Medicine

The Secret to Clustering? Unveiling the Mystery Behind Spinal Cancer Clusters

According to the CDC, over 600,000 people passed away from this leading cause of death, making it the second greatest claimant of casualties. Upon being diagnosed, one experiences a lifetime of stress and a load of rigorous treatment in the form of chemotherapy in an attempt to kill all the cells before the illness could spread to the remainder of the body. It doesn’t always stop at this point though, many go on to have progressing stages that may either require more treatment, a verdict of ‘X months to live,’ or the first followed by the second. This illness is cancer. 

There are over a hundred and fifty types of cancer, ranging from the head to the toe and everything in between. Some cancers are heavily influenced by gender (such as breast cancer), others by age (such as prostate cancer), and so on and so forth. The specific one that ought to be highlighted though for its increased presence (clustering) of cancerous cells relative to the body is spinal cancer. Although most (if not all) cancers have the ability to cluster its cells in a couple of specific areas, this one can cause cancer cells to become three to five times more apparent in the spine relative to other limbs.

Without the assistance of modern medicine and technology necessary to probe deeper, scientists just considered this specific clustering of cells a medical mystery.

But we have access to that technology now. At least, researchers from Weill Cornell Medicine and the Hospital for Special Surgery in New York do. With these resources, they were available to figure out what exactly causes these clusters to emerge: vertebral skeletal stem cells in the spine. What makes these stem cells unique relative to other ones is their production of a protein that attracts these tumor (cancerous) cells to come to them.

So what can be done with this? Excellent question. 

Through identifying what may exactly cause this clustering, researchers can work on targeting these vertebral skeletal stem cells to disrupt their function (i.e., attracting cancerous tumor cells to them). 

That seems like the perfect plan, no? However, when an experiment on mice where these cells are targeted took place, it didn’t completely eliminate the amount of bone (and, by extension, the number of cancerous cells) in that area. This then begs the question: is there a second stem cell type that we aren’t accounting for? Or is it something else?

Sources

  • https://www.cdc.gov/nchs/fastats/leading-causes-of-death.htm
  • https://www.washingtonpost.com/science/2023/11/28/new-stem-cell-spine-cancer/
  • https://pubmed.ncbi.nlm.nih.gov/37704733/

Sleep Paralysis: Conscious Yet Frozen

You are in your bed after a long day, about to fall asleep. You finish reading your book, scrolling on your phone, sending an email, and hit the hay. Then, you wake up the next day in your bed. You might have been dreaming about frolicking in a field, cleaning your house (I hope not), going on vacation, or a variety of other things. But… you wake up in your bed. Not in a different country, not in a different area outside of your home, not even in a different room in your home. You wake up in the exact same place where you went to sleep: your bed. How is this possible?

Sleep paralysis is a deeply researched phenomenon in which, during sleep, you are unconscious and yet unable to move (prompting the apt name). Now, you can still curl your toes, flex your hands, or twist and turn, but you can’t actually get out of your bed and say, clean your house (provided you don’t have night terrors or some other conflicting sleep disorder). But how does sleep paralysis occur? Why can’t we just do our chores when we are dreaming, or rather dreading, them the next day? 

Our brain is considered to be one of the most complex objects there is. From being able to have half of it removed and still function just about perfectly (in another phenomenon referred to as plasticity, or the brain’s ability to repair itself), to being able to not feel pain and yet regulate pain for all the other parts of the body, it’s a pretty unique and powerful organ. Millions of neurons and hundreds of parts within it work to make it function as it does, all without making us sweat even a little. But there are three particular things that explain sleep paralysis: the brain stem, the motor cortex, and movement signals. 

The motor cortex is responsible for initiating your movements. Whether it’d be raising your arms to stretch, climbing a step with your legs, or even scrolling on your phone, you can thank your motor cortex. In all of these actions, the motor cortex sends movement signals to your brain in order to actually cause you to, well, move. During sleep, although you are not conscious, your brain still is active (as it doesn’t ever ‘shut off’). The body acknowledges this and programs your brain stem to block all movement signals from the motor cortex in an effort to protect you by preventing you from wandering off and, say, doing some chores. 

