Decades of chaos have been unleashed by a generation of voters that barely possesses the digital literacy to use a USB stick. By Lauren Razavi Lauren Razavi is a feature writer specializing in busi…
Global millenials lessons from BREXIT
Decades of chaos have been unleashed by a generation of voters that barely possesses the digital literacy to use a USB stick.
By Lauren Razavi
Lauren Razavi is a feature writer specializing in business, technology and innovation stories. She lives in Norwich, England.
Mixed reactions to Brexit from Brits overseas
British travelers in a Paris train station have mixed reactions to the outcome of the historic referendum back home to leave the European Union. (Reuters)
Today has been a day of bitterness, resentment and betrayal for British millennials like me. Overnight, my generation has lost the right to call ourselves Europeans, as well as the right to live, love and work in the 27 other countries of the European Union. Among the many divisions the referendum has revealed in the U.K., the chasm between generations is becoming the most pronounced. While the Leave campaign achieved a two-point victory in the referendum, 75 percent of voters between 18 and 24 wanted to remain.
For all intents and purposes, the referendum result is just the latest in a series of attacks on my generation’s future. First came the financial crisis, caused by poor decision-making on the part of baby boomers across the world. Soon after came austerity measures that disproportionately affected young people in favor of protecting British pensions. Now we are being forced from the European Union — against the wishes of the vast majority of young people — in an attack from a generation that will live to see very little of its consequences.
Workers can get enough hours
In Silicon Valley, we work more than two jobs. I am calling all workers to band to help each other get all the work hours we need to live in the valley. In the caregiving industry, at times we only…
Source: Workers can get enough hours
Workers can get enough hours
In Silicon Valley, we work more than two jobs. I am calling all workers to band to help each other get all the work hours we need to live in the valley.
In the caregiving industry, at times we only work 4hrs so Motherhealth will ensure to connect with other agencies and care home owners/facilities who might need caregivers.
Dear Home health agency,
We would like to invite you to partner with us, Motherhealth, in our new app CareMe.live to match caregivers/providers with clients, allow video and appointment set with doctors, and have curated health tools that will help the community manage chronic disease and wellness.
In England, they have the PUB located within a community and a residence of the owner. Each one in the community update each other about what is going on and help each other while playing balls, having dinner or drinking light alcoholic beverage.
In the valley, we help caregivers and care home owners by word of mouth when they need a reliever, gardener, housekeeper, driver, cook or part time caregiver.
Please email me for collaboration at motherhealth@gmail.com
For health and wellness,
Connie
To what extent can we stave off Alzheimer’s?
To what extent can we stave off Alzheimer's? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
The following may help slow the progression of this degenerative brain disease: Coconut oil, omega 3, Vitamin B (anti-stress), Vitamin D, exercise, sleep and a happy environment.
Ketones were first discovered in the urine of diabetic patients in the mid-19th century; for almost 50 years thereafter, they were thought to be abnormal and undesirable by-products of incomplete fat oxidation. In the early 20th century, however, they were recognized as normal circulating metabolites produced by liver and readily utilized by extrahepatic tissues. In the 1920s, a drastic "hyperketogenic" diet was found remarkably effective for treatment of drug-resistant epilepsy in children. In 1967, circulating ketones were discovered to replace glucose as the brain's major fuel during the marked hyperketonemia of prolonged fasting. Until then, the adult human brain was thought to be entirely dependent upon glucose. During the 1990s, diet-induced hyperketonemia was found therapeutically effective for treatment of several rare genetic disorders involving impaired neuronal utilization of glucose or its metabolic products. Finally, growing evidence suggests that mitochondrial dysfunction and reduced bioenergetic efficiency occur in brains of patients with Parkinson's disease (PD) and Alzheimer's disease (AD). Because ketones are efficiently used by mitochondria for ATP generation and may also help protect vulnerable neurons from free radical damage, hyperketogenic diets should be evaluated for ability to benefit patients with PD, AD, and certain other neurodegenerative disorders.
PMID: 14604265
[PubMed – indexed for MEDLINE]
What causes diabetic neuropathy?
