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This page features articles which tackle imminent health problems such as smoking, childhood obesity and depression, and pre-diabetes. Skin disease, Crohn's disease, anaemias, and endometriosis are also explored.  Medicine Articles This page features articles which tackle imminent health problems such as smoking, childhood obesity and depression, and pre-diabetes. Skin disease, Crohn's disease, anaemias, and endometriosis are also explored. You may also like: Dentistry , Biology Interventions for smoking cessation Public smoking health interventions The problem with childhood obesity What is childhood obesity? How many does it affect, and what can we do to tackle this? Pre-diabetes Pre-diabetes is the period before the onset of diabetes Anaemias Anaemia is a blood disease. Article #1 in a series about anaemia. Endometriosis breakthrough The latest breakthrough in endometriosis: the bacterium theory AI in medicinal chemistry How can it help the field? Depression in children And how we can help them Iron-deficiency anaemia Anaemia is a blood disease. Article #2 in a series about anaemia. The power of probiotics And how they are effective Blood: a vital fluid The role and importance of blood Smart bandages What are they and how can they be better than traditional bandages? Why whales don't get cancer Discussing from Peter's Paradox perspective Anaemia of chronic disease The second most-common anaemia. Article #3 in a series about anaemia. Erasing memory Is it possible to wipe your memories clean? Herpes vs. skin disease From foe to ally: a Herpes-based gene therapy treats dystrophic epidermolysis bullosa. Article #3 in a series on Rare diseases. The foremothers of gynaecology An International Women's Month collab with Publett Healthcare serial killers A disturbing reality The gut microbiome Also known as: the microbiota, gut microflora Crohn's disease A summary of the condition Sideroblastic anaemia A problem synthesising haem. Article #4 in a series about anaemia. Next

Uncovering the truth behind the origins of the virus Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Origins of COVID-19 03/05/26, 17:31 Last updated: Published: 08/10/23, 16:07 Uncovering the truth behind the origins of the virus The quest for the crime of the century begins now! Suspicion of the Wuhan Institute of Virology Since the early epidemic reports in Wuhan, the origin of COVID-19 has been a matter of contention. Was SARS-CoV-2 the outcome of spontaneous transmission from animals to humans, or scientific experimentation? Although most of the recorded initial cases occurred near a seafood market, Western Intelligence Agencies knew that the Wuhan Institute of Virology (WIV) was situated nine miles to the south. Researchers at the biosafety centre combed Yunnan caves for bats harbouring SARS-like viruses. They have been extracting genetic material from their saliva, urine, and faeces. Additionally, bat coronavirus RaTG13 (BatCoV RaTG13) shared 96% of its genome with SARS-CoV-2. Suspicion increased when it was discovered that WIV researchers dealt with chimeric versions of SARS-like viruses capable of infecting human cells. However, similar "gain-of-function" studies in Western biosecurity institutions have shown that such slow virulence increases may occur naturally. The coincidence that the pandemic began in the same city as the WIV outbreak was too obvious to ignore. According to two Chinese specialists , "the likelihood of bats flying to the market was quite remote". Chan and Ridley's "Quest for the Origin of COVID-19" Chan and Ridley have created a viral whodunit titled "Quest for the origin of COVID-19" to excite the curiosity of armchair detectives and scientific sceptics. Both need clarification as to why a virus of unknown origin was detected in Wuhan and not in Yunnan, 900 kilometres to the south. The stakes could not be more significant; if the virus were deliberately developed and spread by a Chinese laboratory, it would be the crime of the century. They are prudent in not going that far. They are, however, within their rights to cast doubt on the findings since their concerns were shared by numerous coronavirus experts who openly discounted the possibility of a non-natural origin and declared that the virus displayed no evidence of design at the time. Is this the impartial and fair probe the world has been waiting for? They present no evidence for the development of SARS-CoV-2. For example, Chan asserts that it seemed pre-adapted to human transmission " to an extent comparable to the late SARS-CoV-2 outbreak ". This statement is based on a single spike protein mutation that appears to "substantially enhance" its potential to connect to human receptor cells, meaning it had "apparently stabilised genetically" when identified in Wuhan. Nonetheless, this is a staggeringly misleading statement. As seen by the alphabet soup of mutations, the coronavirus has undergone multiple alterations that have consistently increased its suitability. Additionally, viruses isolated from pangolins attach to human receptor cells more efficiently than SARS-CoV-2, indicating the possibility of additional adaptation. According to two virologists, although the SARS-CoV-2 virus was not wholly adapted to humans, it was "merely enough". Evidence for design of SARS-CoV-2 and possible natural origins of the virus Another concerning feature of SARS-CoV-2 is a furin cleavage site, which enables it to infect human cells by interfering with the receptor protein. The identical sequence is present in highly pathogenic influenza viruses and was previously utilised to modify the spike protein of COVID-19. Chan and Ridley explain that this is the kind of insertion that would occur in a laboratory-modified bat virus. As a result, 21 leading experts have concluded that the furin sequence is insufficient. Coronaviruses have been shown to possess " near identical " genomes that often can infect humans and animals. Because the furin cleavage site characteristic is not seen in known bat coronaviruses, it is possible that it evolved naturally. Surprisingly, Chan and Ridley do not suggest that the SARS virus's high human