You might be wondering why you can still curl your toes, toss and turn, or even move away from something unpleasurable. After all, the motor cortex is responsible for movement, no? Well, that’s true to an extent: it’s responsible for all voluntary movement, that is. Remember your last doctor’s appointment where they used the tiny rubber hammer to test your knee’s reflexes? That wasn’t voluntary, so instead of going up to the brain, it is only sent to the spinal cord, which the brain stem does not block movement signals from. As such, all reflexes (and certain small movements) are permissible by the brain because, well, they don’t actually go through it.

The brain is an intricate thing. It’s responsible for every single facet of your life, and yet does its job so seamlessly that we hardly even think about it. It even protects us at night when we are sleeping. What else can the brain do that we haven’t discovered? What else does the brain do that we marvel about? 

Sources

  1. https://www.sleepfoundation.org/parasomnias/sleep-paralysis
  2. https://my.clevelandclinic.org/health/diseases/21974-sleep-paralysis
  3. https://sleepdoctor.com/parasomnias/sleep-paralysis/

Quantum-Inspired AI model helps CRISPR Cas9 Genome Editing for Microbes


A team of scientists at the Oak Ridge National Laboratory (ORNL), have embarked on a groundbreaking venture, leveraging quantum biology, artificial intelligence (AI), and bioengineering to revolutionize the effectiveness of CRISPR Cas9 genome editing tools. Their focus is on microbes, particularly those earmarked for modifications to produce renewable fuels and chemicals, presenting a unique challenge due to their distinct chromosomal structures and sizes.

Traditionally, CRISPR tools have been tailored for mammalian cells and model species, resulting in weak and inconsistent efficiency when applied to microbes. Recognizing this limitation, Carrie Eckert, leader of the Synthetic Biology group at ORNL, remarked, “Few have been geared towards microbes where the chromosomal structures and sizes are very different.” This realization prompted the ORNL scientists to explore a new frontier in the quest to enhance the precision of CRISPR tools.

The team’s journey took an unconventional turn as they delved into quantum biology, a field at the intersection of molecular biology and quantum chemistry. Quantum biology explores the influence of electronic structure on the chemical properties and interactions of nucleotides, the fundamental building blocks of DNA and RNA, within cell nuclei where genetic material resides.

To improve the modeling and design of guide RNA for CRISPR Cas9, the scientists developed an explainable AI model named the iterative random forest. Trained on a dataset of approximately 50,000 guide RNAs targeting the genome of E. coli bacteria, the model took into account quantum chemical properties. The objective was to understand, at a fundamental level, the electronic distribution in nucleotides, which influences the reactivity and stability of the Cas9 enzyme-guide RNA complex.

“The model helped us identify clues about the molecular mechanisms that underpin the efficiency of our guide RNAs,” explained Erica Prates, a computational systems biologist at ORNL. The iterative random forest, with its thousands of features and iterative nature, was trained using the high-performance Summit supercomputer at ORNL’s Oak Ridge Leadership Computer Facility.

What sets this approach apart is its commitment to explainable AI. Rather than relying on a “black box” algorithm that lacks interpretability, the ORNL team aimed to understand the biological mechanisms driving results. Jaclyn Noshay, a former ORNL computational systems biologist and first author on the paper, emphasized, “We wanted to improve our understanding of guide design rules for optimal cutting efficiency with a microbial species focus.”

Graphical Abstract https://academic.oup.com/nar/article/51/19/10147/7279034

Validation of the explainable AI model involved CRISPR Cas9 cutting experiments on E. coli, using a large group of guides selected by the model. The results were promising, confirming the efficacy of the model in guiding genome modifications for microbes.

The implications of this research extend far beyond microbial genome editing. “If you’re looking at any sort of drug development, for instance, where you’re using CRISPR to target a specific region of the genome, you must have the most accurate model to predict those guides,” highlighted Carrie Eckert. The study not only advances the field of synthetic biology but also has broader applications in drug development and bioenergy research.

