AP Biology class blog for discussing current research in Biology

Author: allyle

How CRISPR Can Help Individuals Overcome Obesity

Fat, which is made up of cells that have been distended with greasy or oily materials, or triglycerides, is required for the body to function, but it may also be hazardous if consumed in excess. Fat cells are distinct from other cells such that they lack surface receptors and constitute only a small percentage of the cells in fat tissue. While restricting diets can assist those who are obese lose weight, the results are typically solely temporary. If only there were a way to target fat cells specifically… Well, there just might be!

Breast tissue showing fat necrosis 4X

A group of doctors discuss a potential prospective breakthrough utilizing CRISPR-Cas9, a technology that has proven particularly elusive in the study of adipose tissue, in a recent publication published in the Journal of Biological Chemistry. Their study was tested on mice, in order to see how it worked and what it targeted. The gene-editing technology CRISPR-Cas9 changes genes by precisely cutting DNA and then allowing natural DNA repair mechanisms to take charge. This technology has changed the ability of deleting or inserting certain genes of interest into an organism. Cas9, an enzyme that can break DNA strands as well as a piece of RNA that directs the Cas9 enzyme to a specific location in the genome for modification, is encased in a non-harmful virus and supplied to the cells being studied. The equipment has also been used to study the heart, liver, neurons, and skin cells, to name a few. However, brown fat adipose cells have never been studied.

Brown fat cell

Using CRISPR-Cas9 components, the physicians were eventually able to target brown fat adipose cells. In mature mice, they were able to knock off the UCP1 gene, which specifies brown adipose tissue and allows it to generate heat. They discovered that knockout mice were able to adjust to the absence of the gene and maintain their body temperature under freezing settings, indicating the existence of additional mechanisms involved in temperature regulation. Overall, the CRISPR interference system assisted mice in losing about twenty percent of their body weight, proving that CRISPR can accurately target fat cells.

3LFM FAT Mass and Obesity Associated (Fto) Protein

Genetics can have a significant impact on the quantity of fat cells you are born with. However, the proportion of tendency to becoming overweight differs by individual. For example, in some people, genes account for just 25 percent of the tendency, but in others, the genetic effect might be as high as 70 percent to 80 percent. Obesity is most commonly associated with the FTO gene. This FTO gene is not found in everyone. For example, around 20 percent of white people have a variation of the gene that increases their risk of obesity. The FTO gene is located on chromosome 16, which is one of the 23 pairs of chromosomes in humans. While this chromosome pair represents under 3 percent of the total DNA in cells, if FTO is present, it can affect whether if one is obese or not, depending on the alleles of the gene. CRISPR has the potential to target this gene as well as other genes that affect body weight, such as brown fat adipose cells.

Diagram of Chromosome 16

Your health is essential for the rest of your life! A healthy lifestyle can aid in the prevention of chronic diseases and long-term ailments. The alleles on the FTO gene can have an impact on your health and are linked to type 2 diabetes, obesity, and other health concerns.

Do Genetics Play A Role In Attraction?

Have you ever met someone with whom you instantly wanted to be friends but couldn’t put your finger on why or how you felt so drawn to them? There is a reason why you might be drawn to a specific person or group of people that may be explained by biology.

Double stranded DNA with coloured basesChromosome Terminology

According to a book by a well-known author, Malcolm Gladwell, a “unconscious” region of the human brain helps us to digest information spontaneously while encountering someone or something for the first time or making a rash decision. The University of Maryland School of Medicine has expanded on this hypothesis with a new study, indicating that these reactions may have a biological foundation related to heredity. The experiment was carried out on a group of mice. Variations in a particular enzyme discovered in a portion of the brain that affects mood and drive appear to influence which mice desire to actively engage with other mice; genetically related mice favored one another. Similar circumstances, such as disorders linked with social withdrawal, such as schizophrenia or autism, might also influence people’s decisions. Consequently, researchers do not agree with the phrase “opposites attract,” because genetics have a significant role in attraction. Instead, experts propose that we choose friends based only on their similarities to ourselves. Unlike the concept of “opposites attracting,” the expression “people like their own kind” is accurate. While genes definitely contribute to an individual’s attractiveness, they only account for around one-third of the reasons why we choose someone else to be our friend.

In a separate study, researchers examined a range of variables, that often are most inheritable and those that are less inheritable, to evaluate the role genes function in our human conduct, and they discovered that “people are genetically inclined to choose as social partners those who resemble themselves on a genetic level.” Rushton discovered in this study that humans prefer to choose partners based on inheritable attributes, even when we are unaware that such characteristics are genetically determined. For example, the middle-finger length is inherited, although the upper-arm circumference is not. Spouses who took part in the study had identical middle finger lengths but not the same upper-arm circumference. The function of heredity also influences personality, which explains why “people like their own kind.” What you inherited biologically from your parents, which is defined by the genes in your DNA, is the key to personality traits. Genetic heredity accounts for almost half of our cognitive differences, from personality to mental capabilities.


