Researchers Reveal Connection Between Insulin and Human Lactation

A new study conducted by a research team from the Cincinnati Children’s Hospital, from the United States, reveals a connection between insulin and lactation. This study adds more information to their precedent studies regarding mothers who experience insufficient lactation. It is also the first study that describes the increased sensitivity of the mammary gland towards insulin during lactation. Furthermore, it is the first study the accurately depicts the activation of specific genes during lactation.

The research team used RNA sequencing in order to create an extremely detailed blueprint of the lactation process in the human mammary glands. The study, authored by Laurie Nommsen-Rivers was recently published in the online journal PLOS ONE. Professor Nommsen-Rivers has conducted previous studies regarding the lactation process of female patients suffering from a sub-optimal glucose metabolism. This type of metabolism occurs in patients that are overweight, obese or in patients with an advanced maternal age. A sub-optimal glucose metabolism causes the lactation process to slow down, thus, milk takes longer to form. Her study was one of the first to suggest a link between insulin and lactation. Her current paper reveals how the human mammary gland increases its sensitivity towards insulin during the lactation process.

Scientists thought for many years that insulin doesn’t have a role in the regulation of cells that produce milk, due to the fact that insulin isn’t needed by the cells for glucose intake. However, Nommsen-Rivers’ study reveals that insulin plays a more important role, other that just facilitating glucose intake. According to the authors of the study, during the transition of the breast towards a bio-factory for proteins, carbohydrates and fats necessary for newborn feeding, there is a major increase in activated insulin receptors, which eventually causes a dysregulation of insulin. Due to the fact that approximately 20% of women between the ages of 20 and 44 are diagnosed with pre-diabetes, authors say that there is a probability of up to 20% that future mothers will have an insufficient milk supply for their newborns.

Through the use of a non-invasive maneuver called RNA sequencing, researchers were able to observe the RNA sequences found in the cells of the mammary gland. These RNA sequences are responsible for the production of the specific proteins found in the human milk. Furthermore, the research team created the first database of genes expressed in the mammary gland available to the general public. The RNA sequencing method allows for the creation of highly detailed portraits of the genes that are expressed in the milk-producing cells found in the human mammary glands. Researchers discovered the synchronous activation and deactivation or several genes throughout the lactation process, starting with the colostrum and ending with the mature milk.

More specifically, the PTPRF gene, known to play an important role in the suppression of intracellular signals that would normally be triggered by the binding of insulin to its cellular receptor, might be used as a biomarker that would link insulin resistance to an insufficient milk secretion. The research team is currently planning a phase I/II clinical trial regarding the action of a drug that is already used to control the glucose levels of type 2 diabetes patients. The clinical trial will be conducted in order to discover whether or not the drug is able to improve the action of insulin on the cells from the mammary gland, thus increasing the quantity of produced milk. Even though the use of a drug is not the best way to treat the sub-optimal glucose metabolism, Dr. Nommsen-Rivers agrees that it would be an excellent start to prove or disprove her recent discovery through the use of a placebo-controlled double-blind clinical trial.

Sleep Restriction Revealed to be Cause of Weight Gain in Healthy Adults

A recently published study shows that adults who suffer from chronic sleep restriction are more susceptible to gaining weight due to an increased calorie consumption during night hours. The study is one of the largest and most diverse study regarding healthy patients with bad sleeping habits and who suffer from sleep restrictions. According to the results, patients who slept for only 4 hours every night, for 5 consecutive nights experienced a higher weight gain than patients who slept for 10 hours every night.

Researchers report that the higher weight gain for the patients who were experiencing sleep restrictions is due to the fact that they had a higher calorie intake during the additional hours of wakefulness. Moreover, the calorie consumption derived from fat was higher during night hours, compared to that of day time meals. The author of the study, Andrea Spaeth, reports that although precedent studies have already shown that sleep deprivation is linked to weight gain, the results of her study show that even in laboratory conditions, the results were similar.

The study, set to be published in the July edition of the journal Sleep, was conducted in a laboratory from the University Hospital of Pennsylvania. Researchers examined a group of 225 healthy subjects, between the ages of 22 and 50, which were randomly assigned to one of two groups. The first group consisted of patients who were to be deprived of sleep, while the other group consisted of patients who received a normal amount of sleep. The study span over a period of 18 days.

