LionMed Autumn 2025

AUTUMN 2025

EDITION 3

FIGHTING HUNTINGTON’S PHENOMENAL PHAGES DEEP DIVE: RITUXIMAB THE NBA AND INJURIES HIGHLIGHTING HYPERTROPHY REGENERATING DENTISTRY

Hello and welcome to the Autumn 2025 issue of LionMed, Hampton School's very own health sciences magazine.

The Lower Sixth MVD Society meets every week to share ideas and talk about the latest advancements within medicine and dentistry. The number of exciting topics within healthcare is boundless - there are always interesting news articles to read about the latest health science advancements. And so, we wanted to share our passions for subjects that really interest us - from regenerative dentistry to research into bacteriophages.

However, we could not have created this magazine on our own. We would like to thank Mr Langton, for bringing us all together for stimulating discussions during MVD Society, and reprographics expert Mr Cobb, who helped to put this magazine together. We must also thank the 2024 team of Sixth Form writers for the handing the baton over to us. Finally, I must personally thank all MVD Society members for their hard work and dedication in writing for the magazine.

Joshua Ripon

Contributors: Editor: Joshua Ripon Writers: Joshua Ripon, JR Ozen, Emir Aljubouri, Ian Leung, Ibrahim Ameen, and Azam Ahmad

FIGHTING HUNTINGTON’S Neurodegenerative disease refers to any disease which cause neuronal loss (the nerve cells which are responsible for transmitting nerve signals). This family of diseases include Alzheimer's, Multiple Sclerosis, and Parkinson's, but Huntington's Disease has recently been in the news because of a promising new drug trial.

Dr. George Huntington, an American doctor, first described this particular condition in a medical journal at just 22 years old, after he had noticed that members of the same family exhibited the same characteristic symptoms of a disease, which was later named after Huntington. 1 Research conducted in the last few decades has revealed that it is a mutation of the Huntington gene (HTT) which causes the condition. In essence, this gene normally codes for the huntingtin protein which contributes to various processes within the neurons, such as helping to transport other important proteins and neurotransmitters (chemical messengers) to their final destinations in the cell.

However, mutations, which are rare and random changes to the order of the bases (building blocks) of DNA, can occur to this HTT gene. The mutation, in this case, is a repeat of the codon (a set of three bases) which codes for an amino acid called glutamine. As there are more glutamine molecules being coded for by the gene, the fundamental shape of the overall huntingtin protein is altered, and the abnormal proteins clump together. This clumping is what ultimately causes neurodegeneration. 2

A recent drug trial has provided hope to many su ering with Huntington's Disease. Joshua Ripon investigates…

The image on the bottom left shows how the brain of a person who had Huntington's was atrophied (smaller) compared to the non-Huntington's brain. This is evidence of neural loss.

Huntington's is an autosomal dominant condition - this means that a person who has one parent with Huntington's and one without it has a 50% chance of inheriting the condition.

Huntington’s presents with a wide variety of symptoms from cognitive issues, such as being unable to organise oneself or becoming more inflexible. Whilst mental health issues, such as depression and mental health issues, are symptoms of Huntington's due to damage to the brain, Huntington's is most commonly associated with chorea. Chorea, which comes from the word χορεία (dance) in Ancient Greek, is characterised by a number of involuntary movements of muscles. This could mean that a person with Huntington's could no longer keep their balance whilst walking or might make abnormal eye movements. In fact, this condition was originally named Huntington's Chorea but was renamed Huntington's Disease to reflect how varied the symptoms can indeed be.1, 3 Whilst many symptoms of Huntington's could be treated by di erent medications, there was no treatment for Huntington's up until very recently.

However, a UCL team has, for the first time, pioneered a new treatment which can slow down the advancement of Huntington's by up to 75%.

This treatment (known as AMT-130) is a type of gene therapy, in which a person's faulty disease-causing genes are altered. It works by surgically inserting a small, harmless virus (the adeno-associated virus) into the striatum, a part of the brain which is particularly a ected by Huntington's. The virus contains microRNA molecules which bind to mRNA molecules which make the huntingtin protein. This binding process is important because it means that the bad mRNA is destroyed by the cell, in a process called autophagy, and so, ultimately, the amount of mutant huntingtin protein being made is reduced. 4, 5

An image of the microRNA molecules within the virus (represented by an icosahedron) inhibiting huntingtin production is shown below.

