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Dr. Marie Gabrielle Laguna

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Medical doctor-internist

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Novel Method to Diagnose Anxiety Disorders in Autistic Children

Jan 28, 2017

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According to a recent study, a new method effectively diagnosed the symptoms of anxiety, which had the tendency to be one of the autism symptoms.

Connor Kerns, PhD, who serves as an assistant research professor in the A.J. Drexel Autism Institute, devised this new method. She mentioned that Anxiety is an internal symptom, others may not notice it. It can be felt internally only by the person within their minds and bodies. A child may stay away from a social event since they are not socially motivated which is one of the symptom of autism spectrum disorder � or as they are scared of social rejection � a common symptom of anxiety.�

As children with autism may have troubles in expressing themselves, it is generally up to their parents to differentiate whether their behavior is really a symptom of autism or of anxiety. Even the child's parent cannot distinguish those symptoms, since broad clinical guidelines may highly enhance the ability to reliably diagnose anxiety disorders.

By keeping this in mind, Kerns devised an autism-specific variant for an already existing anxiety assessment tool. The new method, Kerns’ Autism Spectrum Addendum (ASA), added to the Anxiety Disorders Interview Schedule — Child/Parent (ADIS-IV-C/P) that includes new questions merged into the original interview to help find out what behaviors might be related to the child’s autism and what might be part of anxiety.

Those children could not receive treatments for anxiety, because there is no proper diagnosis method for it earlier.

Anxiety treatment in autistic children

Kerns emphasized, Anxiety treatment is vital in conditions like autism spectrum disorder, because anxiety is connected with high impairment for the family and their child. That may add stress, depression, self-injurious behavior, physical ailments and more social problems.�

Kern's research showed that the autistic children, who were treated for their diagnosed anxiety disorders, were rated as improved� or very improved� on a majority, after the treatment.

Kerns initially devised this ASA method in 2014. She tested the ASA method in a study recently, among 69 autistic children who had anxiety concerns, but no previous diagnosis.

“All children involved in the study done a complete evaluation to determine if they did, in fact, revealed clinically important symptoms of anxiety and autism as per the ADIS/ASA interview,” Kerns noted. “All of these ADIS/ASA interviews were recorded as video or audio and listened to a next time by a blind assessor, who came up to their own decisions about the child’s diagnosis.”

Subsequently, those results were also verified against other measures of anxiety to review if they came to the similar conclusions.

At last, Kerns’ autism-specific addition to the anxiety evaluation along with the blind assessors and additional measures of anxiety represented its reliability as a diagnostic tool.

“These findings are highly important to those who need to use the ADIS/ASA in their research or in their clinical study with youth on the spectrum,” Kerns stated, “They propose that the ADIS/ASA can be used for widely assessing anxiety in children with autism that may decrease the possibility that anxiety goes unobserved and untreated, while also minimizing inconsistencies in research.

Kerns' study was published in the Journal of Clinical Child and Adolescent Psychology.

Finally, having a reliable method to diagnose anxiety in autistic children will play a major role in their future.

“Anxiety may be an obstacle to look at your challenges and strengths and autism may make it hard to know what to do in social occasions,� Kerns remarked. This is specifically harmful threat, in my opinion, since it may prevent people from dealing with and, ultimately, overcoming actual challenges in their lives and seeking out education, social relations and employment opportunities, that are important to their growth.�

Kerns concluded, In other words, you tend to focus only on survival rather than living, when you struggle with high anxiety and this will reflect consequently on your physical, mental and emotional health.�

New Gene Regulation Essential for Proper Brain Functioning

Jan 27, 2017

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Researchers from the Johannes Gutenberg University Mainz (JGU) and Institute of Molecular Biology (IMB) have discovered a new way of gene regulation that is deemed important for nervous system activity. This gene regulation involves a chemical alteration on RNA known as m6A which plays a significant role in determining whether flies would be males or females. In this study, the importance of RNA modifications is highlighted.

