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Dr. Marie Gabrielle Laguna

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Medical doctor-internist

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Living cells Can Be Observed With New Ultrasound Technique

Feb 20, 2017

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A promising ultrasound technique developed to observe inside living cells could be used for stem-cell transplants and diagnosing cancers. This breakthrough technique has been developed by the researchers at The University of Nottingham.

The new nanoscale ultrasound technique utilizes shorter-than-optical wavelengths of sound and might even challenge the optical super-resolution techniques that were awarded with the 2014 Nobel Prize for Chemistry. This new type of sub-optical phonon imaging offers precious information about the structure, mechanical properties and activities of individual living cells at a scale not accomplished before.

Advantages of�ultrasound technique

“People are aware that ultrasound is a way of imaging inside the body — in the simplest terms we’ve engineered it to the focus where it can see inside an individual cell. Nottingham is now the only place in the world with this facility,” remarked Professor Matt Clark, who contributed to the study.

In traditional optical microscopy which uses light, the size of the tiny object you can see (or the resolution) is limited by the wavelength. For biological specimens, the wavelength cannot be lesser than that of blue light since the energy carried on photons of light in the ultraviolet and shorter wavelengths is very high that it can break the bonds that hold biological molecules together to damage the cells.

Optical super-resolution imaging also has unique limitations in biological studies. This is because the fluorescent dyes it uses are frequently toxic and needs huge amounts of light and time to examine and reconstruct an image which is harmful to cells. Not like light, sound does not contain a high-energy payload. This has allowed the Nottingham researchers to make use of smaller wavelengths and observe smaller things and get to higher resolutions without disturbing cell biology.

“The best part is that, similar to ultrasound on the body, ultrasound in the cells does no damage and does not require any toxic chemicals to work. Due to this we can observe that one day what is inside cells could be put back into the body, for example as stem cell transplants,” mentioned Professor Clark.

Image credit:�University of Nottingham

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Bacterial Secret Code Responsible For Antibiotic Resistance

Feb 19, 2017

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Researchers discovered how pathogenic bacteria use secret code language for them to be resistant to antibiotics and understanding this code language can help researchers develop new antibiotics in the days to come.

Pathogenic bacteria have the ability to be hidden from the immune system and treatment as they go through an inactive state, where they are not discovered. For many years, researchers at Aarhus University have examined the molecular process that allows bacteria to hide in this way, and recent research suggests that they also utilize code language in their effort to avoid being controlled.

Palindrome Secret Code

A palindrome is a word that reads the same both forwards and backwards, such as the word “kayak.” A team of researchers from Aarhus University, Denmark, under the leadership of Associate Professor Ditlev Egeskov Brodersen, has found out that a high number of pathogenic bacteria make use of cryptic palindromes embedded in the sequence of amino acids in their proteins to decide whether the inactive state should be launched or disrupted.

The findings have been published in the journal Nucleic Acids Research, and include detailed three-dimensional structures of particular cell toxins that are triggered during treatment with antibiotics, and reveal what occurs to them when they attach to specific regions of the DNA of the bacterial cells. The toxins are normally kept in check by their partners, the so-called “anti-toxins,” and the researchers have found that the palindrome codes make the anti-toxins block two toxins simultaneously. The amino acid sequence of the codes binds like key in a lock, and the palindromic sequence is essential since the two toxins to be blocked are turned 180 degrees corresponding to each other.

And also, it appears that such codes are seen in unprecedented numbers among bacteria. In the study of over 4,000 bacterial genomes, the researchers have further shown that up to 25 percent of all known bacteria make use of such codes for resistance. Hence, the research findings denote that a better understanding of the code language of the bacteria is important in maximizing the possibilities of making new antibiotics in the future.

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Study Reveals Cellular Process Behind Premature Aging

Feb 18, 2017

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Researchers uncovered the process behind premature aging. Two genes, namely spns1 and atp6v0ca, are involved in regulating normal cell function. A disturbance in spns1 can trigger degradation and premature aging while atp6v0ca can inhibit that degradation. The study was conducted by scientists from the Florida campus of The Scripps Research Institute (TSRI).

Their trials in zebrafish propose that these combined genetic disturbances can work against premature aging and can expand developmental lifespan.”We discovered that the double defects did really work against senescence throughout development and expanded the animal’s survival and life span,” mentioned TSRI Associate Professor Shuji Kishi. The results, published recently in the journal Autophagy, could also guide the discovery of future therapies for diseases that involve the body’s failure to degrade unwanted or harmful compounds.

