Cases are levelling off in the north east of England, even as they rise overall.
Glimmer of hope even as Covid cases rise
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Category Archives: Mind Building
Health24.com | Exposure to man-made chemicals influences genes controlling ageing, immune system and metabolism
Today humans are exposed to thousands of man-made chemicals. Yet the effects on people’s health are still not fully understood.
In 2020 the number of registered chemicals reached 167 million. Every day people are exposed to them through food, water, contaminated air, drugs, cosmetics and other man-made substances. Less than 1% of these chemicals were tested for toxicity, and those that were tested demonstrate ability to disrupt almost every biological process in our body. Can we infer how cumulative exposures shape our health?
I am an environmental toxicologist studying effects of man-made chemicals on our health. I decided to develop a computational approach to objectively compare sensitivity of all genes to all chemicals and identify the most vulnerable biological processes.
Unbiased approach
For our study, my research colleagues and I used data from the Comparative Toxicogenomic Database. The Comparative Toxicogenomic Database collects information from thousands of published studies on how chemicals change the activity of genes. Genes are sections of DNA that encode proteins which perform a broad range of functions in cells, from building tissues to metabolisng nutrients. When chemicals affect genes, that results in increased or decreased production of proteins.
Modern methods of molecular biology can detect changes in activity of all genes in the genome in response to a chemical insult. I developed an approach that overlays lists of altered genes from different studies to calculate how many times each gene was affected. The resulting numbers reflect sensitivities of genes to chemicals generally.
Using 2 169 studies on mice, rats, humans and their cells, my research group ranked the sensitivity of 17 338 genes to chemical exposures. These studies tested the impact of 1 239 diverse chemicals ranging from prescription drugs to environmental pollutants.
At the next step we ran tests to ensure that this sample of over 1 000 chemicals was large enough to reliably represent all classes of man-made chemicals people are exposed to. To do so, we measured sensitivity of genes for one half of this list and then for another to test if even a smaller number of chemicals can reliably identify sensitive genes. The results were encouraging – the values of gene sensitivities were almost identical in the two trials.
Cellular defense system responds to chemicals
Our cells are not completely helpless when exposed to chemical insults. In fact, they possess strategies for dealing with stress and damage induced by chemicals. Our data confirm that these safeguards become active in response to exposures.
This line of defense includes enzymes that eliminate toxic chemicals, alleviate oxidative stress (the accumulation of reactive radicals in cells), repair damaged DNA and proteins, and identify highly damaged cells to trigger their death and prevent them from turning cancerous.
Metabolism of lipids and carbohydrates is vulnerable
Surprisingly, we found that molecular networks involved in the regulation of cellular metabolism are most sensitive to chemical exposures. One of them is PPAR signaling. PPARs are a group of proteins that regulate energy balance and metabolism of lipids and glucose.
Rises or falls in PPARs activity contribute to obesity, metabolic syndrome, diabetes and fatty liver disease. The ability of some environmental chemicals to affect PPARs was shown before. However, we didn’t expect to see sensitivity of PPARs to a very broad range of compounds.
We also discovered that genes involved in the development of pancreatic beta cells, which secrete insulin and play a key role in glucose metabolism, are suppressed by a majority of chemicals in our list. Dysfunction of beta cells results in diabetes. Thus, cumulative chemical exposures may be a significant risk factor for diabetes.
Today an epidemic of metabolic disease is a major public health issue. The prevalence of obesity nearly tripled between 1975 and 2016. Approximately 40% of Americans will develop Type 2 diabetes during their lives, and 33%-88% have fatty liver. Connection between exposures and metabolic diseases was shown before for some chemicals with endocrine disruptive properties. However, the role of a broadest range of man-made chemicals in this epidemic was not recognised before but can be significant.
Growth, ageing and the immune system
Two hormones involved in growth – growth hormone (GH) and insulin-like growth factor (IGF1) – are also affected by exposure to chemicals.
IGF1 is a hormone secreted mostly by the liver. It is recognised as a major regulator of body growth. Additionally, multiple mouse experiments show that decreased GH-IGF1 signaling results in longer lifespan. This pathway also determines if cells will use energy to build new molecules the body needs, or if they will break down existing molecules to release energy for the organism to use.
