AP Biology class blog for discussing current research in Biology

Author: jauharna

Away With Treadmills and Low Carb Diets: Is CRISPR the New Hack For Fat Loss?

Are you sick and tired of spending all of your time running on the treadmill and eating restrictive diets? Are you looking for a way to hack fat loss without ruining your way-of-life? Look no further than CRISPR gene-editing!

In humans, stubborn body fat can be attributed to either white or brown fat. Brown fat, specifically, is used in humans primarily for insulation, and can be tapped into when we are cold or need to ramp up our metabolism to generate heat. This fat is caused by a caloric surplus in humans, and is burned off by engaging in caloric deficit. However, in mice studies conducted by Steven Romanelli, Ormand MacDougald, and colleagues, CRISPR gene-editing offers promising results regarding the topic of brown fat loss in humans. CRISPR-Cas9 Editing of the Genome (26453307604)

But what exactly is CRISPR gene-editing? CRISPR, or Clustered Regularly Interspaced Short Palindromic Repeat, gene-editing entails organizing short, palindromic DNA sequences of bacteria. These DNA sequences are surprisingly important in the immune function of these bacteria and other microorganisms, making CRISPR an incredibly promising and innovative tool in science research. 

Bacteria have short sequences of variable DNA called “spacers” in between CRISPR DNA sequences. This DNA helps protect the bacterium from reinfection from viruses. If any virus were to attack the bacterium, the CRISPR DNA sequences would cut up that viral DNA matching any spacer within the genetic code of the bacterium, preventing it from reinfection. 

CRISPR gene-editing works by processing invading viral DNA into short fragments that are inserted into the CRISPR DNA as spacers. Then, CRISPR replicates and spacers in the DNA of the bacterium experience transcription, in which DNA becomes RNA and CRISPR RNAs. These CRISPR RNAs help bacteria kill viruses, as they match the exact DNA as the viral DNA attacking the bacterium. 

In mice experiments conducted by Romanelli, MacDougald, and colleagues, has used CRISPR gene-editing to have an enzyme named Cas9 break strands of DNA and a single piece of RNA to be packed into a harmless virus cell that will be delivered into cells in the study, which are brown fat cells in this case. This process has shown to delete several genes, namely the UCP1 gene in mice, that allows brown fat to exist and create heat. However, the mice in the study did not die when exposed to cold environments. They were able to survive despite a huge loss in brown fat. 

Accordingly, using CRISPR gene-editing as a tool for brown fat loss in humans provides incredibly promising results. It is certain that, once CRISPR gene-editing becomes available for use in the reduction of brown fat in humans, I will no longer be using the treadmill as my mode of fat-burning and shift toward this method instead.

How Chewing Gum(If You’re a Pregnant Woman) Might Just Prevent You From Having Preterm Birth

In the United States alone, 1 out of every 10 infants is born prematurely. While this might not initially seem to be very significant, this statistic entails hundreds of thousands of infants born prematurely every year. Premature infant birth can cause a myriad of problems – ranging from mild consequences, like small body size, to more severe ones, respiratory distress. Even further, babies born prematurely are more likely to die in their first year alive than babies born according to term. 

If you are a pregnant woman, these facts may scare you. However, there may be a simple fix – the next time someone offers you a stick of sugar-free gum, accept their offer. 

More specifically, xylitol gum, in a large study in Malawi, has been shown to reduce preterm births. In the study, 36.6% of women who did not receive the gum birthed their babies preterm, while only 12.6% of women who regularly chewed xylitol gum birthed their babies preterm, displaying a 24% decrease in preterm births. 

Despite it being a simple solution, the mechanism for xylitol as a saver of infant life is more complex. Oral bacteria is one of the largest hubs for bacteria life in your body; second only to gut flora. However, harmful bacteria growth poses the risk of infected gum tissue, which leads to bacterial infection of the bloodstream and internal organs, including the placenta in pregnant mothers. Although the scientific reasoning is still shaky, certain bacterial infections of the placenta originating from oral flora may cause complications leading to premature childbirth.