The subjects received meals at pre-scheduled hours, while additional food was available in the kitchen for the subjects who wanted to eat more than just the pre-scheduled meals. Subjects were not allowed to exercise during the testing period. Sedentary activities, such as reading, playing video games and watching TV were permitted. The study also reports that male subjects gained more weight due to sleep deprivation, when compared to female subjects. Another observation made by the research team is that Africa American subjects also gained more weight than Caucasian subjects.

According to Spaeth, the results showed significant differences between races and genders, regarding weight gain, when patients were deprived of sleep. She also notes that African Americans are more susceptible to weight gain due to the fact that they are more likely to suffer from sleep deprivation outside laboratory conditions as well. Spaeth reports that further studies regarding the behavioral and psychological mechanisms involved in this susceptibility should be conducted in order to better understand the causes.

The AASM (American Academy of Sleep Medicine) declares that weight gain is one of the most important risk factors for OSA (obstructive sleep apnea). OSA is a common disorder with a large impact on the quality of life of the affected patients. The risk of OSA gradually increases with weight gain, reaching the highest prevalence between patients suffering from morbid obesity. Earlier this week, AASM supported the new policy of the AMA (American Medical Association), which recognizes obesity as a medical disorder.

New Cancer Regulation Pathway Discovered by Research Team

A research team from the University of Florida have determined a molecular pathway closely linked to the deadly proliferation of the cancerous cells of glioblastoma, a form of cancer that is considered to be the most malignant form of brain cancer. The study will be  published shortly in the journal EMBO Molecular Medicine. According to the researchers, their study could aid physicians towards a better understanding of cancer treatment, while also offering a new target for drugs against glioblastoma.

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According to the NCI (National Cancer Institute), approximately 23 thousand patients (13 thousand men and 10 thousand women) were diagnosed with brain and nervous system tumors in the past year alone. Estimates show that almost 50% of these patients have died since. The main author of the study, Florian Seibzehnrubl from University of Florida, collaborated with researchers from various disciplines, including pathology, immunology and neuroscience, from the United States and Germany.

Siebenzehnrubl affirms that glioblastoma is the most malignant type of nervous cell cancer, and one of the most common brain tumors in adults worldwide. He also mentions that currently there is no cure for glioblastoma, and the prognosis is very poor due to the fast proliferation of the cancerous cells, which can quickly spread throughout the whole brain. Glioblastoma is a chemotherapy-resistant tumor, and as such, even if surgery and irradiation are able to eradicate the initial tumor, most patients suffer from a recurrence shortly after existing therapy.

The current study reveals a new pathway, called ZEB1, which is responsible for metastases and chemotherapy resistance. Professor David Sandak, of the Accelerate Brain Cancer Cure philanthropy organisation, reports that ZEB1 is known to be found in various types of cancer, however little information is known about it being a transcription factor for brain tumors. “We are excited about the finding as it integrates a single regulatory pathway with multiple oncogenic mechanisms and provides promise for a new therapeutic target for glioma”, added Sandak.

Siebenzehnrubl says that patients who have the ZEB1 pathway active suffer from a more sever form of brain cancer than other patients. According to his report, the disease of patients with the ZEB1 pathway spreads more rapidly, is resistant to chemotherapy and causes an earlier death. Apparently, the ZEB1 protein is responsible for controlling the genetic information that passes through the pathway. However, unlike other proteins, the ZEB1 protein doesn’t have a specific receptor that can be targeted with drugs, making therapy against the pathway more difficult that previously thought.

As a conclusion, Siebenzehnrubl says that this study revealed a new target for brain cancer therapy. Further research is still needed in order to find if there are other pathways that are responsible for the regulation of these cancerous cells, due to the fact that the ZEB1 pathway is only present in approximately 50% of the cases of glioblastoma.

Researchers Suggest Possible Cause for Narcolepsy

More than a decade ago, in the year 2000, researchers at the Sleep Research Center, from UCLA (University of California, Los Angeles), revealed that patients suffering from narcolepsy had almost 90% less neuropeptide hypocretin producing nervous cells, when compared to healthy patients. Narcolepsy is a neurological disorder that causes excessive sleepiness and uncontrollable periods of daytime sleep. The brain of narcoleptic patients is unable to control their circadian rhythm and clock. Another symptom that is common with narcoleptic patients is cataplexy, a sudden loss of muscle tone that causes patients to fall. Thought to affect approximately 3 million people worldwide, narcolepsy is still a disease without a cure.