The ability of chemicals to affect this central regulator of growth and ageing is a novel finding. What health problems may be due to the sensitivity of GH-IGF1 is yet to be uncovered.
Our analysis indicates that genes that control the immune response are also highly sensitive to chemicals.
Two major outcomes of a dysfunctional immune system are allergy and autoimmunity. Prevalence for both conditions follows upward trends. Food allergies increased from 3.4% to 5.1% between 1997 and 2011 among children in the U.S. Skin allergies increased from 7.4% to 12.5% during the same period. Another study showed a 5% increase in blood marker of autoimmune disease in Americans during the period 1988-2012.
All molecular pathways are sensitive to chemicals
Overall we found that almost every known pathway may be affected by chemicals. That finding has significant implications for regulatory toxicology.
With ever-increasing numbers of man-made chemicals, society needs to develop rapid and cost-efficient methods of toxicity testing.
One important question that remains unanswered is what pathways should be covered by testing to ensure that regulators do not approve chemicals that harm or disrupt critical molecular circuits. Our data suggests that we need to develop tests that cover every known molecular pathway without exception.
Our study outlines new priorities for toxicological research, including the role of chemical exposures for metabolic health, immune system, development and ageing.
Alexander Suvorov, Assistant Professor, University of Massachusetts Amherst
This article is republished from The Conversation under a Creative Commons license. Read the original article.
Health24.com | Increased risk of breast cancer for teen smokers
- According to the World Health Organization (WHO), tobacco kills up to half of its users
- Teenage girls who smoke are especially vulnerable to developing breast cancer later in life
- In South Africa, Protect Our Next aims to improve tobacco control legislation and educate the public on its harmful effects
The month of October is breast cancer awareness month.
It marks a special time for survivors of breast cancer, reminding them of what they have overcome. It is also a painful reminder of the dreadful effect of the disease on those who have lost loved ones as a result. Most importantly, Breast Cancer Awareness Month allows us to reflect and educate ourselves on ways in which we can lower our risk of developing cancer.
Protect Our Next is a partnership between CANSA, the National Council Against Smoking (NCAS), the South African Medical Research Council (SAMFC), and the Heart and Stroke Foundation South Africa (HSFSA). The aim of this partnership is to improve tobacco control legislation and also educate the public on the harmful effects of tobacco usage.
Lowering the risk of developing cancer
In a press release, Protect Our Next recently expressed that teenage girls who smoke are especially vulnerable to developing breast cancer later in life. The risk is even higher for those who have a family history of cancer.
While the risk for breast cancer can be due to family history, a study published in the Journal of Breast Cancer confirmed that smoking is associated with an increased risk of breast cancer. A fact sheet on the World Health Organization (WHO) website also shows that tobacco kills up to half of its users.
Controlling the consumption of tobacco, especially among the youth, is therefore a vital part of lowering the risk of developing cancer. Lorraine Govender of the Cancer Association of South Africa (CANSA) expressed, “We must ensure that we have policies in place that protect young people from these toxic, carcinogenic products. Too many lives are lost through cancers resulting from tobacco addiction, and we need to reduce every risk factor.”
Govender went on to say that implementing a new Bill that makes it harder to obtain and use tobacco-related products will be a step in the right direction.
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Stronger treatments could cure Chagas disease
Researchers in the University of Georgia’s Center for Tropical and Emerging Global Diseases have found that a more intensive, less frequent drug regimen with currently available therapeutics could cure the infection that causes Chagas disease, a potentially life-threatening illness affecting up to 300,000 people in the United States.
Trypanosoma cruzi is a single-celled parasitic organism that causes Chagas disease. At least 6 million people are infected by T. cruzi, mostly in South America. Current drug therapies have been ineffective in completely clearing the infection and are associated with severe adverse side effects.
A single dose of benznidazole has been shown to be highly effective in killing more than 90% of parasites. However, after a CTEGD team found some of the parasites enter into a dormancy stage, the researchers hypothesized that an intermittent treatment schedule could be effective.