Credit: uniQure

Of course, the development of this treatment is very much in its early stages. Drug trials can take many years, from the moment that research has identified that a particular treatment could be e ective to the moment that that treatment is actually o ered to patients. Only 30 people participated in this initial trial stage, and so we do not really know much about the side e ects of gene therapy and about the complications that could possibly occur due to surgery on the striatum. 5 The hurdles that this trial has to overcome are numerous, from problems with regulation and funding to problems with finding willing participants to take part in the next few rounds of trials. Therefore, it's impossible to say whether this treatment will actually be routinely used within the NHS. However, on a personal note, I think that the main message, perhaps, of this trial is not that of the clinical or medical details: it is one of hope. There is hope that treatments will eventually be found for those debilitating conditions which are currently incurable or untreatable. There is hope that trials will progress and that new discoveries will be made. And so, this is a promising medical advancement that we should keep our eyes on.

By Joshua Ripon

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PHENOMONAL PHAGES

JR Ozen o ers a window into the hidden world of bacteriophages, and their potential uses within medicine…

Bacteriophages, commonly known as phages, are viruses that infect bacteria. Even though they were discovered over a century ago, Western medicine has largely overlooked them, until now. Today, phages are finally attracting the attention that they deserve. They are needed for our fight against infection and antibioticresistant bacteria, as they can be used to kill bacteria.

Bacteria can, though, become resistant to phages by modifying their antigens so that they are no longer complementary to that of the phages.

Phages are incredibly diverse. Some carry DNA, whilst others carry RNA. However, they all store their nucleic acids in protein shells that, under a microscope, can look like tiny lunar spaceships or intricate geometric puzzles. Additionally, most are extremely specific and only have the capability to target a singular bacterial species or, in some extreme cases, a single strain from a species. 1 Phages are everywhere. They are found in oceans, soil, sewage, and even within our own body systems. The gut “phagosome” likely plays a role in keeping our microbial communities balanced, but scientists do not know exactly how this works.

Phages attach to the bacteria via tail fibres or antigens (binding proteins), which are complementary to the bacteria’s own antigens.

Once attached, the phage, like other viruses, injects its genetic material into the bacteria. This means that the viral phage can now reproduce, via either the lytic or lysogenic cycles.

In the lytic cycle, the phage hijacks the bacteria’s machinery to make copies of itself, which eventually means that the cell bursts open and releases hundreds of new phages.2, 3 The number of viruses produced increases astonishingly quickly.

In the lysogenic cycle, the phage integrates its DNA into the bacterial genome and lies dormant until triggered.

However, some lysogenic phages can transfer genes for toxins to the surroundings. 4 Bacteria rarely live isolated from each other. In nature, they form communities called biofilms. They can be very dangerous as they often are resistant to antibiotics. They often appear in chronic wounds, the lungs of cystic fibrosis patients, and in prosthetic joints.

Scientific centres in countries, such as the Eliava Institute in Georgia, are pioneers in phage research.

Their early studies, which were originally overlooked, are now being re-examined by scientists who want to use their work clinically.

In phage therapy, phages attack the bacterial biofilms by either producing depolymerase enzymes to break down the protective bacterial matrix, or by replicating within the bacterial cluster.

There are a number of significant challenges associated with phage therapy. Phages do not penetrate into the biofilm uniformly, and so this means that some bacteria living deep in the biofilm may remain shielded. This is because phages cannot communicate or act in a coordinated manner.

Creating phages for therapy isn’t simple. Scientists must carefully purify the phages, remove any bacterial debris, and screen for harmful genes, such as those that can release harmful toxins. Furthermore, phages constantly evolve and so it is di icult to monitor how the phage changes genetically. 5 The image below shows this process.

Credit: MDPI The fact that phages are so specific can be a doubleedged sword. The right phage must match the right bacterium and so phage therapy rarely works like a onesize-fits-all treatment.

Scientists also need to determine how to introduce a phage into a human body, without it being killed o by the human’s white blood cells, before it even reaches its targets.