infectivity feature was inserted on purpose since "there is no way to determine". There is also no way to determine if a RaTG13 is the pandemic virus's progenitor since history is replete with pandemics that began with zoonotic jumps. This argument is based on the strange fact that WIV researchers retrieved the bat isolate in 2013 from a decommissioned mine shaft in Yunnan. Six people were removing bat guano from the cave that year when they suffered an unexplained respiratory ailment. As a consequence, half of them perished. The 4% genetic diversity between RaTG13 and SARS-CoV-2, on the other hand, is similar to 40 years of evolutionary change. While exploring caves in northern Laos, researchers discovered three more closely related bat coronaviruses, which have a higher affinity to attach to human cells than the early SARS-CoV-2 strains. This indicates an organic origin, either through another animal host or directly from a bat, maybe when a farmer went into a cave. This is arguably the most reasonable explanation since it is consistent with forensic and epidemiological data. The food sample isolates collected from the Wuhan seafood market are similar to human isolates, and the majority of original human cases had a history of market exposure, in contrast to the absence of an epidemiological connection to the WIV or any other Wuhan research institution. Lack of evidence for a laboratory origin If scientists could demonstrate prior infection at the Wuhan market or other Chinese wildlife markets that sell the most likely intermediary species, including pangolins, civet cats, and raccoon dogs, the case for a natural origin would be strengthened. Although multiple animals tested positive for sister human viruses during the SARS epidemic, scientists have yet to find evidence of earlier infections in animals in the instance of Sars-CoV-2. Nonetheless, the absence of evidence does not confirm the absence and may indicate that samples were not taken from the appropriate animal. The same may be said of the lab leak argument's lack of evidence. However, even though history is littered with pandemics, no significant pandemic has ever been traced back to a laboratory. In other words, the null hypothesis is a zoonotic occurrence; Chan and Ridley must demonstrate otherwise. The irony is their drive to construct a compelling case for a laboratory accident. They are oblivious to the much more pressing story of how the commerce in wild animals, global warming, and habitat degradation increase the likelihood of pandemic viral development. This is the most plausible origin story that should concern us. Summary and future direction Although Chan and Ridley's "Quest for the Origin of COVID-19" has cast suspicion on the Wuhan Institute of Virology, there is still insufficient evidence to support the lab leak theory. There is, however, growing evidence for a natural origin of SARS-CoV-2, with multiple animals testing positive for sister human viruses during the SARS epidemic and the discovery of more closely related bat coronaviruses in northern Laos. A World Health Organization advisory group in 2025 has concluded its independent assessment of how the COVID pandemic started . As mentioned, most of the peer-reviewed scientific evidence supports the hypothesis that SARS-CoV-2 has a zoonotic origin. "But," the group say, "until requests for additional information are met or more data become available, there can be no certainty about when, where and how SARS-CoV-2 entered the human population. There is a continued need for a thorough, unbiased investigation". As such, we should be more concerned with the increasing likelihood of pandemic viral development due to the commerce in wild animals, global warming, and habitat degradation. Written by Sara Maria Majernikova Project Gallery

Antimicrobial Resistance (AMR) is a growing concern for healthcare systems globally Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Are we doing enough to fight anti-fungal resistance? 26/04/26, 14:30 Last updated: Published: 04/11/24, 15:29 Antimicrobial Resistance (AMR) is a growing concern for healthcare systems globally Introduction to fungi Fungi are a fascinating yet relatively untouched area of microbiology. From growing in damp forest soil to the human body, these eukaryotes (surprisingly more closely related to animals than plants!) reproduce sexually and asexually, producing hyphae (long, branching filaments) to absorb nutrients. Even in the human body, fungal infections can range from athletes' foot to severe cases of invasive pneumonia. Despite its diverse and incredibly interesting nature, only 5% of all estimated fungal species worldwide have been discovered. There is a significant lack of knowledge regarding these amazing microorganisms. The challenge of antimicrobial resistance Antimicrobial Resistance (AMR) is a growing concern for healthcare systems globally. AMR is the process by which microbes develop decreased sensitivity to antimicrobial drugs, meaning they can evade drug and immune response, creating the potential for superbugs (i.e. Multi-Drug Resistant Staphylococcus Aureus/MRSA). An increasing number of resistant fungal species are emerging, with more than 90% of Candida Auris strains in the US now fluconazole resistant. Microorganisms can confer resistance in various ways, such as the misuse of antimicrobial drugs and pesticides in healthcare and agriculture or random genetic evolution (secondary vs primary resistance). Biofilm formation can also contribute to this, particularly for those with inserted medical devices. This can be seen in Candidiasis, for example on inserted catheters, as can be seen in Figure 2 . AMR was thought to be responsible for 1.27 million deaths globally in 2019, with an 8% increase in resistant infections in the UK from 2021-22. Global efforts regarding resistance appear to focus on antibiotic resistance, much reflective of worldwide research efforts. This leaves us wondering, are we doing enough to fight antifungal resistance? Mechanisms of fungal resistance Fungal infections, although typically mild, often present most severely in the immunocompromised, particularly those with cancer or who