The research from UCLA was the first study to have revealed a possible cause for narcolepsy. Following studies conducted by the same research team revealed that hypocretin is a chemical compound responsible for elevating alertness levels and mood. According to the studies, the death of cells called hypocretin cells, could be a possible cause of narcolepsy. However, their assumptions weren’t proven. Their newest study, published in the journal Annals of Neurology, reveals that an increased number of histamine-containing cells found in the brain could be the cause of death for the hypocretin cells.

Professor Jerome Siegel, one of the leaders of the study, reports that patients suffering from narcolepsy have approximately 65% more histamine-containing cells, when compared to healthy patients. The study suggests that the high number of histamine-containing cells is responsible for the loss of hypocretin-containing cells in patients suffering from narcolepsy. Histamine is a chemical molecule involved in the immune system. It is responsible for causing allergies in many patients with defective immune systems. However, histamine is also present in a type of cell found in the brain.

In their study, scientists examined the brains of 5 narcoleptic and 7 healthy brains taken from human cadavers. All 5 patients suffering from narcolepsy were diagnosed, prior to their death, as narcolepsy with cataplexy. Both dog and mouse models were examined in this study. The research team discovered that the brains taken from narcoleptic patients contained approximately 65% more histamine neurons that the brains of healthy patients. However, this observation wasn’t the same for the animal models.

Professor Siegel reports that even though both humans and animals with narcolepsy suffer from the same symptoms, it seems as the amount of histamine-containing cells found in the brains of narcoleptic animals remained unchanged. According to precedent studies, narcolepsy in animals is caused by a genetic mutation that blocks the function of hypocretin. However, until now, the cause of narcolepsy in humans was unknown.

“Our current findings indicate that the increase of histamine cells that we see in human narcolepsy may cause the loss of hypocretin cells”, affirmed professor Siegel. Furthermore, Siegel explains that the study might lead to further understanding of the brain’s plasticity and neurogenesis.

Red and Processed Meats Linked to Higher Colon Cancer Mortality

According to a new study, the survival rate of patients suffering from colon cancer decreases if patients consume excessive red mead and processed meats. The study was recently published in the Journal of Clinical Oncology. Led by professor McCullough, the study comes as a support for precedent studies that suggest that a diet rich in fruits and vegetables is more beneficial to colon cancer patients, unlike a diet rich in red meat and processed meats. McCullough affirms that the study accentuates the importance of a healthy diet throughout one’s lifetime.

After studying data from almost 2,300 patients suffering from colon cancer, the research team revealed that patients on a rich meat diet had a lower survivability rate than patients with a diet rich in vegetables and fruit. More specifically, the data published in the study shows that patients who served red meat and processed meat at least 4 times a week had a mortality rate as much as 79% higher than that of other patients. Moreover, patients with a high-intake of meat prior to their colon cancer diagnostic had a higher mortality rate than others.

Nevertheless, according to Dr. Jeffrey Meyerhardt, the study doesn’t show that the cause of the higher mortality is in fact red meat or processed meats. Meyerhardt affirms that there isn’t enough information about the role of meat in the mortality rates of colon cancer patients. However, the study is still suggestive for the role that meat plays in the overall health of these patients.

The data taken from more than 2,300 United States patients who were diagnosed with colon cancer was examined for this study. During the study, more than 1,000 of the studied patients have died, with approximately 400 patients dying from colon cancer. All of the  patients who took part in the study were also part of a larger study involving nutrition and cancer. They had been regularly completing questionnaires about their diet, prior to their colon cancer diagnostic. Due to this fact, McCullough and his team managed to analyze the impact of the patient’s diet on their survivability.

The analysis of data received from patients prior to their cancer diagnostic reveals that a high intake of meat, specifically more than 7 meat meals per week for men and more than 6 meat meals per week for women, increased the mortality rate by almost 30%. However, most of the recorded deaths were caused by cardiovascular problems. Only the patients who continued to eat a large amount of meat after being diagnosed with colon cancer were found to have an increased mortality rate.

The reasons behind a higher mortality rate between meat consumers is not yet fully understood, according to Meyerhardt. However, precedent studies have shown that meat is responsible for the production of chemical compounds, such as N-nitroso compounds and heterocyclic amines, that are responsible for damaging the colon cells. In theory, this is the one of the processes that can lead to the onset of colon cancer, yet it doesn’t explain how it could affect patients’ survivability.