Genetics is the scientific study of genes and heredity, which transfer particular characteristics from parents to offspring due to variations in DNA sequences. The genome contains all of an organism’s genetic code, including its genes and additional components that govern the activation of those genes. We are drawn to others because of the features that we share with them through genetic material. Our DNA is stored in chromosomes, and each of the 23 pairs of chromosomes has the same genes that are handed down from parent to offspring. When a baby is being formed, DNA is handed down, and each parent sends half of their chromosomes to their kid, thus each of your parents contributes 50% of your DNA. The term “genetic love” refers to the idea of matching partners for romantic relationships based on their biological compatibility. “Genetic love” describes the notion of attraction based on heredity.

Difference DNA RNA-EN

Is it possible that you want to be friends with someone of the same genetics as yourself? Yes! It is! However, it is not the only thing that accounts for maintaining a friendship.

How Diabetes Is Emerging In Patients With COVID-19

COVID-19 has a plethora of underlying effects. However, researchers may have just identified the most dangerous long-term impact.

3D medical animation still of Type One Diabetes

While researchers have been studying COVID-19 for the past two years, pharmacy technician Nola Sullivan of Kellogg, Idaho, has uncovered the virus’s extending underlying conditions. Sullivan faced an additional struggle as a result of being infected with COVID-19 last year, despite the virus’s long-term effects, which included a loss of taste and smell, nausea, and diarrhea. Many COVID-19 patients too are grappling with an additional struggle: the onset of diabetes. In a research involving nearly 3,800 patients infected with the virus, cardiologist James Lo and colleagues discovered that just under half of the patients acquired elevated blood sugar levels that were not previously present. How is it conceivable for COVID-19 patients to develop diabetes? Many researchers have been tackling this exact issue for a long time.

WHO EN Be SAFE from CORONAVIRUS COVID-19 9Mar2020COVID-19 biểu trưng

When a patient develops diabetes, he or she must learn to control the illness and live an active life due to an insulin shortage. Because diabetes is incurable, the prospect that it is a long-term side effect of COVID-19 is very troubling. Insulin is essential in the human body because it lowers triglycerides by boosting lipoprotein lipase activity, which degrades triglycerides into glycerol and fatty acids. A lack of pancreatic B-cells, which release proper quantities of insulin, has a direct impact on mitochondria and the glycolysis process which is utilized for energy synthesis by all cells in the human body, eventually prompting the pyruvate product to join the Krebs cycle for ongoing energy production. Both processes are required for continual energy generation. Glucose is broken down into pyruvate and energy during glycolysis. The process can take place in the absence of oxygen, making it anaerobic. Insulin promotes glycolysis by raising the rate of glucose transport across the cell membrane and the rate of glycolysis by boosting the activities of hexokinase and 6-phosphofructokinase.

Glycolysis metabolic pathway 3

Nonetheless, people with COVID-19 have experienced sugar surges. The elevated blood sugar levels were new after infection for the majority of the patients, suggesting that many of them had not been diagnosed with diabetes prior to contracting the virus. According to Lo and other experts, the mechanism by which COVID-19 causes diabetes is currently being investigated. Patients with ARDS caused by COVID-19 and a high blood sugar level were in the hospital three times longer than those with normal blood sugar levels. While the exact cause of diabetes is unknown, researchers have discovered evidence that the coronavirus attacks pancreatic B-cells, which produce insulin. This does not yet address the question because patients who received COVID-19 continued to generate significant amounts of C-peptide, indicating that pancreatic cells were still generating insulin. Despite this, their blood sugar levels remained elevated, suggesting that something else was at fault. The virus-infected fat cells must be stimulating other cells in a detrimental way, resulting in diabetes. As a result, Lo and colleagues observed that individuals with COVID-19 had low amounts of adiponectin, a hormone generated by fat cells that helps other cells respond to insulin’s urge to take up sugar. COVID-19 can clearly infect fat cells. The virus may also cause replication in human fat, which provides another indication as to how fat is implicated in the virus and, as a result, diabetes. While obesity has a significant impact on the onset of diabetes as a result of the virus, this is not always the case. The miscommunication of fat cells is to blame. 

How may fat cell miscommunication be controlled, and who is directly affected? This is the next question that has to be addressed in order to develop a deep understanding of the long term effects of the virus.

An Antidepressant Is The Next “Weapon” Against COVID-19

Is the COVID-19 vaccine the only way to lower death rates and hospitalization rates? While more individuals are becoming vaccinated against COVID-19, researchers have looked at how a low-cost antidepressant prescription could potentially tackle the virus. Fluvoxamine (Luvox), an antidepressant medication, has the capacity to reduce hospitalization and morality rates after patients receive COVID-19 within a few days. Although fluvoxamine is licensed by the FDA for the treatment of obsessive-compulsive disorder (OCD) and other disorders such as depression, it is not approved for the treatment of COVID-19. In a study, conducted in Brazil, 1,500 newly diagnosed COVID-19 patients were assessed. 741 of the participants received a 100 mg pill of fluvoxamine twice a day for 10 days and the remaining 756 participants received a placebo twice a day. 16 percent of those who took the placebo twice a day got ill enough to necessitate a lengthy hospital stay compared to 11 percent of those who took fluvoxamine. Researchers discovered that participants who took at least 80% of the fluvoxamine administered to them had a two-thirds lower chance of hospitalization! Furthermore, there was only one fatality among individuals that took fluvoxamine, compared to 12 fatalities in the placebo group. According to The Lancet Global Health, this research has shown that the drug has reduced morality rates by roughly 91 percent. The antidepressant drug can be easily prescribed by doctors for COVID-19 using their clinical judgement.