What causes diabetic neuropathy? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
Statin drugs and most acidic medications (OTC or prescribed). Source: Dr Mercola.
Do take Vitamin B complex (esp B12), Vitamin D, omega 3, CQ10, eat whole foods and balance gut flora with probiotic and prebiotic.
Which psychiatric medications are known to cause diabetes?
Which psychiatric medications are known to cause diabetes? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
Statins are associated with a slightly increased risk of diabetes (2-17% in one review).[66] Higher doses have a greater effect, but the decrease in cardiovascular disease outweighs the risk of developing diabetes. Neuro meds affects the brain and metabolism.
I’ve got really awful muscle pain from doing barbell squats and lunges etc. What can I do to relieve the muscle pain most effectively?
I've got really awful muscle pain from doing barbell squats and lunges etc. What can I do t… by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
CQ10, Vitamin C and turmeric/ginger. Eat some cherries, and magnesium rich whole foods. Massage with fresh ginger and coconut oil in one direction/motion. Rest and sleep more.
Receptor suppresses the immune response in order to save it
When viruses enter the body, they activate receptors on the surface of cells that allow viruses to invade those cells. A Yale-led team has found that one of the receptors, known as AXL, actually plays an essential role in the immune system’s ability to fight viral infections.
Prior studies have shown that the AXL receptor served as an immune “checkpoint,” limiting resistance to infection by suppressing immune cells. But those studies were only performed in tissue culture. To examine the role of AXL in animals, the research team tested the immune response to influenza A and West Nile viruses in mice. They found that mice lacking AXL were more susceptible to infection because their immune cells did not have enough information to marshal an adequate defense.
“In an organism, it turns out it’s good for some immune system cells to get infected—to ‘see’ the virus—so you can mount a good immune response,” said Carla Rothlin associate professor of immunobiology and pharmacology, and senior author on the study. The finding should inform the development of drugs designed to inhibit AXL for treatment of flu and West Nile, as well as cancer, she noted.
Edward T. Schmid, a former graduate student in Rothlin’s lab, was first author. The study was published June 28 in eLife.
Explore further: Scientists pinpoint pathway of resistance to viral infections in the gut
More information: Edward T Schmid et al. AXL receptor tyrosine kinase is required for T cell priming and antiviral immunity, eLife (2016). DOI: 10.7554/eLife.12414
Journal reference: eLife search and more info website
Provided by: Yale University
From Wiki:
AXL gene
Tyrosine-protein kinase receptor UFO is an enzyme that in humans is encoded by the AXL gene.[1][2] The gene was initially designated as UFO, in allusion to the unidentified function of this protein.[3]
Function
The protein encoded by this gene is a member of the receptor tyrosine kinase subfamily. Although it is similar to other receptor tyrosine kinases, the Axl protein represents a unique structure of the extracellular region that juxtaposes IgL and FNIII repeats. It transduces signals from the extracellular matrix into the cytoplasm by binding growth factors like vitamin K-dependent protein growth-arrest-specific gene 6 (GAS6). It is involved in the stimulation of cell proliferation. This receptor can also mediate cell aggregation by homophilic binding. The Axl gene is evolutionarily conserved between vertebrate species. This gene has two different alternatively spliced transcript variants.[2]
Clinical significance
Axl is a chronic myelogenous leukemia-associated oncogene and also associated with colon cancer and melanoma. It is in close vicinity to the BCL3 oncogene, which is at 19q13.1-q13.2.[2] There is ongoing research to develop possible drugs to target this signalling pathway and treat cancers.[4]
Interactions
AXL receptor tyrosine kinase has been shown to interact with TENC1.[5] Axl is an essential epithelial-to-mesenchymal transition-induced regulator of breast cancer metastasis and patient survival.
C1-TEN is a negative regulator of the Akt/PKB signal transduction pathway and inhibits cell survival, proliferation, and migration.