have had recent organ transplants. Invasive infections are cleared using five classes of antifungal drugs: azoles, polyenes, allylamines, flucytosine, and echinocandins, the two most common being azoles and echinocandins. Azoles aim to inhibit ergosterol synthesis, which is crucial for cell membrane stability, whilst echinocandins interfere with beta-1,3-D-glucan synthesis (a major component of fungal cell walls). Fungi can come in two forms: mould fungi (multicellular units containing branching hyphae), and yeast fungi (unicellular with the ability to ferment carbohydrates). In yeasts, azoles target the Erg11 protein (or Cyp51A for mould fungi), which disrupts ergosterol synthesis and causes the build up of 14a-methyl sterols. In turn, this disrupts membrane activity. Azole resistance can develop through different pathways: changes in the Erg11 amino acid structure, changes in Erg11 expression, and alterations to drug efflux pathways. For Candida species, amino acid substitutions occurring at the Erg11 enzyme binding site often lead to azole resistance, whilst in Aspergillus fumigatus, changes occur at codons 54-220 in Cyp51A. Resistant Candida albicans can also overexpress Erg11, meaning a higher drug concentration is needed to combat infection. Some fungal species, such as Candida spp. confer azole resistance by utilising drug efflux systems, particularly the ABC transporter MDR1, where a gain of function mutation can lead to multidrug resistance. Loss of heterozygosity, for example, by aneuploidy, can lead to resistance if this occurs across Erg11 or MDR1 gene loci. Inhibition of the Hsp90 pathway (a component of the cellular stress response) can alleviate both azole and echinocandin resistance and regulate biofilm resistance. Hsp90 stabilises the terminal MAPK component, increasing cell wall integrity (most antifungal drugs target the fungal cell wall). Global nature of AMR Global schemes have emerged to combat AMR, with fungal efforts appearing to lag behind its bacterial equivalent; The WHO published its first priority bacterial pathogens list in 2017, which has been effectively used by pharmaceutical companies, researchers, and local health trusts to target bacterial species, asserting themselves as an increasing risk. WHO Fungal Priority lists didn’t emerge until 2022, which was the first global effort to establish fungal species of risk. The One Health approach, another global strategy, aims to combat AMR by emphasising collaboration between multiple sectors, increasing innovation and creating clear communication. Its main aims lay in identifying knowledge gaps, involving policymakers, creating networks and sharing data. In addition to global strategies, national ones exist. The UK government made its own five year AMR-combatting plan, implementing a One Health approach; Previous plans have proven successful; antimicrobial exposure was reduced by 8%, with a further 81% reduction in antibiotic sales for food-producing mammals. It is clear AMR (particularly fungal resistance) is becoming an increasingly worrying issue. In 2019, UK deaths directly arising from drug resistant infections nearly matched those from stomach cancer, with an estimated further 35,000 deaths indirectly resulting from resistant infections. Hence, measures must be in place to contain its potential for worldwide damage. Insufficient action against AMR was predicted to have long-lasting effects like the COVID-19 pandemic every five years. Since drug-resistant fungi have the potential to cause significant burden on healthcare systems globally, what is currently being done to combat Fungal AMR? What more can we do? Fungal infections are the fifth leading cause of death worldwide, yet less than 1.5% of infectious disease funding goes towards research of fungal infections. This could be because fungal infections present mildly in most healthy people. However, we cannot ignore the fatal consequences for those with pre-existing illnesses or the devastating effects that could ensue if we do not make significant efforts to eliminate fungal resistance. In its most recent five-year plan, the UK government stated its support for initiatives to increase agrochemical stewardship, particularly focussing on fungicides. The efforts outlined include establishing a pharmaceutical monitoring programme, funding research into AMR-driving chemicals, and a pilot AMR surveillance scheme. This is significant progress, however, it focuses on environmental fungal resistance, with a tendency to ignore research efforts and failing to actively address fungi in most sections. In April 2026, £4.5 million was awarded to an international collaboration including the University of Edinburgh, to help improve understanding of fungal diseases. This is a significant contribution, and can accelerate endeavours in research. To move forward, more efforts are needed to drive antifungal research - whether in expanding the number of antifungal classes available to patients or improving existing antifungal therapies (e.g. improvements in pharmacokinetics and efficacy). This is evidenced by the sheer number of antibiotics and respective classes compared to fungal counterparts; bacterial infections can be treated with a whopping two-fold more drug classes than their fungal equivalent. Moreover, the One Health approach emphasises the importance of diagnostics and testing; whilst most modern fungal testing methods are very sensitive and specific, some tests can only report positive results very late into disease progression (read more about One Health ). Hence, fungal diagnostic and testing approaches need to be optimised. This all can be achieved by pushing more funding towards fungal research and development, encouraged with government spending, and an emphasis on collaboration between academia and industry. How can we relay the importance of stewardship in agriculture, or bring more treatments to the bedside without collaboration and education? Written by Eloise Nelson Related article: The increasing threat of anti-microbial resistance REFERENCES Gaya E., Fungarium: Welcome to the Museum, 2019. Kundu R, Srinivasan R. Cytopathology of Fungal Infections. Current Fungal Infection Reports. 