Positive Health Online

Women's Hospital Targeted by Seven Air Strikes in Syria; Newborns Evacuated 

The Iman Obstetrics and Gynecology Hospital in Orum Al Kubra in the Aleppo countryside was targeted today, August 31, 2019, by seven airstrikes at 1 a.m. Damascus time. The hospital was damaged and put out of service. No casualties were reported but two patients and one staff were injured. Newborn babies that were still in incubators had to be evacuated.

This marks the 50th medical facility to be targeted since April 28 2019. At least 10 of those hospitals, including Alzerbeh Hospital attacked yesterday, were deconflicted with coordinates provided to the UN.

Dr Khaula Sawah, Vice President of UOSSM USA said, “Seeing pictures of newborn babies being evacuated from a hospital they were just born in is absolutely unacceptable. These war crimes cannot continue to happen with no consequences. We call on the international community to intervene and take action such as the UNGA

"Uniting For Peace" Resolution. I have no words…. hospitals are not a target.”

Since April 28, 2019:

• At least 892 civilians have been killed including at least 226 children and 179 women;
• Over 1912 civilians have been injured;
• Over 750,000 people have been internally displaced in North Western Syria;
• 50 medical facilities have been bombed, 30 aid workers have been killed and 40 have been wounded;
• Five ambulances were hit by different airstrikes while serving patients, killing eight staff;
• Eight water facilities were destroyed.

Numbers are constantly changing due to situation on the ground.

About UOSSM

UOSSM (Union des Organisations de Secours et Soins Médicaux) provides free medical aid to the people of Syria regardless of nationality, ethnicity, gender, religion or political affiliation. UOSSM international, founded by Syrian Doctors around the world, started in 2012 and operates 12 major hospitals and supports 120 clinics inside Syria. UOSSM has performed over 1,000,000 medical treatments inside Syria since inception. UOSSM International,  22 Avenue Saint Clotilde, Geneva, 1205 Switzerland. 

Source, Contact and Further Information

Please contact Avi D'Souza, Director Of Communications, UOSSM Intl on Tel: (647) 528-5029; press@uossm.org   www.uossm.org

Drug Discovery Offers New Hope To Halt Spread of Malaria

Breakthrough research has revealed a new drug that may prevent the spread of malaria, and also treat people suffering with the deadly parasitic disease.

The findings, which were delivered by an international team of scientists led by the University of Glasgow[1] and published today in Science,[2] offer fresh hope in the global fight against malaria.

Malaria, a mosquito-borne infectious disease, currently affects over 200 million people, and kills nearly half a million people – mostly children – every year.

Malaria is caused by the Plasmodium parasite, which infects humans through the bite of a mosquito. The parasite then grows in the liver and in red blood cells in our blood. Parasites can also change in the blood to take on a male and female form, which can re-infect mosquitoes when they bite and suck blood from infected people.

Now, scientists led by Professor Andrew Tobin of the University of Glasgow, have discovered a drug that can kill the parasite at all three stages of its life cycle – when it is in the liver, in red blood cells, as well as preventing sexual development of the parasite.

The new drug works by stopping the activity of an essential protein called PfCLK3, which controls the production/activity of other proteins that are involved in keeping the parasite alive. By blocking this protein’s activity, the drugs can effectively kill the malaria parasite, which not only prevents it spreading, but also holds the possibility of treating the disease in humans too.

Professor Tobin, Professor of Molecular Pharmacology at the University of Glasgow, said:

“We are tremendously excited about these new findings, and hope they pave the way for the first step in the eradication of malaria. Our work has shown that by killing the parasites at the various stages of parasite development, we have not only discovered a potential cure for malaria but also a way of stopping the spread of malaria from person to mosquito which can then infect other people.”

The drug – a potent compound found by scientists after a rigorous screening process – works by stopping the activity of the essential protein PfCLK3. This protein forms part of a system that controls the production of proteins in the parasite, and by inhibiting it, the parasite cannot make many of the proteins that it requires to survive.

Professor Andy Waters, Director of the Wellcome Centre for Integrative Parasitology at Glasgow and a co-author of the study says:

“By inhibiting PfCLK3 we have shown that the production of proteins necessary for the survival of the parasite is stopped and this kills the parasite at multiple stages.