There are an increasing number of bacteria which are becoming resistant to antibiotics and so scientists are racing to find a new treatment to treat these bacterial infections. Therefore, phages are so useful because phages can be engineered in a way to kill o resistant strains of bacteria.6

A patient with Acinetobacter baumannii managed to recover after receiving a customised phage treatment.7 This shows that phages could be an important treatment against bacterial biofilms in the future. 8 Whilst promising, more research needs to be conducted to ensure that this treatment is overall safe.

Even if phages do not completely replace antibiotics, and only act in conjunction with them, phages could be a powerful new treatment. It is, ultimately, incredibly exciting to see what new advancements will be made within phage research.

By JR Ozen

DEEP DIVE: RITUXIMAB

Cancer treatments have significantly improved in the last few decades. Emir Aljubouri examines the use of a promising new treatment…

Non-Hodgkin’s Lymphoma (NHL) is the most prevalent adult blood cancer, representing a major challenge in modern oncology. Annually, the UK records around 13,000 new cases of NHL, reputing itself as the UK’s 6th most common cancer. B-cell lymphomas account for about 85% of all NHL diagnoses. 1

The late 20th century saw quiet yet transformational advancements in cancer treatments: the rise of targeted therapies. Among these was Rituximab (which is also called Rituxan), the world’s first monoclonal antibody (mAb) therapy approved for cancer by the FDA (the US’ Food and Drug Administration).

The disease often announces itself quietly: a painless swelling of lymph nodes° typically in the neck, armpits or groin. Other symptoms include persistent fatigue, chest pain, unexplained weight loss, and drenching night sweats. Beneath these symptoms lie a molecular drama involving genetic mutations that transform healthy, normal immune cells into cancerous, malignant clones. 1, 2

Rituximab binds to the CD20 protein° on B-cell lymphocytes. The monoclonal antibody treatment simply marks out the B-cell lymphocytes to guide the body’s immune system to destroy the cancerous, NHLa ected B-cells as well as being able to destroy these cancerous B-cells on its own. 4, 5

In NHL, acquired genetic mutations (spontaneous changes in DNA which develop during a person’s lifetime, which are not inherited) disrupt the normal cell cycle of mature B-cell lymphocytes (which produce antibodies and are involved in humoral immunity°). The neoplasm° of these B-cells cause the uncontrollable division of these rogue cells forming tumours within the lymphatic system, which is the network of vessels and glands that are involved in producing immune responses. As a result of this, B-cells become defective, and the immune system becomes weakened.3 To confirm NHL, a biopsy° of the lymph nodes is taken.

Under a microscope, non-Hodgkin’s lymphoma cells are identified by their absence of Reed-Sternberg cells° (below) which are found in Hodgkin’s lymphoma (a di erent type of blood cancer).

Rituximab triggers an immune-mediated cell destruction of malignant NHL cells. This means that Rituximab enables a mechanism called antibodydependent cellular cytotoxicity (ADCC) to occur, in which e ector cells, such as Natural Killer (NK) cells, bind to a receptor in the antibody’s fragment crystallisable region. This ultimately leads to NHL-cells dying (cell apoptosis). 6, 7 Although rituximab is generally well-tolerated by its patients, if it is given in combination with chemotherapy, it can harm healthy, fast-dividing cells in the body, like most cancer treatments. Healthy cells a ected include hair follicles, which means that a person might lose their hair temporarily. After treatment, hair follicle cells can repair themselves, but in some cases, damage is permanent and, therefore, so is the hair loss. Other side e ects of Rituximab itself include a severely weakened immune system due to the death of B-cells. Rituximab, an immunosuppressant drug, in combination with compromised immune systems from other underlying diseases such as HIV (which causes AIDS) give way for fungal and viral opportunistic infections such as the Epstein Barr Virus (EBV) which infect B-cells. Furthermore, other associated side e ects include nausea, vomiting, dizziness, headaches and fevers. 8, 9 Immunotherapies (treatments that use the body’s own immune system typically to attack cancer) have been circulating in the medical world for over a century.

Credit: Webpathology

However, the process of finding e ective antibody therapies has not been a breeze. The first mAbs were produced using hybridoma technology, where Köhler and Milstein immunised mice with sheep red blood cells. 10

Rheumatoid Arthritis (RA), Multiple Sclerosis (MS) and Systemic Lupus Erythematosus (SLE) are all autoimmune conditions that can also be treated with Rituximab. This demonstrates the wide range of diseases and conditions that Rituximab can treat.