We have previously identified C1 domain-containing phosphatase and TENsin homologue (C1-TEN) as being an intracellular binding partner for Axl receptor tyrosine kinase (RTK). C1-TEN is a tensin-related protein that houses an N-terminal region with predicted structural similarity to PTEN. Here, we report our observations on the effects of ectopic expression of C1-TEN in HEK293 cells, which resulted in profound molecular and phenotypic changes.
Stable expression of C1-TEN altered cellular morphology, with less cell spreading and weaker filamentous actin staining. Cells overexpressing C1-TEN were inhibited greatly in their proliferation and migration rates as compared with mock-transfected cells.
Furthermore, serum starvation-induced apoptosis caused a twofold increase in caspase 3 activity in C1-TEN-overexpressing cells vs. mock cells. In addition, C1-TEN-overexpressing cells showed a markedly reduced phosphorylation of Akt/PKB kinase and its substrate GSK3, as well as reduced Akt enzymatic activity. No such effects on JNK were observed.
Also, serum-stimulated activation of Akt was delayed in C1-TEN-overexpressing cells, while no difference in profile of ERK activation was observed.
Furthermore, cells expressing a C1-TEN mutant where the putative phosphatase active site cysteine at position 231 was substituted for a serine displayed full restoration of both cell proliferation and Akt activation. In conclusion, C1-TEN appears to be a novel intracellular phosphatase that negatively regulates the Akt/PKB signaling cascade, and is similar to its relative PTEN in this respect.
However, the particular domain organization of C1-TEN may enable it to regulate RTK and other signaling complexes that are linked to Akt/PKB signaling in a unique manner.
PMID: 15817639 DOI: 10.1096/fj.04-2532fje
Non-invasive method to kill cancer cells
Matthew Gdovin, an associate professor in the UTSA Department of Biology, has developed a newly patented method to kill cancer cells. His discovery, described in a new study in The Journal of Clinical Oncology, may tremendously help people with inoperable or hard-to-reach tumors, as well as young children stricken with cancer.
Gdovin’s top-tier research involves injecting a chemical compound, nitrobenzaldehyde, into the tumor and allowing it to diffuse into the tissue. He then aims a beam of light at the tissue, causing the cells to become very acidic inside and, essentially, commit suicide. Within two hours, Gdovin estimates up to 95 percent of the targeted cancer cells are dead.
“Even though there are many different types of cancers, the one thing they have in common is their susceptibility to this induced cell suicide,” he said.
Gdovin tested his method against triple negative breast cancer, one of the most aggressive types of cancer and one of the hardest to treat. The prognosis for triple negative breast cancer is usually very poor. After one treatment in the laboratory, he was able to stop the tumor from growing and double chances of survival in mice.
“All forms of cancer attempt to make cells acidic on the outside as a way to attract the attention of a blood vessel, which attempts to get rid of the acid,” he said. “Instead, the cancer latches onto the blood vessel and uses it to make the tumor larger and larger.”
Chemotherapy treatments target all cells in the body, and certain chemotherapeutics try to keep cancer cells acidic as a way to kill the cancer. This is what causes many cancer patients to lose their hair and become sickly. Gdovin’s method, however, is more precise and can target just the tumor.
In the past two years, he’s developed his photodynamic cancer therapy to the point where it’s non-invasive. It now requires just an injection of the nitrobenzaldehyde fluid followed by a flash of an ultraviolet light to cause the cancer-killing reaction. Gdovin has now begun to test the method on drug-resistant cancer cells to make his therapy as strong as possible. He’s also started to develop a nanoparticle that can be injected into the body to target metastasized cancer cells. The nanoparticle is activated with a wavelength of light that it can pass harmlessly through skin, flesh and bone and still activate the the cancer-killing nanoparticle.
Gdovin hopes that his non-invasive method will help cancer patients with tumors in areas that have proven problematic for surgeons, such as the brain stem, aorta or spine. It could also help people who have received the maximum amount of radiation treatment and can no longer cope with the scarring and pain that goes along with it, or children who are at risk of developing mutations from radiation as they grow older.
“There are so many types of cancer for which the prognosis is very poor,” he said. “We’re thinking outside the box and finding a way to do what for many people is simply impossible.”
