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Dr. Marie Gabrielle Laguna

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Medical doctor-internist

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Nosebleeds Can Be Treated By A Simple Saline Spray

Nov 11, 2016

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Squirting saline spray into the nostril twice a day alleviates continual nosebleeds simply as efficiently as spraying with any one of three distinctive medications, reports a study posted online inside the Journal of the American Medical Association (JAMA). According to corresponding author Kevin Whitehead, M.D., F.A.H.A., associate professor of internal medicine at the University of Utah School of Medicine and director of the Utah HHT Clinical Center, This research highlights that there could be a benefit even in the simplest of interventions. No drug proved to be any better than the saline placebo, but the majority of patients improved over the course of treatment — even those using saline.�

While nosebleeds are an occasional nuisance for many people, they may be an ugly truth for people with hemorrhagic telangiectasia (HHT). One bloody nose per week happens, and some have it more than twice a day. Doctors have tried prescribing medicines off-label to treat nosebleed but they have varied results. The NOSE (North American Study of Epistaxis in HHT) phase 2 scientific trial determined how three of those medicines: bevacizumab, estriol, and tranexamic acid, can stop nosebleeds.

Nosebleeding and Saline Spray

Most severity ratings dropped, and by using almost equal amounts, from between 5 to 6 to between3 to 4. An extensive improvement, says the author. Participants pronounced a superb change regardless of which drug they used, or whether they sprayed their nostrils with placebo. According to Gossage, The results suggest that medicines that people all over the world have used appear to have no benefit over plain saline�.

The idea that easy hydration from any nasal spray, even saline, ought to prevent nosebleeds certainly makes sense, says Whitehead. Humans are at a better chance for nosebleeds while their nose dries out, like when they’re in arid weather for extended durations of time. In addition, the most dreaded but validated treatment that is, surgically sealing the nose, correctly makes the nasal cavity permanently moist.

But the investigators can’t completely rule out the possibility that signs may additionally have improved because of a placebo impact: that participants said higher outcomes because they anticipated seeing an improvement. It may also be that medicine could work well if taken at a higher dose, or if carried out as a gel or polymer that adheres better to the internal lining of the nasal hollow space.

Nonetheless, the effects from this scientific trial were sufficient to convince the researchers to automatically advise saline nasal spray to their sufferers with HHT. According to Whitehead, We tell them that something as simple as a morning and night saline spray could offer them some benefit.�

Nosebleeds resulting from HHT are not essentially distinctive from usual nosebleeds, however scientists haven’t checked whether saline works simply as well for anyone. According to Gossage, There are no data for extrapolating these results to patients with nosebleeds who don’t have HHT. But certainly it’s an easy thing to try.�

Brain Gene Rap1 as Potential Drug Target for Obesity

Nov 9, 2016

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Scientists from Baylor College of Medicine, the National Institutes of Health and Virginia Tech Carilion Research Institute have determined a new mechanism (Rap1 gene) inside the mouse brain that regulates obesity. The new study, which appears in the journal Cell Reports, suggests that this new mechanism can potentially be focused to treat weight problems.

According to the senior author Dr. Makoto Fukuda, assistant professor of pediatrics at Baylor and the USDA/ARS Children’s Nutrition Research Center at Baylor and Texas Children’s Hospital, It’s well known that the brain is involved in the development of obesity, but how a high-fat diet changes the brain so it triggers the accumulation of body fat is still unclear.�

Fukuda and associates studied the mouse Rap1 gene, that’s expressed in many tissues, consisting of the brain where it’s involved in functions along with memory and learning. Little was recognised, however, of the role brain Rap1 plays in energy balance.

To explore the function brain gene�plays in a mouse model, the scientists selectively deleted the Rap1 gene in a collection of neurons in the hypothalamus, a vicinity of the brain that is concerned in regulating entire-body metabolism.

The scientists had two groups of mice. In one group, the mice had been genetically engineered to lack the Rap1 gene, at the same time as the control group had a functional Rap 1 gene. Then, the scientists fed the mice in both groups with a high-fat eating regimen in which 60 percent of the energy came from fats. As anticipated, the mice with the Rap1 gene received weight, however, in evaluation, the mice that lacked Rap 1 had markedly decreased body weight and less body fats. Apparently, whilst each groups of mice were fed a normal diet, both confirmed comparable weights and body fats.