This led to a domino e ect in research. The first use of the first mAb was approved by the FDA in 1986, where it was used to treat an acute kidney transplant rejection.

Rituximab, a chimeric (created from two species - mice and humans) antibody, eventually was created by Ronald Levy to target malignant B-cells and, in 1982, his first mAb cancer patient was successfully treated with the mAb. Furthermore, research showed that Rituximab could kill CD20 cells in vitro.

To conclude, Rituximab has o ered an insight into the e ectiveness of the use of monoclonal antibodies in the treatment of cancer. Since it was introduced, it has transformed the prognosis of B-cell NHL, especially when combined with chemotherapy. This has paved the way for modern immunochemotherapy treatments.

Since the initial approval of rituximab use in oncology patients in 1997 for a follicular lymphoma° case, outcomes of patients with non-Hodgkin’s lymphoma subtypes have improved substantially. The successful use of the monoclonal antibody has triggered widespread use of CD20 antibodies such as ofatumumab, which are also involved in binding to CD20 proteins on B-cells. mAbs are personalised therapeutics (a medical treatment tailored to an individual’s unique characteristics) which have come as a result of advances in research of immunology°.

Moreover, its reduced toxicity compared to cytotoxic treatments like chemotherapy means patients su er less from adverse e ects from treatments of nonHodgkin’s lymphoma. Finally, Rituximab continues to inspire the development of new anti-CD20 antibodies and for this reason, and so it would not come as a surprise if prognosis and survival rates of patients with NHL continued to improve significantly.

Glossary: Lymph nodes° – a part of lymphatic system which is composed of small areas of tissue that filter fluid in your body for harmful cells which act as a disposal unit for immune cells to get rid of damaged cells and foreign substances.

Humoral immunity° – a part of the immune system which involve antibodies neutralising pathogens.

Neoplasm° – an abnormal growth of tissue.

Biopsy° – taking a small sample of tissue or cells from the body which are then to be examined under a microscope by pathologists.

Reed-Sternberg cells° – large, abnormal cells that look like owl eyes.

Credit: Dana-Farber Cancer Institute A retrospective study on patients with di use large Bcell malignant lymphoma (DLBCL), which is a type of Bcell non-Hodgkin’s lymphoma, was carried out to investigate the increase in survival of patients after taking Rituximab. Out of 65 newly-diagnosed patients with DLBCL, 32 were in the pre-rituximab group (with a median follow-up time 60 months) and 33 were in the post-rituximab group (with a median follow-up time of 29 months). Progression-free survival rates increased substantially in the post-rituximab group. The 18-month progression-free survival rate increased from 59.4% to 81.8% and the overall survival rate at 18 months significantly increased from 65.5% to 81.8%. This led to the conclusion that conventional CHOP chemotherapy (a combination of chemotherapy with rituximab) resulted in a better prognosis for patients with DLBCL.12

CD20 Protein° – a glycosylated transmembrane phosphoprotein marker for B-cells; involved in regulating calcium ion concentration and cell cycle progression during B-cell activation.

Follicular lymphoma° – a type of slow growing nonHodgkin’s lymphoma that develop when malignant Bcells accumulate in follicles of lymph nodes.

Immunology° – the study of the immune system.

By Emir Aljubouri

INJURIES IN THE NBA

NBA matches have captivated millions of people around the world. Ian Leung analyses why NBA players seem to su er so many injuries…

As I was thinking of what to write for the Hampton Medical Magazine, a thought occurred to me: injuries in the NBA. I was intrigued by the fact that players in the NBA seemed to su er constantly with injuries despite the advances in injury prevention, medicine, and treatments.

League Mismanagement

This constantly frustrates me as the team that I support, the Charlotte Hornets, is repeatedly struggling with injuries every year. The Hornets’ star player, Lamelo Ball, has missed around 40% of his games due to constantly struggling with the same recurring ankle injury. Ankles injuries are the most common, with over 1,800 game-related ankle injuries in an average year.

This equates to 14.% of all NBA injuries. Researchers have shown an increase in injury rates ranging from 12.4% to 15% within the NBA.1 Knee injuries are the second most common in the NBA. Knee injuries usually take the form of Anterior Cruciate Ligament (ACL) or meniscal tears. ACL injuries are usually the most serious, requiring surgery and a long recovery and rehab time. An ACL tear happens when your knee moves or twists more than it naturally can.