The ORNL researchers envision collaborative efforts with computational science colleagues to further enhance the microbial CRISPR Cas9 model using additional data from lab experiments and diverse microbial species. The ultimate goal is to refine CRISPR Cas9 models for a wide range of species, facilitating predictive DNA modifications with unprecedented precision.

The study, supported by the DOE Office of Science Biological and Environmental Research Program, ORNL’s Lab-Directed Research and Development program, and high-performance computing resources, signifies a significant leap forward in the quest to improve CRISPR technology. As Paul Abraham, a bioanalytical chemist at ORNL, remarked, “A major goal of our research is to improve the ability to predictively modify the DNA of more organisms using CRISPR tools. This study represents an exciting advancement toward understanding how we can avoid making costly ‘typos’ in an organism’s genetic code.” The findings hold promise for applications in fields ranging from bioenergy feedstock enhancement to drug development, marking a pivotal moment in the evolution of CRISPR technology.

Sources

https://doi.org/10.1093/nar/gkad736

Unraveling the Enigma of SSRIs: How Do They Work, and Do They Really?

Image from: https://www.google.com/url?sa=i&url=https%3A%2F%2Fwww.verywellmind.com%2Flist-of-ssris-380594&psig=AOvVaw0XM6qzBGJgJ5sqoor-jvoP&ust=1697051716630000&source 

SSRIS, or Selective Serotonin Reuptake Inhibitors, are a type of psychiatric drugs used to treat symptoms of depression and anxiety, or depressive and anxiety disorders. They are the most commonly prescribed antidepressants, and first began being used clinically in the late 1980s. The first ever SSRI, fluoxetine, was cleared for prescription usage in the United States in 1988, and paved the way for a new, much more reliable form of antidepressants. As of 2018, it is estimated that 13.2% of Americans above the age of 12 are on some form of SSRIS. The question is, what are they, really, and how do they work? 

It’s important to first understand the Serotonin Hypothesis of Depression. This hypothesis states that low levels of serotonin (a neurotransmitter related to mood, sleep, digestion, and much more) in the brain, or an inability to process serotonin correctly, is the leading cause of depression. Within this hypothesis lays the groundwork for SSRIS; the theory being that increasing serotonin in the brain lowers symptoms of depression. Therewithal, it is incredibly difficult for scientists to measure serotonin levels, as when done through bodily fluids, such as blood, urine, or cerebrospinal fluid, deficits do not appear, even when the person has been clearly diagnosed with depression. This is because neurotransmitter levels in the brain are extremely localized, and therefore not well reflected by levels throughout the rest of the body. This makes it difficult for scientists to objectively ‘prove’ the serotonin hypothesis, and as of 2022, many psychiatrists no longer accept the serotonin hypothesis, claiming there is no direct correlation between serotonin levels and depression. But, if the serotonin hypothesis is false, why are SSRIS so commonly used, and do they really work? 

Here’s what we do know. After a few doses of an SSRI, serotonin levels in the brain increase. This happens because the SSRI blocks the reabsorption (or reuptake) of serotonin into the neurons, allowing the neurotransmitter to better send messages between neurons. SSRIS are classified as selective because they only block the reabsorption of serotonin, and not of other neurotransmitters. If the SSRI works properly, the patient should see decreased symptoms of depression within the first two weeks to a month. And that’s it. That’s how they work. It seems quite simple, and foolproof, but many psychologists have begun to find holes in the argument for this. 

Research done by Moncrieff et al includes compelling data suggesting that there is no consistent evidence linking lowered serotonin concentration or activity to depression. They therefore suggest it is “time to acknowledge the serotonin theory of depression is not empirically substantiated.” This leads many to question the effectiveness of SSRIS. But how could that be? For the most part, patients who use SSRIS report their symptoms of depression and anxiety decreasing significantly, as well as their mood stabilizing. It is possible that this is partially because of a placebo effect, which is when a person’s belief in the treatments is what is causing their improvement, and not the treatment itself. It is also possible that researchers claims do not hold as much truth as they believe. Despite there clearly being evidence of a lack of a correlation, there is also decades worth of evidence that SSRIS do work. 

