Lifeboat Foundation

Blood pressure is one of the most important indicators of heart health, but it’s tough to frequently and reliably measure outside of a clinical setting. For decades, cuff-based devices that constrict around the arm to give a reading have been the gold standard. But now, researchers at The University of Texas at Austin and Texas A&M University have developed an electronic tattoo that can be worn comfortably on the wrist for hours and deliver continuous blood pressure measurements at an accuracy level exceeding nearly all available options on the market today.

“Blood pressure is the most important vital sign you can measure, but the methods to do it outside of the clinic passively, without a cuff, are very limited,” said Deji Akinwande, a professor in the Department of Electrical and Computer Engineering at UT Austin and one of the co-leaders of the project, which is documented in a new paper published today in Nature Nanotechnology.

High blood pressure can lead to serious heart conditions if left untreated. It can be hard to capture with a traditional blood pressure check because that only measures a moment in time, a single data point.

In a surprise finding, researchers have found that getting at least one flu shot makes it 40 percent less likely for people over the age of 65 to be diagnosed with Alzheimer’s disease, up to four years later.

While it’s still far too early to determine if there are any direct causal links between the common vaccine and neurological health outcomes like Alzheimer’s — in other words, we don’t know if it’s the flu vaccine itself or something else responsible for the results — the research is certainly an eyebrow-raising new development that could, potentially, point in the direction of easily accessible treatments.

In a peer-reviewed study in the Journal of Alzheimer’s Disease, researchers at UTHealth Houston compared the incidence rate of the disease in patients with and without at least one flu vaccination in a nationwide sample of US adults aged 65 and up, which included 935,887 vaccinated and 935,887 non-vaccinated individuals.

Neurograins might be the future of implantable Brain Computer Interfaces due to their advantages in terms of abilities and safety in terms of implantation. Due to being the smallest Microchips ever made, in addition to being very powerful, they can make very high resolution recordings of brain activity and even stimulate areas in the brain for medical treatments for people suffering from brain disorders.

The field of neuroscience is developing at a rapid pace, which constantly improves on our BCI Technology and enabling more and more treatments and applications for Brain Computer Interface. It’s clear that this is very advanced future technology and who knows, maybe these new Neurograin Brain Computer Interfaces may play a part in it. Or maybe Elon Musk’s Neuralink’s approach will win in the end. People willingly microchipping their brains will be more common in the future.
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Continue reading “Why People are Microchipping their Brains — Next-Gen BCI’s: Neurograins” »

The preclinical drug works by inhibiting the kinase Cdk5 which is found in mature neurons. Cdk5 has long been linked to neuropsychiatric and neurodegenerative disorders, but prior inhibitors have largely failed to cross the blood-brain barrier and enter the brain.

A new preclinical drug reported by James Bibb, Ph.D., and colleagues has the potential to combat depression, brain injury, and cognitive disorders. The drug, which is notable for being brain-permeable, works by inhibiting the kinase enzyme Cdk5.

Cdk5 is an important signaling regulator in brain neurons. Over three decades of research, it has been linked to neuropsychiatric and degenerative disorders such as Alzheimer’s.

Circa 2017

Zipline, a U.S. startup, is helping deliver life-saving blood supplies to rural areas of Rwanda by drones in record time.

Circa 2020 Immortality of the heart and heart regeneration.