There is a high risk of sustaining ACL tears in basketball, as it requires pivotal stop-and-start motions. In the US, ACL injury treatment costs $1 billion per year. 3

League Mismanagement and organisational pressure have increased the number of injuries in the League.

The NBA is big business: it generated $12.25 billion in the 2024-2025 season. This seems small in comparison to the Premier League which only made $8.29 billion in the same 2024-2025 season.

Perhaps in attempts to maximise profits, the NBA puts pressure on medical sta to clear players for play too soon, even if they are not in good shape, to attract fans and sell out venues.

A prominent example of this is when Kevin Durant (KD) su ered a minor calf strain in 2019 during the 2nd round playo series against the Rockets. Although this strain was later determined to be more serious, just a month into recovery, KD returned to play for Game 5 of the 2019 finals.

The Achilles tendon, the largest tendon in the body, connects the 2 major calf muscles (the gastrocnemius and the soleus) to the heel bone. It is likely that the rushed return from his calf strain meant that he tore his Achilles, as a weak calf can place excessive stress on the Achilles tendon, which increases the risk of an Achilles tear or rupture.

This injury was controversial as some think that he was misdiagnosed in the first place. Dr. David Chao, an orthopaedic surgeon and Team Physician for an NFL team, wrote in the San Diego tribune that Durant’s expression when he sustained the initial injury on May 8th indicated a possible Achilles tendon rupture, instead of it just being a calf injury. He said that the team specifically avoided the term “calf muscle” and opted for the more ambiguous and broad term “calf,” as an attempt to cover up a more serious injury, so that fans wouldn’t be concerned for his health during the Finals run.

An ultrasound image of an Achilles tear (not KD’s one) is shown below .

Credit: International Day of Radiology The potential misdiagnoses, along with his rushed return, were perhaps important factors leading to KD’s season ending injury. If KD continued to be sidelined, perhaps he would not have su ered the Achilles rupture.

This was likely due to KD being one of the star players in the team, and so many fans would have wanted to have seen him play. The team’s competitive nature put pressure on medical sta to clear him so that he could play.4

The Sport The demands of the sport itself could be the root cause of many injuries, particularly due to the rise of Amateur Athletic Union (AAU) sports in the US. Children start playing at a very young age, and often have to play 3+ games each day during tournaments, whilst undergoing high intensity training sessions, with little time for rest.

This can lead to injuries such as patellar tendinitis (jumpers knee) and stress fractures.

Rapid, sudden movements, including abrupt stops, change of directions, and fast movements can place tremendous stress on the joints, particularly the ankles and knees.

Constant jumping and landing are key in all aspects of basketball: rebounding, dunking, shooting, and in layups. These can cause awkward or hard landings which can lead to freak injuries such as ACL tears.

However, given that previous research suggested that NBA players su ered twice as many game-related injuries compared to college basketball players, it is most likely that the NBA training schedules contribute more to NBA injuries than the actual sport itself.

Schedules Intense NBA schedules can also contribute to many recurring injuries. Players have to play 82+ games per season, excluding playo s.

This, as well as having back-to-back games (playing 2 games on consecutive days), where teams have to travel to other cities, can make it incredibly exhausting for the players. As players have very little time for rest and recovery, fatigue also plays a big part in injury.

Research showed that injuries were associated with greater fatigue and game load. Furthermore, studies show that athletes who sleep less than 8 hours a night (which is most NBA players!) are at a much higher risk of sustaining a sport related injury.

This has led to many stars resting in the 2nd game of a back-to-back to reduce the risk of injury, to manage fatigue, and to prepare for the playo s This can then, in turn, mean that people who are specifically wanting to see that star player are disappointed. This can lead to attendance figures dropping, as well as TV ratings. 5, 6, 7

Conclusion In conclusion, despite other contributing factors, such as shortcomings within the League’s organisation and the nature of the sport itself, it is overall the demanding NBA timetable which mainly contributes to the increased number of basketball injuries. This is ultimately because NBA players do not have the time, between games or training sessions, to rest their bodies to ensure that they can play without fatigue. It is, therefore, up to NBA owners to put the wellbeing and health of their players before their financial aims, to ensure that basketball is a safer sport for all.