The Rap1 Gene

The scientists then looked nearer at why the mice lacking the Rap1 gene had not gained weight despite consuming a high-fats diet. Fukuda remarked, We observed that the mice lacking Rap1 were not more physically active. However, they ate less and burned more body fat than mice with Rap1. These observations were associated with the hypothalamus producing more of a hormone that reduces appetite, called POMC, and less of hormones that stimulate appetite, called NPY and AgRP�. Those mice also had lower ranges of blood glucose and insulin than controls.

The scientists also were inquisitive about studying whether or not leptin modified in mice missing brain gene. Leptin, the ‘satiety hormone’ produced by fatty tissue, allows changes in body weight by inhibiting the urge for food. Overweight humans however do not reply to leptin’s indicators of satiety, and the blood stages of leptin are higher than those in non-overweight human beings. Leptin resistance is a trademark of human weight problems.

Mice that lacked Rap1 and ate an excessive-fats diet, then again, did not increase leptin resistance; they were capable of responding to leptin, and this turned into the hormone’s decrease blood levels.

Fukuda and co-workers also tested the impact of inhibiting Rap1 with medicines rather than deleting the gene on mice on a high-fat food regimen. The scientists inhibited brain gene�action with inhibitor ESI-05. Fukuda remarked, When we administered ESI-05 to obese mice, we restored their sensitivity to leptin to a level similar to that in mice eating a normal diet. The mice ate less and lost weight. This new mechanism involving Rap1 in the brain may represent a potential therapeutic target for treating human obesity in the future�

The scientists have proven a new mechanism by which the brain can affect the development of obesity by means of eating a high-fat food regimen. Ingesting a high-fats weight loss program results in adjustments inside the brain that increase Rap1 activity, which in turn leads to a decreased sensitivity to leptin, and this sets the body on a direction to weight problems.

Low Vitamin B in Pregnancy Linked to Child Eczema

Nov 8, 2016

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A higher level of a particular type of vitamin B during pregnancy makes infants have a lower risk of eczema at age 12 months, new Southampton research has shown. This is the finding of a study from the Medical Research Council Lifecourse Epidemiology Unit, University of Southampton and is the first evidence that links serum levels of nicotinamide in mothers with risk for atopic eczema in children. Nicotinamide is a naturally occurring form of vitamin B.

The researchers of this study believe that eczema is caused by conditions originating to the baby's development in the womb and these conditions when altered could reduce the risk for the skin condition. The study's lead researcher from the University of Southampton, Dr. Sarah El-Heis remarked, Nicotinamide cream has been used in the treatment of eczema but the link between the mother’s levels of nicotinamide during pregnancy and the offspring’s risk of atopic eczema has not been previously studied.. The findings point to potentially modifiable influences on this common and distressing condition.�

The Wonders of Nicotinamide

Nicotinamide, also known as vitamin B3, is maintained in the body by the consumption of foods such as meat, fish, nuts, chicken, mushrooms and coffee as well as tryptophan, an amino acid commonly found in proteins. This vitamin along with other nutrients is important for energy metabolism and for boosting immune resistance.

The study which was published in Clinical and Experimental Allergy estimated the amount of nicotinamide and related tryptophan metabolites during pregnancy in 497 women that took part in the Southampton Women’s Survey. The researchers then looked at the rates of eczema in their children at ages 6 and 12 months. The results showed that children of mothers with higher than normal levels of nicotinamide had a lower chance of developing eczema at 12 months by 30%.

Nicotinamide is said to improve the elasticity, moisture and structure of skin and could possibly affect the disease process in eczema, the researchers have remarked. There was a gradual relationship between high nicotinamide levels and anthralic acid levels in mothers and a lower risk for atopic eczema. This suggests that the development of eczema was not prevented just by the presence of these nutrients.

According to Professor Keith Godfrey, Director of the NIHR Southampton Biomedical Research Centre in Nutrition, More research is needed to investigate this interesting association, but the findings are further evidence of the potential benefits of eating a healthy balanced diet during pregnancy.�

Reading Skills in Kids Are Boosted By Consuming Fatty Acids

Nov 5, 2016

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A supplement of omega-3 and omega-6 fatty acids may enhance reading capabilities of schoolchildren, according to new research from Sahlgrenska Academy, at the University of Gothenburg, Sweden. Kids with attention problems, particularly, can be helped in their reading with the addition of these fatty acids in their diets.

