases represented more than 10 percent of the 600 passengers tested.

Today, people living with HIV/AIDS can remain healthy if they are able to engage in routine care and take the medicines that reduce their virus to undetectable levels. But for people with HIV who are also struggling with depression, that’s often an insurmountable challenge, especially in South Africa, home to the highest number of cases in the world and a significant shortage of mental health professionals.
But a new study in the Journal of the International AIDS Society has local and global implications for successfully treating both mental health and HIV/AIDS in settings like South Africa — or even Miami, the epicenter of new cases in the United States.
In the study, an international team of researchers — led by the University of Miami’s Steven Safren and two colleagues — demonstrated the effectiveness of training nurses in public HIV clinics to deliver a specially adapted cognitive behavior therapy (CBT) to help people with depression and uncontrolled HIV adhere to their prescribed medication regiment. CBT is a proven approach for changing faulty or unhelpful thinking or behavioral patterns.
“We know that treating HIV-positive people who are clinically depressed with antidepressants alone does not affect their viral loads. Their depression may improve, but their adherence does not,” said Safren, professor of psychology and director of the University’s Center for HIV/AIDS Research and Mental Health. “So, given the global shortage of mental health professionals, we showed it is possible to train nurses to deliver cognitive-behavioral therapy for adherence and depression (CBT-AD), an intervention that successfully addresses both clinical depression and uncontrolled HIV.”
Safren, who joined the University in 2015 from Harvard Medical School, conducted the study in a poor township just outside of Cape Town, South Africa, with fellow researchers John A. Joska, director of the HIV Mental Health Research Unit and professor of psychiatry at the University of Cape Town, and Conall O’Cleirigh, associate professor of psychology at Harvard and director of Behavioral Medicine at Massachusetts General Hospital.
For their study, the researchers recruited 161 patients with uncontrolled HIV/AIDS and clinical depression from four public health clinics in the township of Khayelitsha. Although a medical officer could prescribe antidepressants to the patients, the clinics have limited psychological services — as does the country in general. According to the study, South Africa only has 0.28 psychiatrists and 0.32 psychologists per 100,000 people.

Biomedical engineers at Duke University have demonstrated a method for increasing the depth at which optical coherence tomography (OCT) can image structures beneath skin.
The gold standard for imaging and diagnosing diseases within the retina, OCT has yet to find widespread use as an imaging technique for other parts of the body due to its inability to return clear images from more than a millimeter beneath the skin’s surface.
Duke researchers found that tilting the light source and detector used in the technique increases OCT’s imaging depth by almost 50%, putting skin diagnoses within reach. The “dual-axis” approach opens new possibilities for OCT to be used in applications such as spotting skin cancer, assessing burn damage and healing progress, and guiding surgical procedures.
The results appear online on December 1 in the open access journal Biomedical Optics Express.
“It’s actually a fairly simple technique that sounds like something out of Ghostbusters — you get more power when you cross the beams,” said Adam Wax, professor of biomedical engineering at Duke. “Being able to use OCT even 2 or 3 millimeters into the skin is extremely useful because there are a lot of biological processes happening at that depth that can be indicative of diseases like skin cancer.”
Standard OCT is analogous to ultrasound but uses light instead of sound. A beam of light is shined down into an object, and by measuring how long it takes for it to bounce back, computers can deduce what the internal structure of the object looks like. It has become the go-to technology for imaging and diagnosing retinal diseases because the retina is so thin and easily accessible through the eye’s transparent cornea and lens.

