AP Biology class blog for discussing current research in Biology

Author: alagapplasmamembrane

Bias in Science: History, Representation, and Medicine

Science is not objective. Scientists may value fact, but they are still people too, influenced by identity and implicit and explicit biases in their research. Racism has pervaded every aspect of society since the country’s founding, and scientific institutions are no exception. From historical racist research practices to a modern reluctance to support Black Lives Matter or actively diversify the field, scientists have participated in and promoted racism for centuries. Scientists cannot claim objectivity now as an excuse to not be antiracist.

Throughout American history, unethical, racist research has contributed to scientific “progress”, but that is not regularly acknowledged. Although the past cannot be undone, fields should at least recognize the horrific means by which some research was done. For example, gynecology was borne of unethical experiments done on enslaved women and children. The “Tuskegee Experiment” withheld treatment of syphilis from hundreds of Black men just to see how the disease progressed. Henrietta Lacks, a Black woman with cervical cancer in 1951, had some cells taken from her tumor without being informed of this. The cells from her tumor, now known as HeLa cells, have been used since the 1950s for biomedical research. Since cancer is characterized by an improperly regulated cell cycle, with either too much cell growth or too little cell death, cancer cells can grow and divide excessively. This particular line of cells has been able to grow and divide endlessly, due to the presence of an active version of telomerase during cell division. This enzyme prevents the typical shortening of telomeres in cell division that leads to cell aging and death, making the cells “immortal” and the cell line usable to this day. Though they have been used in various research advances, her name was only connected to them in the 1970s. Her family, still with limited access to healthcare themselves, received no financial benefits and had no say in how the cells were used. Henrietta Lacks’ case is a more recent example of unethical research practices affecting Black people.

The questions scientists choose to study, whom they choose to include, and how they apply their results all bias research. Scientists of marginalized identities are much more likely to explore topics relevant to minority groups. So then, the lack of diversity among scientists also contributes to biased research priorities. In 2016, only 9% and 13.5% of science bachelors degrees were given to African Americans and Latinos respectively, and only 5% and 3.8% of doctoral degrees in science and engineering went to women and men from underrepresented minorities. Almost 70% of scientists and engineers employed full time are white. When issues like COVID-19 and climate change disproportionately affect marginalized groups, the lack of diverse representation can prevent representative research or solutions. Scientific institutions need to work on hiring and retention of Black, Latinx, and Indigenous scientists, in part by creating less hostile work environments and increasing DEI efforts.

The lack of diversity in clinical trials also decreases the inclusivity of science and medicine. Even though about 40% of Americans are nonwhite or Hispanic, the clinical trials for new drugs tend to have much whiter samples, with some having 80 to 90% white participants. Since these drugs will be used to treat all people, diverse samples are needed to determine the efficacy and side effects that can vary across ethnicity and sex. The 1993 National Institutes of Health Revitalization Act that required greater inclusion of women and minorities in NIH research samples did improve the proportion of female subjects, but not so much for minority groups. Even for diseases that disproportionately affect marginalized groups, those groups are grievously underrepresented in the clinical trials. 

One such disease is COVID-19. Even though the rates of infection, severity, and death are greater for Black, Latinx, and Indigenous Americans, these groups are underrepresented in clinical trials. Trials for drugs to treat COVID-19 did not accurately reflect the most affected populations at the research sites. Some studies also did not report the race and ethnicity of participants as required by the FDA. Remdesivir has shown to somewhat decrease recovery time, but since disease severity and outcomes are worse for minority groups, the benefits of improvement may not necessarily extend to them. This is why proportional representation of affected populations is so important in clinical trials for drugs.

One cause for lack of diversity in clinical trials is that minority groups can be unwilling or unable to take part, for reasons including fear of discrimination, lack of time or resources, inaccessibility of recruitment centers, language barriers, and fear of exploitation based in historical precedent. However, these barriers should be on the researchers to address, not on the marginalized groups. A possible solution could be to have the FDA enforce that drugs should be tested on samples that demographically reflect the populations that will be using them.

In the end, research institutions and scientists need to examine their biases in order to determine who they are serving, and then who they mean to serve. Efforts to increase diversity cannot be passive, but instead should involve active recruitment and work to eliminate the barriers in place. In an academic institution, that might mean a more inclusive work environment and better outreach and mentorship programs. For clinical trials, this could be reducing the financial burden of participation and building better relationships with minority communities that may have been hurt in the past. Science is meant to help people, so we need to be better moving forward, as well as acknowledge the damage scientists have done in the past.

We have vaccines- is the pandemic over?

Does a vaccine mean the end of this pandemic?

For this portfolio project, I will be focusing on the vaccine development process and how the developing vaccines each prepare the immune system to fight COVID-19. The goal will be to explore the stages of development, testing, and distribution to the public and how these new vaccines function. Since there has been recent progress with a few vaccine candidates, namely the Pfizer and Moderna vaccines, this blog post will be about the implications of vaccine distribution in coming months.

Firstly, a new vaccine does not mean that it will be safe for society to return to normal just yet. While we’re all definitely excited about the news of successful vaccine trials, the effects of vaccination are not immediate, and the goal of herd immunity will not be reached for a little while. Also, the vaccines have not been tested yet on children and pregnant women, and since women around childbearing age are highly represented in the population of health care workers, it is important that the vaccine work for pregnant women. With the trials so far, we do know that there have been no unexpected negative side effects to vaccination, just the typical mild ones such as injection-site soreness and fatigue.