Explore further: Mouse study: Triple-therapy cocktail shrinks triple-negative breast tumors
More information: Photodynamic acidification therapy to reduce triple negative breast cancer growth in vivo, meetinglibrary.asco.org/content/170361-176
Journal reference: Journal of Clinical Oncology search and more info website
Provided by: University of Texas at San Antonio search and more info
What chemicals in your brain make you attracted to a person?
What chemicals in your brain make you attracted to a person? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
Pheromones, oxytocin – love hormone, ovulation (days), frontal lobes (judgment, as women are turned on by men in power), dopamine (happy hormone), and many other areas.
Wiki:
Human sexuality has many aspects. In biology, sexuality describes the reproductive mechanism as well as the basic biological drive that exists in all sexually reproducing species and can encompass sexual intercourse and sexual contact in all its forms. There are also emotional and physical aspects of sexuality. These relate to the bond that exists between individuals, which may be expressed through profound feelings or emotions. Sociologically, it can cover the cultural, political, and legal aspects; philosophically, it can span the moral, ethical, theological, spiritual, and religious aspects.
Which aspects of a person's sexuality attract another is influenced by cultural factors, and has varied over time, as well as personal factors. Influencing factors may be determined more locally among sub-cultures, across sexual fields, or simply by the preferences of the individual. These preferences come about as a result of a complex variety of genetic, psychological, and cultural factors.
A person's physical appearance has a critical impact on their sexual attractiveness. This involves the impact one's appearance has on the senses, especially in the beginning of a relationship:
Visual perception (The symmetry of the face, physical attractiveness, health and how well they act or move, for example while dancing);
Audition (how the other's voice and movements sound);
Olfaction (how the other smells, naturally or artificially; the wrong smell may be repellent).
As with other animals, pheromones may also have an impact, though less significantly in the case of humans. Theoretically, the "wrong" pheromone may cause someone to be disliked, even when they would otherwise appear attractive. Frequently, a pleasant-smelling perfume is used to encourage the member of the opposite sex to more deeply inhale the air surrounding its wearer,[citation needed] increasing the probability that the individual's pheromones will also be inhaled. The importance of pheromones in human relationships is probably limited and is widely disputed,[unreliable source?][6] although it appears to have some scientific basis.[7]
Many people exhibit high levels of sexual fetishism, and are sexually stimulated by other stimuli not normally associated with sexual arousal. The degree to which such fetishism exists or has existed in different cultures is controversial.
Pheromones have been determined to play a role in sexual attraction between people. They influence gonadal hormone secretion, for example follicle maturation in the ovaries in females and testosterone and sperm production in males.[8]
What chemicals in your brain make you attracted to a person?
What are some important considerations for a patient with neurological conditions?
What are some important considerations for a patient with neurological conditions? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
If one of my family members has neurological conditions, I would also seek advice from internist, metabolic disorder specialist, immune system and endocrine specialist and get support from love ones. Often times, the loving support of the family is what keeps the person feeling more secure. Provide a loving environment, free from noise and things that can cause anxiety. A caregiver to assist in daily living is also important.
What are some important considerations for a patient with neurological conditions?
How do malignant brain tumors degrade the blood-brain barrier?
How do malignant brain tumors degrade the blood-brain barrier? by Connie b. Dellobuono
Answer by Connie b. Dellobuono:
A huge part of stopping cancer and finding new treatments comes from understanding metastasis, or the way cancer spreads through the body. It’s undoubtedly complex, occurring in different ways in different parts of the body. Studies have shown everything from cancer cells following healthier ones as they try to escape to the protein Rac1 becoming more active in cancer cells, helping them to spread. A new study now brings to light how metastasis occurs with the brain cancer glioblastoma.
Metastatic cancers are cancers that have spread from their primary site (where the tumor is) to other parts of the body. The blood vessels and lymph system — vessels that carry fluid and immune system cells — provide highways within the body for the cancer cells to spread efficiently. Glioblastomas are some of the fastest growing tumors in the body because their cells reproduce quickly and the blood vessels within the head provide support for metastasis.