SharecloseShare pageCopy linkAbout sharingImage source, EPAEuropean Union countries should consider mandatory vaccination to combat Covid and the Omicron variant, the head of its Commission has said.Ursula von der Leyen said vaccines would be crucial in the fight against the “highly contagious” new variant.Some two dozen countries have reported cases of Omicron, and the EU has tightened travel restrictions since it was first reported earlier this month.European countries have also been facing a wider spike in cases.The World Health Organization (WHO), meanwhile, said early signs were that most cases of the Omicron variant were “mild”.On Wednesday, Ms von der Leyen said it was “understandable and appropriate” for EU members to discuss mandatory Covid vaccinations given that a third of the bloc’s population was unvaccinated.”How we can encourage and potentially think about mandatory vaccination within the European Union? This needs discussion. This needs a common approach, but it is a discussion that I think has to be led,” she told a news conference in Brussels.Only individual EU states can enforce vaccine mandates and some are already taking steps in that direction. Austria has announced compulsory Covid vaccinations from February next year, while Greece is fining all unvaccinated over-60s €100 (£85) a month.Germany’s incoming Chancellor, Olaf Scholz, has said he supports compulsory jabs. In an interview with Bild television, Mr Scholz said he wanted compulsory vaccinations from March and also said a faster rollout of booster jabs was needed. ‘No sign vaccines won’t work’The WHO, which declared Omicron “of concern” on Friday following its rapid spread in South Africa, says it will know more about the new variant within days. Omicron is becoming the dominant Covid strain in South Africa, where the daily number of recorded cases doubled on Wednesday. Officials there say the variant could be fuelling the surge.However, the WHO has already said it believes existing vaccines “will still prevent severe disease” among people who contract the new variant.Omicron may need ‘stringent response’ – scientistsIs Omicron more harmful than other Covid variants?How can I tell I have Omicron? How fast is worldwide progress on vaccines?Asked about the severity of cases, WHO epidemiologist Dr Maria van Kerkhove said: “There is some indication that some of the patients are presenting with mild disease.”There is still suggestion of increased hospitalisations across South Africa but this could be the sheer fact that we have more cases, and if you have more cases you have more hospitalisations.”The US on Wednesday became the latest country to report a case of Omicron. Other nations include Nigeria, Norway and South Korea. Several countries have tightened their borders to halt the spread of Omicron. This video can not be playedTo play this video you need to enable JavaScript in your browser.But the WHO warned against “punitive” travel measures imposed on southern African countries.WHO head Tedros Adhanom Ghebreyesus said he was concerned about “blunt, blanket measures”, which “will only worsen inequities”.Dr Van Kerkhove said travel bans imposed on South Africa had created problems for shipping virus samples.The US, which has already banned foreign travellers from eight African countries, has ordered airlines to tell it the names of passengers who have been there.

In a recent study published in Nature Biomedical Engineering, a team led by researchers at Massachusetts General Hospital (MGH) has demonstrated that magnetic resonance imaging (MRI) and artificial intelligence (AI) can be used to detect early signs of tumor cell death in response to a novel virus-based cancer therapy.
Recently, a promising therapeutic virus that selectively kills cancer cells while sparing normal tissue has sparked hope for treating aggressive brain tumors. To further optimize the virus-based therapy, frequent non-invasive monitoring of the treatment response must be performed. This monitoring is crucial for understanding the interactions between the virus and cancer cells, such as the extent of virus spread within the tumor and therapeutic response.
The researchers used quantitative molecular MRI images to measure multiple tissue properties, including tissue pH and protein concentration, that are altered with cell-death. This method allows therapeutic response monitoring much earlier than with previous techniques. The treatment responses were visible just 48 hours after viral-therapy, long before any changes in tumor volume were observed.
“We programmed an MRI scanner to create unique signal “fingerprints” for different molecular compounds and cellular pH. A deep learning neural network was then used to decode the fingerprints and generate quantitative pH and molecular maps,” says Christian Farrar, PhD, an investigator and faculty at the Athinoula A. Martinos Center for Biomedical Imaging. “The MRI molecular fingerprinting method was validated in a mouse brain tumor study where the tumors were treated with a novel virus-based therapy that selectively killed cancer cells.”
To maximize the efficiency of this treatment approach, the researchers developed a method for the detection of tumor cell death caused by the virus. This has allowed for the early and rapid detection of treatment-responsive tumor regions. Recently, the researchers have implemented this method to quantify cellular pH and molecular compounds in the healthy human brain. Future investigation of this approach in human brain tumor patients would help to optimize these virus-based therapies
“This study demonstrates the strength and promise of implementing computerized AI-based technology in medicine for the noninvasive investigation of biological processes that underlie disease,” says Or Perlman,PhD, a research fellow at the Athinoula A. Martinos Center for Biomedical Imaging. “One of the most interesting and key components for the success of this approach was the use of simulated molecular fingerprints to train the machine learning neural network. This concept could potentially be expanded and investigated for solving other medical and scientific challenges.”