The study, published in Nature, shows that the m6A RNA modification is important in the development of the fly's nervous system and is also essential for this system to function well. When the researchers disrupted the molecular pathway that changes the RNA, the flies behaved abnormally. These flies had problems in folding their wings correctly and could not orient themselves anymore. They also moved slowly than the flies who did not have alteration in RNA.

The researchers explained that motion impairment results from impairments in the function of the brain. They also found out in this study that m6A is important in determination of sex, whether the fly would become male or female.

The study group leader at IMB and the corresponding author of the study, Dr. Jean-Yves Roignant, also commented that the effect of RNA modifications on messenger RNAs were not anticipated until recently and that their study findings are one of the most exciting discoveries in the field for the last 15 years. This study sheds light on the role of RNA modifications in living organisms and it also shows that m6A modifications is important in the proper functioning of the nervous system and in the sex determination of the fruit fly, Drosophila.

The RNA modification system is found within the vertebrate nervous system and may have similar roles in humans.

RNA modification and gene regulation

For the human body to function normally, genes have to be either switched on or switched off in the right cells at the proper time. It is already a known fact that DNA modification is important in the regulation of gene activity. The DNA molecular markers act as signals to the cells to convert information within genes into a protein and will help us know how a gene is regulated. The signals may be added and removed and will determine whether genes will be active or inactive.

There are many modifications that have been identified in RNA but what they do inside cells is not well known. m6A is said to be the most common of these RNA modifications and it can be added or removed in a similar way as what happens in DNA modifications. To date, this is the first comprehensive study to investigate the role of all components which are involved in m6A RNA modification in organisms.

The researchers also identified a new component that regulates RNA modification: Spenito. They will work in the coming years in how this machinery works in detail.

Localized immunotherapy a promising treatment for bladder cancer

Jan 26, 2017

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Unfavorable side effects are often the drawback of current treatments. A new method used for cancer treatment called antibody-based immunotherapy� holds promise. This method showed an alternative way of drug administration that has the desired effect on cancer cells but is less harmful on normal body cells.

Currently, antibody-based immunotherapy is being used to treat bladder cancer and melanoma. In this method, administered drugs will stimulate the body's immune cells to kill cancerous cells. On the other hand, the major drawback of the treatment is that the injected drug in the bloodstream will result in whole body exposure and thus lead to unfavorable side effects.

Alternatively, the drug would be administered directly inside or adjacent to the cancerous cells, given that this also stimulates immune cells as expected. In the current study at IGP by Sara Mangsbo and her research group, it was revealed that a localized immune stimulation within the area of the tumor had that similar tumor-suppressing ability as when the drug was administered through the blood stream.

Localized immunotherapy

Sara Mangsbo remarked, We tested the therapy in a model bladder cancer system and discovered that even if it was distributed locally, it could activate the immune cells to locate and destroy the tumor cells. These outcomes are highly promising as they denote that whole body immune system stimulation is not required, but merely the tumor area should be treated. This approach can minimize the adverse side effects of the drug.�

In the study, immune stimulation was accomplished by localized administration of blocking antibodies near the tumor. The findings match previous results of the researchers when they discovered that the anti-cancer capacity of direct immune stimulatory antibodies were superior on localized administration than when compared to injecting into blood.

The potential lies in the fact that, the immune cells, not the drug itself, could identify possible metastases and remove them. Further research is needed to understand this process. The current findings are derived from studies in mice; clinical research is required to determine if localized administration of drug into the cancerous cells can minimize side effects, as compared to injections into blood.

Researchers in Lund and Canada collaborated for this study, which was recently featured in the European Journal of Immunology.