Image from: https://www.google.com/url?sa=i&url=https%3A%2F%2Fhopes.stanford.edu%2Fssris%2 

Furthermore, it is important to note that we do not understand everything about SSRIS. The brain, and therefore, psychiatric medications, are incredibly complex. We tend to find that there isn’t just one answer to the psychology questions we seek, especially when considering that everyone is different, and there are lots of things we still don’t know about the brain. Psychiatrists and psychologists alike do not suggest stopping SSRIS if you are on one, especially not without consulting your physician. As research continues, we hope to find more of the answers we seek, although it’s hard to say what the near future holds for current theories about SSRIS and other psychiatric medications. 

Sources: 

https://www.mayoclinic.org/diseases-conditions/depression/in-depth/ssris/art-20044825

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9669646/#B17

https://www.psychologytoday.com/us/blog/denying-the-grave/202209/we-still-don-t-know-how-antidepressants-work

https://www.nhsinform.scot/tests-and-treatments/medicines-and-medical-aids/types-of-medicine/selective-serotonin-reuptake-inhibitors-ssris#:~:text=It’s%20 thought%20to%20have%20a,messages%20between%20 nearby%20never%20 cells.

https://www.cdc.gov/nchs/products/databriefs/db377.htm

Unlocking Limb Regeneration: The Salamander’s Clue to Ending Phantom Pain

You wake up in the morning with some arm pain. Sounds pretty normal, no? But what if you were told that that pain was all in your head? Alright, well obviously it’s in your head, your brain is what detects the pain, but bear with me. What if your arm wasn’t… there? What if your arm hadn’t been there for years, only for you to still feel it being there despite this objective truth? If all of that applies to you, then you are a victim of phantom pain. 

Over 500 people lose their limbs each day, whether it’s through the brutality of warfare, a freak accident at a job, or otherwise. Of these individuals, approximately 80% of them experience phantom pain. Not to mention that all of them suffer some degree of reduction in quality of life and even mental health for some. For what seems like its conception, limbs and their loss seemed like an unfortunate reality of the world. We all are only given one pair of parts, if we lose them somehow, that’s on us. That’s it. No redos, no replacements, no takesies-backsies. 

But what if there were redos? What if there was a way to replace the irreplaceable? What if there was a way to grow the ungrowable? That may very be possible through researching an animal that most of us have yet to encounter in the flesh: the humble salamander. 

What makes the salamander so special lies in its capability to regrow its limbs in its entirety. It could lose all of its arms and legs: as long as the stump is not destroyed, it can regrow them again and again without fail. These were only possible through the salamander’s natural capabilities to salvage what was left and prevent the wound from festering. The blood vessels quickly contract and a layer of skin cells swiftly encase the wound site. This wasn’t what made the salamander’s capability to regrow limbs so odd though, it was that it had other parts of its body (namely the opposite side of the missing limb) chip in to regrow the lost part. Although it would sometimes appear in a slightly different place, it would, for all anatomically sound purposes, be a perfectly functional limb. 

Although humans and salamanders are not the same, we both possess some form of a regeneration factor (with the former resorting to healing and the latter resulting in completely regrowing a limb). It is just a matter of time before we transform our natural capability to heal into being able to regrow lost limbs, perhaps indefinitely. No more will those who are missing an arm or a leg through horrid circumstances have to suffer a poor quality of life. No more will they have to make do with painkillers and accept the never-ending pain. No more will they have to live their life to a fraction of their potential all because of an unfortunate sequence of events. With the help of some salamanders, these circumstances may very well become a thing of the past. 

Image Credit: CAS.org, depiction of limbs regenerating.