Premature aging

Cellular senescence is when cells halt dividing and is a natural part of aging. Interestingly, senescence is not only found in later aging stages but is also observed during embryonic development in vertebrates.

In the recent study, the researchers observed the gene spns1. In vertebrates such as zebrafish and humans, the protein encoded by spns1 is significant in a cellular activity called autophagy, when the cell moves unwanted stuff to a cellular structure called the lysosome. Earlier research had described that defects in this gene can also lead to senescence in the embryonic stage and premature aging symptoms in adulthood.

But, Kishi and his colleagues discovered that a simultaneous interruption of another gene called atp6v0ca, whose sole defect still leads to senescence — causes inhibition of the process triggered by the defective spns1 gene. “Our results propose that these two defects, in fact, function at a balance point that is critically associated with the regulation of developmental senescence — and that balance permits normal cell function,” explained Kishi.

The scientists are currently considering ways to control the balance between these genes as an approach to treat lysosomal storage diseases like Pompe disease, where the excessive accumulation of glycogen leads to severe muscle weakness. They consider there may also be purpose in treating age-associated degenerative diseases related to late-stage autophagy disruption.

“The use of proper inhibitors, selective for key steps in the biosynthesis of cellular macromolecules in general, may repair normal dynamics in the autolysosomal section and rectify the pathological storage that is the ultimate reason of these types of disease,” said TSRI Research Associate Shanshan Lian, the co-first author of the study.

The results may also lead to the development of tools to facilitate the identification of new genes that are involved in the aging process without the need for carrying out lengthy adult lifespan analyses. This strategy could be applied to the high-throughput identification of pharmacological agents that regulate aging and lifespan by means of improved resistance to various stressors, including oxygen radicals.

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The Novel Drug PAI-039 Prevents Blood Vessel Blockage

Feb 17, 2017

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According to a recent study, a new drug called PAI-039 could prevent heart problems like stroke, heart attack and other diseases by avoiding blockages in blood vessels. The study revealed that this drug acts as a protein inhibitor and could be a novel therapeutic approach to prevent cardiac diseases related to blockage of blood vessels. When there is a blockage in blood vessels, they could not effectively deliver oxygen and nutrients to the heart and brain, which consequently leads to stroke or heart attack.

“Arteries are living tubes that contract and expand in order to normalize blood flow to organs and muscles,” explained William Fay, M.D., senior author of the study, who works as a research scientist at the Harry S. Truman Memorial Veterans’ Hospital in Columbia, Missouri. “Soft muscle cells in the artery control blood flow by narrowing and expanding. But, when chronic inflammation happens in a blood vessel because of diabetes, high cholesterol and cigarette smoking, the soft muscle cells in the walls of arteries alter their activities. They slowly accumulate within the artery and narrow the blood vessel. On coronary arteries, which deliver blood to heart muscle cells, this activity creates blockages that can result in a heart attack.”

Efficiency of PAI-039 Drug

Plasminogen activator inhibitor-1, or PAI-1, is a naturally occurring protein inside blood vessels that regulates cell migration. Because of diseases such as diabetes and obesity, PAI-1 over-accumulates in blood vessels. This increases blockage formation. This activity happens not only in arteries, but also in vein grafts in patients who have undergone coronary artery bypass graft surgery.

Fay’s research team examined PAI-039, also called as tiplaxtinin, an experimental drug not yet used to treat humans. The researchers discovered that PAI-039 blocked the migration of cultured human coronary artery smooth muscle cells, and avoided the formation of blockages in arteries and bypass grafts in mice.

“We discovered that PAI-039 reduced blockage development by about 50 percent, which is a potent result in the models we used,” noted Fay. “Other than reducing vascular blockages, inhibiting PAI-1 also creates a blood thinning effect that avoids the blood clots that induce most heart attacks and strokes.”

Fay anticipates that if further studies are successful, PAI-039 or same kind of drugs could be used to avoid blockages in arteries and bypass grafts.

“I don’t believe there will be any single ‘magic pill’ that avoids arterial diseases, particularly for those with other high-risk conditions,” Fay said. “But, possibly someday a PAI-1 inhibitor can be used together with other approaches such as right diet and exercise, aspirin and cholesterol medicines to avoid blood vessel blockages and decrease heart attack and stroke risk.”