“In this way we have found a way to stop the transmission of the parasite by killing the form of the parasite that infects mosquitoes, thereby preventing the parasite from being transferred from one person to another.”

The study was funded by Wellcome, The Medical Research Council (MRC) and Tres Cantos Open Lab Foundation. The work was done in collaboration with GlaxoSmithKline, the University of California, University of Leicester, Royal Melbourne Institute of Technology, the University of Oxford and The MRC Unit the Gambia.

More on Malaria and this discovery

The malaria parasite exists in a number of different forms in humans. When the parasite enters the human body through the bite of a mosquito, the parasite makes its way to and then enters the liver. This is called the liver stage, and at this stage the parasite grows within the liver cells and divides into many thousands of parasites. These new parasites are then released into the blood stream where they invade our red blood cells (the oxygen-carrying cells in our bodies).

When the parasite invades the red blood cells, this begins the stage of the disease that results in the symptoms of malaria, and which can result in the death of the infected person in serious cases.

The next stage of the parasite is to develop into male and female parasites. This happens only to a small number of the parasites, but it is an important stage because it is these male and female parasites – so called gametocytes – which are the forms of the parasite that can infect mosquitoes.

When a mosquito bites an infected person, and takes up a blood meal, they take up the male and female gametocytes which turn into gametes. Then, in the gut of the mosquito the male gamete fertilises the female gamete to generate a new moving parasite capable of infecting the mosquito. Parasite multiplication on the outside of the gut produces lots of infectious parasites that are then able to migrate to the salivary gland of the mosquito where they can be released into the next person through the bite of the infected mosquito.

Importantly, inhibition of the PfCLK3 protein can kill the parasite at all three stages of its life cycle – in the liver, in the red blood cells, and by preventing the formation of male and female gametocytes. This means that the drug would be predicted to successfully treat people with malaria, relieving the symptoms and prevent the spread (transmission) of the parasite. 

References

1. https://www.gla.ac.uk/news/headline_669067_en.html

2. Mahmood M. Alam et al. Validation of the protein kinase PfCLK3 as a multistage cross-species malarial drug targetScience: 365, (6456) eaau1682. DOI: 10.1126/science.aau1682.  https://science.sciencemag.org/content/365/6456/eaau1682 . 30 Aug 2019.

Further Information

For more information contact Elizabeth McMeekin or Ali Howard in the University of Glasgow Communications and Public Affairs Office on Tel: 0141 330 4831 or 0141 330 6557; Elizabeth.mcmeekin@glasgow.ac.uk  or ali.howard@glasgow.ac.uk  

Scientists Develop Novel Nano-Vaccine for Melanoma

Injection of nanoparticle has proven effective in mouse models, researchers say

Researchers at Tel Aviv University have developed a novel nano-vaccine for melanoma, the most aggressive type of skin cancer. Their innovative approach has so far proven effective in preventing the development of melanoma in mouse models and in treating primary tumours and metastases that result from melanoma.

The focus of the research is on a nanoparticle that serves as the basis for the new vaccine. The study was led by Prof. Ronit Satchi-Fainaro, chair of the Department of Physiology and Pharmacology and head of the Laboratory for Cancer Research and Nanomedicine at TAU's Sackler Faculty of Medicine, and Prof. Helena Florindo of the University of Lisbon while on sabbatical at the Satchi-Fainaro lab at TAU; it was conducted by Dr Anna Scomparin of Prof. Satchi-Fainaro's TAU lab and postdoctoral fellow Dr João Conniot. The results were published on August 5 in Nature Nanotechnology.[1]

Melanoma develops in the skin cells that produce melanin or skin pigment.

"The war against cancer in general, and melanoma in particular, has advanced over the years through a variety of treatment modalities, such as chemotherapy, radiation therapy and immunotherapy; but the vaccine approach, which has proven so effective against various viral diseases, has not materialized yet against cancer," says Prof. Satchi-Fainaro.

"In our study, we have shown for the first time that it is possible to produce an effective nano-vaccine against melanoma and to sensitize the immune system to immunotherapies."