The study covered 154 schoolchildren from western Sweden in grade 3, from nine to ten years old. The youngsters took a computerized test (known as the Logos test) that measured their reading abilities in a selection of ways, which includes analyzing reading speed, ability to study nonsense words and vocabulary.

The youngsters had been randomly assigned to consume either omega-3 and omega-6, or equal capsule that contained a placebo (palm oil) for three months. The children, parents and researchers did no study until the research was completed which children had obtained fatty acids and which had received the placebo. After 3 months, all kids acquired actual omega-3/6 capsules for the last 3 months of the study.

Mats Johnson, who is chief physician and researcher at the Gillberg Neuropsychiatry Centre at Sahlgrenska Academy, University of Gothenburg remarked, Even after three months, we could see that the children’s reading skills improved with the addition of fatty acids, compared with those who received the placebo. This was particularly evident in the ability to read a nonsense word aloud and pronounce it correctly (phonologic decoding), and the ability to read a series of letters quickly (visual analysis time)�.

No children identified with ADHD were included in the study; however with the assistance of the kid’s parents, the researchers may want to perceive kids who had milder attention problems. Those youngsters attained even greater improvements in several exams, along with faster reading already after 3 months of receiving fatty acid dietary supplements.

Polyunsaturated Fatty Acids For The Brain

Polyunsaturated fat and their role in kids' behaviour and learning is a growing research interest. Mats Johnson further adds, Our modern diet contains relatively little omega-3, which it is believed to have a negative effect on our children when it comes to learning, literacy and attention,” says Mats Johnson. “The cell membranes in the brain are largely made up of polyunsaturated fats, and there are studies that indicate that fatty acids are important for signal transmission between nerve cells and the regulation of signaling systems in the brain.�

Preceding research wherein researchers examined the effect of omega-3 as a supplement for mainstream schoolchildren have not shown positive results, something Mats Johnson believes that this may be due to how these studies had been organized and what aggregate and doses of fatty acids have been used. That is the primary double-blind, placebo-controlled study showing that omega-3/6 improves studying among mainstream schoolchildren.

Mats Johnson said, Our study suggests that children could benefit from a dietary supplement with a special formula. To be more certain about the results, they should also be replicated in other studies.�

Brain Vesicles Play A Role in Septic Shock

Nov 3, 2016

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Researchers at VIB and Ghent University have located an essential mechanism of sepsis and septic shock, an overreaction of the body’s immune machine to an infection. On this circumstance, the brain is unable to decrease an inflammatory response, causing organ failure or ‘septic shock’. This scenario is the most frequent reason of death in hospitals.

As it turns out, data about infections is handed to our brain thru extracellular vesicles which are small particles in cerebrospinal fluid. Those insights can provide upward thrust to new strategies to treat sepsis or even different inflammatory situations.

In sepsis, early inflammation is associated with low blood pressure and the formation of blood clots, inflicting the organs to stop operating. At the same time as the root is an infection, comparable inflammatory responses can arise in the case of injury, which includes severe burns or accidents caused by accidents. These conditions are labeled under SIRS (Systemic Inflammatory Response Syndrome). Even as medical doctors can every now and then deal with the underlying infection with antibiotics or provide synthetic help for essential features, no real treatment for SIRS or sepsis has been developed to this point.

Brain-Blood Communication

The VIB-Ghent University Research venture, led by professor Roosmarijn Vandenbroucke, explored an underrepresented research field, which is the characteristic of extracellular vesicles. It was long thought that these small structures in organic fluids have been released from cells to rid them of cell waste. But, the scientists proved that blood inflammation affects the brain’s choroid plexus, the component that produces brain fluid, to release extracellular vesicles which switch the inflammatory sign to the brain.

Professor Vandenbroucke again remarked, When trauma or an infection occurs, a specific part of the brain detects abnormal blood levels or the presence of foreign substances such as bacteria. Consequently, extracellular vesicles are released containing vital information about the body’s condition. These vesicles then travel through the brain fluid to eventually reach the central nervous system and alert the brain. In brief, we found a new way of blood-to-brain communication that is detrimental in septic shock.�

The findings may be seen as the missing link among infections and inflammation. The significance of those consequences was illustrated with the study team’s successful blockage of vesicle secretion in mice by an inhibitor of vesicle production. This shows that, in time, inflammatory conditions consisting of sepsis could be handled this way in humans.