Rheb protein depletion leads to memory loss

Life Style

Jan 25, 2017

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Scientists from The Scripps Research Institute (TSRI) have made an essential discovery to drug development when they discovered a way to treat age-related memory loss in conditions like Alzheimer's through Rheb protein. They discovered that decreased levels of a Rheb protein leads to memory loss in animal models and are connected to elevated levels of BACE1 in the brain, as discovered in autopsies of patients with Alzheimer's disease.

Srinivasa Subramaniam who serves as an Associate Professor at TSRI led this study, which was published in the Neurobiology of Aging journal ahead of print.

Rheb and Alzheimer’s

In the recent study, researchers investigated the connection between Rheb and BACE1 enzyme. BACE1 levels are elevated in aged people and patients with Alzheimer’s.

Subraminam remarked, We know that BACE1 is regulated by Rheb. BACE1 is a main drug target in Alzheimer's. Studies of brain autopsies of patients who suffered from Alzheimer's have shown a remarkable decrease in Rheb, hence, it is promising that a raise in Rheb levels might revert the buildup of amyloid plaques or facilitate a decrease or even revert age-related memory loss.”

To discover the effect of removing Rheb, Subramaniam's team placed genetically-altered mice on a series of behavior analyses starting at six months of age.

Rheb removal had no effect on body weight or motor activity of the mice, but has slight and discerning changes on some memory-based activities like memory recall and navigating a maze. Subramaniam and his colleagues analogized these symptoms to memory loss that was found in humans with dementia and Alzheimer's.

They also discovered that Rhed reduction elevated the levels of BACE1 enzyme, which was constant with earlier research demonstrating that elevated BACE1 may be a causative agent for memory loss.

As previous research in fruit flies have shown that, protein starvation may stimulate Rheb mRNA,� Subramaniam's team claimed that a high-protein intake could be a risk factor for Rheb depletion with age, further leading to mild to severe cognitive deficiency in humans, as observed in animal models.

This indicates that nutrient signaling in mammals could control cognitive functions by altering Rheb-BACE1 pathway,� Subramaniam noted.

Neelam Shahani, the first author of the study mentioned, “On the whole, our study shows that forebrain Rheb reduction favors aging-related cognitive disorders. Rheb pathway could be a target and could provide therapeutic potential for age-related or Alzheimer’s disease-related memory loss.”

MEG Is An Efficient Way Of Detecting Concussion

Jan 24, 2017

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Researchers from Simon Fraser University have shown that magnetoencephalography (MEG), a high-resolution scan of the brain, along with computational analysis, might play a vital role in detecting concussions that can be missed by regular scans.

In a recently published study, Vasily Vakorin and Sam Doesburg demonstrate how magnetoencephalography (MEG), which plots relations between the brain regions, might identify higher levels of the changes in neurons than usual clinical scans like MRI or CAT.

To diagnose concussion, clinical practitioners commonly use those tools, together with self-reporting indications like fatigue or headache. They also remarked that associated conditions like mild traumatic brain injury usually found in collisions of football player, don't show on traditional scans.

Vakorin says, Changes in interaction between brain regions as recorded by MEG, helped us to identify concussion from single scans, when CT or MRI scans couldn't detect.�

Concussion Detection With MEG

The researchers scanned 41 men aged from 20 to 44. Within the past three months, half of them had been diagnosed with concussions.

They observed that concussions were connected with changes in communications between various areas of the brain. There were noticeable alterations in how the brain areas interact with each other.

The researchers mentioned that MEG provides a novel combination of good temporal and spatial resolution� for understanding activities of the brain and for improved concussion diagnosis when other traditional methods could not be efficient.

Association between severity of the symptom and MEG- based grouping also demonstrated that these scans can offer essential measurements of brain changes throughout recovery of concussion.

The researchers look forward to improve their perception of specific changes in neurons connected with concussions to further enhance detection, treatment and process of recovery.