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Computational Tool Icages Facilitates Cancer Treatment

Feb 16, 2017

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Researchers built a tool that can quickly predict which genes are responsible for cancer so that cancer treatments can be earlier suggested. It is among the most complete tools of its kind, and the first that contains a user-friendly web interface that needs little knowledge of bioinformatics.

The researcher noticed that iCAGES recognizes individual cancer “drivers” for 77 percent of the time when given a pair of randomly selected driver genes and non-driver genes, in comparison with about 51 percent for other computational tools.

Majority of cancers are caused by the accumulation of somatic versus inherited genetic mutations, or variants. A lot of variants involved in several types of cancer have been recognized with genetic sequencing studies of large numbers of patients. But, this information is not always clinically helpful on an individual level. Cancer “drivers” can differ from patient to patient, and there are no practical clinical tools available for predicting which variants in an individual’s genome are driving his or her disease and which are present but not responsible for the disease. “Even when the genes driving cancer are identified, clinicians don’t have an effective way of selecting among the hundreds of possible drug therapies,” mentioned the lead researcher of the study Kai Wang, PhD, who serves as the associate professor of biomedical informatics and the director of clinical informatics at the Institute for Genomic Medicine at CUMC.

How does iCAGES work?

To overcome all these issues, Dr. Wang and his team built a computational tool named integrated CAncer GEnome Score (iCAGES). First, iCAGES examines the patient’s entire genome, comparing it to the genomic sequence of the patient’s tumor to find possible cancer-causing variants. Then, iCAGES cross-references these variants to databases of known cancer-causing genes, with the help of statistical analyses and machine learning techniques to prioritize the most possible driver genes. In the end, iCAGES matches the prioritized variants to FDA-approved and investigational drug therapies that particularly address those variants or genes. The whole process requires only 30 minutes. In comparison, traditional approaches need multiple separate steps involving human input, taking more than many weeks.

In a test designed to demonstrate how the tool would be used in real practice, Dr. Wang tested iCAGES by means of detailed sequencing data from a patient with lung cancer. Out of 129 possible cancer drivers, iCAGES pointed out a gene called ARAF. iCAGES utilized the genomic sequencing data to choose sorafenib as the best drug candidate out of 122 possible treatments. The patient’s oncologists also had the same conclusions, but they used a much more difficult and time-consuming strategy, which requires expert knowledge during the decision-making process. “The patient was provided with sorafenib and had an outstanding clinical response,” noted Dr. Wang. “It is worth to notice that sorafenib is not FDA-approved. However, the result proposes that iCAGES may facilitate in identifying new treatment strategies and off-label use of available approved drugs.”

When tested on various cancer patient databases, iCAGES seemed to be better than other computational tools at indicating cancer drivers from personal genomes and at recognizing helpful treatment.

“We expect that iCAGES can aid clinicians take full gain of the huge amounts of data on genomic sequencing and cancer variants, and elucidate personalized cancer therapy,” remarked Dr. Wang.

Image credit:�CUMC

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How B Lymphocytes Prevents Preterm Birth?

Feb 15, 2017

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A recent study uncovers the important role of a type of mother’s immune cells called B lymphocytes ��in resisting preterm birth triggered by inflammation. The study was conducted under the leadership of Kang Chen, Ph.D., assistant professor at Wayne State University.

Preterm birth can be defined as child birth before normal 37 weeks of pregnancy which affects up to one in every six births in the United States and many other countries. It is the primary cause of infant death and long-term illnesses and enforces heavy social and economic burdens. Even though preterm birth is a difficult condition, infection of the mother and resulting inflammation in pregnancy are very familiar causes.

Role of B lymphocytes

As per Chen, B lymphocytes produce antibodies to protect the body against infections, but scientists and clinicians have always considered that these cells are uncommon or absent in the uterine lining and not significant for pregnancy.

Chen’s lab found that in late pregnancy, mothers’ B lymphocytes not only exist in the uterine lining in both humans and mice, but also sense inflammation and uterine stress, which are main causes of preterm birth, and consecutively, make molecules such as PIBF1, inhibit uterine inflammation and premature birth.