The researchers harnessed tiny particles, about 170 nanometres in size, made of a biodegradable polymer. Within each particle, they ‘packed’ two peptides – short chains of amino acids, which are expressed in melanoma cells. They then injected the nanoparticles (or "nano-vaccines") into a mouse model bearing melanoma.

"The nanoparticles acted just like known vaccines for viral-borne diseases," Prof. Satchi-Fainaro explains. "They stimulated the immune system of the mice, and the immune cells learned to identify and attack cells containing the two peptides – that is, the melanoma cells. This meant that, from now on, the immune system of the immunized mice will attack melanoma cells if and when they appear in the body."

The researchers then examined the effectiveness of the vaccine under three different conditions.

First, the vaccine proved to have prophylactic effects. The vaccine was injected into healthy mice, and an injection of melanoma cells followed.

"The result was that the mice did not get sick, meaning that the vaccine prevented the disease," says Prof. Satchi-Fainaro.

Second, the nanoparticle was used to treat a primary tumour: A combination of the innovative vaccine and immunotherapy treatments was tested on melanoma model mice. The synergistic treatment significantly delayed the progression of the disease and greatly extended the lives of all treated mice.

Finally, the researchers validated their approach on tissues taken from patients with melanoma brain metastases. This suggested that the nano-vaccine can be used to treat brain metastases as well. Mouse models with late-stage melanoma brain metastases had already been established following excision of the primary melanoma lesion, mimicking the clinical setting. Research on image-guided surgery of primary melanoma using smart probes was published last year by Prof. Satchi-Fainaro's lab.

"Our research opens the door to a completely new approach – the vaccine approach – for effective treatment of melanoma, even in the most advanced stages of the disease," concludes Prof. Satchi-Fainaro. "We believe that our platform may also be suitable for other types of cancer and that our work is a solid foundation for the development of other cancer nano-vaccines."

This project was funded by EuroNanoMed-II, the Israeli Ministry of Health, the Portuguese Foundation for Science and Technology (FCT), the Israel Science Foundation (ISF), the European Research Council (ERC) Consolidator and Advanced Awards, the Saban Family Foundation–Melanoma Research Alliance (MRA) Team Science Award, and the Israel Cancer Research Fund (ICRF).

Reference

1. João Conniot, Anna Scomparin, Carina Peres, Eilam Yeini, Sabina Pozzi, Ana I. Matos, Ron Kleiner, Liane I. F. Moura, Eva Zupančič, Ana S. Viana, Hila Doron, Pedro M. P. Gois, Neta Erez, Steffen Jung, Ronit Satchi-Fainaro, Helena F. Florindo. Immunization with mannosylated nanovaccines and inhibition of the immune-suppressing microenvironment sensitizes melanoma to immune checkpoint modulators. Nature Nanotechnology  DOI: 10.1038/s41565-019-0512-0. 2019.

Source and Contact

George Hunka <ghunka@aftau.org>

Communications Manager, American Friends of Tel Aviv University, Tel: 212.742.9070, ext. 117

Jordan Isenstadt Marino <jisenstadt@marinopr.com>, Tel: 212.402.3510

Apathy: The Forgotten Symptom of Dementia

Apathy is the most common neuropsychiatric symptom of dementia, with a bigger impact on function than memory loss – yet it is under-researched and often forgotten in care.

A new study has found that apathy is present nearly half of all people with dementia, with researchers finding it is often distinct from depression. Although common, apathy is often ignored as it is less disruptive in settings such as care homes than symptoms like aggression.

Defined by a loss of interest and emotions, it is extremely distressing for families and it is linked with more severe dementia and worse clinical symptoms.

Now, research led by the University of Exeter and presented at the Alzheimer’s Association International Conference in LA has analysed 4,320 people with Alzheimer’s disease from 20 cohort studies, to look at the prevalence of apathy over time.

At the start of the study, 45% presented with apathy, and 20% had persistent apathy over time. Researchers found that a proportion had apathy without depression, which suggests that the symptom might have its own unique clinical and biological profile when compared to apathy with depression and depression only.

