Murj wants to give data collection from implantable medical devices an upgrade

Murj, a new company backed by $4.5 million in new venture financing, is looking to make data collection from implantable heart monitoring and management devices easier and more manageable.

The company was founded by a former Medtronic sales rep who’d previously worked as a product manager on Apple’s iPads. After a few years in sales, Murj founder Todd Butka began thinking about ways to make the data collected by cardiac technologies more easily available to physicians and diagnosticians.

Now the company is coming to market with backing from True Ventures and Social Capital.

Unlike existing technologies that deliver data in static .pdf documents, Murj collects the data and stores it in its own off-premise data warehouses. Using dashboards and other visualization tools doctors can get a better read on what’s going on with their patients’ heart health, Butka claims.

“The information comes from the devices to the implantable devices’ servers… We ping the servers,” Butka explained.

The Murj launch wraps up three years of work developing the technology, which was founded in 2014 and raised its first money in 2015.

The company, based in Santa Cruz, brought on Chris Irving as its lead designer and Patrick Beaulieu, an 18 year veteran of the medical device business, as its chief technical officer.

I think of the company as sort of an Apple Healthkit for implantable devices. If it can expand its scope beyond pacemakers and heart monitors to a broader range of implantables, it could be a pretty big business.

As the population ages, and technologies improve, demand for more persistent diagnostic tools will grow.

In a sense this is part of a number of companies that are trying to provide better tools to manage the data coming off of the sensors that we’ve got all around us.

 

Read More: http://snip.ly/kvqol#https://techcrunch.com/2017/04/18/murj-wants-to-give-data-collection-from-wearable-devices-an-upgrade/

Study finds link between increased brain glucose levels and Alzheimer’s

A new study published yesterday in Alzheimer’s & Dementia: the Journal of the Alzheimer’s Association, found a link for the first time between abnormalities in the mechanism of glucose breakdown in the brain and the severity of tangles and amyloid plaques in the brain, as well as the commencement of visible symptoms of Alzheimer’s disease.

Credit: Juan Gaertner / Shutterstock.com

This National Institute on Aging-supported study analyzed the brain tissue samples at autopsy from participants involved in the Baltimore Longitudinal Study of Aging (BLSA). BLSA, which is one of the world’s longest-running scientific studies on human aging, records neurological, psychological as well as physical data of participants over many decades.

In the study, glucose levels in various areas of the brain, such as the temporal and frontal cortex that are prone to Alzheimer’s disease pathology as well as some resistant areas like the cerebellum, were evaluated.

The researchers investigated three different categories of BLSA participants during the study — (a) participants with Alzheimer’s symptoms throughout life and with confirmed pathology of Alzheimer’s disease, including neurofibrillary tangles and beta-amyloid protein plaques in the brain at the time of death; (b) those who lacked symptoms throughout life, yet had notable levels of Alzheimer’s pathology identified during the brain post-mortem; and (c) healthy controls.

The findings indicated discrete abnormalities in glycolysis, which is the major process involved in the breaking down of glucose in the brain, and provided evidence associating the severity of the abnormalities with the severity of the disease pathology.

Poorer glycolysis rates and increased levels of brain glucose were linked with more severe tangles and plaques in the brains of people affected with Alzheimer’s. Also, the more serious declines in brain glycolysis were associated with the manifestation of disease symptoms like memory issues during life.

Richard J. Hodes, M.D, the NIA Director, commented that this kind of research initiates novel ideas on how to investigate the connections between glycolysis, symptoms, and the disease pathology in escalating the search for better and more effective treatment and prevention methods for Alzheimer’s disease.

Even though the likenesses between Alzheimer’s and diabetes had been suspected for a long time, an evaluation of the link has remained difficult, as insulin is not required for the entry of glucose to the brain or to the neurons.

Glucose used by the brain was tracked by calculating ratios of the amino acids serine, alanine and glycine to glucose, which allowed the assessment of rates of the vital steps involved in glycolysis.

The researchers identified that in comparison with samples of normal brain tissue, the enzyme activities that controlled those vital glycolysis steps were lesser in Alzheimer’s cases.

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Statins ‘should be given to children with heart risks before the age of 10’

Statins 'should be given

Statins should be given to thousands of children by the age of 10 under radical new NHS guidance.

GPs are being urged to identify those who have an inherited risk of high cholesterol, amid warnings that the vast majority of cases are going undetected.

Estimates suggest up to 260,000 people – including 50,000 children – are suffering from genetic deficts which affect the body’s ability to break down cholesterol.