By Ian Leung

HIGHLIGHTING HYPERTROPHY

As social media influencers share their opinions on how to build muscle, Ibrahim Ameen turns to science to examine hypertrophy...

What is Hypertrophy?

Myofibrillar Hypertrophy is the growth of the muscle fibres, actin and myosin. This can be triggered by lifting heavier weights for less reps, and by doing compound movements, such as deadlifts or squats. This produces stronger, more dense muscles (like the ones that Eddie Hall has).

Muscle hypertrophy simply means an increase in the cross-sectional area of skeletal muscle fibres. your body adapts to repeated exercise-induced stress, your muscles grow back stronger and thicker. This is how bodybuilders develop the shape and tone of their muscles. The two types of hypertrophy are myofibrillar hypertrophy and sarcoplasmic hypertrophy.

Before we dive into the intricacies of muscle hypertrophy, it is essential to understand how muscles actually work.

The sliding filament muscle theory suggests that muscles are composed of small, contractile units.

These are called sarcomeres, which each consists of smaller filaments: actin, the thinner filament, and myosin, the thicker filament. During muscle contraction, calcium ions are released, which will bind to proteins on actin. This allows myosin to attach onto actin, forming a cross bridge. This ultimately means that ATP (an energy-carrying molecule) helps to pull the actin filament inwards, to shorten the sarcomere. This repeated pulling action is called a muscle contraction.

When our muscles relax, the reverse simply occurs: calcium is pumped away, the cross-bridges release, and the muscle returns to its length at rest.1

Sarcoplasmic Hypertrophy is the growth of the fluid and energy-providing substances, such as glycogen and enzymes, in the muscle cells, which is referred to refer to as the sarcoplasm. This can be achieved by lifting less heavy weights less quickly, but more frequently, and with reduced rest periods. Controlled isolation exercises like lateral raises, preacher curls or tricepspushdowns all increase sarcoplasmic hypertrophy, which in turn produces larger, more “full” muscles.

However, this will result in a lower direct increase in strength. 1, 2 Myofibrillar hypertrophy can be thought of as the thickening of the actual ropes that pull weights, whereas sarcoplasmic hypertrophy can be likened to adding layers of paint or string to the rope, which makes it thicker, but not necessarily stronger.

Stimuli for Growth Mechanical tension, muscle damage, and metabolic stress all stimulate muscular growth.

Mechanical Tension:

Intensity

When a person lifts a heavy weight slowly (i.e. they are reducing their momentum), they stretch their contracting fibres. This in turn activates sensors in the muscle that triggers mTORs, which regulates muscle protein synthesis. This means that a person can synthesise more muscle when under mechanical tension, leading to hypertrophy.

When lifting weights, a high degree of intensity is required to trigger hypertrophy. Studies suggest that the ideal degree of intensity ranges from 65 to 85% of one’s ‘one-rep-max. Doing 6 reps would trigger myofibrillar hypertrophy, and 12 would trigger sarcoplasmic hypertrophy. 3, 4

Muscle Damage: Microscopic tears tend to form during intense exercise, especially during the eccentric (basically the lowering part) half of the movement. In response to this, the body activates satellite cells, which are basically muscle stem cells. These fuse to damaged fibres, to repair them. Once repaired these muscle fibres become thicker, and so they grow. 2 Metabolic Stress: Metabolic stress is best described as the ‘pump’ or ‘burn’ a person feels when working out, especially with high rep exercises, such as lateral raises. This is caused by lactate, hydrogen ions and low oxygen in the muscle, which means that muscle cells swell up, and trigger hormonal signals, that will stimulate growth. The most famous of these hormones is probably testosterone, which enhances protein synthesis and muscle recovery.

Maximising Hypertrophy A keen athlete would want to maximise hypertrophy during their workout sessions, and there are a number of di erent methods to do this. The guiding principles to maximising hypertrophy remain the same for all athletes, whether they are bodybuilders, rugby players, or goalkeepers.

Progressive Overload: Muscles will only grow and adapt if they are pushed to their limits. Just like anything in life, a person will not see progress unless they really push themselves. To achieve this, a person needs to either lift a little bit more weight or a few more reps per week (as demonstrated below.