Sources

  1. https://acl.gov/sites/default/files/programs/2021-04/llam-infographic-2021.pdf
  2. https://www.montefiore.org/limb-loss-facts
  3. https://my.clevelandclinic.org/health/diseases/12092-phantom-limb-pain
  4. https://www.ucl.ac.uk/news/2014/jun/limb-regeneration-do-salamanders-hold-key

Synthetic Biology: A Brave New World of Cures and Cautions

As a recent and ever-changing form of medicine and science, synthetic biology is paving the way for the future of medicine. Defined as a “research and engineering domain of biology where a human-designed genetic program is synthesized and transplanted into a relevant cell type from an extant organism” (A.M. Calladine, R. ter Meulen, 2013), synthetic biology offers possible solutions to some of society’s most pressing medical issues. Through DNA sequence modification and genome editing, scientists have been able to edit genetic material in living organisms with tools such as CRISPR (Clustered regularly interspaced short palindromic repeats). This ability allows scientists to provide organisms with genetic tools that nature has not yet apportioned. CRISPR also allows for the creation of ‘living therapeutics’ and introduction of immunity cells into the human body. 

So, what does this all mean? Well, synthetically creating genetic tools has already allowed for a breakthrough in different areas of production, such as the ability for silkworms to produce spider silk, as well as genetically engineered food, such as cheese, plant-based meat, etc., some of which are already available on a market scale. This provides society with a more sustainable way of creating different materials, which may be necessary as we continue to experience the impacts of consumerism on our planet’s environment. Living therapeutics and immune cells can help treat patients with various diseases, including multiple forms of cancer, providing them with a better chance of recovery and survival. Synthetic biology also assisted in the mass production of certain COVID-19 vaccines by manufacturing the SARS-CoV-2 genome sequence. 

It’s clear that an abundance of benefits derive from the usage of synthetic biology. Consequently, as with most technological advancements, there is also a profusion of risks. A majority of these risks appear to be ethical and extremely dangerous. According to The University of Oxford, synthetic biology, although promising, gives biologists a concerning way of ‘playing god.’ Misusing synthetic biology could potentially destroy existing ecosystems and undermine our crucial distinction between living organisms and machines. The loss of this distinction could be catastrophic for humans’ view on the importance of different organisms and creates an ethical concern of prioritizing machines and technology over nature and living organisms. Synthetic biology also introduces the risk of the synthesization of known human pathogens, such as Influenza or Smallpox, which could be released in much more dangerous forms than what they currently are. Although some of these associated risks are unlikely, the potential danger they inflict could be devastating. 

When considering the sad reality of human greed, it is essential to question whether the findings of synthetic biology will continue to be used for good. If put into the wrong hands, the technology could cause the decimation of multiple existing species, ultimately jeopardizing the balance of our ecosystem. Synthetic biology also poses the genuine risk of bioterrorism, as creating hazardous and genetically mutated organisms could be maliciously and violently released. Control of this technology is seen more in richer first-world countries, creating an inequality regarding access and usage. This gives certain countries, such as the U.S., an extensive scientific advantage over other countries, which could be used at the expense of other nations. 

It is still being determined what the future of synthetic biology holds, but it is imperative that both the benefits and drawbacks are considered. Naturally, we hope synthetic biology continues to be used for the greater of humankind, but that could very easily and swiftly change. Therefore, and when considering that we are already in the midst of multiple ethical, moral, and environmental crises, it is necessary to be aware of the information we consume and promote, specifically regarding the ongoing evolution of technology and science. 

Sources

New drug clinically slows down cognitive decline in Alzheimer’s patients by 35%

CC: Unsplash

Donanemab, “seen as a turning point in dementia fight,” as per a report from the BBC, is a drug that has slowed cognitive decline of the symptoms of dementia/Alzheimer’s by 35% (as per data presented July 17 at the Alzheimer’s Association International Conference in Amsterdam).

This antibody can temporarily put a hold to the effects of the disease on the patient. “The rationale behind Donanemab is that targeting deposited plaque itself is necessary to clear existing amyloid burden from the brain, rather than merely prevent deposition of new plaques or growth of existing plaques.” (Source: https://www.alzforum.org/therapeutics/donanemab)

Donanemab is primarily targeted towards patients in the early stages of the disease, and has shown significant results depicting an optimistic future in finding a cure/cures for the disease. 