“This research not only describes the long-neglected role of B lymphocytes in supporting healthy pregnancy, but also promotes therapeutic approaches of utilizing B lymphocyte-derived molecules like PIBF1 to avoid or treat preterm birth,” explained Chen.

Chen’s team has conducted proof-of-concept and efficiency studies in animal models, and with the support of the Wayne State University’s Technology Commercialization Office, applied for a patent for this potential therapeutic approach.

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Why Hypercholesterolemia A Dangerous Genetic Disorder Goes Underdiagnosed?

Feb 14, 2017

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A life-threatening genetic disorder called as Familial Hypercholesterolemia (FH) is both underdiagnosed and undertreated says a recent study conducted by Geisinger Health System in collaboration with the Regeneron Genetics Center (RGC).

It was published alongside another important study from the same Geisinger-RGC collaboration called as DiscovEHR. That other study explains exome sequencing and analyses of the initial 50,726 adult participants in the DiscovEHR cohort — all members of the Geisinger MyCode Community Health Initiative.

In the FH study, the researchers observed genetic variants causing FH in the DiscovEHR cohort and then compared the results against the de-identified medical histories of these patients as present in Geisinger electronic health records. Conventionally, in the United States, FH is diagnosed in patients with high cholesterol who also have a family history of stroke and early heart attacks. Genetic testing for FH is now rare in clinical practice.

FH is caused by a defect that makes the body incapable of eliminating “bad” cholesterol from the blood. This low density lipoprotein cholesterol or LDL-C then builds up, frequently undetected, and can result in early death from heart attacks or stroke, even in very young patients.

Findings of the recent study discovered many undiagnosed cases of FH and described the extent of FH in the general population.

Hypercholesterolemia and medical records

“The study explains to us that FH is about twice as frequent as it was once thought to be, and that large-scale genetic testing for FH facilitates detecting cases that would otherwise be missed,” noted Michael F. Murray, M.D.,who serves as Geisinger director of clinical genomics. “We currently hope to use DNA sequencing to have better management for patients.”

Among the various findings of the study are that one in every 256 people have a disease-causing mutation, or variant, in one of the three FH genes. It described that participants with a toxic FH gene variant had considerably higher “bad” cholesterol levels than those lacking an FH gene variant. They also had remarkably raised chances of both general and premature coronary artery disease.

“Accessing patients' that are de-identified medical records with their DNA data is a benefit that few others in this field have. Combined with the RGC’s exclusive technological and analytical resources, we are able to make significant discoveries that may lead to the implementation of precision medicine today and the development of new or advanced medicines tomorrow,” mentioned Noura Abul-Husn, M.D., Ph.D., associate director of translational genetics at the RGC and the co-author of this paper.

The study recognized 35 mutations, or variants, in the genes LDLR, APOB, and PCSK9 that have been verified to cause FH. Only 24 percent of people who carry FH-causing variants had enough criteria within their electronic health records to help make a probable or definite FH diagnosis, meaning that without genetic verification, many of these patients would go undiagnosed and are likely to be undertreated. Certainly, 42 percent of people with these FH-causing variants did not have a current active prescription for statins, the primary therapy for lowering cholesterol levels. Among those statin-treated people with FH-causing variants, only about a half of the population met goals for cholesterol lowering.

“Geisinger is dedicated to translating this significant research directly into advanced care for our patients,” said Geisinger Executive Vice President and Chief Scientific Officer David H. Ledbetter, Ph.D. “We have started a key effort to verify individual patient findings and notify individual participants and their doctors when genetic findings, that are known to cause illness, are discovered in our population,” he stated.

FH is one of the 27 genetic conditions being aimed at Geisinger. So far, nearly 200 patients — together with 29 FH carriers — have previously been reported to carry one or more disease-causing genetic mutations with consequences that can be treated. These conditions are mostly linked to risk for cancer or cardiovascular illness. The effort to return individual results will carry on as more results are verified.

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The Myth Behind Sudden Infant Death Syndrome Revealed

Feb 13, 2017

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A recent study could explain the mystery behind sudden infant death syndrome (SIDS) in human babies, which is considered to be linked with dysfunctional airway sensory neurons.

A newly discovered protein called Piezo2 at The Scripps Research Institute (TSRI) seems to be associated in how the body controls breathing, according to a recent study performed by scientists at TSRI and Harvard Medical School.