Even more technically, xylitol affects the energy-production processes of oral bacteria, such as Streptococcus mutans (MS). When xylitol is consumed by MS bacteria, MS transports the xylitol sugar into the cell using facilitated diffusion, and transports it via the same processes that happen to control growth inhibition. Xylitol is converted to xylitol-5-phosphate, which MS then dephosphorylates. After, the bacteria expels this dephosphorylated molecule out of the cell actively, requiring energy. However, the metabolism of xylitol by MS does not provide it with any significant energy as a product. Thus, MS repeats this process until it starves to death due to lack of energy, as MS is not taking in enough energy to meet its energy demands from xylitol metabolism. 

In conclusion, chewing xylitol gum as a treatment for premature childbirth has yielded promising results thus far. And due to its high efficacy to cost ratio and high availability, chewing xylitol gum seems to be an effective treatment for premature childbirth in poorer nations like Malawi. Xylitol chewing gums

Paxlovid and Molnupiravir: Our First Steps Toward Covid-19 Treatment?

Currently, the new Covid-19 variant Omicron is taking the world by storm. Originating in South Africa as of late November, it was considered a variant of concern(VOC) by the WHO on November 26th and the first US case was identified on December 1st. While masks and current vaccination provide significant protection against Covid-19 strains, there is always a chance of breakthrough infections

In response, both Merck and Pfizer have developed novel antiviral pills in attempts to treat Covid-19 symptoms. It is known that cures for viral diseases do not exist, since viruses tend to mutate extremely fast. However, there exist novel drugs that promise to alleviate Covid-19 symptoms in the early stages of infection, like Pfizer’s Paxlovid and Merck’s molnupiravir. 

It is known that Covid-19 infects human cells by its outer spike proteins attaching to ACE2 receptors on the outside of the cell membrane. When in the cell, Covid-19 viral pathogens insert their viral RNA into our cytoplasmic ribosomes, which then codes for the creation of new viruses that then get excreted by the human cell. Merck’s molnupiravir consists of a five day treatment in which mutations to the viral RNA are introduced, since molnupiravir resembles viral nucleosides, causing irregular viral replication and, ultimately, an inability for the Covid-19 viral population to collectively survive in their human host. Pfizer’s Paxlovid pill, on the other hand, is administered in the early stages of Covid-19 infection to stop the progression of the disease and to prevent severe Covid-19 symptoms by inhibiting protease enzymes from functioning, which leads to the inability of virus proteins to become segmented and to spread, leading to dysfunctional Covid-19 viral pathogens and the ultimate death of Covid-19 viruses in the human host.Omicron

Fortunately, these two treatments are showing promising results in current clinical data trials. According to a Merck Sharp and Dohme (MSD) clinical study, 14.1% of placebo-treated patients were admitted to the hospital or had died of Covid-19, while only 7.3% of molnupiravir-treated patients were either hospitalized. In addition, at the end of the trial, 0 deaths were recorded in the monopiravir trial, while 8 deaths were reported among the placebo group. These results lead MSD scientists to deduce that the novel molnupiravir to reduce hospitalization or death by 50%. 

Pfizer’s Paxlovid, on the other hand, is especially promising in its clinical results. According to a recent Pfizer clinical data trial, 7% of the placebo group was hospitalized, and 7 died, while a staggering .8% of Paxlovid-treated Covid-19 patients were hospitalized, with 0 deaths by the end of the trial. These results lead Pfizer to state that “Paxlovid is 89% effective at patients in risk of serious illness,” as reported by Pfizer CEO Albert Bourla. 