Meyerhardt suggests that based on recent findings, patients diagnosed with colon cancer should reduce the intake of red meat and processed meat. The results of the study also suggest that cutting down on the meat intake improves survival rates of patients, whether they are diagnosed with colon cancer or not. However, according to both Meyerhardt and McCullough, reducing the amount of red meat is not enough. According to them, a healthy diet also includes an increased amount of vegetables, fruits, whole-grains and vegetable oils.

Researchers Reveal Dopaminergic Neurons Derived from PSCs Could Treat Parkinson’s

A research team consisting of members from three major United States universities (Colorado, Rush and Yale) and scientists from the St. Kitts Biomedical Research Foundation, managed to transplant embryonic stem cells from humans to primates suffering from a laboratory modeled Parkinson’s disease. 6 weeks after the transplant, researchers report that the cells are still viable and are very well integrated into the host primates. The study was recently published in the online journal Cell Transplantation.

Parkinson’s disease is a neurodegenerative condition that affects the central nervous system. Approximately one and a half million U.S. citizens and more than ten million people worldwide. Symptoms include postural instability, bradykinesia, rigidity and tremor. These motor symptoms are caused by the death of the dopamine-generating cells found in the substantia nigra. The cause of the disease is not yet fully understood by scientists, but there are several therapies currently targeting the symptoms.

According to Professor Eugene Redmond, from the School of Medicine at the Yale University, Parkinson’s disease was among the first neurological disorders to which neuron-replacement therapy was considered. Starting in the early 1970s, researchers made progress towards learning the requirements to differentiate stem cells into dopamine-generating nervous cells. Since then, researchers progressed towards discovering the correct gene expression, the right amount of growth factors and the propitious culture factors that would result in the creation of dopamine-generating neurons.

Dopamine1

However, precedent studies show that if dopamine-generating neurons are transplanted into animal models, such as primates and rodents, the effects are only short-lasting. Furthermore, only a very small amount of studies reveal functional improvement. According to the authors of the current study, they tested the long-term effects, survival rates and functional benefit of the dopamine-generating neurons implanted into laboratory primates suffering from Parkinson’s disease. As also shown in previous studies, the gene expression responsible for the activity of the enzyme known as TH (tyrosine hydroxylase), is only transitory. Tyrosine hydroxylase is an enzyme that plays an important role in the synthesis of catecholamines. Researchers have been trying to discover the best cellular stage and the best culture environment in order to increase the survivability of the transplanted cells. One factor that was underlined was the need for a stronger immunosuppression.

Professor Redmond affirms that the results of this study reveal that these dopamine-generating neurons, derived from PSCs (pluripotent stem cells), maintain their responsive abilities once they were transplanted into the brains of primates. However, the absence of a continuous TH expression shows that further research is needed in order to create and maintain the correct form of dopamine-generating neurons.

Although the study shows that the transplanted neurons are capable of surviving in the brain of primates, the research team concluded that further long-term studies need to be don in order to better understand the factors that contribute to a functional long-term replacement of dopamine-generating neurons.

 Development of the Bionic Eye

In collaboration with multiple research centers, through the Artificial Retina Project, researchers from Los Alamos participated in the production of the first bionic eye. The first bionic eye, named Argus II, was recently approved by the United States FDA (Food and Drug Administration). It will be used for patients suffering from either retinitis pigmentosa or sever AMD (age-related macular degeneration). Retinitis pigmentosa is a rare, inherited, degenerative eye disease that eventually causes severe vision impairment and even blindness. AMD is a medical condition which affects adult and elderly patients, consisting of vision loss in the macula, due to retinal damage. The research team from Los Alamos was part of the Advanced Concepts team of the Artificial Retina Project.

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Argus II operates through the use of a mini-camera mounted in a pair of eyeglasses. The camera captures images and sends the information to a microprocessor through wireless technology. The microprocessor, worn by the patient on a belt, further converts the images to electrical signals. These electrical signals reach the retina of the patient through an electrode array, which stimulates the optic nerve, and through the optic nerve, the stimuli reach the brain. Blind patients can be taught how to interpret these visual signals.