Professor Vandenbroucke further added, Our data show that the frequently occurring cytokine TNF, which is a substance released upon the occurrence of inflammation, also stimulates the release of extracellular vesicles. One of the next steps is to investigate the therapeutic potential of changing the process of extracellular vesicle release. All of this strengthens our hope in further exploring the links between vesicles and inflammation.�

New “Molecule Chaer Can Prevent Heart Failure

Oct 29, 2016

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Scientists at UCLA have discovered a molecule called Chaer that appears to play an important role in the development of heart failure. The scientists observed that blockading the molecule, called chaer, in animal studies avoided the animals from developing heart failure.

Although the studies continue to be at an early level, future medicines that concentrate on chaer or associated signalling pathways may be promising for treating or preventing heart failure, a situation that afflicts about 5.7 million people and is a contributing motive to more or less one in nine deaths within the US. The outcomes of the study were posted in Nature Medicine journal.

The Mystery of Chaer

Chaer isn’t a protein; it is a product of RNA, DNA’s simpler cousin, and belongs to a category of RNA molecules referred to as lengthy non-coding RNA, or lncRNA. It is referred to as “non-coding” due to the fact the molecules don’t encode and get translated into proteins, as do other RNAs. Non-coding RNAs had been taken into consideration as part of the “dark matter” of biology due to the fact that they’re considerable and diverse in cells, and the DNA that encodes them is responsible for many plant and animal genomes, but their roles have been unexplored.

According to Yibin Wang, the study’s senior author and a professor in the departments of anesthesiology, physiology and medicine at the David Geffen School of Medicine at UCLA, The observation that a single IncRNA molecule can activate a broad set of heart-failure related genes was a big surprise. The findings provide us a better understanding of the molecular processes of heart failure, which we hope eventually to target with effective therapies.�

With heart failure, the muscle groups progressively thicken and stiffen, impairing the heart’s capacity to pump blood. Damage to the heart that occurs from heart ailments, heart attacks, persistent excessive blood pressure strain (high blood pressure) or diabetes can increase one’s chance of heart failure. Current treatment options can slow the disorder in its early stages however regularly comes to be much less effective because the ailment progresses.

Scientists understand that the normal, healthy sample of gene activity goes awry in heart cells in the course of heart failure. However the info of how high blood pressure and other heart stresses can result in this vast exchange in gene expression had been elusive.

In current years, researchers have begun to investigate the feasible roles of non-coding RNAs in this system. For his or her study, Wang and associates focused on chaer, which they’d determined in earlier research to be at surprisingly high stages in mouse heart cells at the outset of coronary heart failure precipitated by excessive blood pressure.

Whilst the researchers removed chaer in mice that were further caused by excessive blood stress, they discovered that the animals had been basically blanketed from coronary heart failure, having little of the usual heart overgrowth (hypertrophy), scar-like remodeling of tissue (fibrosis), and lack of cardiac function. The knockout of chaer additionally blocked the usual heart failure-associated pattern of gene activity inside the mice’s heart muscle cells. Experiments in human heart cell-primarily based models of heart failure yielded comparable outcomes.

The researchers decided that chaer ranges spike in heart cells after a jump in blood stress, and cause a cascade of heart failure activities by binding to a huge protein complex known as PRC2. Typically, PRC2 works as an “epigenetic” regulator, switching off diverse genes throughout the genome. In heart cells, these PRC2-suppressed genes consist of the ones liable for inducing cardiac hypertrophy and different aspects of heart failure. Chaer interferes with this function of PRC2, basically taking the brakes off heart failure-causing genes.

According to Wang, For heart failure to develop, it has to get past this epigenetic ‘checkpoint. That’s an entirely new idea in the field, and we think it presents opportunities for developing future therapies.�

In principle, a drug that blocks or reduces chaer production within the heart, and thereby restores PRC2's wholesome function, ought to prevent or postpone the improvement of heart failure in humans who have excessive blood pressure or are in any other case prone to the circumstance.

Wang and associates wish to find molecules that might be changed into chaer-blocking drugs. Additionally they have begun to explore other signaling pathways that need to be present for chaer to supply its heart failure-inducing activity, and are already checking out compounds that inhibit the indicators.

