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Scientists are exploring how to edit genomes and even create brand new ones that never existed before, but how close are we to harnessing synthetic life?
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Scientists have made major strides when it comes to understanding the base code that underlies all living things—but what if we could program living cells like software?

The principle behind synthetic biology, the emerging study of building living systems, lies in this ability to synthesize life. An ability to create animal products, individualized medical therapies, and even transplantable organs, all starting with synthetic DNA and cells in a lab.

There are two main schools of thought when it comes to synthesizing life: building artificial cells from the bottom-up or engineering microorganisms so significantly that it resynthesizes and redesigns the genome.

With genetic engineering tools becoming more and more accessible, researchers want to use these synthesized genomes to enhance human health with regards to things like detecting infections or environmental pollutants. Bacterial cells can be engineered that will detect toxic chemicals.

And these synthesized bacteria could potentially protect us from, for example, consuming toxins in contaminated water.

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https://www.youtube.com/watch?v=KmYj2MBfaZc&t=1s

EVANSTON, Ill. — A new Northwestern University study finds that despite human’s close genetic relationship to apes, the human gut microbiome is more similar to that of Old World monkeys like baboons than to that of apes like chimpanzees.

These results suggest that human ecology has had a stronger impact in shaping the human gut microbiome than genetic relationships. The results also suggest the human gut microbiome may have unique characteristics compared to other primates, including increased flexibility.

“Understanding what factors shaped the human gut microbiome over evolutionary time can help us understand how gut microbes may have influenced adaptation and evolution in our ancestors and how they interact with our biology and health today,” said Katherine Amato, lead author of the study and assistant professor of anthropology in the Weinberg College of Arts and Sciences at Northwestern.

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https://www.youtube.com/watch?v=PFw4tSuXIyc&t=1s

Schizophrenia is a severe mental health condition that causes significant disability, and affects 1 in 100 people. Patients with schizophrenia commonly experience negative symptoms, which include lack of motivation, social isolation and inability to experience pleasurable feeling. The current antipsychotics minimally improve these negative symptoms, and there are no currently licensed treatments. In addition, it is estimated that total service costs for schizophrenia in England alone will be £6.5 billion by 2026. In view of this, there is considerable interest in identifying potential treatment targets for these symptoms. However, the nature of the changes in brain chemistry that contribute to these negative symptoms is unknown.

Mu-opioid receptors (MOR) are found in a region of the called the striatum and they play a crucial role in how we experience pleasure and reward. Our bodies naturally produce opioid molecules that include endorphins; which are hormones secreted by the brain that are known to help relieve pain or stress and boost happiness. MORs are receptors that bind these naturally produced endogenous opioid molecules, and stimulation of the MOR system starts a signalling cascade that causes an increase in motivation to seek reward and increase food palatability amongst many other effects. Interestingly, MORs were found to be reduced in the striatum post-mortem in schizophrenia. So, it was unclear whether the availability of these receptors was increased when individuals were alive, or whether reduced MORs was related to the negative symptoms of schizophrenia.

The latest brain scan research from the Psychiatric Imaging group at the MRC LMS published on 3 October in Nature Communications has reported how the MOR system contributes to the negative symptoms displayed in schizophrenia patients. For the first time, this research study showed how MOR levels are significantly reduced in the striatum region of the brain. Thus, a lack of MOR system stimulation in the brain contributes to these negative feelings that schizophrenia patients can experience.

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A new study is the first to report evidence that nonsteroidal anti-inflammatory drugs (NSAIDs) like aspirin may lessen the adverse effects of air pollution exposure on lung function. The team of researchers from the Columbia Mailman School of Public Health, Harvard Chan School of Public Health, Boston University School of Medicine published their findings in the American Journal of Respiratory and Critical Care Medicine.

The researchers analyzed a subset of data collected from a cohort of 2,280 male veterans from the greater Boston area who were given tests to determine their lung function. The average age of participants was 73 years. The researchers examined the relationship between test results, self-reported NSAID use, and ambient particulate matter (PM) and black carbon in the month preceding the test, while accounting for a variety of factors, including the health status of the subject and whether or not he was a smoker. They found that the use of any NSAID nearly halved of the effect of PM on lung function, with the association consistent across all four weekly air pollution measurements from same-day to 28 days prior to the lung function test.

Because most of the people in the study cohort who took NSAIDs used aspirin, the researchers say the modifying effect they observed was mainly from aspirin, but add that effects of non-aspirin NSAIDs are worthy of further exploration. While the mechanism is unknown, the researchers speculate that NSAIDs mitigate inflammation brought about by air pollution.

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CRISPR Gene-Editing Shows Promise As HIV Cure, Research Shows : Shots — Health News Researchers safely used CRISPR gene-editing techniques in a patient with HIV. The research provides evidence the approach may be promising for treating HIV infection.

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The fruit flies in Noah Whiteman’s lab may be hazardous to your health.

Whiteman and his University of California, Berkeley, colleagues have turned perfectly palatable —palatable, at least, to frogs and birds—into potentially poisonous prey that may cause anything that eats them to puke. In large enough quantities, the flies likely would make a human puke, too, much like the emetic effect of ipecac syrup.

That’s because the team genetically engineered the flies, using CRISPR-Cas9 gene editing, to be able to eat milkweed without dying and to sequester its toxins, just as America’s most beloved butterfly, the , does to deter predators.

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A role for the gut microbiome on the health and functioning of many tissues, including the brain, liver, kidney, and adiposity, has been widely reported in the literature. Interestingly, 2019 might be the year that the role of the gut microbiome on skeletal muscle (i.e. the gut-muscle axis) comes into greater focus.

The influence of the gut microbiome on muscle strength

In April, Nay et al. reported that endurance exercise capacity was reduced in mice that do not contain a microbiome (germ-free mice, GFM) when compared with conventionally raised, microbiome-containing mice. This finding suggests that there are microbes in the gut that positively influence aerobic exercise performance.

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