Argus II

The research team examined the pathways through which visual data is encoded as electrical impulses. They managed to improve the visualization and interpretation of neural activity patterns derived from the stimulation of the retina. They used high-performance video cameras and infrared illumination in order to document the birefringence properties of the nervous tissue associated with the electrical stimulation of the retina, whilst also observing the small changes in the scattering of light. The research team from Los Alamos also advised the rest of the research consortium on the usage of technologies capable of mapping the human brain function.

Researchers developed a theory through which they managed to map the retinal function of patients by analyzing polarized light signals, produced by the nerve cells found in the retina. The method consisted in a computer generated model of the retina which is capable of predicting the function of retinal neurons as a result to different patterns of stimulation. Furthermore, the team managed to develop several theoretical models of nervous cells response to electric stimuli. Their models show results towards new strategies for further improvement of the bionic eye and the development of other therapies for the visually impaired patients.

The Artificial Retina Project is conducted by the United States Department of Energy. It consists of a collaborative work effort between national research laboratories (Los Alamos being one of them), national universities (from California, Utah and North Carolina) and private companies. The goal of the team is to develop an artificial eye capable of restoring at least limited vision, so that visually impaired patients would be able to read and recognize friendly faces. So far, researchers managed to develop an instrument that contains an array of micro-electrodes that are implanted in the eyes of patients suffering from forms of retinal disease.

A part of the funds for the Los Alamos laboratory is provided by the U.S. Department of Energy, whilst the rest of the funds come from LDRD (Laboratory Directed Research & Development), NSF (National Science Foundation) and the NIH (National Institutes of Health).

Biomarker That Predicts Breast Cancer Recurrence Risk

A new study, published in the online edition of the Journal of the National Cancer Institute, reveals that a new biomarker could be responsible for accurate predictions on breast cancer recurrence in women previously treated with tamoxifen. Researchers from the MGHCC (Massachusetts General Hospital Cancer Center) report that the ratio between the genes known as HOXB13 (responsible of encoding the homeobox protein Hox-B13) and IL17BR (responsible for encoding the Interleukin-17B receptor) could be used to indicate women that would only need treatment with letrozole (an aromatase inhibitor) and women who are at risk for breast cancer recurrence.

According to Dennis Srgoi, the lead author of the study, the majority of patients with an early stage of ER-positive breast cancer can show no signs of recurrence in the first five years after undergoing treatment with tamoxifen, however, they still have a chance of cancer recurrence after 15 or more years after the initial tamoxifen therapy. He also added that the new biomarker is capable of identifying the subgroup of patients that still have a high risk of breast cancer recurrence after tamoxifen, whilst also revealing the subgroup of patients that will best benefit from the letrozole therapy.

Precedent studies lead by professor Sgroi revealed that the ratio between the expression of two genes, HOXB13 and IL17BR, can determine the cancer recurrence of ER-positive/lymph-node-negative breast cancer, regardless if the patients had received treatment with tamoxifen. Sgroi’s current study was meant to discover the prediction potential of the HOXB13/IL17BR ration for both prognosis and identification. The prognosis part refers to the prediction of recurrence in tamoxifen-treated patients. The identification part refers to identifying the patients who would benefit the most out of a continued treatment with letrozole.

In order to answer these two questions, Sgroi’s team analyzed tumor samples taken from a placebo-controlled trial cohort known as MA.17. This clinical trial had already confirmed that the usage of letrozole after tamoxifen treatment improved the survival rates of patients. The tissue of 83 patients with recurring breast cancer was examined. 52 out of the 83 patients were in the control group, receiving placebo, whilst 31 patients were in the letrozole-receiving group. Tissue samples from another 166 patients without recurring breast cancer were also examined. 75 of these patients were in the placebo-group whilst 91 were in the letrozole-receiving group.

The analysis of the samples revealed that if the expression level of the HOXB13 gene is greater than that of the IL17BR gene, there is an increased risk of breast cancer recurrence after tamoxifen treatment. However, this risk is significantly lowered if the patient receives treatment with letrozole. Professor Paul Goss, the co-author of the study, reports that their findings show that approximately 60% of the women suffering from this type of breast cancer can be spared of unnecessary treatment. Furthermore, the 40% of patients who have an increased risk of cancer recurrence are now identifiable, thus allowing doctors to start treatment with letrozole and reduce mortality rates.