In conclusion, although Covid-19 cannot have a fixed “cure,” outside of a vaccine of course, yet convenient, short-course antiviral pill treatments like Pfizer’s Paxlovid and Merck’s molnupiravir provide promising clinical trial results that show efficacy in reducing hospitalization and death rates due to Covid-19. While clinical data trials provide important markers of understanding Covid-19 treatment, it is still impossible to predict the practical applications of these pill treatments in the real world. Who will have access to these pill treatments? How will they get distributed? Will these treatments create global and regional socioeconomic disparities? In the eyes of these questions, our current vaccination protocols remain firm. While novel Covid-19 antiviral treatments are a huge step against Covid-19, the necessity for society to continue vaccination, as well as attempt to reach herd immunity levels, still holds utmost importance. 















The Dark Truth of Athletic Industry: The Effects of Anabolic-Androgenic Steroids on the Brain

Decades ago, the use of performancing-enhancing drugs, or PEDs, had been reserved for use by only the most elite of athletes, including bodybuilders and competitive sports players. In this day in age, however, PEDs have become ubiquitous amongst not only competitive athletes, but also regular gym-goers. As they play such a drastic role in the betterment of athletic performance, the benefits of PEDS are not without a trade-off: they have innumerable dangerous health consequences that must be understood. 

But what are PEDs in the first place? The most common form of PEDs comes in the form of anabolic-androgenic steroids, or AAS, which are derivatives of the male sex hormone testosterone. In a performancing-enhancing context, AAS such as pure testosterone are used to increase systemic androgenic activity in the body, manifesting in the hyper-development of male sexual characteristics such as hair growth, acne development, low voice, muscularity, and libido. By taking AAS, athletes are also able to reap the competitive benefit of erythropoiesis, or the production of red blood cells, increasing athleticism and endurance. In addition to overall increase in testosterone, many forms of testosterone derivatives other than pure testosterone, have anabolic, tissue-selective properties, directly leading to an increase in muscle mass. By taking AAS, athletes are able to give themselves a competitive edge in beating their counterparts. 

However, the effects of AAS on the body also have overwhelming negatives. It is widely known that taking AAS in the form of exogenous testosterone can shut down endogenous androgenic activity, leading to symptoms such as shrunken testicles, breast tissue development, and low energy. In addition, a new study conducted by Oslo University Hospital suggests that AAS can also lead to premature aging of the brain

Due to their chemical structure, after being injected using a needle into the blood, AAS enter the brain very easily. As steroids, AAS are hydrophobic, non-polar molecules, meaning they are able to passively diffuse through the phospholipid bilayer of cells through passive transport, depending upon concentration. At Oslo University Hospital, Dr. Bjørnebekk and his colleagues lead a study to investigate the effects of AAS on brain aging by scanning the brains of patients with past AAS use and those without it using MRIs. In the study, Dr. Bjørnebekk tested the brain age gap, or the difference between a patient’s chronological age and their predicted brain age, with a high brain age gap marking a higher risk for cognitive disease. Across the board, the AAS group showed significantly higher brain aging, or higher brain age gap, than standard participants, illustrating the underlying risks involved with AAS use. 

While the detrimental effects of exogenous AAS abuse are widespread across the body, unfortunately, technology to aid in the success of PED-using athletes has been flourishing in recent years. As exogenous AAS use often leads to crashed endogenous testosterone production in men, PCT, or Post-Cycle Therapy, drugs have been created to help men regain normal endogenous testosterone production after exogenous steroid abuse. Since AAS users usually experience low testosterone and high estrogen levels, estrogen blockers, such as Clomid or Nolvadex, are used in PCT to regain natural hormonal balance. While this may address the acute hormonal consequences of AAS use, technology, as of now, has not yet been created to ameliorate the long-term effects of AAS use on the brain. Manifested in the higher incidence of brain age gap in AAS users in the study, the neurodegenerative effects of AAS cause neurons to gradually lose function and die, which is often permanent. In conclusion, while PEDs in the form of AAS do exhibit strong competitive benefits for athletes, their long-term negative consequences and role in the acceleration of neurodegeneration make using AAS an unwise choice. 

Depo-testosterone 200 mg ml crop

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