2021;15(3):81-92. The Role of Plant Agricultural Practices on Development of Antimicrobial Resistant Fungi Affecting Human Health: Proceedings of a Workshop Series.: Hearing before the National academies of Sciences, Engineering and Medicine (05.04.2023, 2023). Government U. Confronting antimicrobial resistance 2024 to 2029. In: Care DoHaS, editor. 2024. Fisher CM, Alastruey-Izquierdo A, Berman J, Bicanic T, Bignell ME, Bowyer P, et al. Tackling the emerging threat of antifungal resistance to human health. Nature Reviews Microbiology. 2022;20(9):557-71. Cowen EL, Sanglard D, Howard JS, Rogers DP, Perlin SD. Mechanisms of Antifungal Drug Resistance. Cold Spring Harbor Perspectives in Medicine. 2015;5(7):a019752. Fisher CM, Alastruey-Izquierdo A, Berman J, Bicanic T, Bignell ME, Bowyer P, et al. Tackling the emerging threat of antifungal resistance to human health. Nature Reviews Microbiology. 2022;20(9):557-71. WHO fungal priority pathogens list to guide research, development and public health action. WHO; 2022. Greener M. Why have we neglected fungal infections? Prescriber. 2022;33(8-9):20-3. Baker J, Denning WD. The SSS revolution in fungal diagnostics: speed, simplicity and sensitivity. British Medical Bulletin. 2023;147(1):62-78. Project Gallery

You can have endometriosis and PCOS at the same time Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Are PCOS and endometriosis sisters? 25/02/26, 18:21 Last updated: Published: 30/01/24, 21:33 You can have endometriosis and PCOS at the same time The label of PCOS or endometriosis can have physical and emotional consequences for women. It is important for both male and females to gain a better understanding of such conditions, the symptoms and the challenges they pose. Such knowledge can act as physical and emotional support in times of need. It creates a safe space where the person with PCOS is comfortable discussing their experiences, feelings and concerns knowing they are being heard and supported by the right people. With research fast developing there is a plethora of information out there, so WHAT do you believe in and WHAT do you ignore and WHOM do you believe and WHOM do you ignore? Endometriosis and polycystic ovary syndrome (PCOS) both affect females and can have similar symptoms. However, the causes and some key symptoms are different. Endometriosis is a painful disorder in which tissue that normally lines the inside of your uterus grows outside the uterus. (Read more on Endometriosis breakthrough ). PCOS is an endocrine system disorder where small fluid-filled sacs develop in the ovaries. You can have endometriosis and PCOS at the same time. A 2015 study found that women with PCOS had a higher risk for a diagnosis of endometriosis. Another 2014 study determined that there is a strong link between endometriosis and PCOS with pelvic pain and trouble getting pregnant. What is a normal menstrual cycle? Let’s polish up the basics! The brain, ovaries and uterus work together to prepare the body per month for pregnancy. Follicle-stimulating Hormone (FSH) and Luteinising Hormone (LH) are made by the pituitary gland and progesterone and oestrogen are made in the ovaries. Many females with PCOS do not ovulate regularly and it may take these females longer to become pregnant. Irregular periods results in months where ovulation does not occur. Where the ovaries do not produce progesterone the lining of the uterus becomes thicker but shedding is very irregular which can lead to heavy and prolonged bleeding. PCOS affects 1 in 10 women in the UK. Women with PCOS experience irregular menstrual cycles, acne, excess hair growth, infertility, pregnancy complications and cardiovascular disease. PCOS can be associated with weight gain and obesity in approximately one-half of females. Females with PCOS can also be at increased risk of other problems that can impact quality of life. These include depression and anxiety, sexual dysfunction and eating disorders. Although PCOS is not ‘completely’ reversible there are many ways you can minimise the symptoms. Most females can lead a normal life and are able to conceive without significant complications. A pelvic examination is requested by your GP to assess the ovaries for a diagnosis to be made. Imaging tests for examining the ovaries are pelvic and intravaginal ultrasonography, however, the latter may be extremely uncomfortable if sexually inactive. Note: As of Oct 2025, NICE has announced it will adapt the International PCOS Guideline for the UK. Please be aware this article acts to capture your attention, encouraging you to delve further into the subject and continue your self-education on this topic and by no means is everything about PCOS. It is essential to consult with a healthcare professional if you suspect you may have symptoms of either PCOS or endometriosis. Proper diagnosis and management can help address specific concerns and improve overall reproductive health. Written by Khushleen Kaur Related articles: Endometriosis breakthrough / Underreporting in endometriosis / Gynaecology REFERENCES R. Hart and D. A. Doherty, Fertility Specialists of Western Australia (R.H.), Bethesda Hospital, 6008. K. J. Holoch, R. F. Savaris, D. A. Forstein, P. B. Miller, H. Lee Higdon, C. E. Likes and B. A. Lessey, https://doi.org/10.5301/je.5000181 , 2014, 6, 79–83. R. J. Norman, D. Dewailly, R. S. Legro and T. E. Hickey, The Lancet, 2007, 370, 685–697. Project Gallery