So why is getting a vaccine so important? It’s true that none of the vaccines are 100% effective, but they have been proven to decrease the severity of symptoms. (Both vaccines have reported about 95% efficacy rates in preventing COVID-19.) There are many good reasons to get a vaccine. Not only will it protect you, but it will be a safer path than widespread infection to build herd immunity. Since the trials did not measure rates of infection, it remains unclear whether the vaccines prevent infection and transmission, though results from another vaccine’s trials suggest that it might somewhat protect against infection. Either way, the rate of subjects who became severely ill was lower for those vaccinated in these two prominent vaccines’ trials. The high rates of hospitalization are due to development of severe symptoms, so reducing symptoms would also help to slow the pandemic’s adverse effects.

So, we’ve seen that the Pfizer and Moderna vaccines are effective in reducing symptoms, but that brings us to another question. How do these vaccines work? Both of these vaccines are mRNA vaccines. This means that they deliver synthetic messenger RNA that is taken in by immune cells that then produce the spike protein, just as would happen if the cells came into contact with the actual virus. However, since it is just the proteins, there is no risk of getting infected with COVID-19 from the vaccine itself. The immune system will then recognize the protein as a foreign substance and develop an immune response and produce memory cells that will respond swiftly in the case of seeing that protein again. As we learned, the adaptive immune defense depends on the recognition of the epitope of a virus, in this case the spike protein. After first infection, the memory B and Tc cells that are produced via clonal expansion remain in the lymph nodes until the same virus attacks again. However, this mRNA vaccine removes the need for a first infection in developing adaptive immunity because the spike proteins are produced without the rest of the virus needing to be introduced.

Now, let’s imagine it’s a few months from now, and the distribution of vaccines has begun. Can we skip the precautions we have in place now? Do we still need social distancing and mask-wearing? Well, until most people are able to be vaccinated, it will be important to maintain safety protocols that reduce the spread. Even once somebody is vaccinated, they will need to follow guidelines, because it takes several weeks for the immune defense to build up, and both vaccines require a booster dose about a month after the first one. Also, we’ve already addressed the uncertainty about transmission after vaccination, so it’s best to err on the side of caution. 

So, even though these vaccines may not be perfect, they will help control the pandemic. The main question that remains is how efficiently and fairly vaccines can be distributed to best reduce deaths and bring about an end to the pandemic.

Mice Maintain Muscle in Microgravity

Scientists recently found a molecule that can maintain, and even augment, the muscle mass and bone density of space-faring mice.

That might sound irrelevant (why would mice need to maintain muscle mass in space?), but this could actually help astronauts with a common problem with space travel. Astronauts in space must exercise regularly and intensely to avoid muscle atrophy; due to the microgravity, astronauts have little regular physical exertion and quickly lose muscle mass otherwise. Studies have shown that space journeys as brief as 5 to 11 days lead to a 20% loss of muscle mass for astronauts. The calf muscles, quadriceps, and back and neck muscles (which can be collectively termed antigravity muscles) require minimal contraction for astronauts to move around in space, allowing the muscles to weaken rapidly.

Muscle atrophy isn’t only a problem for astronauts, though. Others to benefit from this research could include “people who are bedridden or in a wheelchair, as well as people with cancer, chronic obstructive pulmonary disease or other causes of muscle wasting.” 

The main focus of this study was the gene myostatin, common to various species, including mice, cattle, and humans. Myostatin plays a role in both the number of muscle fibers in the developing animal and the level of fiber growth in the adult stage, negatively regulating muscle growth in species from dogs to humans. Several studies have shown that myostatin inhibition can help with disorders that cause wasting of the muscles by increasing muscle mass. Some evidence even suggests that myostatin inhibition might increase muscle strength as well. This study, however, targeted a different cause of muscle atrophy.

Study author Se-Jin Lee eliminated the myostatin gene from mice, allowing them to achieve double the muscle mass of regular mice. In December 2019, the mice were launched on a SpaceX craft from Florida’s Kennedy Space Center for a 33 day space journey. In contrast to the normal mice, that lost muscle mass, the myostatin-inhibited mice maintained their augmented muscle mass.

On the left, a regular mouse, and on the right, a myostatin inhibited mouse with about double the muscle mass.

Of course, eliminating the gene from human astronauts is not a feasible approach. To better model a treatment that could be applied to humans, Lee’s team came up with a solution to inhibit myostatin’s expression. Myostatin prohibits growth by attaching to a specific receptor on muscle cells. To prevent this binding, the researchers came up with a molecule that was a “decoy” receptor to be injected into the mice’s bloodstreams, capturing myostatin proteins and activin A proteins, which prevent both muscle and bone growth. The unique chemical structure and folding of the receptor allows it to bind to these two proteins for this effect, and as we learned in class, the shape is very important to the functionality. The mice in the International Space Station injected with this molecule experienced bone and muscle growth while still in space. The treatment also recovered bone and muscle mass for untreated mice landing from space.

Treatments inspired by this research could hopefully be used to help astronauts maintain bone density and muscle mass in space. Though myostatin inhibition alone has not proven effective in humans, such a treatment that inhibits other proteins, like activin A, as well may be plausible.

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