The FDA has approved the first drug to treat the rapid-aging disease progeria by Shalvi Gupta
Hutchinson-Gilford progeria syndrome or progeria for short is a rare genetic disorder in children. This disorder causes premature aging in children. Children with this disorder die before the age of 15. The main common causes of their deaths are heart failure, heart attack or stroke. The US FDA has approved a new drug called Zokinvy to help kids with progeria live longer. While this drug isn’t a cure for this disorder it is one step closer to helping families with kids who have this disorder. Clinical trials have shown that Zokinvy can increase the lifespan of children by 2.5 years on average. Zokinvy does this by slowing the pace of the disease. Kids with progeria have a mutation in their genetic code that interferes with the gene responsible for making lamin A. Lamin A is a protein that holds the cells’ nuclei together. Children with progeria end up with high amounts of defective proteins called progerin. This is the same as lamin A, but it has an extra piece attached. These proteins get stuck in the cells’ membrane causing cells to prematurely age and male the blood vessels and connective tissues stiffer. Everyone makes progerin and as we get older the body produces more. Children with progeria produce lots of progerin at a young age. The Zokinvy works to block the production of progerin, lowering the amount that gets stuck in the cells’ membrane. While this isn’t a long timer cure, it is a step in the right direction to help kids with this disorder. More research is being conducted on how this new drug and other drugs or therapeutics can help discover a cure for this disease.
Source: https://www.sciencenews.org/article/fda-approved-first-drug-treat-rapid-aging-disease-progeri
Hutchinson-Gilford progeria syndrome or progeria for short is a rare genetic disorder in children. This disorder causes premature aging in children. Children with this disorder die before the age of 15. The main common causes of their deaths are heart failure, heart attack or stroke. The US FDA has approved a new drug called Zokinvy to help kids with progeria live longer. While this drug isn’t a cure for this disorder it is one step closer to helping families with kids who have this disorder. Clinical trials have shown that Zokinvy can increase the lifespan of children by 2.5 years on average. Zokinvy does this by slowing the pace of the disease. Kids with progeria have a mutation in their genetic code that interferes with the gene responsible for making lamin A. Lamin A is a protein that holds the cells’ nuclei together. Children with progeria end up with high amounts of defective proteins called progerin. This is the same as lamin A, but it has an extra piece attached. These proteins get stuck in the cells’ membrane causing cells to prematurely age and male the blood vessels and connective tissues stiffer. Everyone makes progerin and as we get older the body produces more. Children with progeria produce lots of progerin at a young age. The Zokinvy works to block the production of progerin, lowering the amount that gets stuck in the cells’ membrane. While this isn’t a long timer cure, it is a step in the right direction to help kids with this disorder. More research is being conducted on how this new drug and other drugs or therapeutics can help discover a cure for this disease.
Source: https://www.sciencenews.org/article/fda-approved-first-drug-treat-rapid-aging-disease-progeri
History of Disease Eradication and potential COVID-19 applications by Saumya Shah
Eradicating a disease is no easy feat, but it is a noble endeavor. Through aggressive vaccination programs, 2 diseases have been fully eradicated: human smallpox and a cattle disease called rinderpest, both of which were highly infectious and deadly. Currently, the World Health Organization prioritizes polio and dracunculiasis (guinea worm disease); because of decades of effort, these two diseases have survived only in pockets around the world. Found mostly in Africa, the guinea worm parasites develop inside human hosts who drink contaminated water. The human hosts incubate the parasites for one year until the worm painfully erupts through the human’s skin and when the human dips their arms in water, the worm can breed in that water and continue the cycle. To control guinea worm infections, activists provide clean water sources, larvicide, sanitation, and education. In contrast, polio can be spread through ingesting fecal matter or respiratory droplets and produces flu-like symptoms and in a small proportion of cases, muscle paralysis. Due to political instability, remoteness, and rumors about the vaccine, polio still exists in Afghanistan and Pakistan. The oral polio vaccine developed in 1962 is inexpensive and mostly effective albeit rare cases of the attenuated virus regaining its severity and transmitting between people.
Regarding the COVID-19 pandemic, we see that past strategies can be applicable to eradicating the coronavirus one day. The first step to controlling the highly infectious poliovirus was creating an effective and inexpensive vaccine. Like the coronavirus, even though the minority of cases causes life-threatening symptoms, those certain cases are severe and motivate people to avoid catching the virus. In cases where a vaccine is not an option, like in the guinea worm disease, educating the population on preventing the spread and managing the symptoms was also effective. In industrialized countries, masks, sanitation, public understanding of coronavirus, and virtual work can reduce the spread of coronavirus. Beyond coronavirus, issues like political conflict, population’s fear of immunization, outside transmission, and costs are the major barriers to disease eradication. Eradication of disease has been accomplished with smallpox, is in progress with polio and guinea worm disease, and can one day happen with the coronavirus with enough money, effort, and public will.
Source: Hopkins, Donald R. “Disease Eradication.” New England Journal of Medicine, vol. 368, no. 1, 3 Jan. 2013, pp. 54–63., doi:10.1056/nejmra1200391. <https://www.nejm.org/doi/full/10.1056/NEJMra1200391>
Eradicating a disease is no easy feat, but it is a noble endeavor. Through aggressive vaccination programs, 2 diseases have been fully eradicated: human smallpox and a cattle disease called rinderpest, both of which were highly infectious and deadly. Currently, the World Health Organization prioritizes polio and dracunculiasis (guinea worm disease); because of decades of effort, these two diseases have survived only in pockets around the world. Found mostly in Africa, the guinea worm parasites develop inside human hosts who drink contaminated water. The human hosts incubate the parasites for one year until the worm painfully erupts through the human’s skin and when the human dips their arms in water, the worm can breed in that water and continue the cycle. To control guinea worm infections, activists provide clean water sources, larvicide, sanitation, and education. In contrast, polio can be spread through ingesting fecal matter or respiratory droplets and produces flu-like symptoms and in a small proportion of cases, muscle paralysis. Due to political instability, remoteness, and rumors about the vaccine, polio still exists in Afghanistan and Pakistan. The oral polio vaccine developed in 1962 is inexpensive and mostly effective albeit rare cases of the attenuated virus regaining its severity and transmitting between people.
Regarding the COVID-19 pandemic, we see that past strategies can be applicable to eradicating the coronavirus one day. The first step to controlling the highly infectious poliovirus was creating an effective and inexpensive vaccine. Like the coronavirus, even though the minority of cases causes life-threatening symptoms, those certain cases are severe and motivate people to avoid catching the virus. In cases where a vaccine is not an option, like in the guinea worm disease, educating the population on preventing the spread and managing the symptoms was also effective. In industrialized countries, masks, sanitation, public understanding of coronavirus, and virtual work can reduce the spread of coronavirus. Beyond coronavirus, issues like political conflict, population’s fear of immunization, outside transmission, and costs are the major barriers to disease eradication. Eradication of disease has been accomplished with smallpox, is in progress with polio and guinea worm disease, and can one day happen with the coronavirus with enough money, effort, and public will.
Source: Hopkins, Donald R. “Disease Eradication.” New England Journal of Medicine, vol. 368, no. 1, 3 Jan. 2013, pp. 54–63., doi:10.1056/nejmra1200391. <https://www.nejm.org/doi/full/10.1056/NEJMra1200391>
Newsletter Interferon Deficiency leads to COVID Adith Velavan
The coronavirus pandemic has completely changed our way of life. Many of the details regarding the virus and its mechanism of action are still unknown, and will require many more months of additional research. However, the future looks promising, with the release of efficient vaccines, and more questions being answered. COVID mortality data indicates that it is the most lethal for elderly men, and for those with comorbidities and immunodeficiency. However, there are still multiple cases of younger people developing severe cases of Covid-19, and recent research may have divulged why that occurs. Research groups have identified deficiencies of type 1 Interferon proteins as critical to causing these severe cases.
The IFN-1 family, composed of IFN-⍶, IFN-β, and IFN-⍵, are innate immune defense that are activated by the presence of viral RNA. They are cytokines, and function as immune signals by complexing with other proteins in the presence of viral RNA to transcribe multiple genes that are active in fighting against infections.
The study suggests that low levels of IFN proteins could be a result of antibodies, or genetic mutations that reduce the protein concentration. One team, headed by researchers at Rockefeller University, examined people with fatal cases of pneumonia related to COVID-19 for 13 unique genes involved in the IFN production pathways and found that 4% did not have the ability to properly synthesize this protein due to mutations in 8 of those genes. In contrast, 534 people with asymptomatic or mild covid were analyzed for these mutations, and only one was identified to have a mutation in a single related gene. Thus, it is highly plausible that IFN protein levels are reduced in the face of viral challenges, when particular genes are mutated, causing more severe cases of covid.
Another possible explanation for the link between IFN reduction and severe Covid cases could be that autoantibodies are reducing the protein’s level. Individuals with autoimmune diseases can produce antibodies targeted at IFN, and people with the autoimmune disease APS-1 do produce these antibodies, and it was even found that people with this condition have more severe cases.The second group, led by a team at a paris laboratory, found that nearly 14% of people they tested had antibodies for some IFN protein, while .3% of healthy people had these. Interestingly, more than 90% of these individuals with antibodies were male. Typically, B cells that produce these antibodies are selectively eliminated in early development, and an issue in that process could be the cause of these autoantibodies. Furthermore, many B cell checkpoint genes are encoded in the X chromosome, which could explain the skew towards men.