Why The Body’s Circadian Clock Disturbs Metabolic Processes

Jan 23, 2017

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Researchers from Charité � Universitätsmedizin Berlin have demonstrated that the body's carbon monoxide metabolism is highly associated with the circadian clock of the body. Carbon monoxide, a toxic gas, is an endogenous by-product of heme degradation and is also present in cigarette smoke and exhaust fumes. Carbon monoxide production is controlled by the body's circadian clock and this clock, in turn, is managed by carbon monoxide.

Metabolism and Circadian Clock

A close connection between the body's circadian clock and metabolism assures that our bodies are favorably adapted to various environments like timing of meals and availability. Cell-based internal clock senses signals from metabolism and makes the appropriate cellular metabolic process adjust according to these signals.

The interruption of one of these regulatory systems disturbs the other; this is evident in diabetes or metabolic syndrome, since the internal clocks are disturbed. A team of researchers led by Prof. Dr. Achim Kramer, who serves as Head of the Chronobiology Research Unit at Charite's Institute for Medical Immunology, has been analyzing the role of heme in the body's internal clocks. Heme is a part of various other proteins and functions as a metabolic sensor.

Prof. Kramer explained, Our research has revealed that toxic gas � carbon monoxide is also a by-product of the heme degradation and plays a major role in maintaining the body's circadian clock.�

Heme production inside the liver cells can be disturbed by external pharmacological inhibition or genetically blocking the expression of the enzyme heme oxygenase � the enzyme which synthesizes heme. Eventually, the clock is slowed down since the regular internal rhythm is disturbed.

Disruption of this type leads to the deregulation of many other genes, which is also required for important metabolic processes like glucose synthesis. Findings from this study make us understand more about metabolic disorders and the body's circadian clock. By finding the molecular interactions behind the body's internal clocks, we can be able to refine therapeutic targets.

3-D Structure of Chemokine Receptor Facilitates Drug Discovery

Jan 22, 2017

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A new chemokine receptor study offers new drug development approaches for autoimmune and inflammatory diseases.

Inflammation reactions in our bodies fight against infections; however, too much of these reactions may result in cancer or autoimmune diseases.� To reduce inflammation, scientists rely on CC chemokine receptor 2 (CCR2), a protein which plays a significant role in inflammation. CCR2 binds on the immune cells like an antenna and senses and transmits inflammatory signals that stimulate cellular movement towards inflammation sites.

A team of researchers at the Pharmaceutical Sciences at University of California San Diego and the Skaggs School of Pharmacy have determined the 3D structure of CCR2 with two inhibitors.

Analyzing how these molecules bind with each other could be a potential target to create anti-inflammatory medicines that could bind and block CCR2 in the same way.

CCR2 and related signaling molecules play major roles in many inflammatory diseases and neurodegenerative disorders such as cancer, multiple sclerosis, diabetic nephropathy and asthma. Many pharmaceutical companies have tried to produce drugs which block CCR2, though not one are available in the market till date.

Tracy Handel, PhD, one of the lead authors of this study who serves as a professor in the Skaggs School of Pharmacy said, Up to now, that target CCR2 has always failed in clinical trials. To work as a therapeutic agent, CCR2 should be turned off entirely, all the time. We can't manage the ups and downs of CCR2 activity. To be efficient, any drug molecule that blocks CCR2 should fit the receptor firmly and stay there, which is a hard thing to do.�

The study was led by Irina Kufareva, PhD, project scientist at Skaggs School of Pharmacy, and Laura Heitman, PhD, of Leiden University. The first author of the study, Yi Zheng, PhD, is a postdoctoral researcher at Skaggs School of Pharmacy.

CCR2 covers the membrane of immune cells. CCR2 has two parts, one of which binds outside the cell and another binds inside. Chemokines, which are inflammatory molecules, stick to the outer part of CCR2, after which the receptor transmits a signal to the inner part of the cell. In the interior part of the cell, CCR2 modifies shape and attaches to other interaction molecules such as G proteins, further stimulating a series of activities. In the end, the immune cells will be in motion, following the chemokine path that directs them to areas in the body where help is required.