Duchenne Muscular Dystrophy Treatment

A research team from Duke University, in the United States, managed to repair the mutation of a gene responsible for the onset and development of DMD (Duchenne muscular dystrophy). For their study, the researcher used cellular samples taken from patients suffering from DMD. Rather than using gene therapy in order to repair the genetic mutations, the research team from Duke created a novel technique that is able to change the mutated gene into a healthy gene. The study was recently published in the online journal Molecular Therapy.

According to the research team, this new technique might prove to be safer and more stable than any current genetic therapy method. Currently, they are conducting several other tests on animal models with DMD. DMD is a genetic muscular disorder which affects 1 in almost 3,600 male newborns. The genetic mutation responsible for the disease is located on the X chromosome, meaning that there is only one copy of the mutation. Scientists presume that females have a healthy copy of the gene, thus only rarely exhibiting the symptoms of the disease.

Duchenne Muscular Dystrophy

The gene affected in DMD is called dystrophin gene. It regulates the production of dystrophin, a protein that is essential for the structural integrity of the muscle fibers. Due to the lack of dystrophin protein, patients with DMD suffer from a gradual deterioration of their muscles, which eventually leads to paralysis and even death. Patients with DMD most often die before the age of 25. Charles Gersbach, an assistant professor at Duke affirms that current genetic therapies focus on adding healthy genes in order to stop the expression of the mutated genes. However, this approach can sometimes cause unforeseen problems.

“Our approach actually repairs the faulty gene, which is a lot simpler”, said David Ousterout, a graduate student from Gersbach’s laboratory, and the leader of the study. He explained that the newly developed technique finds the faulty gene and the repairs it in order to recover its initial functionality. The technique consists in synthesizing proteins known as TALENs (transcription activator-like effector nucleases). These are artificial enzymes capable of altering most of the genetic sequences found in the DNA. TALENs bind to the faulty gene and correct its defect, thus recovering its normal function. According to professor Gersbach, there are no known treatments for DMD at this time. “Patients usually are in a wheelchair by the age of ten and many die in their late teens or early twenties”, he added.

DMD has been intensively studied by researchers from around the world. The currently developed technique is believed to be capable of treating more than 60% of DMD patients. According to Ousterout, precedent studies have revealed that some DMD symptoms were alleviated when dystrophin protein levels were raised through other techniques. Professor Gersbach concluded that if the technique proves to be able to treat DMD, it could be used to treat other genetic diseases, such as hemophilia or drepanocytosis.

 Understanding Heart Failure Mechanisms

Researchers from the University of Bristol, in the United Kingdom, recently managed to resolve the mystery behind the mechanism through which the heart regulates its contractions. Their findings, which could lead to better understanding of heart failures, have been published at the end of this week in the journal Biophysics. The contraction of the heart’s muscles is switched on by the influx of calcium within the muscular cells. When the electrical signal ” action potential, mediated by very small amounts of calcium, reaches the cell it causes the release of calcium from intracellular storing organelles. Researchers showed interest in this mechanism due to the fact that both the action potential and the response involves the use of calcium, and the amount of calcium that triggers the release of intracellular calcium is very small.

Professor Mark Cannell and his research team from the School of Physiology, within the University of Bristol, found an answer to this problem almost 20 years ago, in the early 90’s. They found out that the release of calcium was time-dependent, which allowed for the calcium releasing events to be graded. The micro-events leading to the release of intracellular calcium from their storing organelles, called  sarcoplasmic reticulum, are known as ‘calcium sparks’. In the heart muscle, these sparks occur when clusters of ryanodine receptors are activated by the calcium influx. Even though each micro-event should have a regenerative effect, the time-dependence results in ‘calcium sparks’ not activating due to the fact that the trigger had already passed its location. However, their discovery did not find out why these calcium sparks eventually terminated themselves.

For the current study, a team formed by researchers led by Professor Cannell and Doctor Laver, discovered the answer to the question. The research team created a 3D model of the releasing mechanism and its sensitivity towards calcium. Their computer model revealed what they call ‘induction decay’ ” a process through which there is an automatic release termination, without the need of other  mechanisms. As a result, one of the keys to understanding the cardiac contraction regulation might have been resolved. This discovery could lead to the better understanding of heart failures, due to the fact that precedent studies have shown that in case of a heart failure, the calcium releasing mechanism is involved. “Thanks to sophisticated computer modeling, we have been able provide the necessary insight into the complex behavior of this fundamental system”, concluded Professor Cannell