“In this system we can see what a single dose of drug does,” said Rick Tarleton, Regents’ Professor in UGA’s department of cellular biology. “Does it make sense to give a drug twice daily when the remaining dormant parasites are insensitive to it?”
The investigators found that giving as little as two-and-a-half times the typical daily dose of benznidazole, once per week for 30 weeks, completely cleared the infection, whereas giving the standard daily dose once a week for a longer period did not.
“Current human trials are only looking at giving lower doses over a shorter time period, which is the exact opposite of what we show works,” said Tarleton.
Since Tarleton’s team worked with a mouse model, how this change in treatment regimen will translate in humans is yet unknown, as are any potential side effects of the higher doses. Adverse reactions already are a problem with current treatments; the hope is that side effects from a less frequent dosage would be more tolerable.
Assessing the success of treatments in Chagas disease is a significant challenge. Tissue samples from infected organisms might not be representative of the entire organ or animal, since low numbers of persistent, dormant parasites can be difficult to detect. Therefore, Tarleton’s group used light sheet fluorescence microscopy to view intact whole organs from infected mice.
“With light sheet fluorescence microscopy, you have a broad view of potentially any tissue in the mouse that allows for dependable assessment of parasite load and persistence,” said Tarleton. “It gives you an incredible view of the infection.”
Using this technology, they learned something new about the dormant parasites: Some were still susceptible to drug treatment. This provides hope that new drug therapies could be developed to target these parasites.
“Discovery of new drugs should continue,” Tarleton said. “We still need better drugs.”
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Materials provided by University of Georgia. Original written by Donna Huber. Note: Content may be edited for style and length.
Comparing sensitivity of all genes to chemical exposure
A University of Massachusetts Amherst environmental health scientist has used an unprecedented objective approach to identify which molecular mechanisms in mammals are the most sensitive to chemical exposures.
The study, published in the journal Chemosphere, advances the understanding of the interaction of chemicals, both pollutants and pharmaceuticals, on gene expression and the impact on human health.
“When we identified all the sensitive genes, we were very much surprised that almost every well-known molecular pathway is sensitive to chemicals to a certain degree,” says lead author Alexander Suvorov, associate professor in the School of Public Health and Health Sciences.
The study identified genes and molecular pathways most sensitive to chemical exposures, including mechanisms involving aging, lipid metabolism and autoimmune disease. “These findings for the first time prove that current epidemics in metabolic and autoimmune disorders may be partly due to a very broad range of chemical exposures,” Suvorov says.
To carry out their analysis, Suvorov and five students — undergraduates Victoria Salemme, Joseph McGaunn and Menna Teffera, and graduate students Anthony Poluyanoff and Saira Amir — extracted data on chemical-gene interactions from the Comparative Toxicogenomics Database, which includes human, rat and mouse genes.
The UMass Amherst team created a database of 591,084 chemical-gene interactions reported in 2,169 studies that used high-throughput gene expression analysis, which means they looked at multiple genes. Low-throughout analysis focuses only on a single gene.
“In the recent past, everything that we knew about molecular mechanisms affected by chemicals was coming from low-throughput experiments,” Suvorov says, which led toxicology researchers to focus on those already identified genes, rather than looking for chemical sensitivity among a fuller range of genes.
“I wanted to find some approach that would tell us in a completely unbiased way which mechanisms are sensitive and which are not. I wondered if we were missing a significant toxic response just because no one ever looked for it,” Suvorov says. “By overlaying many high-throughput studies, we can see changes in the expression of all genes all at once. And that is unbiased because we are not cherry-picking any particular molecular mechanisms.”
The interactions analyzed encompassed 17,338 unique genes and 1,239 unique chemicals. The researchers split their database of chemicals into two parts — pharmaceutical chemicals, which are designed to target known molecular cascades; and other chemicals such as industrial, agricultural, cosmetics and pollutants. When the sensitivity of genes to pharmaceutical chemicals was compared to the sensitivity of genes to the other chemicals, the results were the same. “That proves that when analysis is done on really big numbers of chemicals, their composition does not matter,” Suvorov says.