Time Under Tension To improve muscle growth, a person must try to control their movements, so that the eccentric phase of their exercise lasts for 2 to 4 seconds, depending on the exercise. If the eccentric phase lasts for too long, the muscle will become more fatigued. For example, when one is doing a bicep curl, it is important to lower the weight, straighten the elbow, and slow down the extension to 2-4 seconds.

There are, though, many di erent things that a person can do at home to continue to maximise muscle hypertrophy, and to ensure that they are staying healthy.

Nutrition The one word which is synonymous with muscles is protein. Protein can be found in red meat, eggs, and soya. 1.6 to 2.29g of protein per kilogram of bodyweight is enough for most people, but this amount can be adjusted to better fit a person’s needs. Proteins makes the amino acids we need for actin and myosin, which is needed for muscle contraction. Protein also repairs the exercise-induced microscopic tears in the muscle. 5 Sleep Many people, including myself, do not get enough sleep, but it is actually one of the most important things to do to maximise hypertrophy. Most of the muscle protein synthesis, which repairs muscular microscopic tears, happens during sleep. Furthermore, 70 to 80% of growth hormone, which helps to repair muscle tissue, is released during sleep. 6

Our Final Set! The science behind hypertrophy is, of course, fascinating. However, perhaps more importantly, these scientific principles can be applied readily whilst exercising. This demonstrates how science is not theoretical, but is actually tangible and applicable to our personal development.

By Ibrahim Ameen Credit: Colin DeWaay Training

REGENERATING DENTISTRY

Innovative technologies in dentistry have been developed to improve patient care. Azam Ahmad finds out more…

Dentistry is evolving from repair to regeneration.

Instead of simply patching damaged teeth with artificial filling, researchers are learning to coax nature itself into rebuilding enamel, dentin, and even pulp. This emerging field - regenerative dentistry - draws heavily on biomimetics, the science of imitating natural structures and processes to engineer materials that behave like real tissue.

The nacre of seashells (the iridescent inner layer known as mother-of-pearl) has inspired the design of layered composites with remarkable toughness and selfhealing capabilities. By replicating the microstructure of natural materials, these biomimetics systems can endure chewing stresses while facilitating biological repair. 4

At the very core of this transformation are biomimetic materials, designed to mimic the mechanical and biochemical properties of tooth tissues. Recent reviews describe how nanoscale fabrication and smart polymers have accelerated progress in crafting materials that don't just fill, but heal. By integrating calcium phosphate, hydroxyapatite, and bioactive glass (the same components that form natural enamel and dentin), scientists are creating restorations that can bond seamlessly with the tooth surface.1 One striking example is the development of bioactive composites capable of releasing ions that stimulate dentin remineralization and pulp repair. The materials encourage stem cells to regenerate lost or damaged dental tissue, e ectively blending the boundary between restorative and regenerative dentistry.2, 3 Another innovative approach takes cues from marine organisms.

Modern regenerative dentistry also explores tissue engineering, combining sca olds, growth factors, and dental stem cells. Researchers highlight the potential of bioactive sca olds that support periodontal and pulp regeneration. These materials provide the 'blueprint' that cells need to rebuild functional dental tissues; that's a big change from the old days when dentists just used metal or plastic filling that didn't really fix the tooth, just covered the damage.5 However, challenges do still remain. Biocompatibility, long-term stability, and cost all limit clinical adoption.

Despite this, optimism is high. The convergence of nanotechnology, biomaterials science, and stem cell research is setting the stage for a new era in dental care, one where dentists act less like engineers and more like gardeners of tissue, guiding natural healing. 6 The ultimate dream of regenerative dentistry is not just restoring a smile, but reviving it, making teeth that grow, adapt, and endure as living parts of the human body.

It's crazy to think how science and nature are starting to mix together, as if technology is learning to grow teeth back, bit by bit.

Glossary: Dentin - The hard layer beneath the enamel that makes up most of the tooth. It protects the pulp and carries tiny tubes that sense heat and pressure.

Pulp - The soft inner part of the tooth that contains nerves and blood vessels. It keeps the tooth alive.

Bioactive - A material that can interact with living tissue to help it heal or grow, instead of just sitting there passively.

Remineralization - The natural process where minerals like calcium and phosphate are added back into the tooth to repair early damage.

Biocompatibility - How safely a material can exist inside the body without causing harm or rejection.