The resultant effect of a reduced IFN concentration is an excess of viral replication and spread without many of proper immune checkpoints and responses. However, there are other auxiliary responses like an overactive inflammatory response, which is often the reason why Covid-19 can be lethal. Ultimately, this research begets even more questions, but creates hope that this virus can be better understood for newer treatments on top of the vaccines.
The coronavirus pandemic has completely changed our way of life. Many of the details regarding the virus and its mechanism of action are still unknown, and will require many more months of additional research. However, the future looks promising, with the release of efficient vaccines, and more questions being answered. COVID mortality data indicates that it is the most lethal for elderly men, and for those with comorbidities and immunodeficiency. However, there are still multiple cases of younger people developing severe cases of Covid-19, and recent research may have divulged why that occurs. Research groups have identified deficiencies of type 1 Interferon proteins as critical to causing these severe cases.
The IFN-1 family, composed of IFN-⍶, IFN-β, and IFN-⍵, are innate immune defense that are activated by the presence of viral RNA. They are cytokines, and function as immune signals by complexing with other proteins in the presence of viral RNA to transcribe multiple genes that are active in fighting against infections.
The study suggests that low levels of IFN proteins could be a result of antibodies, or genetic mutations that reduce the protein concentration. One team, headed by researchers at Rockefeller University, examined people with fatal cases of pneumonia related to COVID-19 for 13 unique genes involved in the IFN production pathways and found that 4% did not have the ability to properly synthesize this protein due to mutations in 8 of those genes. In contrast, 534 people with asymptomatic or mild covid were analyzed for these mutations, and only one was identified to have a mutation in a single related gene. Thus, it is highly plausible that IFN protein levels are reduced in the face of viral challenges, when particular genes are mutated, causing more severe cases of covid.
Another possible explanation for the link between IFN reduction and severe Covid cases could be that autoantibodies are reducing the protein’s level. Individuals with autoimmune diseases can produce antibodies targeted at IFN, and people with the autoimmune disease APS-1 do produce these antibodies, and it was even found that people with this condition have more severe cases.The second group, led by a team at a paris laboratory, found that nearly 14% of people they tested had antibodies for some IFN protein, while .3% of healthy people had these. Interestingly, more than 90% of these individuals with antibodies were male. Typically, B cells that produce these antibodies are selectively eliminated in early development, and an issue in that process could be the cause of these autoantibodies. Furthermore, many B cell checkpoint genes are encoded in the X chromosome, which could explain the skew towards men.
The resultant effect of a reduced IFN concentration is an excess of viral replication and spread without many of proper immune checkpoints and responses. However, there are other auxiliary responses like an overactive inflammatory response, which is often the reason why Covid-19 can be lethal. Ultimately, this research begets even more questions, but creates hope that this virus can be better understood for newer treatments on top of the vaccines.
Deep Brain Stimulation in Parkinson's Disease by Raabiah Chaudhry
A study published in the peer-reviewed neurology journal, American Academy of Neurology, displays the impact of subthalamic nucleus deep brain stimulation (DBS) in early-stage Parkinson’s disease. Individuals with early PD were split into two groups, each with a different treatment plan. One group was given only medications, in the form of optimal drug therapy and the other group was given the medications, as well as, DBS.
The results showed that the group given the additional DBS required lesser doses of the main medication for PD treatment, levodopa, which generally needs to be given in increasing doses over time. With needing lower doses of this medication, the individuals receiving DBS treatment, also had less symptoms associated with the drug, including dyskinesis and dizziness. Further, as PD progresses, polypharmacy is generally required. However, this likelihood for requiring multiple medications was much lower for individuals receiving the DBS. The individuals treated with the DBS also exhibited significantly less tremors, which is common in the hands of PD patients, as well as slower progression of tremors.
The study shows that early use of DBS in PD is effective in minimizing the doses and number of medications needed overtime, as well as their associated side effects and, in regards to motor function, helps with dyskinesias and slowing tremor progression as PD progresses. Thus, in using DBS treatment in early PD, there is potential for improving daily living activities and overall quality of life long-term for individuals with the disease.
Source: https://n.neurology.org/content/95/4/e436
A study published in the peer-reviewed neurology journal, American Academy of Neurology, displays the impact of subthalamic nucleus deep brain stimulation (DBS) in early-stage Parkinson’s disease. Individuals with early PD were split into two groups, each with a different treatment plan. One group was given only medications, in the form of optimal drug therapy and the other group was given the medications, as well as, DBS.
The results showed that the group given the additional DBS required lesser doses of the main medication for PD treatment, levodopa, which generally needs to be given in increasing doses over time. With needing lower doses of this medication, the individuals receiving DBS treatment, also had less symptoms associated with the drug, including dyskinesis and dizziness. Further, as PD progresses, polypharmacy is generally required. However, this likelihood for requiring multiple medications was much lower for individuals receiving the DBS. The individuals treated with the DBS also exhibited significantly less tremors, which is common in the hands of PD patients, as well as slower progression of tremors.
The study shows that early use of DBS in PD is effective in minimizing the doses and number of medications needed overtime, as well as their associated side effects and, in regards to motor function, helps with dyskinesias and slowing tremor progression as PD progresses. Thus, in using DBS treatment in early PD, there is potential for improving daily living activities and overall quality of life long-term for individuals with the disease.
Source: https://n.neurology.org/content/95/4/e436
"COVID-19 Antibodies in Production After Initial Infection" by James He
Not only marking the beginnings of COVID-19 infection, this past Tuesday, December 1st, was also World AIDS Day, which commemorates the deaths of those inflicted with human immunodeficiency virus (HIV) infection and raises awareness of the spread and terrible outcomes of the deadly disease. Since the first case of HIV/AIDS in 1981, the infection has ravaged over 37 million people, amassing over 750,000 deaths worldwide. Unfortunately, infection rates have been steadily increasing over the last couple of years, and the COVID-19 pandemic may introduce severely problematic trends in disease incidence and progression as the virus lingers across the globe.
One bright outlook that has risen from the COVID-19 pandemic is the efficacy of the scientific community’s efforts in the management of widespread disease, as headlined by successes in Pfizer/BioNTech and Moderna’s vaccine development along with Eli Lilly’s new antibody treatment. Likewise, ViiV Healthcare, a partnership coalesced by Pfizer, has developed a new FDA-approved infant formulation of an HIV/AIDS medication called dolutegravir, which belongs to a class of integrase inhibitors that has recently entered the therapeutic landscape for retroviral disease. This berry-tasting medication is designed to dissolve in fluids friendly for infant consumption, like water and juice, and provides a promising therapeutic route for the 160,000 newly infected children each year. Such represents a dramatic improvement, simply due to the newfound treatment option that can hopefully reduce the number of infants who fall to the disease, often without anyone knowing they had it.
Simultaneously, significant efforts are being made to combat transmission of disease to women, who may inadvertently pass the virus to newborns during pregnancy or via breastfeeding. Currently, a vaginal insert called a dapivirine ring serves as a preventative measure that can avoid social stigmas accompanying concerns about infection, and is being promoted for use. While the data displays mixed results surrounding the efficacy of the ring, consistent usage has been shown to significantly enhance its effectiveness. This is crucial - perhaps the best form of medicine is preventative care, so tackling infection rates among children from both a therapeutic and preventative perspective should combine to induce a decrease in infection. A similar idea surrounds COVID-19, as both vaccine and treatment developments have the potential to induce compounding benefits on the state of the world today.
Source: Mcneil, Donald G. “Berry-Flavored H.I.V. Medication Is Ready for Babies.” The New York Times, The New York Times, 30 Nov. 2020, www.nytimes.com/2020/11/30/health/hiv-aids-medication-babies.html.
Not only marking the beginnings of COVID-19 infection, this past Tuesday, December 1st, was also World AIDS Day, which commemorates the deaths of those inflicted with human immunodeficiency virus (HIV) infection and raises awareness of the spread and terrible outcomes of the deadly disease. Since the first case of HIV/AIDS in 1981, the infection has ravaged over 37 million people, amassing over 750,000 deaths worldwide. Unfortunately, infection rates have been steadily increasing over the last couple of years, and the COVID-19 pandemic may introduce severely problematic trends in disease incidence and progression as the virus lingers across the globe.
One bright outlook that has risen from the COVID-19 pandemic is the efficacy of the scientific community’s efforts in the management of widespread disease, as headlined by successes in Pfizer/BioNTech and Moderna’s vaccine development along with Eli Lilly’s new antibody treatment. Likewise, ViiV Healthcare, a partnership coalesced by Pfizer, has developed a new FDA-approved infant formulation of an HIV/AIDS medication called dolutegravir, which belongs to a class of integrase inhibitors that has recently entered the therapeutic landscape for retroviral disease. This berry-tasting medication is designed to dissolve in fluids friendly for infant consumption, like water and juice, and provides a promising therapeutic route for the 160,000 newly infected children each year. Such represents a dramatic improvement, simply due to the newfound treatment option that can hopefully reduce the number of infants who fall to the disease, often without anyone knowing they had it.