This study describes a new method for detecting tumor cell death non-invasively using MRI. The capacity to do this could be useful for non-invasive monitoring of cancer treatment, potentially improving patient care and tailoring the treatment to an individual patient. The same approach might also be beneficial for detecting and characterizing other medical conditions where elevated cell death occurs, such as stroke and liver disease. While the study was mainly validated using a mouse brain tumor model, the researchers have demonstrated the ability to use the same method for producing quantitative pH and molecular maps in rat stroke models and healthy humans. In the future, they plan to further explore the applicability of this non-invasive imaging approach in patients with brain tumors and stroke.
Story Source:
Materials provided by Massachusetts General Hospital. Note: Content may be edited for style and length.

A new study from Texas Biomedical Research Institute (Texas Biomed) and collaborators has identified a promising drug candidate to minimize uncontrolled, erratic muscle movements, called dyskinesia, associated with Parkinson’s disease.
The small molecule, called PD13R, reduced dyskinesia by more than 85% in the marmoset animal model of Parkinson’s disease. And, the animals got much better sleep taking this compound compared to another drug often prescribed for dyskinesia. The results were published in the journal Experimental Neurology.
Dyskinesia is a common side effect in patients with Parkinson’s disease. It is not a symptom of the disease itself, but typically emerges about five years into taking levodopa, the leading medication used to restore balance, reduce shaking and manage other motor control issues patients experience.
“Levodopa is amazing, it works like magic, but it has side effects. If we can eliminate these side effects, it could change the life of patients with Parkinson’s,” says Marcel Daadi, PhD, an associate professor at Texas Biomed and lead paper author.
Designing drugs for Parkinson’s and its side effects is notoriously difficult. This is in part due to the progressive nature of the disease as neurons deteriorate, and because it involves the neurotransmitter dopamine. There are five types of dopamine receptors, all with different functions, yet very similar structures. Finding a compound that only interacts with the desired receptor is a major challenge.
To try to identify a compound that only binds to dopamine receptor #3 (D3), Daadi teamed up with Southwest Research Institute. SwRI’s drug discovery software RhodiumTM identified PD13R as a likely candidate and predicted how it would bind to D3. Daadi reached out to medicinal chemists at Temple University to synthesize the compound, who are currently working on this class of compounds for their antipsychotic properties.
Daadi and his team at Texas Biomed explored how well the compound targeted the D3 receptor compared to the other dopamine receptors in cell culture tests. They found it had a 1,486-times higher selectivity for D3 than for D2, which is the most similar in structure.
The team then administered PD13R to the marmoset animal model of Parkinson’s. Like human patients, the nonhuman primates developed dyskinesia after receiving levodopa. When treated with PD13R, dyskinesia dropped dramatically.
“We were very excited to see the robust antidyskinetic effect of the drug,” Daadi explains.
The animals wore activity monitors, and with PD13R, their activity was low at night, when they normally sleep. In contrast, when given a different drug currently on the market for dyskinesia, their nighttime activity was significantly high, suggesting that PD13R may be a good treatment option without this side effect.
Daadi and his team plan to continue with safety and efficacy studies required by the U.S. Food and Drug Administration (FDA) before human clinical trials can begin. “I am very hopeful we can move this into Phase 1 clinical trials within two years,” Daadi says. 
This investigation used resources that were supported by the Southwest National Primate Research Center grant P51 OD011133 from the Office of Research Infrastructure Programs, National Institutes of Health. This work was supported by the Worth Family Fund, The Perry and Ruby Stevens Charitable Foundation, The Robert J. Jr. and Helen C. Kleberg Foundation, The Marmion Family Fund, The William and Ella Owens Medical Research Foundation, the National Institute on Aging R56 AG059284.