Before continuing, it should be known that though the symptoms of Alzheimer’s disease and dementia diseases are similar, their causes are usually different. Generally, all diseases that contribute to memory loss are due to nerve cell damage and plaque build up, and Alzheimer’s disease is no different.

It is caused due to the abnormal or excess build up of protein in and around brain cells, and all diseases that come under dementia are due to nerve cell damage. Amyloid is one such protein that is most commonly present in Alzheimer’s disease patients. 

Dementia is somewhat of an umbrella term, and includes various diseases and conditions that contribute to memory loss and odd behavior, Alzheimer’s disease being one, Parkinson’s disease, Chronic Traumatic Encephalopathy (CTE) among others. 

Denenomab specifically targets the Amyloid protein, and is therefore subjected for Alzheimer’s disease, not other dementia diseases.

Previously, the FDA (food and drug administration) gave approval to another drug, Lecanemab, another drug whose main goal is to slow down cognitive decline as well. Both of these drugs aim to remove amyloid plaque from the brain, which is presumed to be the cause of the disease in the first place.

In a nutshell, the main purpose of Donanemab is to clear amyloid plaque present in the brain, which is usually present in Alzheimer disease patients. 

It should be noted that these drugs do have side effects, some concerning, such as internal brain bleeding and/or swelling, and even four deaths – three of whom were tested in the Donanemab group. Though the probability of such risks are rare, intensive research and development is still required until they can officially be licensed as drugs. 

It should also be understood that the drug doesn’t stop cognitive decline, it is just that it slows or delays the symptoms of cognitive decline, and that the known symptoms are bound to be visible in patients over an extended period of time.

As per JAMA, “Donanemab significantly slowed Alzheimer disease progression, based on the iADRS (Integrated Alzheimer’s Disease Rating Scale) score.” 

This new drug could possibly open doors to finding a temporary cure for the disease, and make it long lasting instead of permanent – similar to diabetes or asthma. 

References:

John R. Sims, MD. “Trial of Donanemab in Early Symptomatic Alzheimer Disease.” JAMA, JAMA Network, 17 July 2023, jamanetwork.com/journals/jama/fullarticle/2807533. 

MC, Irizarry, et al. “Donanemab.” ALZFORUM, www.alzforum.org/therapeutics/donanemab. 

FDA Grants Accelerated Approval for Alzheimer’s Disease Treatment, https://www.fda.gov/news-events/press-announcements/fda-grants-accelerated-approval-alzheimers-disease-treatment

Defeating Time: A breakthrough in Aging.

Something you can’t see or hear until years go by. Something you recognize as simple and yet impossible to avoid. Something that is known as both the cruelest and most beautiful law in all of nature. Something that neither the richest nor poorest person can escape from. That something is time. 

Throughout mankind, humans have been able to conquer just about everything, from their minuscule problems to global affairs. However, with all of our minds combined, we still failed to defeat the toughest opponent of all: time. For what seems like since the origin of the universe, it appeared as the one unstoppable force that nobody could fight.

That is until 2022. While this year beckoned the end of the COVID-19 pandemic, it also brought along news about a case study conducted by David Sinclair, a molecular biologist who spent the vast majority of his career (twenty years) searching for ways to reverse aging and undoing time in the process. While the beginning of his journey was unsuccessful, he didn’t give up. 

The study split up two different mice (siblings born from the same litter) and genetically altered one of them to make them considerably older, something that was a marked success. While this alone is not indicative of a reversal in aging, it does bring up an important question: if time could be sped up, could it also be slowed down or even undone altogether? However, before we get to that, we need to understand just how the mice were genetically altered and why. 

Image credit: https://www.cnn.com, depiction of two mice from the same litter being drastically different in age appearance.