“The findings here might offer essential clues on how to treat patients with respiratory disorders” noted senior author Ardem Patapoutian, who serves as a professor at TSRI and also as a Howard Hughes Medical Institute (HHMI) investigator.

Using genetically engineered mouse models, the researchers discovered that newborn mice without the Piezo2 channel exhibit critical respiratory distress that causes death. Adult mice without the Piezo2 channel in sensory neurons show remarkable raise in tidal volume which is the amount of inhaled air in lungs, in addition to an impaired Hering-Breuer reflex (an inhibitory respiratory reflex that blocks lung over-expansion).

Piezo2 And Lung Functions

The Piezo2 ion channel was at first discovered as a new mechanosensor which means that the sensor of mechanical stimuli such as pressure or stretch, in Patapoutian’s lab in 2010. Further studies revealed that the Piezo2 channel seen in sensory neurons is needed for sensing touch sensation and muscle stretch in mice. These studies made researchers to speculate if Piezo2 has a role as a common stretch sensor in other organs such as lungs.

“Earlier studies proposed the occurrence of lung inflation sensors; though, their molecular identity or physiological significance has not been explained,” said Patapoutian.

The researchers dealt this question by making and characterizing Piezo2 “knockout” mice, in which the Piezo2 channel is removed throughout the animal or only from sensory neurons (more particularly, vagal sensory neurons that are recognized to manage breathing). They discovered that Piezo2 is important for proper breathing and lung expansion in newborn mice. Piezo2-deficient newborn mice exhibited unexpanded lungs and considerably shallow breathing.

“The lungs interact with the brain via sensory neurons. The Piezo2 channel in sensory neurons creates a message about lung volume changes, and Piezo2-containing sensory neurons convey this message to the brain,” explained TSRI Research Associate Keiko Nonomura, who is the co-first author of the study and along with TSRI Research Associate Seung-Hyun Woo. “Piezo2-deficient mice were unable to create an accurate message regarding their lung volume changes. Consequently, these mice were unable to receive appropriate output from the brain.”

Prominently, as per recently published papers, Piezo2-deficient human infants also exhibit shallow breathing and need medical attention.

“Piezo2-deficient newborn mice grow normally until birth. The problem only arises when the mice are born and try to breathe on their own,” stated Nonomura.

Understanding sudden infant death syndrome and other respiratory diseases

The researchers were amazed to notice a surprising result of removing Piezo2 in sensory neurons of adult mice. When the Piezo2 channel was removed either in all sensory neurons or only from vagal sensory neurons, adult mice could do breathing, but they inhaled remarkably more air than Piezo2-intact mice.

Under standard conditions, animals halt breathing when they are forced to breathe in more air, but Piezo2-deficient adult mice without the Hering-Breuer reflex keep on breathing when they were forced to inhale more air.

Why this variation between adults and newborns? The researchers discovered that Piezo2 has different roles in newborns and adults because establishing independent breathing in newborns is more difficult.

“At birth, the respiratory system of newborn experiences drastic structural modifications, as liquid-filled compressed fetal airways are being cleared out and filled with air,” noted Patapoutian. “Hence, newborn airways undergo larger mechanical changes when compared to adult airways which have previously established regular breathing.”

These data, for the first time, describe the significance of mechanosensory transduction in adult respiration. This research is also applicable for understanding respiratory diseases, such as chronic obstructive pulmonary disease (COPD) and sleep apnea, which seems to be linked to disruption of the airway sensory feedback system.

The team mentioned that future studies could also utilize the same genetic manipulations to better understand the work of Piezo2 in other physiological processes such as heart rate control and bladder function.

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The First Oral Capsule To Treat Hemophilia

Feb 12, 2017

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Researchers are working on a pill to treat hemophilia, which would let patients with type B hemophilia have oral formulations of clotting factor IX instead of many weekly injections to keep bleeding under control. The study was funded by National Institute of Biomedical Imaging and Bioengineering. A team of researchers are working under the leadership of Professor Nicholas Peppas at the University of Texas at Austin’s Institute of Biomaterials, Drug Delivery, and Regenerative Medicine

Hemophilia B can be defined as a genetic disorder, which affects boys who have a defective factor IX gene that exists on the X chromosome they obtained from their mother. This leads to a deficiency of the factor IX protein, which the body needs for blood to clot. Though mothers transfer the defect, they do not have the disorder, as they have a normal factor IX gene on their other X chromosome. It is very uncommon, but there is a possibility that a daughter might inherit hemophilia if her father has it and her mother also carries the gene for hemophilia.