The risk of developing cardiovascular disease is strongly associated with the “bad” LDL cholesterol. A large study by scientists at Karolinska Institutet now shows that two proteins that transport cholesterol particles in the blood provide early and reliable risk information. The researchers now advocate introducing new guidelines for detecting cardiac risk and say the results may pave the way for early treatment, which could help lower morbidity and fatality rates.
Cardiovascular disease is the most common cause of death globally and includes a wide range of conditions, such as stroke and myocardial infarction with atherosclerosis in different organs of the body. In many cases the disease can be prevented and arrested with lifestyle changes and lipid-lowering treatments using statins and other methods.
The data generally used to assess elevated cardiac risk are reference values for the “bad” LDL cholesterol. In some medical conditions, other types of fat particles are also measured along with apolipoproteins, which transport cholesterol in the blood. International guidelines for cardiovascular disease recommend using the apolipoprotein apoB, which transports the “bad” cholesterol, as an alternative risk marker for people with type 2 diabetes, overweight (high BMI) and very high levels of blood lipids.
Recent research has, however, indicated the importance of also factoring in the apolipoprotein apoA-1, which transports the “good” protective and anti-inflammatory HDL cholesterol. Calculating the apoB/apoA-1 ratio gives a risk quotient reflecting the balance between the “bad” fat particles that expedite atherosclerosis and the “good” protective apoA-1 particles that arrest the process.
In this present study, the researchers have analysed the link between cardiovascular disease and apoB/apoA-1 values in more than 137,000 Swedish men and women between the ages of 25 and 84. The individuals were followed for 30 years, during which time 22,000 suffered some form of cardiovascular event. The analysis methods are simple, inexpensive and safe, and do not require pre-test fasting, as is the case with LDL and non-HDL tests. Basing their study on a large database (AMORIS), the researchers linked the laboratory analyses to several clinical diagnosis registers.
“The results show that the higher the apoB/apoA-1 value, the greater the risk of myocardial infarction, stroke and need for coronary surgery,” says Göran Walldius, senior author and professor emeritus at the Institute of Environmental Medicine, Unit of Epidemiology, Karolinska Institutet. “The study also showed that the risk was amplified in the presence of low protective levels of apoA-1.”
Individuals with the highest apoB/apoA-1 values had a 70 percent greater risk of severe cardiovascular disease and almost triple the risk of non-fatal myocardial infarction compared with those with the lowest apoB/apoA-1 values. Individuals with the highest risk quotient were also more affected by severe cardiovascular diseases many years earlier than individuals with the lowest apoB/apoA-1 values.
The relationship was observed in both men and women and the elevated levels could be detected as early as 20 years before the onset of cardiovascular disease.
“Early preventive treatment and information about cardiovascular risk is, of course, important in enabling individuals to manage their risk situation,” Walldius says. “Early treatment can also reduce the cost burden on the public health services.”
All in all, the results indicate that the apoB/apoA-1 ratio is a better marker for identifying more individuals at risk of future cardiovascular disease than the apoB method alone, according to the researchers.
“It should be possible to introduce cut-values for apoB, apoA-1 and the apoB/apoA-1 ratio into new guidelines as a complement to current guidance on the detection and treatment of dyslipidaemia,” Walldius says.
The study was financed by the Gunnar and Ingmar Jungner Foundation for Laboratory Medicine.
Story Source:
Materials provided by Karolinska Institutet. Note: Content may be edited for style and length.

Monash University’s Biomedicine Discovery Institute researchers have made a vital breakthrough in the understanding of a new facet of the immune response to malaria, which will help in the development of a vaccine.
Malaria is caused by an infection with a deadly parasite species called Plasmodium falciparum and although it is one of the world’s most prevalent global diseases, efforts to develop an effective vaccine have been restricted by a lack of understanding of the immune response that drives immunity. The World Health Organization estimates there are 200 million infections and 500,000 deaths each year as a direct result of malaria.
The new study found that a poorly understood group of immune cells, called gamma delta T cells, were directly involved in promoting clinical protection from malaria. These gamma delta T cells express a unique T cell receptor (TCR) that was involved in the recognition of P. falciparum parasite fragments.