Simultaneously, significant efforts are being made to combat transmission of disease to women, who may inadvertently pass the virus to newborns during pregnancy or via breastfeeding. Currently, a vaginal insert called a dapivirine ring serves as a preventative measure that can avoid social stigmas accompanying concerns about infection, and is being promoted for use. While the data displays mixed results surrounding the efficacy of the ring, consistent usage has been shown to significantly enhance its effectiveness. This is crucial - perhaps the best form of medicine is preventative care, so tackling infection rates among children from both a therapeutic and preventative perspective should combine to induce a decrease in infection. A similar idea surrounds COVID-19, as both vaccine and treatment developments have the potential to induce compounding benefits on the state of the world today.
Source: Mcneil, Donald G. “Berry-Flavored H.I.V. Medication Is Ready for Babies.” The New York Times, The New York Times, 30 Nov. 2020, www.nytimes.com/2020/11/30/health/hiv-aids-medication-babies.html.
COVID-19 Vaccine: Who Gets it First? By Will Odell
As the spread of COVID-19 continues in the United States and worldwide, a glimmer of hope for beginning to end the pandemic emerged as two companies, Pfizer and Moderna, announced that their vaccine candidates had proven highly effective. While this is unequivocally great news, this only represents the first step in the vaccination process. An equally daunting process looms as decisions must be made on how to get these vaccines to into the public.
On December 2nd, the US Centers for Disease Control formally released their suggested priority list as to who should receive the vaccine first. Why is it necessary to assign priority? The answer is manufacturing. While most attention was focused on the scientific steps to develop the vaccine, it was as important to develop the infrastructure to produce millions and billions of doses of the vaccine. With this in mind, the US is set to receive 40 million doses of the vaccine by the end of December, enough to vaccinate 20 million people. Due to this fact, not everyone who wants to receive a vaccine will initially be able to do so.
So, who is getting the vaccine first? The CDC guidance recommends that two groups of people should be first in line: health care workers, and residents of long-term care facilities. Health care workers are given priority due to their front-line exposure to the virus and integral role within the healthcare system, and long-term care residents are given priority due to their disproportionate risk of COVID complications and death. The decision was not reached lightly, representing the culmination of months of debate and model analysis. However, the CDC feels that this best represents the combination that will reduce the rate of infection and reduce loss of life.
Fortunately for the rest of Americans, production will rapidly ramp up beginning in January, with an estimated 10 million doses set to be available each week. There has been preliminary discussion as to the next groups of people to be assigned priority, with current thinking pointing towards essential workers, older, and at-risk Americans as next in line. However, this is not yet agreed upon, and has been subject to political debate.
In the broader scheme, it is the hope that by the end of the spring the vaccine will available to everyone. The development of a successful COVID-19 vaccine is an incredible scientific achievement and will hopefully mean a return to normal life soon.
Source: https://www.washingtonpost.com/health/2020/12/01/vaccine-priority-groups-covid/
As the spread of COVID-19 continues in the United States and worldwide, a glimmer of hope for beginning to end the pandemic emerged as two companies, Pfizer and Moderna, announced that their vaccine candidates had proven highly effective. While this is unequivocally great news, this only represents the first step in the vaccination process. An equally daunting process looms as decisions must be made on how to get these vaccines to into the public.
On December 2nd, the US Centers for Disease Control formally released their suggested priority list as to who should receive the vaccine first. Why is it necessary to assign priority? The answer is manufacturing. While most attention was focused on the scientific steps to develop the vaccine, it was as important to develop the infrastructure to produce millions and billions of doses of the vaccine. With this in mind, the US is set to receive 40 million doses of the vaccine by the end of December, enough to vaccinate 20 million people. Due to this fact, not everyone who wants to receive a vaccine will initially be able to do so.
So, who is getting the vaccine first? The CDC guidance recommends that two groups of people should be first in line: health care workers, and residents of long-term care facilities. Health care workers are given priority due to their front-line exposure to the virus and integral role within the healthcare system, and long-term care residents are given priority due to their disproportionate risk of COVID complications and death. The decision was not reached lightly, representing the culmination of months of debate and model analysis. However, the CDC feels that this best represents the combination that will reduce the rate of infection and reduce loss of life.
Fortunately for the rest of Americans, production will rapidly ramp up beginning in January, with an estimated 10 million doses set to be available each week. There has been preliminary discussion as to the next groups of people to be assigned priority, with current thinking pointing towards essential workers, older, and at-risk Americans as next in line. However, this is not yet agreed upon, and has been subject to political debate.
In the broader scheme, it is the hope that by the end of the spring the vaccine will available to everyone. The development of a successful COVID-19 vaccine is an incredible scientific achievement and will hopefully mean a return to normal life soon.
Source: https://www.washingtonpost.com/health/2020/12/01/vaccine-priority-groups-covid/
COVID and Blood Clots by Defne Alpdogan
As more individuals continue to research COVID and learn about the properties of the disease, a recent discovery would be that COVID could potentially trigger blood clots. While it is known that COVID causes excessive inflation from the overactive immune response to the disease, a recent pathway indicates that it might cause neutrophils to release a web of genetic material to trap the virus particles in the bloodstream. In tissues, this mechanism is an effective way to control the spread of disease and trap the particles from further infecting the body; however, in the bloodstream, this is a one way ticket to disaster as it can cause clotting. In the recent report, blood clots in the lungs have been seen to cause a significant cause of death in COVID patients and these blood clots can form from the trapped red blood cells and platelets which clog the blood vessel in the lungs. Another point that the researchers use to back up their theory would be that severely ill COVID patients have high levels of neutrophils, indicating that there is a trigger for the release of the neutrophils in the bloodstream. While, this is just the first step in the research, the colleagues on the report hope to further study the antibodies that could be causing the neutrophils to release the traps for the trigger clotting.
This is a significant finding in the current pandemic, as it helps build the piece of how to best target the disease, The presence of the neutrophils can helps establish certain links to cell signaling and the immune system’s role in the spread of the disease inside of the body. In addition, the researchers are also looking into the effect of phospholipid auto-antibodies and their affect with the blood clots. Currently, while it is a small case study, researchers have looked at 11 patients who developed blood clots and found that half of them had phospholipid auto-antibodies. In short, the global participation on finding and researching COVID affects are not only interesting but also vital when discussing the future of science.
Source: https://www.sciencenews.org/article/coronavirus-covid-19-dangerous-blood-clots
As more individuals continue to research COVID and learn about the properties of the disease, a recent discovery would be that COVID could potentially trigger blood clots. While it is known that COVID causes excessive inflation from the overactive immune response to the disease, a recent pathway indicates that it might cause neutrophils to release a web of genetic material to trap the virus particles in the bloodstream. In tissues, this mechanism is an effective way to control the spread of disease and trap the particles from further infecting the body; however, in the bloodstream, this is a one way ticket to disaster as it can cause clotting. In the recent report, blood clots in the lungs have been seen to cause a significant cause of death in COVID patients and these blood clots can form from the trapped red blood cells and platelets which clog the blood vessel in the lungs. Another point that the researchers use to back up their theory would be that severely ill COVID patients have high levels of neutrophils, indicating that there is a trigger for the release of the neutrophils in the bloodstream. While, this is just the first step in the research, the colleagues on the report hope to further study the antibodies that could be causing the neutrophils to release the traps for the trigger clotting.
This is a significant finding in the current pandemic, as it helps build the piece of how to best target the disease, The presence of the neutrophils can helps establish certain links to cell signaling and the immune system’s role in the spread of the disease inside of the body. In addition, the researchers are also looking into the effect of phospholipid auto-antibodies and their affect with the blood clots. Currently, while it is a small case study, researchers have looked at 11 patients who developed blood clots and found that half of them had phospholipid auto-antibodies. In short, the global participation on finding and researching COVID affects are not only interesting but also vital when discussing the future of science.
Source: https://www.sciencenews.org/article/coronavirus-covid-19-dangerous-blood-clots
Dopamine Therapy in Alzhemer’s Disease by Raabiah Chaudhry
A newly published study backed by the Alzheimer’s Drug Discovery Foundation displays the ability of dopamine therapy to improve cognitive function in mild-to-moderate Alzheimer’s disease. Specifically, rotigotine, a drug associated with the brain’s dopamine transmission, has been found to improve cognitive ability in Alzhemier’s patients.
To evaluate the effect of rotigotine on the function and connectivity of the brain, novel biomarker testing involving transcranial magnetic stimulation and electroencephalography recordings was conducted. Results showed that rotigotine amplifies the dopaminergic pathways associated with the frontal lobe of the brain. From judgement and reasoning to working memory and orientation, the drug shows improvement in executive function of the frontal lobe, as well as, patients’ performance of daily living activities, such as shopping, bathing themselves, and planning. This is especially significant as it gives the patients a greater sense of independence, lessening their reliance on caregivers.
The study shows potential for therapeutic options involving dopaminergic transmission for early treatment, when there is only mild impairment of cognitive functions associated with frontal lobe activity and daily life task performance, slowing the onset of full-on Alzheimer’s.