The study confirmed the molecular mechanisms that were previously recognized as being sensitive to chemical exposure, such as oxidative stress. The study’s new findings that the pathways involving aging, lipid metabolism and autoimmune disease are also highly sensitive suggest that chemical exposures may have a role in such conditions as diabetes, fatty liver disease, lupus and rheumatoid arthritis, among others.
“This study represents a significant step forward in the use of genomic data for the improvement of public health policies and decisions,” Suvorov says, “and the public health field will benefit from a future focus of toxicological research on these identified sensitive mechanisms.”
Path to nanodiamond from graphene found
Marrying two layers of graphene is an easy route to the blissful formation of nanoscale diamond, but sometimes thicker is better.
While it may only take a bit of heat to turn a treated bilayer of the ultrathin material into a cubic lattice of diamane, a bit of pressure in just the right place can convert few-layer graphene as well.
The otherwise chemically driven process is theoretically possible according to scientists at Rice University, who published their most recent thoughts on making high-quality diamane — the 2D form of diamond — in the journal Small.
The research led by materials theorist Boris Yakobson and his colleagues at Rice’s Brown School of Engineering suggests a pinpoint of pressure on few-layer graphene, the atom-thin form of carbon known for its astonishing strength, can nucleate a surface chemical reaction with hydrogen or fluorine.
From there, the diamondlike lattice should propagate throughout the material as atoms of hydrogen or fluorine alight on the top and bottom and covalently bind to the surfaces, prompting carbon-carbon connections between the layers.
The pressure applied to that one spot — as small as a few nanometers — is entirely unnecessary for a bilayer but is needed and must be progressively stronger for thicker films, Yakobson said. Making synthetic diamond from bulk graphite at industrial scale requires about 10-15 gigapascals, or 725,000 pounds per square inch, of pressure.
“Only at the nanoscale — in this case, at nanometer thickness — does it becomes possible for the surface chemistry alone to change the thermodynamics of the crystal, shifting the phase-change point from very high pressure to practically no pressure,” he said.
Single-crystal diamond film for electronics is highly desirable. The material could be used as a hardened insulator or as a heat transducer for cooling nanoelectronics. It could be doped to serve as a wide band gap semiconductor in transistors, or as an element in optical applications.
Yakobson and his colleagues developed a phase diagram in 2014 to show how diamane might be thermodynamically feasible. There’s still no easy way to make it, but the new work adds a critical component the earlier research lacked: a way to overcome the energetic barrier to nucleation that keeps the reaction in check.
“So far only bilayer graphene has been reproducibly converted into diamane, but through sheer chemistry,” Yakobson said. “Combining it with a pinch of local pressure and the mechanochemistry it triggers seems like a promising path to be tried.”
“In thicker films, the barrier rises quickly with the number of layers,” added co-author and former Rice postdoctoral associate Pavel Sorokin. “External pressure can reduce this barrier, but chemistry and pressure must play together to deliver a 2D diamond.”
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Materials provided by Rice University. Note: Content may be edited for style and length.
Health24.com | Dangerous Covid-19 syndrome first seen in kids also strikes adults
- There is a different Covid-19 phenomenon called ‘Multisystem Inflammatory Syndrome in Adults’ – or MIS-A
- This is affecting patients’ heart, digestive tract and nervous systems
- MIS-A might not be driven directly by the virus itself but by a post-infectious immunologic response
When the new coronavirus pandemic first began, respiratory distress immediately became the hallmark of severe Covid-19 illness. News reports focused on the inability to breathe, low oxygen saturation levels and the alarming need for ventilators.
But six months later, experts are becoming increasingly concerned about a very different Covid-19 phenomenon, one that spares the lungs only to take direct aim at the patient’s heart, digestive tract and nervous system.
Called “Multisystem Inflammatory Syndrome in Adults” – or MIS-A – the condition was first spotted last spring in children and teens.
“The symptoms are very similar among adults and children,” explained Dr Alisa Femia, director of both in-patient dermatology and autoimmune connective tissue disease at NYU Langone Dermatologic Surgery & Cosmetic Associates, in New York City.
A shock-like state
“Fever is characteristic,” Femia noted, sometimes accompanied by a rash, skin discolouration and chapping, chest pain and gastrointestinal issues.