Cardiovascular diseases represent the major cause of morbidity and mortality worldwide. Multiple studies have been conducted so far in order to develop treatments able to prevent the progression of these pathologies. Despite progress made in the last decade, current therapies are still hampered by poor translation into actual clinical applications. The major drawback of such strategies is represented by the limited regenerative capacity of the cardiac tissue. Indeed, after an ischaemic insult, the formation of fibrotic scar takes place, interfering with mechanical and electrical functions of the heart. Hence, the ability of the heart to recover after ischaemic injury depends on several molecular and cellular pathways, and the imbalance between them results into adverse remodeling, culminating in heart failure. In this complex scenario, a new chapter of regenerative medicine has been opened over the past 20 years with the discovery of induced pluripotent stem cells (iPSCs). These cells share the same characteristic of embryonic stem cells (ESCs), but are generated from patient-specific somatic cells, overcoming the ethical limitations related to ESC use and providing an autologous source of human cells. Similarly to ESCs, iPSCs are able to efficiently differentiate into cardiomyocytes (CMs), and thus hold a real regenerative potential for future clinical applications. However, cell-based therapies are subjected to poor grafting and may cause adverse effects in the failing heart. Thus, over the last years, bioengineering technologies focused their attention on the improvement of both survival and functionality of iPSC-derived CMs. The combination of these two fields of study has burst the development of cell-based three-dimensional (3D) structures and organoids which mimic, more realistically, the in vivo cell behavior. Toward the same path, the possibility to directly induce conversion of fibroblasts into CMs has recently emerged as a promising area for in situ cardiac regeneration. In this review we provide an up-to-date overview of the latest advancements in the application of pluripotent stem cells and tissue-engineering for therapeutically relevant cardiac regenerative approaches, aiming to highlight outcomes, limitations and future perspectives for their clinical translation.

Cardiovascular diseases represent the major cause of morbidity and mortality worldwide, accounting for 31% of all deaths (Organization WH 2016). Myocardial infarction (MI) is associated with necrosis of the cardiac tissue due to the occlusion of the coronary arteries, a condition that irrevocably diminishes oxygen and nutrient delivery to the heart (Thygesen et al., 2007). While effective therapies, including surgical approaches, are currently used to treat numerous cardiac disorders, such as valvular or artery diseases, available therapeutic treatments for the damaged myocardium are still very limited and poorly effective. Furthermore, after an ischaemic insult, the formation of fibrotic scar takes place, interfering with mechanical and electrical functions of the cardiac tissue (Talman and Ruskoaho, 2016).

Mitochondrial uncoupling by agents such as BAM15 may mitigate age-related decline in muscle mass and function by molecular and cellular bioenergetic adaptations that confer protection against sarcopenic obesity.

Background Sarcopenic obesity is a highly prevalent disease with poor survival and ineffective medical interventions. Mitochondrial dysfunction is purported to be central in the pathogenesis of sarcopenic obesity by impairing both organelle biogenesis and quality control. We have previously identified that a mitochondrial-targeted furazano[3,4-b]pyrazine named BAM15 is orally available and selectively lowers respiratory coupling efficiency and protects against diet-induced obesity in mice. Here, we tested the hypothesis that mitochondrial uncoupling simultaneously attenuates loss of muscle function and weight gain in a mouse model of sarcopenic obesity.

A team of researchers at the National Institute of Health Doutor Ricardo Jorge in Portugal, working with a colleague at Lusófona University, also in Portugal, has found that the monkeypox virus has been evolving at a faster rate than expected. In their paper published in the journal Nature Medicine, the researchers describe their genetic study of the virus collected from 15 samples.

Monkeypox is a double-stranded DNA virus from the same genus as smallpox, and it mostly infects people in Africa. Scientist have known of its existence since the 1950s. Despite its name, the virus is more commonly found in rodents than monkeys. Prior research has shown that there are two main varieties of monkeypox: West African and Congo Basin—the former is far less deadly and is the clade that has infected several thousand people outside Africa. Prior research has also shown that viruses like monkeypox typically only mutate once or twice in a given year.

In this new effort, the researchers collected samples from 15 patients and subjected them to genetic analysis to learn more about how quickly the virus is evolving. They found the virus has mutated at a rate six to 12 times as high as was expected. The researchers suggest the sudden accelerated rate of mutation in the virus may be a sign that the virus has developed a new way to infect people—currently, it is believed to move from person to person through close contact with open lesions, through body fluids or by airborne droplets.

Researchers have discovered that the human liver never ages beyond just three years old, no matter how old an individual is.

The liver is an amazing organ. Not only is it capable of regenerating itself to repair damage from toxins, like alcohol, but the liver apparently never ages, either.

According to new research, the liver is almost always just under three years old. The concept of liver age has been a medical conundrum for decades. Studying animal livers has yet to offer any kind of answer, so scientists with TU Dresden looked at human livers to try to discern more about our body’s filter.

Continue reading “Your liver is always less than three years old or younger” »