“Many weekly injections of factor IX is so hard for the boys who require the clotting factor to prevent potentially fatal bleeding incidents, also for their families” explained Peppas. “But, in working with these families, we soon found that there was also an emotionally challenging aspect for mothers, who take the burden that they passed this disease on to their sons. This has added necessity to our research since we know that oral dosage of factor IX could be a better relief for these families.”

Engineering a polymer to deliver factor IX

If a patient were to swallow factor IX protein only, it would be rapidly digested by stomach acids and its biological activity would be lost as a clotting factor. Therefore, the researchers designed a protective polymer capsule that has many critical roles in altering the environment of the digestive tract.

First, the polymer is engineered to be impermeable to harsh stomach acids such as pepsin, in order to avoid factor IX protein from being digested. Second, the capsule passes on through the stomach and into the small intestine which has the protease trypsin. The polymer is designed to be degraded by trypsin, facilitating the intestinal fluids to enter and make the capsule swell. This swelling allows degradation of the capsule and ejection of the clotting factor into the bloodstream for absorption.

The latest version of the polymer has been enhanced from earlier designs since it is highly biodegradable in the neutral pH of the small intestine. The recent biodegradable capsule upholds a several-fold increase in the absorption of factor IX through the intestinal wall. The result is that each capsule can release more of the factor IX protein into the bloodstream.

Due to years of advancement in the polymer design of the capsule, the latest results in investigational cell culture systems denote that taking two capsules of the recent formulation orally can distribute as much factor IX similar to a single needle injection.

After accomplishing this benchmark, Peppas is working together with other players in the industry to speed up the required testing in animals, with the objective of moving forward to human clinical trials and FDA approval as soon as possible.

His research could provide a better treatment for hemophilia in the days to come. For more interesting insights on medical research, visit our site and subscribe to our newsletter.

Cimaglermin Facilitates Heart Repair

Feb 11, 2017

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According to a recent study, Cimaglermin, a novel experimental drug, can be helpful in restoring cardiac function after heart failure.

Heart failure, due to the loss of cardiac function, is one of the major causes of death across the globe. A significant portion of heart failure patients, particularly those with severe left ventricular systolic dysfunction, do not sufficiently respond to current medical therapy.

Efficiency of�cimaglermin

Researchers evaluated the safety and efficiency of a single combination of cimaglermin, which plays the role of a growth factor for the heart, facilitating the structural, metabolic and contractile elements of the heart to repair itself after the injury. The study was conducted among 40 heart failure patients who were undergoing best medical therapy for at least three months earlier to the trial. When compared with patients who received a placebo, patients who given a high dose of cimaglermin had a prolonged increase in left ventricular ejection fraction, or pumping capacity, through 90 days after dosage, with the highest increase reached at day 28.

“These results support continued clinical development of the experimental drug cimaglermin, including further safety assessments and detailing the potential advancement on clinical heart failure outcome measures,” mentioned Daniel J. Lenihan MD, the lead author of the study who works with the division of cardiovascular medicine at Vanderbilt University. “Along with all investigational therapeutics, further studies will be needed and are subject to regulatory review to conclude if the relative risks and benefits of cimaglermin confirm approval.”

The most general side effects were headache and nausea, which were, in the short term, related to drug exposure. One patient who received the maximum planned dosage of cimaglermin had an adverse reaction that met the stopping criteria of Federal Drug Administration guidance for drug induced liver injury.

Limitations of this study include the smaller sample size and that the patients only received a single dose rather than multiple infusions.

“Even though the results of the study must be considered as provisional because of the small numbers of patients, the results of this study are however very exciting,” noted Douglas L. Mann, MD, FACC, editor-in-chief of JACC: Basic to Translational Science. “Rather than blocking the basic mechanisms that lead to cardiac injury, the early results with cimaglermin propose that it can also be possible to administer therapeutics that permit the failing heart to repair itself with the help of its own repair mechanisms. If the findings of this study can be replicated and translated into advancements in clinical results in larger numbers of patients in phase II and III clinical trials, it will symbolize a paradigm shift in the way in which clinicians treat patients with heart failure.”

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