The yearly incidence of TBI is around 27 and 69 million people worldwide Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Beyond the bump: unravelling traumatic brain injuries 30/03/26, 17:08 Last updated: Published: 15/10/24, 11:32 The yearly incidence of TBI is around 27 and 69 million people worldwide A traumatic brain injury (TBI) is one of the most serious and complex injuries sustained by the human body, often with profound and long-term effects on an individual’s physical, emotional, behavioural and cognitive abilities. What is a traumatic brain injury? A TBI results from an external force which causes structural and physical damage to the brain. The primary injury refers to the immediate damage to the brain tissue which is caused directly by the event. Whereas secondary injuries result from the cascade of cellular and molecular processes triggered by the initial injury and develop from hours to weeks following the initial TBI. Typically, the injury can be penetrating, where an object pierces the skull and damages the brain, or non-penetrating which occurs when the external force is large enough to shake the brain within the skull causing coup- contrecoup damage. Diagnosis and severity The severity of a TBI is classified as either mild (aka concussion), moderate, or severe, using a variety of indices. Whilst more than 75% of TBIs are mild, even these individuals can suffer long-term consequences from post-concussion syndrome. Here are two commonly used measures to initially classify severity: The Glasgow Coma Scale (GCS) is an initial neurological examination which assesses severity based on the patient’s ability to open their eyes, move, and respond verbally. It is a strong indicator of whether an injury is mild (GCS 13-15), moderate (GCS 9-12) or severe (≤8). Following the injury and any period of unconsciousness, when a patient has trouble with their memory and is confused, they are said to have post-traumatic amnesia (PTA). This is another measure of injury severity and lasts up to 30 minutes in mild TBI, between 30 minutes and 24 hours in moderate TBI, and over 24 hours in severe TBI. Imaging tests including CT scans and MRIs are used to detect brain bleeds, swelling or any other damage. These tests are essential upon arrival to the hospital, especially in moderate and severe cases to understand the full extent of the injury. Leading causes of TBI Common causes of TBI are a result of: Falls (most common in young children and older adults) Vehicle collisions (road traffic accidents- RTAs) Inter-personal violence Sports injuries Explosive blasts Interestingly, the rate of TBI is 1.5 times more common in men than women. General symptoms The symptoms and outcome of a TBI depend on the severity and location of the injury. They differ from person to person based on a range of factors which include pre-injury sociodemographic vulnerabilities including age, sex and level of education, as well as premorbid mental illnesses. There are also post-injury factors such as access to rehabilitation and psychosocial support which influence recovery. Due to this, nobody will have the same experience of a TBI, however there are some effects which are more common than others which are described: Mild TBI: Physical symptoms: headaches, dizziness, nausea, and blurred vision. Cognitive symptoms: confusion, trouble concentrating, difficulty with memory or disorientation. Emotional symptoms: mood swings, irritability, depression or anxiety. Moderate-to-severe TBI: Behavioural symptoms: aggression, personality change, disinhibition, impulsiveness. Cognitive symptoms: difficulties with attention and concentration, decision making, memory, executive dysfunction, information processing, motivation, language, reasoning, self-awareness. Physical symptoms: headaches, seizures, speech problems, fatigue, weakness or paralysis. Many of these symptoms are ‘hidden’ and can often impact functional outcomes for an individual, such as their capacity for employment and daily living (i.e. washing, cooking, cleaning etc.). The long-term effects of TBI can vary, with some returning to normal functioning. However, others might experience lifelong disabilities and require adjustments in their daily lives. For more information and support, there are some great resources on the Headway website, a leading charity which supports individuals after brain injury. Written by Alice Jayne Greenan Related articles: Why brain injuries affect adults and children differently / Neuroimaging / Different types of seizures Project Gallery

Known as microbial endocrinology, it is a complex field Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Investigating the interplay of hormones and the microbiome 03/05/26, 17:05 Last updated: Published: 08/11/24, 12:00 Known as microbial endocrinology, it is a complex field The microbiome The human body hosts a vast ecosystem of bacteria, with trillions crawling on our skin, colonising our gut, and living throughout our bodies. Most of these microbes serve to protect us against infections influencing our metabolism and even our behaviour. However, scientists have started to question the mechanisms by which these bacteria affect our bodily functions and characteristics. Scientists have studied these communities of microorganisms residing within our bodies and the genes they contain, yielding new and exciting perspectives… …Welcome to the human microbiome. The microbiome is the dynamic community of microorganisms (like fungi, bacteria and viruses) that exist in a particular environment. In humans, the term is most often used to describe the collection of microorganisms that inhabit a particular body area, such as the gastrointestinal tract, mouth or skin. While a person’s core microbiome is established within the first few years of life, its composition can shift over time in response to factors like medication, such as potent antibiotics and environmental factors. Researchers have uncovered that the gastrointestinal microbiota can influence some physiological processes, including a direct line of communication between the gut and the brain. But what facilitates this dialogue? What mechanisms enable the gut to relay signals to the brain? The answer is hormones. Hormones and the endocrine system The endocrine system is a network of glands that produce and release chemical messengers known as hormones. They travel via the bloodstream and bind to specific receptors on their target tissues. This binding of hormones to their receptors triggers a response in the target tissue. For instance, during stressful situations, epinephrine (also known as adrenaline) is produced by the adrenal medulla, the inner region of the adrenal glands. This hormone, released into the bloodstream, acts on target tissues such as the heart, where it increases heart rate. Hormones regulate most of the body’s vital functions through their release. Some of these crucial processes include growth, metabolism, and