“Some patients develop muscle pain and a general feeling of unwellness. And some experience a shock-like state, which means that blood pressure is dropping, the heart rate is up, and the patient appears very, very ill and in immediate need of hospitalisation,” she added.
Femia was part of a team that first reported on the paediatric version of the condition – known as MIS-C – back in July. To date, there have been more than 1 000 cases of MIS-C in the United States, resulting in 20 deaths.
Femia ultimately went on to treat the first reported case of MIS-A. Now, the US Centers for Disease Control and Prevention is zeroing in on the adult version, with an analysis outlined recently in the CDC’s Morbidity and Mortality Weekly Report.
The CDC report focused on 27 MIS-A patients ranging in age from 21 to 50. Of those, 10 ended up in the intensive care unit and two of those patients died.
“The lack of respiratory symptoms at presentation represent the main distinction between patients with severe Covid-19 and MIS-A,” said Dr Sapna Bamrah Morris, lead author of the CDC report. She’s an infectious disease specialist and clinical lead of the Health Care Systems and Worker Safety Task Force for the CDC’s Covid-19 Response Team.
In fact, said Morris, in some cases, MIS-A patients “may have multiorgan dysfunction without [any] history of showing symptoms of Covid-19”.
Many patients show no ‘typical’ COVID-19 symptoms
That speaks to the bewildering nature of MIS-A, Femia said. MIS-A patients are testing positive for Covid-19 antibodies, but absent classic respiratory symptoms, many had no idea they were infected. But several weeks or even months later, they suddenly end up hospitalised with serious MIS-A symptoms. At that point, they are often no longer positive for active Covid-19.
“The timing of all of this is very difficult to establish,” Femia said. “We really don’t know how long after an infection with Covid this can happen, because antibodies can remain positive for a couple of months. I would say that, from a doctor’s perspective, our best guess is that this is likely to happen four to six weeks after infection, but it could be three to four months. We really don’t know.”
Dr David Hirschwerk is an infectious disease specialist at Northwell Health in Manhasset, New York. “The timing of all of this suggests that MIS-A is driven not directly by the virus itself but by a post-infectious immunologic response that causes damage to the body,” he said.
“We think that it is relatively rare,” Hirschwerk added. “But we are all on the lookout for it now.”
Femia acknowledged that wasn’t always the case, given that in the early days of the pandemic “hospitals were overwhelmed, and it was a new disease, and this condition just wasn’t on the radar, which means we honestly don’t really know how many adults have gotten this”.
So, who is most at risk for MIS-A? Hirschwerk pointed to the CDC finding that “the vast majority of patients with MIS-A belonged to racial or ethnic minority groups”.
More prevalent in children
But, “like many things with Covid-19, it is all very new to us,” he added. “It requires more study, more data and more time.”
Femia agreed. But she noted that some characteristics of MIS-A are becoming both clear and worrisome. For example, “this has been seen in otherwise healthy patients, as well as among patients with underlying conditions, like obesity. So, the overall suspicion is that you probably don’t need as may co-morbidities to be at risk,” she explained.
“MIS also seems to be more prevalent in children than adults,” she noted. “Why, we just don’t know.”
The good news: “It is treatable,” Femia said. Apart from anti-clotting meds and aspirin, “the most consistent treatment that’s given is IV immunoglobulins”, which are proteins that function as antibodies. “We don’t usually use that to treat acute Covid infection, but it’s borrowed from treatments for other hyper-inflammatory conditions, like Kawasaki disease,” a pediatric illness that causes blood vessel inflammation.
“There’s a lot we don’t know about this,” said Femia. “And many patients will have a very difficult hospital course before they come back to health. But in the end, the majority of patients do survive.”
Image credit: Getty
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The 23-year-old says she posted the picture to mark three months of breastfeeding her baby girl.
Coronavirus treatment: Experimental drug in trial phase
An experimental drug that could prevent Covid-19 patients from becoming seriously ill is being trialled in England.
Win Before You Begin
If you tend to procrastinate on certain projects, one reason could be that you haven’t created a victory in your mind first.