Source: https://www.prnewswire.com/news-releases/newly-published-study-funded-by-the-alzheimers-drug-discovery-foundation-finds-dopamine-therapy-improves-cognitive-function-in-mild-to-moderate-alzheimers-disease-301094138.html?emci=99e2043b-c0c6-ea11-9b05-00155d03bda0&emdi=ea000000-0000-0000-0000-000000000001&ceid=
A newly published study backed by the Alzheimer’s Drug Discovery Foundation displays the ability of dopamine therapy to improve cognitive function in mild-to-moderate Alzheimer’s disease. Specifically, rotigotine, a drug associated with the brain’s dopamine transmission, has been found to improve cognitive ability in Alzhemier’s patients.
To evaluate the effect of rotigotine on the function and connectivity of the brain, novel biomarker testing involving transcranial magnetic stimulation and electroencephalography recordings was conducted. Results showed that rotigotine amplifies the dopaminergic pathways associated with the frontal lobe of the brain. From judgement and reasoning to working memory and orientation, the drug shows improvement in executive function of the frontal lobe, as well as, patients’ performance of daily living activities, such as shopping, bathing themselves, and planning. This is especially significant as it gives the patients a greater sense of independence, lessening their reliance on caregivers.
The study shows potential for therapeutic options involving dopaminergic transmission for early treatment, when there is only mild impairment of cognitive functions associated with frontal lobe activity and daily life task performance, slowing the onset of full-on Alzheimer’s.
Source: https://www.prnewswire.com/news-releases/newly-published-study-funded-by-the-alzheimers-drug-discovery-foundation-finds-dopamine-therapy-improves-cognitive-function-in-mild-to-moderate-alzheimers-disease-301094138.html?emci=99e2043b-c0c6-ea11-9b05-00155d03bda0&emdi=ea000000-0000-0000-0000-000000000001&ceid=
COVID Vaccine by Amrita Makhijani
The article I read was about the new Pfizer vaccine announcement. I chose to read about this because it is groundbreaking news will impact the entire world if it is as good as they made it seem. To summarize the press conference that Pfizer held, they tested two doses of the vaccine BNT162b2. They began the trial in late July and have been monitoring the 43,538 participants since then. Out of those 38,955 participants were given the second dose of the vaccine and in this sample, they have found an efficacy rate of above 90%. The FDA released a requirement that at least 62 cases have to be analyzed for any data to be released on any vaccine. Pfizer had 94 cases to analyze and after doing so they found this efficacy. This translates to the fact that of the 94 patients, 90% of the ones who did receive the vaccine (rather than the placebo) responded well to it and that it had a great hand in helping them overcome the COVID-19 virus. They found this efficacy seven days after the second dose, which means that it takes about a month for protection to take place and this is after two doses of the vaccine. After this conclusion, the FDA has mandated that there be a new efficacy evaluation 14 days after the second dose as well. Pfizer also announced that they will be monitoring all subjects up to two years after they receive the vaccine in order to rule out any possible long-term side effects. They released that they should be able to produce 50 million doses in 2020 and up to 1.3 billion in 2021. The full data report will be released in the third week of November by Pfizer, as per FDA guidelines. The reason that this article is so important and interesting to me is because no other company has been able to reach such a high efficacy in their Phase 3 trial before. It is also important to acknowledge that even though Pfizer can produce many doses of the vaccine, it is always going to be up to the American people to take or not take the vaccine. Regardless, this news is as close to good news as we have gotten in the past 10 months and therefore it is an important breakthrough in medicine.
Source: https://www.pfizer.com/news/press-release/press-release-detail/pfizer-and-biontech-announce-vaccine-candidate-against
The article I read was about the new Pfizer vaccine announcement. I chose to read about this because it is groundbreaking news will impact the entire world if it is as good as they made it seem. To summarize the press conference that Pfizer held, they tested two doses of the vaccine BNT162b2. They began the trial in late July and have been monitoring the 43,538 participants since then. Out of those 38,955 participants were given the second dose of the vaccine and in this sample, they have found an efficacy rate of above 90%. The FDA released a requirement that at least 62 cases have to be analyzed for any data to be released on any vaccine. Pfizer had 94 cases to analyze and after doing so they found this efficacy. This translates to the fact that of the 94 patients, 90% of the ones who did receive the vaccine (rather than the placebo) responded well to it and that it had a great hand in helping them overcome the COVID-19 virus. They found this efficacy seven days after the second dose, which means that it takes about a month for protection to take place and this is after two doses of the vaccine. After this conclusion, the FDA has mandated that there be a new efficacy evaluation 14 days after the second dose as well. Pfizer also announced that they will be monitoring all subjects up to two years after they receive the vaccine in order to rule out any possible long-term side effects. They released that they should be able to produce 50 million doses in 2020 and up to 1.3 billion in 2021. The full data report will be released in the third week of November by Pfizer, as per FDA guidelines. The reason that this article is so important and interesting to me is because no other company has been able to reach such a high efficacy in their Phase 3 trial before. It is also important to acknowledge that even though Pfizer can produce many doses of the vaccine, it is always going to be up to the American people to take or not take the vaccine. Regardless, this news is as close to good news as we have gotten in the past 10 months and therefore it is an important breakthrough in medicine.
Source: https://www.pfizer.com/news/press-release/press-release-detail/pfizer-and-biontech-announce-vaccine-candidate-against
Rise of Robot Radiologists by Saumya Shah
Computer assisted diagnosis is a hot issue on both the medical and technological fronts, but did you know the development of it began in the 90s? While the prototypes were difficult to use, often inaccurate, and thus unreliable at its advent, decades later the question is whether computers will replace physicians. In an opinion piece published by Nature, MIT computer scientist Regina Barzilay was diagnosed with breast cancer in 2014. However determining the diagnosis was not simple, as imaging tests returned ambiguous results. With her machine-learning background, she and her team trained an artificially-intelligent algorithm with thousands of mammogram images and whether the patient was diagnosed with breast cancer. AI can detect minute anomalies in scans that a radiologist may miss. Besides making diagnoses more reliable, AI can also make radiology more accessible for regions that do not have radiologists on site. Finally, AI can also reduce medical costs by predicting whether the patient needs another imaging appointment.
Rather than replacing radiologists entirely, AI will simply be another tool radiologists can use to make their work faster and more reliable. In fact, AI can prioritize the scans from cases that seem very urgent (eg. a collapsed lung) so that the physician can take action more quickly. The Medscape Radiologist Lifestyle, Happiness and Burnout Report found that 44% of radiologists reported that they were experiencing burnout. For that reason, 84% of radiology clinics had adopted or were planning to adopt AI into their practice in a survey by Reaction Data. The FDA has approved several of these computer programs, most notably the ones by Google which can make 3D organ models from CT scans and determine cardiovascular risk factors from retinal scans. Despite this incredible potential, programs still do not have the medical training that physicians have because the programs cannot differ between causation and correlation. For example, the computer calculates that patients with lower flexibility had higher mortality, except the physician knows that the underlying cause of the inflexibility was age and general lack of wellbeing from the patients. Also, inputting populations with different disease rates or institutions with different labelling methods can cause issues with the AI’s results because it was trained on a specific set of images from a specific population in most cases. Ultimately, physicians who use AI will spend more time talking to their patients and connecting anomalies in the images to underlying biology while the AI programs take over the tedious work of reading scans all day.
Source: Reardon, Sara. “Rise of Robot Radiologists.” Nature News, Nature Publishing Group, 18 Dec. 2019, www.nature.com/articles/d41586-019-03847-z.
Computer assisted diagnosis is a hot issue on both the medical and technological fronts, but did you know the development of it began in the 90s? While the prototypes were difficult to use, often inaccurate, and thus unreliable at its advent, decades later the question is whether computers will replace physicians. In an opinion piece published by Nature, MIT computer scientist Regina Barzilay was diagnosed with breast cancer in 2014. However determining the diagnosis was not simple, as imaging tests returned ambiguous results. With her machine-learning background, she and her team trained an artificially-intelligent algorithm with thousands of mammogram images and whether the patient was diagnosed with breast cancer. AI can detect minute anomalies in scans that a radiologist may miss. Besides making diagnoses more reliable, AI can also make radiology more accessible for regions that do not have radiologists on site. Finally, AI can also reduce medical costs by predicting whether the patient needs another imaging appointment.
Rather than replacing radiologists entirely, AI will simply be another tool radiologists can use to make their work faster and more reliable. In fact, AI can prioritize the scans from cases that seem very urgent (eg. a collapsed lung) so that the physician can take action more quickly. The Medscape Radiologist Lifestyle, Happiness and Burnout Report found that 44% of radiologists reported that they were experiencing burnout. For that reason, 84% of radiology clinics had adopted or were planning to adopt AI into their practice in a survey by Reaction Data. The FDA has approved several of these computer programs, most notably the ones by Google which can make 3D organ models from CT scans and determine cardiovascular risk factors from retinal scans. Despite this incredible potential, programs still do not have the medical training that physicians have because the programs cannot differ between causation and correlation. For example, the computer calculates that patients with lower flexibility had higher mortality, except the physician knows that the underlying cause of the inflexibility was age and general lack of wellbeing from the patients. Also, inputting populations with different disease rates or institutions with different labelling methods can cause issues with the AI’s results because it was trained on a specific set of images from a specific population in most cases. Ultimately, physicians who use AI will spend more time talking to their patients and connecting anomalies in the images to underlying biology while the AI programs take over the tedious work of reading scans all day.