By using human samples from clinical trials exploring the natural immune response to malaria, the scientists were able to obtain a detailed map of how gamma delta T cells and the gamma delta TCR respond to repeated seasonal and experimental P. falciparum infections.
While many aspects of the immune system’s defence mechanisms are actively avoided or dampened by the complex life cycle of P. falciparum, gamma delta T cells were highly responsive and evolved to tolerate repeated P. falciparum infections. This work reshapes the understanding of how these T cells interact with dangerous pathogens and provides new avenues for future discoveries.
The findings are published today in Science Translational Medicine.
The study was led by Dr Martin Davey and first author Dr Anouk von Borstel.
Dr von Borstel, a postdoctoral research fellow in the Davey lab, said: “Our findings that gamma delta T cells are an important component of an effective immune response to malaria will be very important for the development of future vaccines.
“Gamma delta T cells are not very well understood and our findings show that the gamma delta TCR is critical to their response to malaria which will open new areas to harness these cells for infectious diseases.”
Lead author Dr Davey said: “These cells have long been thought to be involved in immunity to malaria, but their potential role and how they do this has not been elucidated. This international study provides a breakthrough in our understanding of gamma delta T cell immunity and evidence for their vital importance in combating infectious pathogens.
“These are important T cells that form a major component of the immune response to malaria. With a greater understanding of how our immune system operates in response to infectious disease, we can reveal crucial factors that can be delivered by next-generation vaccines.”
The study represents a cross-disciplinary and international collaboration between researchers from the United States National Institute of Allergy and Infectious Disease (NIAID), Uniformed Services University, University of Maryland, University of California San Francisco, Emory University, Monash Children’s Hospital, Monash University and Walter and Eliza Hall Institute. This research was supported by funding from the Rebecca L. Cooper Medical Research Foundation and the Australian Research Council.
Story Source:
Materials provided by Monash University. Note: Content may be edited for style and length.

A gene mutation linked to Alzheimer’s disease alters a signaling pathway in certain immune cells of individuals with the disease, according to a new study by scientists at Weill Cornell Medicine. The team also found that blocking the pathway — with a drug that’s currently being tested in cancer clinical trials — protects against many features of the condition in a preclinical model. The results could lead to new strategies to block the development of Alzheimer’s disease or slow its progression.
The study, published Dec. 1 in Science Translational Medicine, focused on microglia, immune cells of the central nervous system that are the first to respond when something goes wrong in the brain. Studies have identified many genetic variants linked to Alzheimer’s disease that are highly expressed in microglia, providing compelling evidence that alterations within these cells may play a role in the disease’s onset and progression.
“Microglia are guardians of the brain under healthy conditions, but can turn detrimental in disease conditions. Our goal is to identify how they become toxic and contribute to Alzheimer’s disease pathogenesis and whether we can identify immune modulators to reverse the toxicity without diminishing their normal protective function,” said senior author Dr. Li Gan, director of the Helen and Robert Appel Alzheimer’s Disease Research Institute and the Burton P. and Judith B. Resnick Distinguished Professor in Neurodegenerative Diseases in the Feil Family Brain and Mind Research Institute at Weill Cornell Medicine.
Alzheimer’s disease is the most prevalent neurodegenerative disease in ageing, affecting approximately 46 million people worldwide. Theories point to a number of potential causes, including age-related changes in the brain, along with genetic, environmental, and lifestyle factors. These lead to the accumulation of toxic proteins in the brain — and according to recent evidence, immune system changes — that result in loss of neurons and their connections.
To examine how the brain’s immune cells may contribute to Alzheimer’s disease, Dr. Gan and her colleagues first established the molecule fingerprint of individual microglia in the brains of patients with Alzheimer’s disease who carry a mutation in the TREM2 gene that markedly elevates individual’s risk for developing Alzheimer’s disease. TREM2 is a receptor mainly expressed by microglia in the brain, and among other functions, it signals through an enzyme named AKT to modulate inflammation and metabolism.