When you think about a project that isn’t advancing very well, consider these questions:
- Do you have a clear vision of what success for this project looks like?
- Can you see your desired end result clearly in your mind’s eye, like you’re recalling a vivid memory?
- Is the path forward relatively clear, from start to finish?
- Can you visualize the key action steps to bring the project to completion?
- Have you firmly decided to do the project now (as in this week, this month, or this quarter)?
- Do you have a reasonably clear understanding of your standards for success (and what results would fall short of those standards)?
- Are you confident that you can achieve the results you desire and satisfy your standards?
If you must answer no or maybe to any of these questions, it’s fair to say that you haven’t created a victory in your mind yet.
Without the pre-creation of a mental victory, you’re very likely to be plagued by procrastination, delay, excuses, and hesitation.
Create the Mental Victory
How do you create the mental victory? Let me ‘splain…
Kick back in a chair, and put your feet up on a desk or table. Prepare to do some imagining.
Pick a project where you’ve been stuck and that you’d like to unlock, so you can make some real progress on it.
Start a five-minute timer. Knowing that the time is counting down can help you focus, so your mind doesn’t drift to other topics. If you run out of time and want to keep going, feel free to set another timer. Tell yourself that you only need to focus on this for five minutes.
Now engage your mind by thinking about the project. Start at the end. Imagine that it’s over and done with, and you’ve succeeded. Go to that future time and place in your mind. See the final work product. It’s 100% finished. You did it! The project is complete.
Feel how it feels to be finally done. Look at the outcome in your mind’s eye. Appreciate the results. You achieved what you wanted to achieve. You met or exceeded your standards. You satisfied the requirements for victory.
Engage fully with the outcome in your imagination. See it. Touch it. Experience it. If you were watching this as a movie, get clear about what you’re seeing on the movie screen.
Now after visualizing the outcome, stay in the future in your mind, and reflect back upon what you did to get there. You don’t have to review the steps in linear order. Just let your mind pick a step and show it to you.
Imagine yourself doing some of the action steps. Picture those scenes, one by one, in whatever order they come to you. Hop around the timeline as much as you want. See yourself doing some of the final actions shortly before the project is done. See yourself just getting started. See yourself doing some of the middle actions.
Invite your mind to build the story of how you went from present reality to future victory. Let your mind show you the steps you took to get there. Let it show you how it feels to experience the end result.
If you’re not sure about the outcome, this is your chance to play around with different possible outcomes. Compare the stories to see which you like best. It doesn’t take long to do this several times in a row with different results.
If there are obstacles to be overcome to achieve your goal, see yourself facing and overcoming those obstacles. Imagine solving the problems you expect to encounter along the way. Make the path seem real.
The Flow of Action
When you pre-create the victory and you see enough of the story to get there, you’re likely to feel some motivation to act – possibly even while you’re still visualizing. Great… that’s good evidence that your mind now understands what success is supposed to look like. You’ve given your mind a clear goal that it can achieve.
Let yourself flow into action as the inspiration arises. See if you can invest at least 30 minutes in taking action to get started. Start building some momentum.
If you get stuck again, no worries. Just repeat the visualization exercise. Return to the end result in your mind. Re-experience the achievement. Invite your mind to help you visualize some of the key beats to get there. Realize that you can take the steps and solve the problems to reach your desired outcome.
Try this even with projects that you feel you should do but resist doing. If you really don’t feel like doing them, just tell yourself that you’re only going to visualize the end result for a while, and you don’t need to take action right now. See what happens.
You may find that this little mental trick works nicely. Once you get into visualizing the end result, your mind will often wander into thinking about the steps to get there. Let your mind explore some possible stories around that – without feeling obligated to act. You may find that this alone is enough to bypass the resistance.
If you really want to get into this, make two lists of all of your open and pending projects. For your first list, include the projects where you’re satisfied with your progress, and you expect them to be completed successfully if you just keep doing what you’re doing. For your second list, note the projects that don’t satisfy this criteria. Now compare the projects on those two lists. I’ll bet you’ll see that you’ve pre-created a successful outcome in your mind for the projects that are advancing nicely, and you haven’t properly done this for the stuck projects. And now you know how to fix that.