reproduction. In the following sections, however, we specifically focus on how hormones influence the microbiome. The interactions between hormones and the microbiome Exploring the relationship between hormones and the microbiome is known as microbial endocrinology; it is a complex field because there are numerous interactions to account for, and the effects of each one can have lasting impacts on human physiology. For example, epinephrine and norepinephrine can lead to more bacteria, notably E. coli and Pseudomonas aeruginosa , signifying that imbalance could harm humans. Also, parts of the host, ranging from mood to gender, impact hormones, bacterial presence and activity ( Figure 3 ). An emerging area of microbial endocrinology is how the microbiome and sex hormones engage with each other in disease and female health- this is called microgenderome (this describes "bidirectional interactions between human microbiomes, sex hormones, and immune systems"). This may help to explain why women are more prone to certain autoimmune conditions. One paper noted that disorders from metabolic syndrome (MetS) to type 2 diabetes (T2D) have distinctions in the levels of sex hormones and gut microbiota, indicating that they are essential to understanding in developing those conditions. The influence of gut microbiota on sex hormones can occur through various mechanisms, such as bacteria controlling the activity and expression of endocrine receptors and even bacteria metabolising sex hormones; this knowledge can help create treatments against polycystic ovarian syndrome and ovarian cancer, among other diseases that usually impact females due to gut microbiome imbalances ( Figure 4 ). Another part of microbial endocrinology being researched is how the microbiome impacts human growth. In one study involving adult male mice, decreased growth hormone (GH) led to undeveloped microbiomes, while surplus GH was linked to an expanded microbiome; this depicts that bacteria influences development via the growth hormone-insulin-like growth factor 1 (GH-IGF-1) axis; maintaining a steady dynamic between the microbiome and this axis is vital for development ( Figure 5 ), particularly in children. In puberty, hormones and the gut microbiome interact, as observed in obesity and precocious puberty. Hence, a deeper awareness of the bacteria and sex hormones during puberty is crucial to designing targeted medicines for growth disorders. Moreover, patients with GH-secreting pituitary adenoma (GHPA) have modified gut microbiota, like increased Alistipes shahii and Odoribacter splanchnicus . Still, more research is needed to investigate this. Conclusion The microbiome refers to the millions of microorganisms on and within the human body that influence various physiological functions ranging from digesting food to outcompeting pathogens for resources. Also, the microbiome can affect the endocrine system, which consists of hormones that control glucose and reproduction, among other processes. This bridge, known as microbial endocrinology, has critical applications for understanding women’s health and growth disorders (microgenderome); this emerging area is growing, so it can address knowledge gaps in diseases like cancer and even improve other medical treatments. Written by Sam Jarada and Fozia Hassan The interactions between hormones and the microbiome, and Conclusion sections by Sam The microbiome, and Hormones and the endocrine system sections by Fozia Related articles: The gut microbiome / Dopamine and the gut / The power of probiotics / Vitamins REFERENCES “The Human Microbiome and Its Impacts on Health - PWOnlyIAS.” PWOnlyIAS , 18 Jan. 2024, pwonlyias.com/current-affairs/gut-microbiome-and-health/ . Accessed 17 Oct. 2024. Mittal, Rahul, et al. “Neurotransmitters: The Critical Modulators Regulating Gut-Brain Axis.” Journal of Cellular Physiology , vol. 232, no. 9, 10 Apr. 2017, pp. 2359–2372, www.ncbi.nlm.nih.gov/pmc/articles/PMC5772764/ , https://doi.org/10.1002/jcp.25518 . Accessed 17 Oct. 2024. Neuman, Hadar, et al. “Microbial Endocrinology: The Interplay between the Microbiota and the Endocrine System.” FEMS Microbiology Reviews , vol. 39, no. 4, 1 July 2015, pp. 509–521, academic.oup.com/femsre/article/39/4/509/2467625 , https://doi.org/10.1093/femsre/fuu010 . Hiller-Sturmhöfel S, Bartke A. The Endocrine System: An Overview. Alcohol Health and Research World. 2024;22(3):153. Available from: https://pmc.ncbi.nlm.nih.gov/articles/PMC6761896/ Neuman H, Debelius JW, Knight R, Koren O. Microbial endocrinology: the interplay between the microbiota and the endocrine system. FEMS Microbiology Reviews [Internet]. 2015 Feb 19 [cited 2024 Sep 18];39(4):509–21. Available from: https://academic.oup.com/femsre/article/39/4/509/2467625?login=false Jose Antonio Santos-Marcos, Mora-Ortiz M, Tena-Sempere M, José López-Miranda, Camargo A. Interaction between gut microbiota and sex hormones and their relation to sexual dimorphism in metabolic diseases. Biology of Sex Differences. 2023 Feb 7;14(1). He S, Li H, Yu Z, Zhang F, Liang S, Liu H, et al. The Gut Microbiome and Sex Hormone-Related Diseases. Frontiers in Microbiology. 2021 Sep 28;12. Siddiqui R, Makhlouf Z, Alharbi AM, Alfahemi H, Khan NA. The Gut Microbiome and Female Health. Biology [Internet]. 2022 Nov 1;11(11):1683. Available from: https://www.mdpi.com/2079-7737/11/11/1683 Jensen E, Young JA, Jackson Z, Busken J, List EO, Ronan O’Carroll, et al. Growth Hormone Deficiency and Excess Alter the Gut Microbiome in Adult Male Mice. Endocrinology [Internet]. 2020 Feb 26 [cited 2023 Nov 9];161(4). Available from: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7341558/ Jensen EA, Young JA, Mathes SC, List EO, Carroll RK, Kuhn J, et al. Crosstalk between the growth hormone/insulin-like growth factor-1 axis and the gut microbiome: A new frontier for microbial endocrinology. Growth Hormone & IGF Research. 2020 Aug;53-54:101333. Project Gallery