Many believe that aging is caused due to cell damage, but that’s not exactly accurate. That is one of the reasons, yes, but that’s not the main cause. Instead, we should look at the heart of the matter: the epigenome. It is what determines what each cell becomes and how it works, an instructional manual of sorts for each cell. When the epigenome malfunctions, the “instructions” of the cells are lost, thus resulting in the cell failing to continue functioning. 

So, Sinclair utilized gene therapy to get the cells their instructions to continue working and the results were shocking. Sinclair wasn’t only able to display success in accelerating aging, but also reversing it as well by nearly 60%. What’s more, this appears to be limitless, with Sinclair even citing that “[he’s] been really surprised by how universally it works. [Him and his team] haven’t found a cell type yet that [they] can’t age forward and backward.”

This expands beyond mice: it has already been utilized to reverse aging in non-human primates through the use of doxycycline, an antibiotic with gene reprogramming potential, with rapid success. There has even been some human experimentation, with gene therapy being done on human tissues in lab settings. 

The ability to reverse aging across the board brings up more than just stopping time, it also enables the possibility of halting sickness relating to aging. In retrospect, these illnesses (like dementia and Alzheimers among others) are caused due to cell malfunction. If the reversal of aging is potent enough, it runs the risk of also undoing these illnesses. 

With the potential to halt aging and enable people to live into their hundreds without fear of age-related illnesses, it does bring up countless possibilities. If we can already undo aging on a small scale, imagine what the future ten, fifty, or even a hundred years from now can behold.

  • https://www.cell.com/cell/fulltext/S0092-8674(22)01570-7
  • https://time.com/6246864/reverse-aging-scientists-discover-milestone/
  • https://www.cnn.com/2022/06/02/health/reverse-aging-life-itself-scn-wellness/index.html

Who Would You Trust More: AI or Doctors?

For as long as the profession existed, doctors have been working diligently to perfect their craft and refine any rough edges, diagnosing, treating, and eventually curing their patients in the most efficient way possible in their eyes. However, mistakes are frequently made: medical malpractice is the third leading cause of death in the United States, with over 250,000 deaths occurring yearly. Despite the rigorous education doctors undergo to officially practice their craft, they too still make mistakes. It’s human nature to err sometimes, even in life-or-death scenarios. For the majority of time, it appeared as if this was just a sacrifice that had to be made to keep one of the world’s oldest, and most vital, professions stable. 

But what if the risk of human error was eliminated by having humans removed from the equation when it came to distributing medical care?  This would dynamically pivot the medical industry and the person-to-person interaction we all know today, in a completely different direction. Some speculate that this is possible, through the utilization of artificial intelligence (AI). 

Artificial intelligence has permeated throughout the medical field briefly, but it’s been shut down due to a variety of complications, whether it’d be availability, cost, unreliability, or a combination of these factors (among others). This was especially true of Mycin, an expert system designed by Stanford University researchers to assist physicians in detecting and curing bacterial diseases. Despite its superb accuracy, being even as reliable as human experts on the matter, it was far too rigid and costly to be maintained. Despite not being medically affiliated, Google image software is another example of just how unreliable AI is: it assessed, with 100% certainty, that a slightly changed image of a cat is guacamole, a completely incorrect observation.

However, as modern technology rapidly advances, with special emphasis on machine learning (the ability of a machine to function and improve upon itself without human intervention), some believe that AI can now pick up the slack of physicians. 

This claim isn’t entirely unsubstantiated: artificial intelligence can already assess whether or not infants have certain conditions (of which there are thousands of) by facial markers, something doctors struggle with due to the massive variety of illnesses. MGene, an app that has Ai examine a photo taken of a child by its user, has over a 90% success rate at accurately detecting four serious, potentially life-threatening syndromes (Down, DiGeorge, Williams, and Noonan). AI even detected COVID-19, or SARS-CoV-2, within Wuhan, China (the origin of this virus) a week before the World Health Organization (WHO) announced it as a new virus.

With every passing day, it appears that more and more boxes that are needing to be checked, enabling the possibility of artificial intelligence becoming a dominating presence within the medical field to become one step closer to turning into a reality.