Source: Reardon, Sara. “Rise of Robot Radiologists.” Nature News, Nature Publishing Group, 18 Dec. 2019, www.nature.com/articles/d41586-019-03847-z.
Brains Immune Cells Put the Brakes on Neurons by Adith Velavan
Neurons in the brain convey information by action potentials, which is an electrical signal that involves an initial excitation caused by a neurotransmitter followed by inhibition of this signal so that the neuron can transfer the signal and isn’t constantly stimulated. Initially, it was believed that interneurons, a subtype of neuron, were involved in the inhibition of the neuronal signalling by use of particular inhibitor neurotransmitters such as GABA. Lead researcher Ana Badimon of Mount Sinai identified in experiments with her team that there is another brain cell type that is involved with this inhibition; microglia. The team began by using mice that had the growth factor receptor protein CSF1R blocked which led to a lack of microglia. Afterwards, the mice were given neurostimulants and the result was epileptic seizures, a sign of hyperactive neurons, and a lack of inhibition. Mice without this protein that produced microglia being blocked did not experience the same seizures. Typical neuron synapses have ATP being released, and a microglial enzyme CD39 then converts this ATP in ADP which signals a final P2Y12 receptor found only on microglia, thus attracting them. Blocking P2Y12 receptors not only inhibited microglial attraction, but prevented the typical inhibition of the synapse that is observed when microglia are present.
The authors then wondered how the microglia could be inhibiting the neurons. After removing microglia, they noticed a lack of the molecule Adenosine in the extracellular area. After blocking CD39 enzyme, they once again found a lack of Adenosine and an increased susceptibility for seizures in mice when there were neurostimulants present. ADO works by inhibiting the receptor A1, which usually allows the intracellular messenger cAMP to release an excitatory neurotransmitter called Glutamate. Further assessment allowed the team to realize that microglia have their greatest effect when altered in grey matter, where neuronal cell bodies are located, and where this effect was localized.
The team is now poised to investigate further and future questions such as how the level of neuron excitability can affect the inhibitory action of microglia. Further, the actions of microglia can also be involved with neurological disease considering its effect on epilepsy and seizures, and possibly more. Additional research will revolve around these topics, and will be used to further explore the specific mechanisms of microglial inhibition.
Source: https://www.nature.com/articles/d41586-020-02713-7
Neurons in the brain convey information by action potentials, which is an electrical signal that involves an initial excitation caused by a neurotransmitter followed by inhibition of this signal so that the neuron can transfer the signal and isn’t constantly stimulated. Initially, it was believed that interneurons, a subtype of neuron, were involved in the inhibition of the neuronal signalling by use of particular inhibitor neurotransmitters such as GABA. Lead researcher Ana Badimon of Mount Sinai identified in experiments with her team that there is another brain cell type that is involved with this inhibition; microglia. The team began by using mice that had the growth factor receptor protein CSF1R blocked which led to a lack of microglia. Afterwards, the mice were given neurostimulants and the result was epileptic seizures, a sign of hyperactive neurons, and a lack of inhibition. Mice without this protein that produced microglia being blocked did not experience the same seizures. Typical neuron synapses have ATP being released, and a microglial enzyme CD39 then converts this ATP in ADP which signals a final P2Y12 receptor found only on microglia, thus attracting them. Blocking P2Y12 receptors not only inhibited microglial attraction, but prevented the typical inhibition of the synapse that is observed when microglia are present.
The authors then wondered how the microglia could be inhibiting the neurons. After removing microglia, they noticed a lack of the molecule Adenosine in the extracellular area. After blocking CD39 enzyme, they once again found a lack of Adenosine and an increased susceptibility for seizures in mice when there were neurostimulants present. ADO works by inhibiting the receptor A1, which usually allows the intracellular messenger cAMP to release an excitatory neurotransmitter called Glutamate. Further assessment allowed the team to realize that microglia have their greatest effect when altered in grey matter, where neuronal cell bodies are located, and where this effect was localized.
The team is now poised to investigate further and future questions such as how the level of neuron excitability can affect the inhibitory action of microglia. Further, the actions of microglia can also be involved with neurological disease considering its effect on epilepsy and seizures, and possibly more. Additional research will revolve around these topics, and will be used to further explore the specific mechanisms of microglial inhibition.
Source: https://www.nature.com/articles/d41586-020-02713-7
How COVID-19 May Trigger Dangerous Blood Clots by Shalvi Gupta
While scientists are having a difficult time finding a vaccine for coivd-19. This disease just might have taught us something very interesting about our immune systems. Doctors have been noticing that a lot of the covid-19 patients that have been due to blood clots found in the lungs. They have discovered that these blood clots occur because our immune system starts to attack our body instead of the virus. This happens because auto-antibodies are unable to identify the invader and instead go after the molecules that form the cell membrane. This causes the immune cells known as neutrophils release a web of genetic material that is used to trap the virus particles. This method is generally used in the tissues of the cell, but when this happens in the bloodstream it causes clotting. This discovery has moved scientists one step closer to discovering if auto-antibodies are beneficial or harmful towards the body. In terms of what this means for covid-19, more study needs to be done to understand how the immune proteins are linked to clotting. But, they are currently considering removing the problematic antibodies through a process called plasmapheresis. Plasmapheresis is where they filter the liquid part of the blood. But, if they proceed with this plan, they will have to insert lab-made immune proteins to help fight the virus. They still have a long way to go with this discovery to figure what it really means for our body and covid.
Source: : https://www.sciencenews.org/article/coronavirus-covid-19-dangerous-blood-clots
While scientists are having a difficult time finding a vaccine for coivd-19. This disease just might have taught us something very interesting about our immune systems. Doctors have been noticing that a lot of the covid-19 patients that have been due to blood clots found in the lungs. They have discovered that these blood clots occur because our immune system starts to attack our body instead of the virus. This happens because auto-antibodies are unable to identify the invader and instead go after the molecules that form the cell membrane. This causes the immune cells known as neutrophils release a web of genetic material that is used to trap the virus particles. This method is generally used in the tissues of the cell, but when this happens in the bloodstream it causes clotting. This discovery has moved scientists one step closer to discovering if auto-antibodies are beneficial or harmful towards the body. In terms of what this means for covid-19, more study needs to be done to understand how the immune proteins are linked to clotting. But, they are currently considering removing the problematic antibodies through a process called plasmapheresis. Plasmapheresis is where they filter the liquid part of the blood. But, if they proceed with this plan, they will have to insert lab-made immune proteins to help fight the virus. They still have a long way to go with this discovery to figure what it really means for our body and covid.
Source: : https://www.sciencenews.org/article/coronavirus-covid-19-dangerous-blood-clots
Seeds of Cancer in Normal Skin by Adith Velavan
Cancer continues to be one of the foremost medical challenges facing modern science. Published in Nature, this article recounts novel research conducted by Jessica Tang, a dermatology postdoctoral investigator at the University of California in San Francisco. Tang and her team sequenced the DNA of individual melanocytes, which are mature cells in the skin that form melanin, which in turn is the polymer that pigments our skin. Her research was focused on identifying microscopic DNA changes and differences between melanocytes that could reveal more about the origins of melanoma, an extremely aggressive form of skin cancer.
The common understanding of cancer is that mutations accrued over a lifetime can yield, in the most unfortunate circumstances, a set of changes that could lead to cancer. Somatic cells, those that are non reproductive like the skin, can mutate in key genes that could be oncogenic, or cancer causing, and result in the common cancers like melanoma. However, researchers have yet to understand many minute details of the origins of cancer because of the lack of technology required to sequence single or a few cells. The epidermis, the outermost layer of skin, does not contain many cells and is only “.1 milimeters thick” as the article states, and is constantly bombarded by all kinds of toxins from chemicals to electromagnetic rays that can potentially cause mutations. UV rays continue to be the leading cause of many skin cancers.
A previous study utilized sequencing of small biopsies, and revealed that mutations occur often in these normal cells, and actually favor the growth of these mutated cells. The mutations occurred in keratinocytes, which makes up “90% of the cell types” in the epidermis, unlike melanocytes which are in much smaller quantities.
Thus, to further investigate the origins of a rare cancer originating from these melanocytes, the investigating team decided to sequence single cells. The two most common methods to this were: “single cell sequencing, which relies on error prone, whole genome amplification,” or separating and growing out the single melanocytes into colonies which can then allow researchers to use more conventional sequencing methods. Tang et al. used a combination of methods. Since it is difficult to grow out melanocytes, the group grew out the cells in the colonies of hundreds and then continued the whole genome amplification step to continue the single cell sequence technique while reducing typical system errors.
“133 melanocytes were sequenced, from 19 body sites of 6 deceased donors,” with two of the people having skin cancer and others without. The colonies that were grown out had sequencing done to confirm particular mutations, and other controls were included. The results the researchers found were that most of the mutations were similar to UV ray mutations, and that the number of mutations per melanocyte on average was around 20,000, which is quite similar to the level of mutations found in melanoma cells. An additional result the researchers found was that, “around 20% of melanocytes had melanoma-driving mutations.” This, interestingly, leads to the growth of “scattered fields” of mutated clone melanocytes, an understanding that is now emerging as a feature of ageing.