Comparative oncology Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link What can our canine friends tell us about cancer? 14/07/25, 15:12 Last updated: Published: 02/07/24, 10:04 Comparative oncology Comparative oncology is a field of study within cancer that has been adopted to study cancer and develop new therapies. It involves studying cancer in animals to uncover similarities between human and animal cancers. By combining scientific findings across a range of species, including companion animals such as dogs and horses or non-human primates such as monkeys, comparative oncology will advance cancer research and help develop effective novel therapies. This approach not only explores cancers in both animals and humans but also aims to bridge the gap between human and veterinary medicine. By examining similarities and differences in cancer biology, progression and treatment responses across species, comparative oncology provides valuable insights that can benefit both fields. Understanding how cancer behaves in animals can offer new perspectives and potential therapies for human patients. Conversely, while findings in human oncology can inform veterinary medicine, leading to improved diagnostics and treatments for animals. ( Figure 1 summarises the aims of comparative oncology). This article aims to explore this field of oncology further by discussing what it entails, the methodologies utilised, some recent advancements, and finally, things to look out for in the future. Comparative oncology has been developed and expanded into two areas of study. This includes spontaneous oncology and experimental oncology. Spontaneous oncology focuses on naturally occurring tumours in animals by investigating aspects of carcinogenesis, epidemiology, diagnosis, and treatment. It provides unique insights by drawing comparisons with human oncology research. These results can then be extrapolated to human oncology to gain a better understanding of cancer. This is because the similarities and differences observed in naturally occurring tumours across species provide valuable insights into underlying mechanisms within tumours and treatment responses. Experimental oncology serves as a distinct discipline where there are specialisations such as studying viral, chemical, and radiation oncogenesis alongside studying environmental factors such as pollution residues and food additives. This area involves studying both spontaneous tumours in animals and lab settings, where controlled conditions are used to explore different parts of cancer biology and treatment strategies. Additionally, the primary methodology utilised in comparative oncology involves studying spontaneous tumours in animals. Unlike artificially induced tumours in lab animals, these spontaneous tumours in pets closely mimic the complexity and heterogeneity of human cancers. For example, canines will live in similar living environments and experience similar external stimuli to their owner, such as pollution. The nature of these external stimuli means that they develop cancer in similar ways caused by epigenetic alterations, metabolic, and immune changes. (Figure 2 illustrates this process). Furthermore, comparative oncology uses advanced imaging techniques, genetic analysis, and immunological studies to predict pathways that may be shared among animals and humans which, could drive cancer development. Overall, these methods will allow the identification of promising therapies which directly target cancer and expand on current treatment choices such as chemotherapy and immunotherapy. One of the recent advancements in comparative oncology relates to osteosarcomas. This refers to cancer cells which begin to grow in the bones. For this specific form of cancer, molecular signatures were identified to predict clinical outcomes for both humans and canines, which can help improve treatment outcomes. Led by Amy K. LeBlanc, scientists have identified gene activity patterns in osteosarcoma tumours in nearly 200 dogs, revealing distinct groups with varying prognoses. These findings help us understand the biology behind osteosarcomas further and can potentially help us develop targeted therapies that take advantage of the immune system to treat the disease in both species. This potentially includes a range of therapies including PD-L1 inhibitors and cancer vaccines targeting the immune system. Moreover, breakthroughs in immunotherapies such as checkpoint inhibitors and CAR-T cell therapy are effective in treating haematological malignancies in both humans and canines. Furthermore, studies in canine melanoma reveal similar gene expression changes to human melanoma, such as in the PI3K/AKT/mTOR and MAPK pathways, even when the driver mutations are different. (Figure 3 shows how the pathway contributes to cancer). Useful data was provided in trials using companion animals with spontaneous tumours, providing an insight into safety, dosage, and efficacy, which have paved the way to develop treatments for both species. To conclude, it is clear with comparative oncology, researchers will be able to identify new molecular targets, assess novel drugs, and identify patient populations which will benefit the most from these therapies. It holds great promise in helping streamline cancer diagnosis further and even plays a role in preventing cancer. While the field shows great potential, more studies still need to be conducted to understand the similarities and differences in cancers between animals and humans. Additionally, more collaboration is needed amongst oncologists, veterinarians, and researchers across these disciplines to harness collective expertise to address questions relating to cancer diagnosis, treatment, and prevention. Ultimately, this field will help us identify new avenues of treating and diagnosing cancer whilst improving healthcare outcomes for humans and animals alike. Written by Harene Elayathamby Related articles: Why blue whales don't get cancer / Rare zoonotic diseases REFERENCES Schiffman, J.D. and Breen, M. (2015) ‘Comparative oncology: What dogs and other species can teach us about humans with cancer’, Philosophical Transactions of the Royal Society B: Biological Sciences , 370(1673), p. 20140231. doi:10.1098/rstb.2014.0231. Oh, J.H. and Cho, J.