Heart Problems May Result From Gallstone Disease

Oct 5, 2016

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A history of gallstone ailments may expand your risk of heart problems, according to a new study featured by the American Heart Association’s journal Arteriosclerosis, Thrombosis and Vascular Biology.

Gallstone disease is one of the most common problems affecting the hepatobiliary system. Gallstone ailments and heart disease have the same risk factors, such as diabetes, obesity, high cholesterol, hypertension and an imbalanced diet.

In a meta-evaluation of seven studies including 842,553 participants and 51,123 instances of coronary heart disease, researchers analyzed the relationship between past medical history of gallstones and the progress of coronary heart disease. They discovered that a past medical history of gallstones is related to a 23 percent risk of having coronary heart sickness. According to Lu Qi, M.D., Ph.D., study senior author and professor of epidemiology at Tulane University in New Orleans, Louisiana, Our results suggest that patients with gallstone disease should be monitored closely based on a careful assessment of both gallstone and heart disease risk factors. Preventing gallstone disease may also benefit heart health.�

In a separate evaluation of 269,142 subjects from three different reports, the researchers found out that coronary heart disease are found more often with a history of gallstones due to similar risk factors. Moreover, the expanded risk was identical between women and men. Interestingly, in the three reports, subjects with a history of gallstones who have been healthy, who were not chubby, diabetic or had hypertension had a higher risk of heart problems than subjects who actually have these diseases.

Previous studies have stated a multiplied risk of cardiovascular disease with past medical history of gallstones, however these studies had been carried out over brief durations, didn’t verify the circumstances of gallstones or didn’t account for important risk factors for gallstones such as lifestyle and eating habits, researchers stated.

The researchers didn’t determine why gallstones and coronary heart diseases had been linked in this study, but one conception is that gallstones may just impact bile acid secretion, which has been related to heart disease risk. Furthermore, changes in gut microbiota had been implicated in cardiovascular disorders. According to Qi, Patients with gallstones also have abnormal abundance and metabolism in their gut microbiota.�

Figuring out the explanations that link gallstones and coronary heart disorder and clinical trials to check the consequences of cardiovascular diseases are foremost for applying study findings to clinical practice.

To know more about diseases and their treatment and prevention, feel free to read our other articles on this site.

Pollution and High Fat Diet among Dementia Risks

Oct 4, 2016

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Dementia strikes one in 14 people in the UK over 65, and 47 million people around the world. Yet scientists are nonetheless urgently looking why the ailment affects some however not others.

Dr Ruth Peters, a neuropsychologist from Imperial College London, is one such scientist. Her research entails trying to pinpoint the risk factors for dementia. Dr Peters, from the School of Public Health at Imperial College investigates about the factors which might be in our power to change like weight, blood pressure and alcohol intake.

Utilizing the latest expertise from clinical trials and reports on dementia, she has created an infographic that indicates what explanations do — and do not — cut back the chance of dementia. She has compiled this along woth Professor Kaarin J Anstey, Director of the Centre for Research on Ageing at Australian National University.

Among the findings from the latest research, represented within the infographic, are that eating a significant amount of fatty foods and residing in a polluted area may increase dementia risk, whereas taking regular exercise and maintaining cholesterol at healthy levels may lower risk. Dr Peters said, The evidence is increasingly suggesting that keeping a healthy blood circulation throughout the body is crucial for lowering dementia risk — in other words, what is good for your heart is good for your brain.�

A healthy heart, arteries and veins ensures that the mind receives a sufficient supply of oxygen and nutrients, which maintains our neurons functioning efficiently.

Dr Peters’ present work is investigating whether or not any targeted blood pressure medicinal drugs appear to improve cognitive function. Her most contemporary study, released this week in the journal Current Hypertensive Reports observed that no type of medication seems to work higher than the other. She said, Previous work has suggested a type of blood pressure medication called calcium channel blockers may improve cognitive function, though the latest findings don’t suggest this. There are still large gaps in our knowledge when it comes to dementia risk, which scientists are working hard to fill — but in the meantime keeping yourself fit, active and healthy will keep your brain — and body — in good shape.�

Professor Anstey further added, Keeping healthy in middle age is important for brain aging and reducing risk of dementia in old age — but it’s never too early or too late to take steps to reduce your risk�

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Laser Pointers Can Lead to Blindness

Oct 3, 2016

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Laser pointers bought cheaply in stores are a risk to eyesight — with one pointer discovered to be 127 instances over the Australian legal limit. RMIT school researchers in Melbourne, Australia, have found out that green lasers have been most unsafe, with all four units validated failing Australian specifications.