Dr Miguel de Silva Vasconcelos, of the University of Exeter and King’s College London, said:

“Apathy is an under-researched and often ignored symptom of dementia. It can be overlooked because people with apathy seem less disruptive and less engaging, but it has a huge impact on the quality of life of people living with dementia, and their families. Where people withdraw from activities, it can accelerate cognitive decline and we know that there are higher mortality rates in people with apathy. It’s now time this symptom was recognized and prioritised in research and understanding.”

Professor Clive Ballard, of the University of Exeter Medical School, said:

“Apathy is the forgotten symptom of dementia, yet it can have devastating consequences. Our research shows just how common apathy is in people with dementia, and we now need to understand it better so we can find effective new treatments. Our WHELD study to improve care home staff training through personalised care and social interaction included an exercise programme that improved apathy, so we know we can make a difference. This is a real opportunity for interventions that could significantly benefit thousands of people with dementia.”

https://www.exeter.ac.uk/news/research/title_725251_en.html

The poster is entitled ‘The Course of Apathy in People with Dementia’.

Further Information and Contact

Louise Vennells <l.vennells@exeter.ac.uk>, Press and Media Manager

University of Exeter Medical School, Tel: +44 (0)1392 724927 or 07768 511866

Study: Fat Cells Play Key Role in Dangerous Transformation of Melanoma

Fat cells allow melanoma cells to penetrate the dermis, from which they spread, causing fatal metastases in vital organs,

Researchers at Tel Aviv University, led by Prof. Carmit Levy and Dr Tamar Golan of the Department of Human Genetics and Biochemistry at TAU's Sackler School of Medicine, have discovered that fat cells are involved in the transformation that melanoma cells undergo from cancer cells of limited growth in the epidermis to lethal metastatic cells attacking patients' vital organs.[1]

"We have answered a major question that has preoccupied scientists for years," explains Prof. Levy.

"What makes melanoma change form, turning aggressive and violent? Locked in the skin's outer layer, the epidermis, melanoma is very treatable; it is still Stage 1, it has not penetrated the dermis to spread through blood vessels to other parts of the body and it can simply be removed without further damage.

"Melanoma turns fatal when it 'wakes up,' sending cancer cells to the dermis layer of skin, below the epidermis, and metastasizing in vital organs. Blocking the transformation of melanoma is one of the primary targets of cancer research today, and we now know fat cells are involved in this change."

The research was conducted in collaboration with several senior pathologists: Dr Hanan Vaknin of Wolfson Medical Center, and Dr Dov Hershkowitz and Dr Valentina Zemer of Tel Aviv Medical Center.

The study was on published July 23 in Science Signaling and is featured on the journal's cover.

In the study, the researchers examined dozens of biopsy samples taken from melanoma patients at Wolfson Medical Center and Tel Aviv Medical Center, and observed a suspicious phenomenon: fat cells near the tumor sites.

"We asked ourselves what fat cells were doing there and began to investigate," adds Prof. Levy. "We placed the fat cells on a petri dish near melanoma cells and followed the interactions between them."

The researchers observed fat cells transferring proteins called cytokines, which affect gene expression, to the melanoma cells.

"Our experiments have shown that the main effect of cytokines is to reduce the expression of a gene called miRNA211, which inhibits the expression of a melanoma receptor of TGF beta, a protein that is always present in the skin," says Prof. Levy. "The tumor absorbs a high concentration of TGF beta, which stimulates melanoma cells and renders them aggressive."

Critically, the researchers have also found a way to block this transformation.

"It is important to note that we found the process reversible in the laboratory: When we removed the fat cells from the melanoma, the cancer cells calmed down and stopped migrating," adds Prof. Levy.

A trial of mouse models of melanoma yielded similar results: When miRNA211 was repressed, metastases were found in other organs, while re-expressing the gene blocked metastases formation.

In the search for a potential drug based on the new discovery, the researchers experimented with therapies that are known to inhibit cytokines and TGF beta, but which have never before been used to treat melanoma.

"We are talking about substances that are currently being studied as possible treatments for pancreatic cancer, and are also in clinical trials for prostate, breast, ovarian and bladder cancers," Dr. Golan said. “We saw that they restrained the metastatic process, and that the melanoma returned to its relatively 'calm' and dormant state."

"Our findings can serve as a basis for the development of new drugs to halt the spread of melanoma — therapies that already exist, but were never used for this purpose," concludes Prof. Levy. "In the future, we are seeking to collaborate with drug companies to enhance the development of the metastatic melanoma prevention approach."