However, the researchers also found discoveries that were unexpected. They found, for example, that places that are more chronically exposed to the sun, like the face, actually had less mutations in melanocytes, than places with intermittent exposure, which may explain why melanomas often arise in places with intermittent exposure. The team further discovered that a select population of the melanocytes did not have the high average of mutations, and they surmised that it could be because these melanocytes originally resided in places not exposed to sun, like hair follicles. The last important result found by the researches was an identification that many of the mutations found in the sequencing data corresponded to a particular signalling pathway for particular genes such as NRAF. However, melanomas typically arise from a common mutation in the BRAF gene. The team has proposed that melanomas, thus, can arise from moles and express BRAF mutations, or arise de novo, or without these moles, and may follow the MAPK pathway to affect NRAF.
Ultimately, this novel study provides insights into the development of melanomas, and how there may be more pathways, mechanisms, and genes involved in their development than previously understood. By following a difficult but new single cell sequencing pathway, Tang et al. were able to observe and identify new discoveries about melanoma.
Source: Martincorena, Inigo. “Seeds of Cancer in Normal Skin.” Nature News, Nature Publishing Group, 7 Oct. 2020, www.nature.com/articles/d41586-020-02749-9.
Cancer continues to be one of the foremost medical challenges facing modern science. Published in Nature, this article recounts novel research conducted by Jessica Tang, a dermatology postdoctoral investigator at the University of California in San Francisco. Tang and her team sequenced the DNA of individual melanocytes, which are mature cells in the skin that form melanin, which in turn is the polymer that pigments our skin. Her research was focused on identifying microscopic DNA changes and differences between melanocytes that could reveal more about the origins of melanoma, an extremely aggressive form of skin cancer.
The common understanding of cancer is that mutations accrued over a lifetime can yield, in the most unfortunate circumstances, a set of changes that could lead to cancer. Somatic cells, those that are non reproductive like the skin, can mutate in key genes that could be oncogenic, or cancer causing, and result in the common cancers like melanoma. However, researchers have yet to understand many minute details of the origins of cancer because of the lack of technology required to sequence single or a few cells. The epidermis, the outermost layer of skin, does not contain many cells and is only “.1 milimeters thick” as the article states, and is constantly bombarded by all kinds of toxins from chemicals to electromagnetic rays that can potentially cause mutations. UV rays continue to be the leading cause of many skin cancers.
A previous study utilized sequencing of small biopsies, and revealed that mutations occur often in these normal cells, and actually favor the growth of these mutated cells. The mutations occurred in keratinocytes, which makes up “90% of the cell types” in the epidermis, unlike melanocytes which are in much smaller quantities.
Thus, to further investigate the origins of a rare cancer originating from these melanocytes, the investigating team decided to sequence single cells. The two most common methods to this were: “single cell sequencing, which relies on error prone, whole genome amplification,” or separating and growing out the single melanocytes into colonies which can then allow researchers to use more conventional sequencing methods. Tang et al. used a combination of methods. Since it is difficult to grow out melanocytes, the group grew out the cells in the colonies of hundreds and then continued the whole genome amplification step to continue the single cell sequence technique while reducing typical system errors.
“133 melanocytes were sequenced, from 19 body sites of 6 deceased donors,” with two of the people having skin cancer and others without. The colonies that were grown out had sequencing done to confirm particular mutations, and other controls were included. The results the researchers found were that most of the mutations were similar to UV ray mutations, and that the number of mutations per melanocyte on average was around 20,000, which is quite similar to the level of mutations found in melanoma cells. An additional result the researchers found was that, “around 20% of melanocytes had melanoma-driving mutations.” This, interestingly, leads to the growth of “scattered fields” of mutated clone melanocytes, an understanding that is now emerging as a feature of ageing.
However, the researchers also found discoveries that were unexpected. They found, for example, that places that are more chronically exposed to the sun, like the face, actually had less mutations in melanocytes, than places with intermittent exposure, which may explain why melanomas often arise in places with intermittent exposure. The team further discovered that a select population of the melanocytes did not have the high average of mutations, and they surmised that it could be because these melanocytes originally resided in places not exposed to sun, like hair follicles. The last important result found by the researches was an identification that many of the mutations found in the sequencing data corresponded to a particular signalling pathway for particular genes such as NRAF. However, melanomas typically arise from a common mutation in the BRAF gene. The team has proposed that melanomas, thus, can arise from moles and express BRAF mutations, or arise de novo, or without these moles, and may follow the MAPK pathway to affect NRAF.
Ultimately, this novel study provides insights into the development of melanomas, and how there may be more pathways, mechanisms, and genes involved in their development than previously understood. By following a difficult but new single cell sequencing pathway, Tang et al. were able to observe and identify new discoveries about melanoma.
Source: Martincorena, Inigo. “Seeds of Cancer in Normal Skin.” Nature News, Nature Publishing Group, 7 Oct. 2020, www.nature.com/articles/d41586-020-02749-9.
Regeneron’s Antibody Cocktail: An Explainer by William Odell
Following President Trump’s recent diagnosis with COVID-19, Regeneron’s experimental antibody cocktail named REGEN-COV2 was thrown into the mainstream as part of his successful treatment. Weeks prior, Regeneron released preliminary clinical findings on the efficacy of the cocktail, and as the pandemic continues its hold worldwide, it is now one of a number of promising emerging treatments for the deadly virus.
Beginning in February, Regeneron began work on an antibody treatment for the then relatively unknown virus, boosted by government funding. Thousands of COVID-19 antibodies, sourced from recovered humans and genetically modified mice, were screened for effectiveness, where REGN10933 and REGN1098 were chosen due their ability to neutralize the spike protein of the virus.
The first wave of trials saw the enrollment of 275 patients confirmed to have COVID-19. These patients were divided into 3 groups, consisting of high dose, low dose, and no dose control. Prior to administration, viral load amount and antibody levels were measured in each patient in order to determine their baseline immune response. Around 45% of patients were seropositive, meaning they mounted an immune response, 41% were seronegative, meaning they didn’t mount an immune response, and 14% were unknown.
Investigators were first able to establish a relationship between immune response and viral load. Seronegative patients exhibited significantly higher amounts of virus as compared to seropositive patients and took nearly double the time for symptom alleviation. Following administration of REGEN-COV2, seronegative patients saw significant decreases in viral load by day 7 as compared to placebo groups, and their time for symptom alleviation was nearly halved. Clearly, this data shows that REGEN-COV2 has potential as a treatment, especially in those with weakened immune systems.
So, what’s next? Regeneron is planning to conduct further trials with more than 1,300 enrolled patients. Fortunately, no adverse health effects were reported from the initial trials, a trend that hopefully continues. Should the treatment receive government approval, Regeneron has already secured manufacturing and distribution partnerships worldwide. Regardless, these results offer a glimmer of hope.
Source: https://investor.regeneron.com/news-releases/news-release-details/regenerons-regn-cov2-antibody-cocktail-reduced-viral-levels-and
Following President Trump’s recent diagnosis with COVID-19, Regeneron’s experimental antibody cocktail named REGEN-COV2 was thrown into the mainstream as part of his successful treatment. Weeks prior, Regeneron released preliminary clinical findings on the efficacy of the cocktail, and as the pandemic continues its hold worldwide, it is now one of a number of promising emerging treatments for the deadly virus.
Beginning in February, Regeneron began work on an antibody treatment for the then relatively unknown virus, boosted by government funding. Thousands of COVID-19 antibodies, sourced from recovered humans and genetically modified mice, were screened for effectiveness, where REGN10933 and REGN1098 were chosen due their ability to neutralize the spike protein of the virus.
The first wave of trials saw the enrollment of 275 patients confirmed to have COVID-19. These patients were divided into 3 groups, consisting of high dose, low dose, and no dose control. Prior to administration, viral load amount and antibody levels were measured in each patient in order to determine their baseline immune response. Around 45% of patients were seropositive, meaning they mounted an immune response, 41% were seronegative, meaning they didn’t mount an immune response, and 14% were unknown.
Investigators were first able to establish a relationship between immune response and viral load. Seronegative patients exhibited significantly higher amounts of virus as compared to seropositive patients and took nearly double the time for symptom alleviation. Following administration of REGEN-COV2, seronegative patients saw significant decreases in viral load by day 7 as compared to placebo groups, and their time for symptom alleviation was nearly halved. Clearly, this data shows that REGEN-COV2 has potential as a treatment, especially in those with weakened immune systems.
So, what’s next? Regeneron is planning to conduct further trials with more than 1,300 enrolled patients. Fortunately, no adverse health effects were reported from the initial trials, a trend that hopefully continues. Should the treatment receive government approval, Regeneron has already secured manufacturing and distribution partnerships worldwide. Regardless, these results offer a glimmer of hope.