New guidance from the National Institute for Health and Care Excellence (Nice) today says statins should be offered to such cases, to reduce their risk of heart or stroke in midlife.

Just 15 per cent of those with the condition are being treated for it, Nice said, including just 600 of 56,000 children with the genetic problem.

Family doctors are being asked to trawl records to idenitfy those with very high cholesterol levels.

Where levels of more than 9 mmol/l are found in those over 30, and those of 7.5 mmol/l are found in those under 30, high-dose statins should be offered, the NHS guidance states.

And it says gene tests should be used to find other family members – including those below the age of 10 – who are at such heightened risk that they should be put on medication.

Around 56,000 children are estimated to suffer from familial hypercholesterolaemia (FH), yet just 600 have been diagnosed, charities say.

The condition gives men a 50 per cent chance of suffering a heart attack or stroke before the age of 50, while women have a one in three chance by the age of 60.

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Orkambi Reduces Main Biomarker of CF, Vertex Says in Updated Results on Four Therapies

Orkambi Reduces

Orkambi (lumacaftor/ivacaftor) reduced levels of the main biomarker of the lung disease cystic fibrosis and improved the nutritional status of children with the condition, according to a Phase 3 clinical trial.

The results were part of a recent update that Vertex Pharmaceuticals provided on Orkambi and three of its other CF therapies, Kalydeco (ivacaftor), tezacaftor (VX-661) and VX-371.

Vertex conducted the Phase 3 trial (NCT02797132) of Orkambi to evaluate its effectiveness and safety in preschoolers with two copies of the CFTR gene’s F508del mutation. The 60 children were aged 2 to 5. Mutations of the gene cause CF by producing faulty versions of the CFTR protein.

An indication of Orkambi’s effectiveness in the trial was that it reduced the production of the children’s sweat chloride and improved their nutritional status.

A sweat test is the gold standard for diagnosing CF because people with the disease have more chloride in their sweat than those who don’t. As for nutrition, the thick mucus that CF produces in the digestive system can prevent patients from absorbing nutrients and fat properly, leading to difficulty gaining weight and slower growth. CF also produces the mucus in lungs and other organs.

The Phase 3 trial also showed that Orkambi was safe and that the children tolerated it well. Researchers reported no adverse events besides those seen in studies of patients aged 6 to 11.

Based on the promising results of the trial, Vertex plans to submit a New Drug Application on Orkambi to the U.S. Food and Drug Administration during the first quarter of 2018. It will also ask the European Medicines Agency to extend the therapy’s availability to very young children.

Another Phase 3 trial (NCT02412111) that Vertex conducted evaluated a combination of tezacaftor and Kalydeco’s ability to reduce respiratory problems in patients more than 12 years old.

The study included 151 participants at 68 sites in the United States, Canada, Australia, and the European Union. The patients had one copy of the F508del mutation and one copy of another CFTR mutation.

Eight weeks of treatment with the combo led to a negligible improvement in a measure of patients’ lung function known as forced expiratory volume in one second, or FEV1. This is the amount of air that people can forcefully blow out of their lungs in one second.

The combo did lead to a reduction in sweat chloride that was larger than Kalydeco generated alone, however.

Given the results, Vertex has decided not to continue pursuing regulatory approval for the combo. One reason is that most patients older than 12 are eligible to receive Kalydeco by itself.

The FDA is expected to make a decision by February 2018 on a related New Drug Application that Vertex has filed. That application involves using the tezacaftor-Kalydeco combo to treat patients aged 12 or older who carry two copies of an F508del mutation or one copy of an F508del mutation plus another mutation. The FDA is giving the request priority review.

European regulators are expected to decide whether to approve the combo therapy in the second half of 2018.

Vertex has completed enrolling children 12 to 24 months for another Phase 3 trial (NCT03277196) of Kalydeco. It will evaluate the therapy’s safety in children less than 2 years old with a CFTR gating mutation and an R117H mutation.

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Video of father comforting newborn son receiving his first vaccines goes viral

Video of father comforting.jpg

On October 26, first-time father Antwon Lee took his two-month-old son Debias King to get his first vaccinations. Lee, 29, said he was very nervous for the appointment, telling People Magazine that he “felt kind of scared a little bit,” as he knew the child was “going to go through some pain.” Before the visit, he also continually reassured his son that he could cry if he needed to.