For this study, the researchers used the X-ray crystallographic technique to find out the 3D structure of CCR2, along with the structures of two molecules that bind to it all together — one at both end.

According to Kufareva, It is difficult to crystallize receptors out of the cell membrane. To enhance crystallization, we have to modify the amino acid sequence of CCR2 to compose the receptor molecules assembly in a regular manner. If not, when taken out of the cellular membrane, receptors have a tendency to randomly cluster together. ”

Handel, Kufareva and the rest of the team also found that the two small molecules attaching CCR2 keep the receptor “off” by different but commonly supporting mechanisms. One of the small molecules attaches the outer region of the receptor and inhibits binding of the natural chemokines that usually turn the receptor “on.” The other small molecule attaches to the surface of the receptor inside the cell, where the G protein usually binds, and blocks inflammatory signal transmission. Handel mentioned that the latter binding location has never been noted before.

Kufareva said, We hope that this new CCR2 structure with two inhibitors will be helpful in optimizing present and future drug discovery efforts.�

PCEM An Effective Technique For Understanding Cell Interactions

Jan 21, 2017

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A new live-cell imaging technique, PCEM, has been invented by researchers from the University of Illinois at Urbana-Champaign. This might be helpful to biologists in understanding the spread of cancer and in understanding the transformation of stem cells into specialized cells.

The Photonic Crystal Enhanced Microscope (PCEM) has the ability to monitor and quantitatively measure cell adhesion, an important process required in various cellular activities like migration, differentiation, division, and cell death.

“This new approach is significant since there are no label-free and high-resolution imaging tools at present, that let interactions of the cell-surface be quantified and imaged dynamically, though these processes are basic to things such as wound healing, tumor invasion, tissue development and cancer metastasis,” mentioned Brian Cunningham, a professor of electrical and computer engineering and of bioengineering at Illinois.

PCEM advantages

Most common imaging methods depend on fluorescent dyes, which bind to and illuminate the components of the cell so they are visible with a microscope. But this method has its limitations. It is invasive and hard for quantitative measurement, and also allows only a short period of time for examining the cells and for measurement because of photo bleaching.

By using the PCEM microscopic technique, the researchers have successfully calculated the effective mass density of cell membranes during stem cell differentiation and the tumor cell response to drugs in an extended period. Their findings, “Quantitative imaging of cell membrane-associated effective mass density using Photonic Crystal Enhanced Microscopy,” were published in the journal Progress in Quantum Electronics, (November 2016, Volume 50).

Yue Zhuo, who led this research, is a post-doctoral Beckman Institute Fellow. �He mentioned that, The common method of fluorescent tagging doesn’t allow researchers to view how a cell or protein alters over time.�

“You can view the cell for only a few hours maximum until the fluorescent tagging dies out, but it requires many days to perform a stem cell experiment,” said Zhuo. “Scientists usually rely on fluorescent tagging since there’s no other better way to observe live cells due to their low imaging contrast among organelles of the cell. That urges us to build up a high-resolution imaging and label-free method to study live cells.”

CD36 Accelerates Cancer Metastasis

Jan 20, 2017

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For the first time, researchers at the Institute for Research in Barcelona (IRB) have found the protein CD36 on cancerous cells which have the tendency to spread. The study was partially supported by UK charity Worldwide Cancer Research and led by Professor Salvador Aznar Benitah at IRB. CD36, seen in membranes of the cancer cells, is playing a major role in fatty acids intake. This distinctive activity of CD36 and fatty acid dependence differentiate cells which initiate metastasis from other cancerous cells.

Cancer is extremely life threatening when it spreads to other parts of the study; at this stage therapy is very complicated. Scientists are now trying to identify how cancer spread happens so they can discover new methods to block it.