Source: https://investor.regeneron.com/news-releases/news-release-details/regenerons-regn-cov2-antibody-cocktail-reduced-viral-levels-and
Stanford scientists solve secret of nerve cells marking a form of schizophrenia by Defne Alpdogan
Stanford scientists recently discovered a gene that leads to the electrical abnormality presented in nerve cells in schizophrenic patients. Usually, nerve cells have a systematic way of responding to signals and exchange information without causing “much disturbance.” However, while studying the nerve cells in schizophrenic patients, the Stanford University School of Medicine investigators saw that the nerve cells were popping up and showing excitement like a “noisy classroom,” illustrating a heightened electrical current present in these cells. One specific gene that the researchers looked at would be the 22q11DS gene, which is a gene that increases the chance of schizophrenia by 30 fold in individuals. During their study, they saw that the 22q11DS carrier had a “less-than-normal voltage different between the inner-facing and outer-facing sides of the cell membranes” which meant that the cells derived from the individuals who carried these genes had more excitable neurons and had an abnormal resting membrane potential. The effects of the more excited neurons led to altered calcium signaling, neurotransmitter signaling and led to abnormalities in the neuron. Furthermore, another side effect of the 22q11DS gene is that it deletes another gene called DGCRB. The researchers wanted to see if there was an association between the function and the excitability of the neurons due to the lack of presence of DGCRB by the 22q11DS. Shockingly, the deletion of the DGCRB led to the weakened resting membrane potential and illustrated the malfunctions present in 22q11DS neurons. However, with the DGCRB gene restored back into the cell, the neurons were largely restored to the “normal” resting potential and normal electrical conductivity. Overall, the studies that Stanford conducted illustrated the electrical malfunctions that can come from one of the genes associated with schizophrenia. One point of further discussion that the scientists and the researchers want to highlight is that while this information can be seen in cell cultures and in experiments, the procedure to apply the same treatments to humans may come with further difficulty. For example, none of the research quite explains the hallucinations and the effects of schizophrenia on the human brain. The entire idea of the research was to identify mechanisms that could help create an environment genetically for drugs or treatment that can help alleviate the symptoms for schizophrenic patients.
Unfortunately, the function of the brain and the systems of the brain still remain a mystery till today. Other genetic diseases that target brain activity like Alzheimer’s are still being investigated; however, the discussion piece at the end really highlights the importance of research and further development. By studying the mechanism that could led to the rise of certain disorders, scientists and researchers can slowly start to piece the puzzle in helping to solve the overarching problem.
Source: http://med.stanford.edu/news/all-news/2020/09/neuronal-abnormalities-in-schizophrenia.html
Stanford scientists recently discovered a gene that leads to the electrical abnormality presented in nerve cells in schizophrenic patients. Usually, nerve cells have a systematic way of responding to signals and exchange information without causing “much disturbance.” However, while studying the nerve cells in schizophrenic patients, the Stanford University School of Medicine investigators saw that the nerve cells were popping up and showing excitement like a “noisy classroom,” illustrating a heightened electrical current present in these cells. One specific gene that the researchers looked at would be the 22q11DS gene, which is a gene that increases the chance of schizophrenia by 30 fold in individuals. During their study, they saw that the 22q11DS carrier had a “less-than-normal voltage different between the inner-facing and outer-facing sides of the cell membranes” which meant that the cells derived from the individuals who carried these genes had more excitable neurons and had an abnormal resting membrane potential. The effects of the more excited neurons led to altered calcium signaling, neurotransmitter signaling and led to abnormalities in the neuron. Furthermore, another side effect of the 22q11DS gene is that it deletes another gene called DGCRB. The researchers wanted to see if there was an association between the function and the excitability of the neurons due to the lack of presence of DGCRB by the 22q11DS. Shockingly, the deletion of the DGCRB led to the weakened resting membrane potential and illustrated the malfunctions present in 22q11DS neurons. However, with the DGCRB gene restored back into the cell, the neurons were largely restored to the “normal” resting potential and normal electrical conductivity. Overall, the studies that Stanford conducted illustrated the electrical malfunctions that can come from one of the genes associated with schizophrenia. One point of further discussion that the scientists and the researchers want to highlight is that while this information can be seen in cell cultures and in experiments, the procedure to apply the same treatments to humans may come with further difficulty. For example, none of the research quite explains the hallucinations and the effects of schizophrenia on the human brain. The entire idea of the research was to identify mechanisms that could help create an environment genetically for drugs or treatment that can help alleviate the symptoms for schizophrenic patients.
Unfortunately, the function of the brain and the systems of the brain still remain a mystery till today. Other genetic diseases that target brain activity like Alzheimer’s are still being investigated; however, the discussion piece at the end really highlights the importance of research and further development. By studying the mechanism that could led to the rise of certain disorders, scientists and researchers can slowly start to piece the puzzle in helping to solve the overarching problem.
Source: http://med.stanford.edu/news/all-news/2020/09/neuronal-abnormalities-in-schizophrenia.html
Covid-19 pandemic increasing disparity in the Latinx community by Saumya Shah
By now, we all know that coronavirus is more likely to produce severe complications for older folks and people with pre-existing conditions. One population that is especially at risk are undocumented immigrant Latinxs who have positive rates twice or thrice as high as non-Hispanic Black or White patients in cities across the country. Transmission is higher for this population for a number of reasons, including the nature of their occupations. Landscaping, agricultural, cleaning, and cooking which still needed in-person workers during the pandemic. Even if a coworker or housemate were sick, they did not have the option of working from home. Hospitals in Baltimore, MD struggled to provide competent care to the inflow of Latinx patients because of cultural and language barriers, in addition to the challenges of caring for the novel coronavirus in a time of equipment shortages and around the clock work shifts. To help the language barrier, the hospital created a team of bilingual social workers, translators, and health professionals to facilitate conversation regarding health and outside resources. For undocumented people in a hostile political climate, reaching out to institutions like hospitals and assisted housing are the last resort. The Coronavirus Aid, Relief, and Economic Security (CARES) Act passed in March covered the costs of undocumented immigrants’ care which was incredibly important to them - even very sick patients worried about missing days of work and having to pay expensive hospital bills. Lack of access, the language barrier, being uninsured, distrust of institutions, and occupational hazards. In a crisis like the pandemic, it is imperative that doctors and hospitals welcome patients regardless of their immigration status to reduce the effect of the pandemic on a vulnerable population and for the country as a whole. Further economic relief and workplace protections for immigrants will reduce the severe disparities that the Latinx community is currently facing and has always faced.
Source: Page, Kathleen R., and Alejandra Flores-Miller. “Lessons We’ve Learned — Covid-19 and the Undocumented Latinx Community.” New England Journal of Medicine, 2020, doi:10.1056/nejmp2024897. <https://www.nejm.org/doi/full/10.1056/NEJMp2024897>
By now, we all know that coronavirus is more likely to produce severe complications for older folks and people with pre-existing conditions. One population that is especially at risk are undocumented immigrant Latinxs who have positive rates twice or thrice as high as non-Hispanic Black or White patients in cities across the country. Transmission is higher for this population for a number of reasons, including the nature of their occupations. Landscaping, agricultural, cleaning, and cooking which still needed in-person workers during the pandemic. Even if a coworker or housemate were sick, they did not have the option of working from home. Hospitals in Baltimore, MD struggled to provide competent care to the inflow of Latinx patients because of cultural and language barriers, in addition to the challenges of caring for the novel coronavirus in a time of equipment shortages and around the clock work shifts. To help the language barrier, the hospital created a team of bilingual social workers, translators, and health professionals to facilitate conversation regarding health and outside resources. For undocumented people in a hostile political climate, reaching out to institutions like hospitals and assisted housing are the last resort. The Coronavirus Aid, Relief, and Economic Security (CARES) Act passed in March covered the costs of undocumented immigrants’ care which was incredibly important to them - even very sick patients worried about missing days of work and having to pay expensive hospital bills. Lack of access, the language barrier, being uninsured, distrust of institutions, and occupational hazards. In a crisis like the pandemic, it is imperative that doctors and hospitals welcome patients regardless of their immigration status to reduce the effect of the pandemic on a vulnerable population and for the country as a whole. Further economic relief and workplace protections for immigrants will reduce the severe disparities that the Latinx community is currently facing and has always faced.
Source: Page, Kathleen R., and Alejandra Flores-Miller. “Lessons We’ve Learned — Covid-19 and the Undocumented Latinx Community.” New England Journal of Medicine, 2020, doi:10.1056/nejmp2024897. <https://www.nejm.org/doi/full/10.1056/NEJMp2024897>
Role of Steroids in Multiple Sclerosis Flare-Ups by Raabiah Chaudhry
Multiple Sclerosis is a disease characteristic of recurring exacerbations. To treat symptoms of such flare-ups, one method is a corticosteroids, which work to make the attacks shorter. Steroids, however, can have varying side effects. For this reason, they are used only for severe relapses, involving intense weakness, balance issues, or vision loss.
Glucocorticoids, the specific steroid involved in treatment of MS relapse, mimic the effects of naturally produced hormones in the body. In effect, they repress inflammation and other MS-related symptoms, by preventing migration of inflammatory cells to the central nervous system.
In terms of duration, high-dosage steroids are administered for a course of three to five days, once a day, intravenously as a form of outpatient treatment in a clinic/hospital. Oral steroids can be given in decreasing doses in the couple of weeks following the treatment. Dosages of such steroid treatments are determined based on the severity of symptoms, as there is no set standard of steroid treatment in MS.
The most common steroid treatment for MS is Solumedrol, which is administered intravenously and given in doses ranging from 500 to 1000 milligrams per day. This treatment generally ranges from three to seven days. Prednisone is an oral steroid, used for more moderate relapses. It can also be used in the coupe of weeks following IV steroid treatment to help with tapering off as well. Decadron, given in daily 30 milligram doses lasting a week, is another oral steroid used to treat MS relapses.