TEARS AS CONJOINED TWINS DIE DAY AFTER BIRTH

When it came time for the vaccinations, Lee held his son in his arms and told the little boy to “stay strong,” while Shamekia Harris, Lee’s girlfriend, recorded the visit on her phone. Little Debias did cry as the nurse gave him his shots, but stopped soon afterward when Lee consoled him.

The video has since gone viral, with about 13 million views, 51 thousand likes, and 186 thousand shares as of Wednesday.

Sadly, Lee’s father, Anthony Lee, 57, died that same day due to complications from drinking. Lee explained to People that he was emotional and very close to his father, and that he later spoke to his son Debias about his hopes for the future.

“I talked to him like a grown up … I told him, before I leave, want to see him succeed,” Lee said.

Lee wishes that the video will remind others of the importance of fatherhood, “I want them to take care of their kids, because when you sign up for something, you have to stick with it,” he told People.

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Lee, however, isn’t the only person to go viral for his vaccination video: In 2014, pediatrician Michael Darden gained attention for his unique approach to giving shots, and the video still doesn’t disappoint:

Read More: http://snip.ly/9obne#http://www.foxnews.com/health/2017/11/01/video-father-comforting-newborn-son-receiving-his-first-vaccines-goes-viral.html

The science of Sad: understanding the causes of ‘winter depression’

The science of Sad

For many of us in the UK, the annual ritual of putting the clocks back for daylight saving time can be accompanied by a distinct feeling of winter blues as autumn well and truly beds in. This might be felt as a lack of energy, reduced enjoyment in activities and a need for more sleep than normal. But for around 6% of the UK population and between 2-8% of people in other higher latitude countries such as Canada, Denmark and Sweden, these symptoms are so severe that these people are unable to work or function normally. They suffer from a particular form of major depression, triggered by changes in the seasons, called seasonal affective disorder or Sad.

In addition to depressive episodes, Sad is characterised by various symptoms including chronic oversleeping and extreme carbohydrate cravings that lead to weight gain. As this is the opposite to major depressive disorder where patients suffer from disrupted sleep and loss of appetite, Sad has sometimes been mistakenly thought of as a “lighter” version of depression, but in reality it is simply a different version of the same illness. “People who truly have Sad are just as ill as people with major depressive disorder,” says Brenda McMahon, a psychiatry researcher at the University of Copenhagen. “They will have non-seasonal depressive episodes, but the seasonal trigger is the most common. However it’s important to remember that this condition is a spectrum and there are a lot more people who have what we call sub-syndromal Sad.”

Around 10-15% of the population has sub-syndromal Sad. These individuals struggle through autumn and winter and suffer from many of the same symptoms but they do not have clinical depression. And in the northern hemisphere, as many as one in three of us may suffer from “winter blues” where we feel flat or disinterested in things and regularly fatigued.

Putting the clocks back for daylight saving time can be accompanied by a distinct feeling of winter blues.

One theory for why this condition exists is related to evolution. Around 80% of Sad sufferers are women, particularly those in early adulthood. In older women, the prevalence of Sad goes down and some researchers believe that this pattern is linked to the behavioural cycles of our ancient ancestors. “Because it affects such a large proportion of the population in a mild to moderate form, a lot of people in the field do feel that Sad is a remnant from our past, relating to energy conservation,” says Robert Levitan, a professor at the University of Toronto. “Ten thousand years ago, during the ice age, this biological tendency to slow down during the wintertime was useful, especially for women of reproductive age because pregnancy is very energy-intensive. But now we have a 24-hour society, we’re expected to be active all the time and it’s a nuisance. However, as to why a small proportion of people experience it so severely that it’s completely disabling, we don’t know.”

There are a variety of biological systems thought to be involved, including some of the major neurotransmitter systems in the brain that are associated with motivation, energy and the organisation of our 24-hour circadian rhythms. “We know that dopamine and norepinephrine play critical roles in terms of how we wake up in the morning and how we energise the brain,” Levitan says. One particular hormone, melatonin, which controls our sleep and wake cycles, is thought to be “phase delayed” in people with severe Sad, meaning it is secreted at the wrong times of the day.