Researchers noticed that CD36 is present on metastatic cancer cells from patients with various tumours such as melanoma lung, breast, ovarian, bladder, skin cancer and oral tumours. To affirm the tendency of CD36 in spreading cancer, they included it to non-metastatic tumor cells which then transformed into metastatic cells.

Even though we have not tested this in all types of cancer, we can say that CD36 is a common marker of metastatic cells, the primary thing I know about that is normally peculiar to metastasis,� explains Professor Benitah, who serves as the Head of the IRB's Stem Cell and Cancer Lab.

We anticipate this study may lead to advancements in metastasis studies.� We hope that we can evaluate the CD36's potential as an anti-metastasis therapy. �

The researchers then observed the role of fat intake on cancer metastasis. They fed mice with high fat food and then injected them with human oral cancer cells. The high-fat food led to frequent and larger metastasis on 50 percent of the mice.

They continued to test a particular fatty acid known as palmitic acid, a key component of animal and vegetable fats which is abundantly present in palm oil and is used in several household items like toothpaste and processed food. The researchers administered palmitic acid on human oral tumor cells for two days then injected them into mice which were provided a normal diet. The research team found that every mice with CD36 had cancer metastatsis compared to those without palmitic acid.

In mice infected with human oral cancer cells, there exists a direct connection between fat intake and a rise in metastatic potential because of CD36. Further studies are required to disintegrate this relationship, especially since developed countries are showing a substantial raise in the intake of sugar and saturated fats,� mentions Professor Benitah. “Fat is essential in the functions of the body, but excess intake may have a bad effect on health, as previously revealed in some cancers such as colon cancer, and in metastasis, as we show here.”

By observing mice with oral cancer, the researchers were then able to demonstrate that stopping CD36 entirely prohibited metastasis. In mice with tumour cells that have previously metastasized, CD36 antibodies resulted in the entire removal of metastases in 20% of the mice, while in others, it resulted to a remarkable decline of 80-90% in terms of metastases and a decrease in size. Prominently, these were all accomplished with no severe side effects.

The researchers are now creating new antibody-based treatments against CD36 that might potentially treat many types of cancers in the days to come.

SPP from Sweet Potato Reduces Blood Fat Levels

Jan 19, 2017

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In a recent study, mice fed with a high fat diet had remarkably lower body weight after one month of consuming SPP, a sweet potato peptide. This peptide was obtained from the enzymatic digestion of proteins in waste water during processing of sweet potato. This indicates that the peptide is responsible for digesting fats but further research is required to find out if this also occurs in human beings.

Dr. Koji Ishiguro from the National Agriculture and Food Research Organization in Japan and his colleagues sought to discover a new way to use waste from sweet potato processing, so they analyzed the effect of proteins present in this waste water on mice.

“We discard large volumes of wastewater that have sweet potato proteins — we assumed that these might show effect on the body weight and fat tissue,” mentioned Dr. Ishiguro. “Finding other uses for the sweet potato proteins in wastewater might be good for the industry, environment, and moreover potentially for health.”

Effects of SPP

The researchers tested three groups of mice with high fat diets. They then fed one group with protein digest — sweet potato peptide (SPP) — at a high concentration and one group with a low concentration. After 28 days, they weighed the mice and assessed their liver mass and fatty tissue. They examined blood cholesterol and triglyceride levels, in addition to leptin which manages appetite and adiponectin which controls metabolic syndrome.

Mice that were provided SPP had remarkably lower body weight and liver mass. Mice given with SPP also had lower cholesterol and triglycerides, and higher levels of the appetite and lipid-controlling hormones. The results indicate that SPP helps in appetite suppression and can manage lipid metabolism in mice provided with high fat diets.

“We were amazed that SPP decreased the levels of fat in mice and that it seems to play a role in managing appetite suppression molecules,” noted Dr. Ishiguro. “These results show potential, while offering new choices for utilizing wastewater rather than throwing it away. We expect SPP to be useful food stuff in the future.”

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