That isn’t to say that there are issues with having artificial intelligence enter the medical industry: beyond the previous problems (of cost and unreliability) being possible, Ai being ever-changing also opens up the doors to bias, ranging from socioeconomic status to race to gender and everything in between. In addition, the usage of AI also is uncomfortable to many due to the removal of the person-to-person interaction that is commonly known to people, another big issue that needs to be addressed to ensure the successful implementation of artificial intelligence into the healthcare sector. 

Regardless of what side you are on, there is a common ground: artificial intelligence will continue to get more and more advanced. While it is uncertain as to whether the general public will want AI to replace doctors, have them serve as back-end helpers, or not exist whatsoever in the office, it is clear that artificial intelligence is a tool that has both a lot of benefits and drawbacks. Whether AI is implemented or not is a question that is left to the future. 

AI can now use the help of CRISPR to precisely control gene expressions in RNA

Almost all infectious and deadly viruses are caused due to their RNA coding. Researchers from established research universities, such as NYU and Columbia, alongside the New York Genome Center, have researched and discovered a new type of CRISPR technology that targets this RNA and might just prevent the spread of deadly diseases and infections.

A new study from Nature Biotechnology has shown that the development of major gene editing tools like CRISPR will serve to be beneficial at an even larger scale. CRISPR, in a nutshell, is a gene editing piece of technology that can be used to switch gene expression on and off. Up until now, it was only known that CRISPR, with the help of the enzyme Cas9, could only edit DNA. With the recent discovery of Cas13, RNA editing might just become possible as well.

https://theconversation.com/three-ways-rna-is-being-used-in-the-next-generation-of-medical-treatment-158190

RNA is a second type of genetic material present within our cells and body, which plays an essential role in various biological roles such as regulation, expression, coding, and even decoding genes. It plays a significant role in biological processes such as protein synthesis, and these proteins are necessary to carry out various processes. 

RNA viruses

RNA viruses usually exist in 2 types – single-stranded RNA (ssRNA), and double-stranded RNA (dsRNA). RNA viruses are notoriously famous for causing the most common and the most well-known infections – examples being the common cold, influenza, Dengue, hepatitis, Ebola, and even COVID-19. These dangerous and possibly life-threatening viruses only have RNA as their genetic material. So, how can/might AI and CRISPR technology, using the enzyme Cas13 help fight against these nuisances?

Role of CRISPR-Cas13

RNA targeting CRISPRs have various applications – from editing and blocking genes to finding out possible drugs to cure said pathogenic disease/infection. As a report from NYU states, “Researchers at NYU and the New York Genome Center created a platform for RNA-targeting CRISPR screens using Cas13 to better understand RNA regulation and to identify the function of non-coding RNAs. Because RNA is the main genetic material in viruses including SARS-CoV-2 and flu,” the applications of CRISPR-Cas13 can promise us cures and newer ways to treat severe viral infections.

“Similar to DNA-targeting CRISPRs such as Cas9, we anticipate that RNA-targeting CRISPRs such as Cas13 will have an outsized impact in molecular biology and biomedical applications in the coming years,” said Neville Sanjana, associate professor of biology at NYU, associate professor of neuroscience and physiology at NYU Grossman School of Medicine. Learn more about CRISPR, Cas9, and Cas13 here

Role of AI

Artificial intelligence is becoming more and more reliant as days pass by. So much so, that it can be used to precisely target RNA coding, especially in the given case scenario. TIGER (Targeted Inhibition of Gene Expression via guide RNA design), was trained on the data from the CRISPR screens. Comparing the predictions generated by the model and laboratory tests in human cells, TIGER was able to predict both on-target and off-target activity, outperforming previous models developed for Cas13 

With the assistance of AI with an RNA-targeting CRISPR screen, TIGER’s predictions might just initiate new and more developed methods of RNA-targeting therapies. In a nutshell, AI will be able to “sieve” out undesired off-target CRISPR activity, making it a more precise and reliable method.