Reference

1. Tamar Golan1, Roma Parikh1, Etai Jacob2,3,4,5, Hananya Vaknine6, Valentina Zemser-Werner7, Dov Hershkovitz7,8, Hagar Malcov1, Stav Leibou1, Hadar Reichman1, Danna Sheinboim1, Ruth Percik8,9, Sarah Amar6, Ronen Brenner6, Shoshana Greenberger10, Andrew Kung11, Mehdi Khaled12, and Carmit Levy1. Adipocytes sensitize melanoma cells to environmental TGF-β cues by repressing the expression of miR-211. Science Signaling 12 (591) eaav6847. DOI: 10.1126/scisignal.aav6847. 23 Jul 2019 .  

https://stke.sciencemag.org/content/12/591/eaav6847  

Source and Contact

George Hunka <ghunka@aftau.org>

Communications Manager, American Friends of Tel Aviv University, Tel: 212.742.9070, ext. 117

Jordan Isenstadt Marino <jisenstadt@marinopr.com>, Tel: 212.402.3510

New Proof of Link Between Obesity and Disease

Health and Medical

Evidence that obesity causes a wide range of chronic health conditions has been strengthened by a new method of analysis developed in South Australia Professor Elina Hypponen of the University of South Australia’s Australian Centre for Precision Health.

The University of South Australia’s Australian Centre for Precision Health researchers examined links between body mass index (BMI) and more than 925 diseases in 337536 UK volunteers, confirming the link between obesity and conditions such as diabetes, cancer and cardiovascular disease. The study was published in digital health journal The Lancet.[1]

Led by Professor Elina Hypponen, researchers developed a multi-dimensional analysis that subjected genetic data to stringent examinations in order to deliver high confidence of causality.

“We conducted five different analyses and the more consistent the evidence for a causal association between obesity and health outcomes across these five different approaches, the more confident we could be that we were looking at the true causal effect,” Professor Hypponen said.

She said while previous research suggested a high BMI was linked with increased risk of chronic diseases, the clinical trials used to asses health risks of obesity were typically too small or too short to assess causation with many of the diseases. To overcome this challenge, Professor Hypponen said they used alternative statistical approaches.

Drawing data from the UK Biobank – a research database holding health and genetic information from half a million UK volunteers – Professor Hypponen said the researchers looked at the link between genetic obesity risks and more than 900 disease outcomes.

“The results were really quite astounding,” she said.

“Fully consistent evidence across all approaches was seen for 14 different diseases, and for 26 different diseases evidence was obtained by at least four of the five methods used.

“What increases the confidence that these associations are largely reflective of real effects is the fact that those effects which came across with consistent evidence are also ones for which we have previous clinical evidence.”

Professor Hypponen said while all five of the approaches used to help prove causation rely on a number of statistical assumptions by working through each of the approaches, they were able to note consistent evidence of causal association.

She said the approach could be used to cement the relationship between disease risks and other health factors and has already been used by researchers to identify the link between serum iron concentration and disease risks.

Professor Hypponen said the study also highlighted the importance of genetic research to further the understanding that genes played in obesity, and the insights it could provide for the future management and treatment of obesity.

One of the key findings, according to Professor Hypponen, was the strong the relationship observed between obesity and diabetes.

“For example, we saw evidence for obesity effects on peripheral nerve disorders, chronic leg and foot ulcers, and even gangrene and kidney failure, which are all known to be diabetic complications.

“This suggests a key aspect to reduce comorbidity risk in obesity is careful monitoring of blood sugar and effective control of diabetes and its complications.”

References

1. Elina Hyppönen et al, A data-driven approach for studying the role of body mass in multiple diseases: a phenome-wide registry-based case-control study in the UK Biobank, The Lancet Digital Health. DOI: 10.1016/S2589-7500(19)30028-7. 2019. www.thelancet.com/journals/landig/article/PIIS2589-7500(19)30028-7/fulltext

Acknowledgement Citation

theleadsouthaustralia.com.au

http://theleadsouthaustralia.com.au/industries/health-and-medical/new-proof-of-link-between-obesity-and-disease/