Although these steroids are effective in helping with a quicker relapse recovery, they do come with a range of potential side effects, both short-term and long-term.Short-term effects may include bursts of energy which make sleeping difficult, mood swings, and feelings of impulsiveness. These symptoms are temporary and tend to go away with tapering off of the steroids. Long-term effects may include diabetes, osteoporosis, and weight gain.
Tapering off is a crucial part of steroid treatments, as it must be done at a monitored pace to prevent symptoms of withdrawal.
Source: https://www.healthline.com/health/steroids-for-ms
Multiple Sclerosis is a disease characteristic of recurring exacerbations. To treat symptoms of such flare-ups, one method is a corticosteroids, which work to make the attacks shorter. Steroids, however, can have varying side effects. For this reason, they are used only for severe relapses, involving intense weakness, balance issues, or vision loss.
Glucocorticoids, the specific steroid involved in treatment of MS relapse, mimic the effects of naturally produced hormones in the body. In effect, they repress inflammation and other MS-related symptoms, by preventing migration of inflammatory cells to the central nervous system.
In terms of duration, high-dosage steroids are administered for a course of three to five days, once a day, intravenously as a form of outpatient treatment in a clinic/hospital. Oral steroids can be given in decreasing doses in the couple of weeks following the treatment. Dosages of such steroid treatments are determined based on the severity of symptoms, as there is no set standard of steroid treatment in MS.
The most common steroid treatment for MS is Solumedrol, which is administered intravenously and given in doses ranging from 500 to 1000 milligrams per day. This treatment generally ranges from three to seven days. Prednisone is an oral steroid, used for more moderate relapses. It can also be used in the coupe of weeks following IV steroid treatment to help with tapering off as well. Decadron, given in daily 30 milligram doses lasting a week, is another oral steroid used to treat MS relapses.
Although these steroids are effective in helping with a quicker relapse recovery, they do come with a range of potential side effects, both short-term and long-term.Short-term effects may include bursts of energy which make sleeping difficult, mood swings, and feelings of impulsiveness. These symptoms are temporary and tend to go away with tapering off of the steroids. Long-term effects may include diabetes, osteoporosis, and weight gain.
Tapering off is a crucial part of steroid treatments, as it must be done at a monitored pace to prevent symptoms of withdrawal.
Source: https://www.healthline.com/health/steroids-for-ms
COVID-19 Antibodies in Production After Initial Infection by James He
Amidst the never-ending concerns of the COVID-19 pandemic, rates of re-infection are now being investigated in the scientific and medical communities. This stems from the uncertainties surrounding this year’s flu season and a seemingly endless trend of infection resurgences after slight improvements across the nation. Most notably, an elderly woman was recently documented in the news as the first death resulting from re-infection with the virus, raising important questions: “Should individuals who have already been infected fear re-infection? How severe is the second infection?”
While there are no absolute answers to these enduring questions just yet, there are come clues available - COVID-19-specific antibodies, one of the circulating security guards of our body’s immune system, have been shown to rise in production following an initial production. A recently published study in the journal, “Immunity,” on Tuesday, October 13th, tested almost 30,000 people in Arizona who displayed positive blood tests for COVID-19. They found that there are levels of active antibodies in production 5-7 months following the initial infection. These antibodies are specific to the SARS-CoV-2 infection, implying that they should effectively recognize the deadly virus once it enters the body. However, the re-infection rates of these individuals has yet to be tested, so the viability of the antibodies in combating the infection is still under question. Regardless, this is good news! Individuals who fight through one bout of infection with COVID-19 likely build up some resistance to a second infection where applicable.
Now, these results should be taken with extreme caution. Although the antibodies are detected at strong levels, this does not yet indicate immunity, so the heralded herd immunity that we are striving to achieve with a successful vaccine is still out of reach. This does provide a promising avenue of research. If scientists and clinicians can probe the specific features of the SARS-CoV2 antibodies further, then we might be able to better define the specific mechanisms by which the virus enters our cells, and how we can effectively counteract its effects once it does. While there are a number of different types of vaccines currently under development, their ultimate goal is to initiate an immune response that can be remembered and sustained to fight the actual virus if it springs upon us. Learning about these antibodies and the possibility of re-infection can further direct us in the right direction for vaccine development and production.
Source: Schimelpfening, Nancy. “How Long Does Immunity Last After COVID-19? What We Know.” Healthline.com, 14 Oct. 2014, www.healthline.com/health-news/how-long-does-immunity-last-after-covid-19-what-we-know.
Amidst the never-ending concerns of the COVID-19 pandemic, rates of re-infection are now being investigated in the scientific and medical communities. This stems from the uncertainties surrounding this year’s flu season and a seemingly endless trend of infection resurgences after slight improvements across the nation. Most notably, an elderly woman was recently documented in the news as the first death resulting from re-infection with the virus, raising important questions: “Should individuals who have already been infected fear re-infection? How severe is the second infection?”
While there are no absolute answers to these enduring questions just yet, there are come clues available - COVID-19-specific antibodies, one of the circulating security guards of our body’s immune system, have been shown to rise in production following an initial production. A recently published study in the journal, “Immunity,” on Tuesday, October 13th, tested almost 30,000 people in Arizona who displayed positive blood tests for COVID-19. They found that there are levels of active antibodies in production 5-7 months following the initial infection. These antibodies are specific to the SARS-CoV-2 infection, implying that they should effectively recognize the deadly virus once it enters the body. However, the re-infection rates of these individuals has yet to be tested, so the viability of the antibodies in combating the infection is still under question. Regardless, this is good news! Individuals who fight through one bout of infection with COVID-19 likely build up some resistance to a second infection where applicable.
Now, these results should be taken with extreme caution. Although the antibodies are detected at strong levels, this does not yet indicate immunity, so the heralded herd immunity that we are striving to achieve with a successful vaccine is still out of reach. This does provide a promising avenue of research. If scientists and clinicians can probe the specific features of the SARS-CoV2 antibodies further, then we might be able to better define the specific mechanisms by which the virus enters our cells, and how we can effectively counteract its effects once it does. While there are a number of different types of vaccines currently under development, their ultimate goal is to initiate an immune response that can be remembered and sustained to fight the actual virus if it springs upon us. Learning about these antibodies and the possibility of re-infection can further direct us in the right direction for vaccine development and production.
Source: Schimelpfening, Nancy. “How Long Does Immunity Last After COVID-19? What We Know.” Healthline.com, 14 Oct. 2014, www.healthline.com/health-news/how-long-does-immunity-last-after-covid-19-what-we-know.
New Ultrasound Treatment Kills Cancer Cells by Shalvi Gupta
Scientists have moved one step closer to finding a new cancer therapy. It might not be a cure to cancer, but it is progress. Most of the current cancer therapies not only, tire the patients out, they also harm the healthy cells in the body. Thus, the scientists have come up with the idea to use ultrasounds to kill cancer cells. This process can still end up killing healthy cells, but they have discovered a way to prevent that. They first tried the ultrasound treatment with high-intensity ultrasounds, meaning sending lots of energy to a small area. This method wasn’t effective because the high-intensity waves would cause the water inside the cells to vibrate. Thus, causing the cells to heat up and die. The downside of this was that the target cells and the healthy cells around the cells would heat up and die. So, instead of using high-intensity, they tried using low-intensity frequency. Low-intensity sound-waves have frequencies greater than 20,000 Hertz. In order to test this, they suspended cancer cells with healthy blood cells and immune cells in liquid. Then they tested different frequencies between 300,000 to 650,000 Hertz for different pulse durations ranging from 2-40 millisecond. They tried one minute of 500,000 hertz, delivered in 20 millisecond. This trial killed every cancer cell, didn’t harm any of the blood cells, and left more than 8 in every 10 immune cells unharmed. This therapy isn’t ready for the patients yet, but it has been taken to the next step of testing.
Source: https://www.sciencenewsforstudents.org/article/ultrasound-treatment-kills-cancer-cells
Scientists have moved one step closer to finding a new cancer therapy. It might not be a cure to cancer, but it is progress. Most of the current cancer therapies not only, tire the patients out, they also harm the healthy cells in the body. Thus, the scientists have come up with the idea to use ultrasounds to kill cancer cells. This process can still end up killing healthy cells, but they have discovered a way to prevent that. They first tried the ultrasound treatment with high-intensity ultrasounds, meaning sending lots of energy to a small area. This method wasn’t effective because the high-intensity waves would cause the water inside the cells to vibrate. Thus, causing the cells to heat up and die. The downside of this was that the target cells and the healthy cells around the cells would heat up and die. So, instead of using high-intensity, they tried using low-intensity frequency. Low-intensity sound-waves have frequencies greater than 20,000 Hertz. In order to test this, they suspended cancer cells with healthy blood cells and immune cells in liquid. Then they tested different frequencies between 300,000 to 650,000 Hertz for different pulse durations ranging from 2-40 millisecond. They tried one minute of 500,000 hertz, delivered in 20 millisecond. This trial killed every cancer cell, didn’t harm any of the blood cells, and left more than 8 in every 10 immune cells unharmed. This therapy isn’t ready for the patients yet, but it has been taken to the next step of testing.
Source: https://www.sciencenewsforstudents.org/article/ultrasound-treatment-kills-cancer-cells