Now they are calling on the government to consider banning green lasers. In the meantime, they are recommending authorities to put in stringent checking out and quality control.

Dr Kate Fox, a senior lecturer in RMIT’s school of Engineering, mentioned the laser pointers would be bought by anyone, together with youngsters, over-the-counter or online. She said, All the green laser pointers we tested were from 51 to 127 times over the 1 milliwatt government safety limit. At that upper level, the beam would cause catastrophic retinal damage.�

Fox, working with RMIT ophthalmologists, Adjunct Associate Professor Marc Sarossy and Alfred Hospital doctor Matthew Hao Lee, tested 4 models of green laser pointer and 4 models of red. Sarossy further added, Three of the four red models were within safety limits. There can still be some risk, but our normal response to visible light is to blink and turn away — and that’s usually enough to avoid any permanent damage. But green lasers produce much more infrared radiation, which does not trigger our natural blink and aversion responses. Green lasers also produce a much more focused spot than red lasers, with a higher risk of damaging the retina.�

The study staff has found out that imported laser pointers were poorly made, with manufacturers tempted to bypass installing infrared-blocking off filters to keep down expenditures. Fox stated that their findings raised important public protection questions and referred to organizations like the Australian Radiation Protection and Nuclear Safety Agency and the Royal Australian and New Zealand College of Ophthalmologists to join their crusade. The staff’s research were presented at the IEEE Engineers in Medicine and Biology Society conference in Orlando, Florida, on August 18.

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Linaglipitin, A Diabetic Drug Can Protect Blood Vessels

Oct 2, 2016

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Weight problems and type 2 diabetes are related to vascular stiffening and the progress of cardiovascular disease. Overweight and diabetic premenopausal females are mostly at risk — even more than men of the same age who’ve similar health problems. A study by University of Missouri School of Medicine researchers observed that a diabetes medication provided defense towards arterial stiffness in obese female mice, a discovery that can have future implications for sickness prevention in people.

According to Vincent DeMarco, Ph.D., a research associate professor of endocrinology at the MU School of Medicine and lead author of the study, The widespread overconsumption of a western diet high in fats and refined sugars is a contributing factor to the epidemic of obesity and diabetes around the world. Our previous studies showed that young female mice consuming a mostly western diet not only gained weight, but also exhibited arterial stiffening consistent with obese premenopausal women. Our current study sought to understand what effects, if any, the diabetes medication linagliptin had on preventing vascular stiffness.�

Linagliptin is a medication prescribed to lower blood glucose in patients with Type 2 diabetes. The treatment works by blocking off the enzyme dipeptidyl peptidase-4, or DPP-four. Earlier studies have shown that the DPP-4 inhibitor additionally appeared to prevent vascular inflammation and oxidative stress — conditions related to arterial stiffening.

DeMarco’s group located 34 female mice that have been fed both normal food regimen or a simulated western diet for four months. The other group of mice have been fed a western food regimen containing a low dose of linagliptin. The team used an ultrasound approach designed specifically for mice to evaluate stiffness of the aorta — the important artery that supplies blood to the circulatory system.

De Marco said, The mice fed a western diet without receiving linagliptin gained weight and developed aortic stiffness. However, a big surprise to us was an almost total prevention of aortic stiffening in the mice that were fed the western diet along with linagliptin, even though this group gained as much weight as the other mice.�

DeMarco cautions that extra research is required to assess if linagliptin might be used as a therapeutic instrument at some point to prevent aortic stiffening and the cardiovascular dangers related to obesity and diabetes. Moreover, Linagliptin, like other DPP-four inhibitors, can be costly without insurance coverage.

He further added, Based on the results of our study, it is tempting to speculate that linagliptin could target arterial stiffness and reduce the risk of cardiovascular disease. However, results from clinical trials already in progress will be needed to determine what, if any, future role linagliptin could play in the management of obesity-related cardiovascular disease.�

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