Another system of particular interest relates to serotonin, a neurotransmitter that regulates anxiety, happiness and mood. Increasing evidence from various imaging and rodent studies suggests that the serotonin system may be directly modulated by light. Natural sunlight comes in a variety of wavelengths, and it is particularly rich in light at the blue end of the spectrum. When cells in the retina, at the back of our eye, are hit by this blue light, they transmit a signal to a little hub in the brain called the suprachiasmatic nucleus that integrates different sensory inputs, controls our circadian rhythms, and is connected to another hub called the raphe nuclei in the brain stem, which is the origin of all serotonin neurons throughout the brain. When there is less light in the wintertime, this network is not activated enough. In especially susceptible individuals, levels of serotonin in the brain are reduced to such an extent that it increases the likelihood of a depressive episode.

The most popular treatments for Sad is bright-light therapy.

Read More: http://snip.ly/25gi4#https://www.theguardian.com/lifeandstyle/2017/oct/30/sad-winter-depression-seasonal-affective-disorder

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Second Death From Flesh-Eating-Bacteria Infection After Hurricane Harvey Is Reported

 

A 31-year-old man who helped to repair homes in Galveston, Texas after flooding caused by Hurricane Harvey was recently diagnosed with flesh-eating bacteria and died on October 16th after being admitted to a hospital on October 10th, according to a statement released by health officials in Galveston on Monday.

He is the second person to die from flesh-eating bacteria since Hurricane Harvey struck the Gulf Coast. Two weeks ago, a 77 year old woman died after a fall inside her flooded home in which she cut her arm and subsequently contracted the flesh-eating bacteria.

When the man initially presented to the hospital on October 10th, officials described an infected wound affecting the upper portion of his left arm.

The aggressive and deadly soft tissue infection is formally referred to as necrotizing fasciitis . It’s a rare infection under normal circumstances, but if promptly recognized, diagnosed and treated with the appropriate antibiotics and surgery to remove dead or dying tissue, the majority of patients recover without any serious consequences.

Necrotizing fasciitis, or “nec fasc”, is most commonly caused by Group A Strep , but a mixed infection with anaerobic bacteria including Clostridium may also develop, leading to what is commonly known as gas gangrene. Necrotizing fasciitis causes pain out of proportion in the affected area, relative to the degree of injury.

A cut, scrape, puncture or any break in the skin may serve as a portal of entry for the dangerous bacteria, which then leads to destruction of blood vessels, fat, nerves and a white fibrous covering of the muscle known as the fascia. The infection then proceeds to enter the muscle, compromising blood flow and leading to death of the tissue.

Its important to realize that bacteria don’t actually digest the tissue, but instead produce a deadly toxin that is responsible for the extensive tissue damage.

As the bacteria enter the bloodstream, fever, chills and vomiting may rapidly develop, leading to a dangerous condition known as sepsis which is characterized by low blood pressure, rapid and difficult breathing and confusion.

Early warning signs include severe pain and tenderness in the infected area, spreading redness and warmth and blue to purple skin discoloration, with darkened tissue in the later stages. The presence of gas or air in the soft tissue known as “crepitus” produces a crackling sound or crunching sensation if the area of skin is palpated. An abscess containing pus may also form as the infection becomes more organized.

Necrotizing fasciitis is a surgical emergency. Aggressive fluid resuscitation along with broad spectrum antibiotics must be started promptly with emergent preparation for surgery to remove or debride the affected area in order to contain the infection.

Persons with diabetes, chronic kidney disease and cancer who are receiving chemotherapy are most at risk for complications, due to poor blood supply to skin, muscle and soft tissue from having such chronic conditions.

Flood waters harboring bacteria (from sewage), along with dirty surfaces or debris contacting the victim’s initial cut or injury, likely led to the onset of this aggressive and deadly infection. As a general rule, it’s best to keep all cuts or blisters covered with a dry gauze and waterproof type dressing if there is any potential to come in contact with floodwater or dirty surfaces or debris.

The CDC describes about 700-1,110 cases annually in the U.S., the result of an active surveillance and reporting network that is set up to monitor such aggressive infections.

Cases of typhoid and cholera, invasive and aggressive diarrheal illnesses typically associated with floods in developing countries, never materialized after the hurricane, according to data from the CDC. In addition, cases of tetanus, which can develop from heavily contaminated wounds after soil exposure, have generally not been a concern with such flooding in the U.S., as supported by data from the CDC.

“Necrotizing fasciitis is caused by strep group A (flesh-eating bacteria) or anaerobic bacteria which thrive in areas without oxygen,” said Debra Spicehandler, MD, Co-Chief of Infectious Diseases, Northern Westchester Hospital.  ”Antibiotics are important but swift surgical debridement is necessary. The cases caused by strep release a toxin which can also cause systemic effects and organ failure leading to mortality.”

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