When the COVID-19 virus enters the body through the eyes, nose, or mouth and travels to the lungs, the immune system strives to protect itself from the invading pathogens by producing antibodies that, on occasion, eliminate invading infections. If the invading pathogen is unfamiliar to the body, B-memory cells will be unable to detect it, and B-plasma cells (antibody secreting cells) will be unable to manufacture antibodies, allowing the virus to enter the cell and flourish in the body.


Fluvoxamine is a 2-aminoethyl oxime ether of aralkylketones. The antidepressant medication, if taken promptly after receiving COVID-19, may be an additional method of minimizing viral transmission and accompanying medical concerns. Fluvoxamine is easy to get and inexpensive to manufacture, particularly as a generic drug. COVID-19 treatments, in general, serve as both a cure for severe sickness and a treatment for the beginning of illness. Fluvoxamine, as an SSRI (selective serotonin reuptake inhibitor), attaches to a cell’s receptor that governs cellular stress response and the generation of cytokines, proteins that alert the body of a problem and lead to extreme inflammation. Nevertheless, fluvoxamine has been shown to minimize inflammation. When people get COVID-19, it’s theorized that the damaged cells produce a slew of cytokines that generate inflammation in the lungs, making it difficult to breathe. Patients would be able to breathe better and require fewer hospitalizations if fluvoxamine was taken to help decrease inflammation.


Who knew that an antidepressant that inhibits the serotonin reuptake pump at the presynaptic neuronal membrane might reduce inflammation and allow you to breathe? Because fluvoxamine works by boosting serotonin levels between nerve cells in the brain, it is impressive that the medicine might be used for purposes other than treating depression or OCD. The lingering question is whether someone with COVID-19 who has been taking these antidepressants for a previous disorder has an edge.

The Potential End To COVID-19: How An Antiviral Pill Could Decrease Death Rates

When will the world return back to normal? In recent years, people have questioned the longevity of the COVID-19 outbreak. While concentrating on vaccine delivery and vaccination capabilities, a pill has been developed in the hopes of preventing future COVID variations. Hopefully, the pill will eventually be administered to patients; this would make it the first oral treatment for the virus.

A current study on molnupiravir, an antiviral pill, has published data demonstrating that the medicine has the ability to lower hospitalization and fatality rates as a result of COVID-19. The study dealt with two groups of people. One group of 377 people were given a placebo, and the other group of 385 people were given molnupiravir to examine how the antiviral affected patients with COVID-19. The findings were substantial. Within 29 days of starting the trial, 14.1 percent of the group given the placebo were hospitalized. Fortunately, of the individuals who were given molnupiravir, only 7.3 percent of them were hospitalized.

Molnupiravir is a prodrug of N4-hydroxycytidine (NHC), a nucleoside analog (meaning that it contains a sugar and a nitrogenous base). Molnupiravir metabolism

Molnupiravir is similar to the genetic coding of the coronavirus’s RNA, as is remdesivir (a FDA-approved medication). By interfering with the polymerase enzyme, the “fake” basic elements impair the coronavirus’s RNA synthesis, preventing the virus from replicating. Despite the fact that the two medications serve the same goal, they serve different actions. Remdesivir penetrates a growing RNA strand, slowing and ultimately blocking the polymerase enzyme. Unlike the COVID-19 vaccine, the structure of molnupiravir gives it the ability to target the polymerase enzyme instead of the virus’s spike protein. Molnupiravir enters the cell and is transformed into RNA-like building components. The active medication binds to the genome of RNA viruses, setting off a chain of mutations; this process is known as viral error catastrophe. In simpler terms, it disrupts how the virus replicates RNA.

Molnupiravir could theoretically be administered as soon as a patient receives a positive COVID-19 test, thereby preventing floods of COVID-19 patients from overburdening medical systems while the highly infectious delta variant continues to spread. Although the side effects of the drug remain unknown, it has been reported that the side effects of COVID-19 are much worse than those of molnupiravir. The antiviral drug has the potential to save lives, but the primary concern is about the long-term repercussions. When contemplating molnupiravir, the fear of birth abnormalities or cancer comes into play because it is a mutagenic medication. In response, the drug’s creator, Merck, stated that there is no indication of the possibility for mutagenicity. Although the manufacturer is confident in the treatment and believes that the long-term consequences are insignificant, it is logical that parents might have concerns about molnupiravir.

Ultimately, if patients receive the vaccination that targets the spike protein and are also able to take molnupiravir, hospitalization and mortality rates may dramatically reduce.

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