The new study, from researchers at the National Institute of Neurological Disorders and Stroke (NINDS), found that glioblastoma cells are able to bypass several protective mechanisms in the head’s blood-brain barrier (BBB) in order to spread.
The BBB usually works to protect harmful materials, like chemicals and pathogens, from entering the brain. It works as both a barrier and a regulator of these chemicals with the help of several mechanisms. One of them, called tight junctions, are a set of tight connections between the blood vessels’ endothelial cells. They form an impermeable seal in order to limit diffusion. Astrocytes, another cell that resides in the blood vessels, contain 50 to 60 branching protrusions with “endfeet” at their tips. These endfeet cover 90 percent of the brain’s blood vessel surfaces and release chemicals that regulate the tight junctions as well as the expanding and contracting of the blood vessels.
Using mice, fluorescent dyes, and several brain imaging techniques, the researchers were able to see how glioblastoma spread within the brain. They found that glioblastoma cells outside of the main tumor were sneakily located between the astrocytes and the outer surface of the blood vessel. By doing this, they were able to displace the astrocytic endfeet from the blood vessels and tap into the blood supply for sustenance. This resulted in the loosening of tight junctions, and the eventual breakdown of the BBB.
Historically, treating brain tumors has been difficult due to the protection the BBB provides. But the new research suggests that some drugs could possibly make contact with the tumor cells. “Evidence from our models suggests that early in the disease, invading tumor cells are not completely protected by the blood-brain barrier and may be more vulnerable to drugs delivered to the brain via blood,” said Dr. Harald Sontheimer, of the University of Alabama, Birmingham, in a press release. “If these findings hold true in humans, treatment with anti-invasive agents might be beneficial in newly diagnosed glioblastoma patients.”
More research will be needed before any kind of drugs can begin to be developed. But the findings offer new insight into possible treatments for glioblastomas, which kills most people diagnosed with it within 15 months.
Source: Watkins S, Robel S, Kimbrough I, et al. Disruption of astrocyte–vascular coupling and the blood–brain barrier by invading glioma cells. Nature Communications. 2014.
How do malignant brain tumors degrade the blood-brain barrier?
Altering Gut Flora Could Reduce Stroke Risk
Changing the profile of the bacteria in the gut led to a reduction in stroke size, a new study in mice suggests. “This was a proof-of-concept study,” study author Costantino Iadecola, M…
Altering Gut Flora Could Reduce Stroke Risk
Changing the profile of the bacteria in the gut led to a reduction in stroke size, a new study in mice suggests.
“This was a proof-of-concept study,” study author Costantino Iadecola, MD, Weill Cornell Medical College, New York, New York, told Medscape Medical News.
“We have demonstrated two important principles: that changes to the microflora in the gut have an effect on how the brain withstands injury, and that changes to the immune system can have a profound effect on stroke,” he said. “This could eventually lead to new therapies to prevent stroke.”
“The hope is that in future we may be able to reduce an individual’s risks of stroke by changing their microbiota profiles in the gut with use of probiotics and/or antibiotics or maybe just with dietary habits,” he added. “This could be targeted to patients at very high risk of stroke, such as those undergoing cardiac or brain surgery, but may also be applicable to secondary prevention.”
Coauthor Josef Anrather, also from Weill Cornell Medical College, said, “We have shown a new relationship between the intestine and the brain in the setting of stroke. Whatever is going on in the microflora in the gut is contributing to the immune response that controls the damage caused by a stroke. The next step is to address how much of this change is relevant in humans and which bacteria are important.”
The study was published online March 28 in Nature Medicine.
”Our findings shed new light on poorly understood immune mechanisms that have an impact on brain injury and have far-reaching and translationally relevant implications for assessing cerebrovascular risk and predicting stroke severity,” the researchers conclude in their paper.
Dr Iadecola explained that a substantial amount of evidence suggests that immunologic factors have some control over stroke occurring in the brain. “So we figured that if the immune system is geared in a certain way this may protect against stroke. As the intestine is the major reservoir of immune cells, we focused on changing the environment here and whether this would have any affect on stroke.”