By Azam Ahmad

Fighting Huntington’s 1) Bhattacharyya KB. The story of George Huntington and his disease. Annals of Indian Academy Neurology. [Online]. 2016 Jan-Mar;19(1):25-8. [Accessed 5 October 2025].

Available from: https://pubmed.ncbi.nlm.nih.gov/27011624/ 2) National Institute of Neurological Disorders and Stroke. Huntington's Disease. [Online] [Accessed 7 October 2025]. Available from: https://www.ninds.nih.gov/healthinformation/disorders/huntingtons-disease 3) Mayo Clinic. Huntington's Disease. [Online] [Accessed 9 October 2025]. Available from: https://www.mayoclinic.org/diseases-conditions/huntingtons-disease/symptomscauses/syc-20356117 4) UCL. Gene therapy appears to slow Huntington’s disease progression. 24 September 2025. [Online] [Accessed 20 October 2025]. Available from: https://www.ucl.ac.uk/news/2025/sep/gene-therapy-appears-slow-huntingtonsdisease-progression

Phenomenal Phages 1) Hyman P and Abedon ST. (2010) Bacteriophage host range and bacterial resistance.

Advances in Applied Microbiology. [Online]. 2010;70:217-48. [Accessed 21 November 2025]. Available from: https://pubmed.ncbi.nlm.nih.gov/20359459/ 2) Abedon ST et al. Phage treatment of human infections. Bacteriophage. [Online].

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[Online]. 8(6), pp. 769–783. [Accessed 21 November 2025]. Available from: https://pubmed.ncbi.nlm.nih.gov/23701332/ 4) Emencheta SC et al. The Role of Bacteriophages in the Gut Microbiota: Implications for Human Health. Pharmaceutics. [Online]. 2023 Oct 3;15(10):2416. [Accessed 22 November 2025]. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC10609668/ 5) Pirnay JP et al. The phage therapy paradigm: a scientific and regulatory challenge.

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Deep Dive: Rituximab 1) Bowzyk Al-Naeeb A. Non-Hodgkin lymphoma. BMJ. [Online]. 2018 Aug 22;362:k3204. [Accessed 9 November 2025]. Available from: https://pubmed.ncbi.nlm.nih.gov/30135071/ 2) Cleveland Clinic. Unknown. Non-Hodgkin lymphoma. [Online]. [Accessed 9 November 2025]. Available from: my.clevelandclinic.org 3) Sapkota S. 2023. Non-Hodgkin Lymphoma. StatPearls. [Online]. 2023 Feb 24. [Accessed 9 November 2025]. Available from: https://www.ncbi.nlm.nih.gov/books/NBK559328/ 4) Tavarozzi R. 2023. Changing Trends in B-Cell Non-Hodgkin Lymphoma Treatment: The Role of Novel Monoclonal Antibodies in Clinical Practice. Cancers (Basel). [Online].

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The NBA and Injuries 1) Moore ML et al. Management of ankle injuries in professional basketball players:

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Sports Health. [Online]. 2010;2:284-90. [Accessed 18 November 2025]. Available from: https://pubmed.ncbi.nlm.nih.gov/23015949/ Alentorn-Geli E et al. Prevention of non-contact anterior cruciate ligament injuries in sports. Part II: systematic review of the e ectiveness of prevention programmes in male athletes. Knee surgery, sports traumatology, arthroscopy. [Online]. 2014 Jan;22(1):16-25.

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Highlighting Hypertrophy 1) Hall JE and Hall ME. 2020. Guyton and Hall Textbook of Medical Physiology. 14th edn.

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Regenerating Dentistry 1) Zafar et al. Biomimetic Aspects of Restorative Dentistry Biomaterials. Biomimetics (Basel). [Online]. 2020 Jul 15;5(3):34. [Accessed 29 October 2025]. Available from: https://pubmed.ncbi.nlm.nih.gov/32679703/ 2) Singer L et al. Biomimetic approaches and materials in restorative and regenerative dentistry: review article. BMC Oral Health. [Online]. 2023 Feb 16;23(1):105. [Accessed 1 November 2025]. Available from: https://pubmed.ncbi.nlm.nih.gov/36797710/ 3) Alsolaihim AN et al. Biomimetic Regenerative Materials in Restorative Dentistry and Endodontics. Journal of International Health. [Online]. 2023 Jun 15(3):p 250-256.

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