The team then established a mouse model by combining two strains; one that carries the AD-linked mutation in the TREM2 gene and another that exhibits Tau aggregates, one of the major pathological hallmarks in Alzheimer brains. Both patients and mice with the mutation demonstrated memory-related deficits, and their microglia expressed high levels of inflammatory molecules and exhibited an overactive AKT signaling pathway. In the mice, inhibiting AKT with a drug called MK-2206 reversed the inflammatory properties of microglia and protected against synaptic toxicity — a type of damage to the brain’s neurons that is a hallmark of Alzheimer’s disease.
Importantly, because AKT signaling also contributes to the pathogenesis of many types of cancer, MK-2206 is currently being evaluated in multiple cancer clinical trials. Therefore, the safety of the drug is already under investigation.
“We identified a small molecule compound that has been tested in patients with cancer, readily enters the brain, potently modulates the brain’s immune responses, and protects against synaptic loss in animal models of Alzheimer’s disease,” Dr. Gan said. “Our findings support further study of this compound as a potential therapy for Alzheimer’s disease.”
Dr. Li Gan is a co-founder with equity and consultant for Aeton Therapeutics, Inc.
Story Source:
Materials provided by Weill Cornell Medicine. Note: Content may be edited for style and length.

Research from the University of Cincinnati College of Medicine shows that use of a topical drug, called AB569, a combination of acidified nitrite and EDTA (or ethylenediaminetetraacetic acid) promotes killing of antibiotic-resistant bacteria while enhancing the healing of wounds in a variety of burn injuries. The study was published in the journal Infection and Immunity.
AB569 was patented in the United States in 2018 by Daniel Hassett, PhD, professor in the Department of Molecular Genetics, Biochemistry and Microbiology at the UC College of Medicine. Hassett’s research has found that AB569 kills virtually all pathogenic bacteria tested with no observed acquired resistance. These, including multidrug resistant Pseudomonas aeruginosa (MDR-PA), are some of the most serious pathogens according to the Centers for Disease Control and Prevention exhibiting multidrug resistance and enhanced virulence properties.
“Multidrug resistant bacteria, often called ‘superbugs,’ are an ever-burgeoning global health problem,” says Hassett. “As a result, there is a critical need to develop novel and effective antimicrobials for the prevention, treatment and eradication and healing of such wounds that are complicated by the most formidable pathogen of burn patients, known as MDR-PA. Injury severity is predominantly due to potentially lethal sepsis caused by MDR-PA.”
Hassett, who is the co-corresponding author on this study with Latha Satish, PhD, director of clinical lab operations at Cincinnati Children’s Hospital Medical Center, says the research shows AB569 acts synergistically to kill all human burn wound strains of the pathogen in vitro.
“AB569 not only kills the bug, it also enhances the wound-healing process,” says Hassett. “At the same time, AB569 topical application significantly increases the anti-inflammatory mediators…that allow improved epidermal restoration and the healing process to occur more rapidly and efficiently.”
AB569 was initially seen as a potential treatment for many antibiotic-resistant organisms that cause pulmonary infections in patients with cystic fibrosis and chronic obstructive pulmonary disease (COPD) and many other opportunistic infections. In addition to tackling COPD and cystic fibrosis, AB569 may also be effective in addressing infections related to severe burns, urinary tract disorders, endocarditis and diabetes, said Hassett.
“This study provides solid foundational evidence that AB569 can be used topically to treat highly problematic dermal [injuries] including wound, burn, blast and likely diabetic infections in civilian and military populations and help relieve the economical burden that MDR organisms have on the global health care system,” says Hassett.
Disclosures: Hassett is a stockholder and principal scientist at Arch Biopartners. AB569 is currently in a Phase 1 human trial at the Cincinnati VA Medical Center in healthy volunteers testing its safety and pharmacokinetic profile. AB569 has been licensed by the University of Cincinnati exclusively to Arch Biopartners, a Toronto-based publicly traded biotechnology company.
Story Source:
Materials provided by University of Cincinnati. Original written by Bill Bangert. Note: Content may be edited for style and length.