For the study, the researchers induced bacteria dysbiosis — changes in the make-up of the bacteria in the gut — by treating mice with antibiotics (amoxicillin and clavulanic acid) for 2 weeks. For controls, they used mice who had been on the same antibiotics for generations, so their flora had become resistant; no bacteria dysbiosis occurred.
When stroke was induced in the mice, the ones that had induced bacterial dysbiosis showed a 60% to 70% reduction in stroke size compared with controls.
As a further verification that it was the dysbiosis rather than the antibiotic itself that was responsible for the reduced stroke, the researchers transplanted the gut contents of the mice with induced bacterial dysbiosis into normal mice and found that these mice also had smaller strokes. “This further suggests that it is the changed composition of the gut flora that is bringing about the benefit on stroke,” Dr Iadecola said.
To address the question of how gut flora can affect the brain in this way, the researchers analyzed the lymphocyte profiles of the mice. They found that the animals with induced dysbiosis and smaller strokes had more protective regulatory T cells and fewer harmful gamma delta T cells. Dr Iadecola commented: “So the change in the gut flora appears to bring about a change in the immune system, which favors smaller stroke injury.”
He explained that these lymphocytes regulate the influx of inflammatory cells, such as neutrophils, into the brain, thereby controlling inflammation in the brain. On further investigation using flow cytometry, the researchers found normal mice had increased neutrophil counts in the brain, whereas the animals with induced dysbiosis had increased neutrophil counts in the meninges but not in the brain itself.
“Our results suggest that the altered gut flora leads to higher amounts of regulatory T cells and fewer gamma delta T cells in the meninges, which somehow causes fewer neutrophils to enter the brain. We believe the gamma delta T cells help neutrophils enter the brain, whereas the regulatory T cells prevent this process,” Dr Iadecola noted.
He added that any clinical application of these findings is still a very long way off. “We need to figure out what is the optimum dysbiotic state in humans. First of all we need to conduct more studies in mice to identify the bacterial species that produce the best changes to the immune system. Then do the same thing in humans.”
Dr Anrather referred to efforts underway at present to better characterize the human microbiome on a large scale. “We might be able to use this data to analyze how certain microbiome profiles influence stroke risk. Then in certain high-risk populations we could try and change the composition of the gut flora to the profile most suited to producing beneficial immunological changes for the cardiovascular system.”
He agreed with Dr Iadecola that the most obvious target is the prevention of stroke, and it would be more difficult to influence the acute phase of stroke because the immunologic changes take time to come into effect.
“In our current study 1 week of antibiotics did not show any change in stroke risk. The reductions in stroke size only became obvious after 2 weeks of treatment. The changes in the microbiota were there at 1 week but the immune changes did not become apparent until 2 weeks. So this approach does not seem appropriate for use in acute situations. But the immune system also plays a role in regeneration and repair, so there may also be possibilities there,” Dr Anrather said.
By Sue Hughes
Nature Med. Published online March 28, 2016. Abstract
From Dr Mercola on Dysbiosis, leaky gut
Dysbiosis, or “leaky gut,” is a bacterial imbalance that leads to inflammation of the intestinal mucosa. Once inflamed, the intestinal lining is compromised and allows undigested food particles and other potential toxins to enter the bloodstream.
- The most common cause of dysbiosis in today’s dogs and cats is, hands down, antibiotic overuse. Antibiotics, other drugs including vaccines, highly processed diets, and stress all contribute to development of dysbiosis in pets.
- Typical signs of a leaky gut include gas, bloating and diarrhea. But dysbiosis can also cause or worsen a wide variety of other disorders and diseases – everything from bad breath to certain types of cancer.
- Every case of dysbiosis is unique, so a customized healing protocol must be designed for each patient based on a specific set of conditions. There is no one-size-fits-all remedy for every leaky gut.
- In most cases, replacing a highly processed diet with balanced, species-appropriate nutrition, and adding appropriate supplements to address inflammation and support the organs of digestion, will relieve symptoms and resolve the root cause of the leaky gut.