-Y. (2023) ‘Comparative oncology: Overcoming human cancer through companion animal studies’, Experimental & Molecular Medicine , 55(4), pp. 725–734. doi:10.1038/s12276-023-00977-3. Al, B. and C., C. (2007) ‘Chapter 1 COMPARATIVE ONCOLOGY ’, in Comparative oncology . Bucharest (RO): The Publishing House of the Romanian Academy, p. 1. Vail, D.M., LeBlanc, A.K. and Jeraj, R. (2020) ‘Advanced cancer imaging applied in the comparative setting’, Frontiers in Oncology , 10. doi:10.3389/fonc.2020.00084. New findings highlight shared features of human and canine osteosarcoma (2023) Center for Cancer Research . Available at: https://ccr.cancer.gov/news/article/new-findings-highlight-shared-features-of-human-and-canine-osteosarcoma (Accessed: 02 March 2024). Mochel, J.P. et al. (2018) Car T-cell immunotherapy in human and veterinary oncology: Changing the odds against hematological malignancies [Preprint]. doi:10.20944/preprints201811.0525.v1. LeBlanc AK, Mazcko CN, Khanna C. (2016) ‘Defining the Value of a Comparative Approach to Cancer Drug Development’, Clinical cancer research : an official journal of the American Association for Cancer Research , 22(9). p. 2133-2138. doi: 10.1158/1078-0432.CCR-15-2347 FIGURE REFERENCES Boddy, A.M., Harrison, T.M. and Abegglen, L.M. (2020) ‘Comparative oncology: New insights into an ancient disease’, iScience , 23(8), p. 101373. doi:10.1016/j.isci.2020.101373. Oh, J.H. and Cho, J.-Y. (2023) ‘Comparative oncology: Overcoming human cancer through companion animal studies’, Experimental & Molecular Medicine , 55(4), pp. 725–734. doi:10.1038/s12276-023-00977-3. Rascio, F. et al. (2021) ‘The pathogenic role of PI3K/Akt pathway in cancer onset and drug resistance: An updated review’, Cancers , 13(16), p. 3949. doi:10.3390/cancers13163949. Project Gallery

And its chemical effects Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Exposing medication to extreme heat 09/07/25, 14:09 Last updated: Published: 08/10/23, 16:18 And its chemical effects Introduction The majority of us look forward to when summer is just around the corner. It is a time for parents to start planning days off to be able to go on holiday with their kids to relax from their studies and enjoy sunsets at the beach. But for people who take medication, whether this just be a week-long course of antibiotics or for long-term conditions, summer may also be a chance for some negligence to occur. Specifically, alongside making sure you have applied SPF to protect your skin from the sun’s rays, you should also protect your medicine as well. This applies to both oral and non-oral drugs. Experts at The Montreal Children’s Hospital say that “many prescription drugs are very sensitive to changes in temperature and humidity”; in this article, we will therefore discuss the effect of extreme heat on drugs from a medicinal chemistry perspective. Factors affecting drug activity due to heat Certain drugs may begin to degrade before their expiry date if not stored appropriately. This affects the efficacy, which is the maximum biological response that is achievable with a certain drug. A dose-response curve can be plotted (see Figure 1 ) to show the relationship between the two variables; the label Emax refers to the efficacy. During hot weather, the structure of the drug can change and therefore unable to bind to its target, causing a lowered and shifted Emax to be seen. Simply put, the medication will not relieve your symptoms as effectively. Another physiochemical property of a drug that can be altered in the heat is the potency. Many people confuse this term with efficacy, but potency refers to the concentration of a drug required to achieve 50% of its maximum therapeutic effect i.e., half the Emax. Potency is therefore also known as EC50, which abbreviates for ‘half maximal effective concentration’. The lower the concentration needed, the more potent your drug is. Like reduced efficacy, the drug’s potency will also decrease in the heat due to altered chemical structure. For drugs like antibiotics, it is crucial to note that if potency is reduced significantly, it could risk infection spreading to other parts of the body as the medication will not fight off bacteria as well as it should. Potentially dangerous! Finally, drug absorption is when a drug moves into the bloodstream after being administered. The chemical structure of the drug and the environment in which it is present hugely affects this; for example, if a lipophilic (‘fat loving’) drug is also present in a lipophilic surrounding, fast absorption is seen as they work well with each other. As you have probably guessed, high temperatures outside of the body can reduce drug absorption due to the above factors mentioned, as the drug is not in its optimal structure to be absorbed effectively. Examples of medicine that are heat sensitive Here is a list of some medicines that require extra care to prevent the above: 1) Nitroglycerin – used to treat chest pains for those with cardiovascular disease. It is especially sensitive to heat or light as it degrades very fast. Dr. Sarah Westberg, a professor at The University of Minnesota College of Pharmacy, says you should follow the storage instructions and replace them regularly. 2) Some antibiotics – research has shown that ampicillin, erythromycin, and furosemide show a reduction in activity in the heat, although this was found after storing them for a year in a car with a temperature exceeding 25 degrees Celsius. Other antibiotics such as cefoxitin are shown to have some “stability in warmer climates”. 3) Levothyroxine – used to treat an underactive thyroid, also known as hypothyroidism. This drug should be stored between 15 to 30 degrees Celsius, although even 30 is quite high so the lower the temperature the better. Interestingly, levothyroxine isn’t heat sensitive itself, it is the fact that the body becomes sensitive to the drug and may make a person feel strange in the heat. 4) Metoprolol succinate – used to treat high blood pressure, also known as hypertension, and heart failure in emergencies . The ideal storage conditions for this drug are 15 to 30 degrees Celsius, like Levothyroxine. Key things to look out for with your medicine in the heat Below are the 2 main things you should be checking for before taking your medicine in the summer: 1) Change in colour – Light can initiate all sorts of reactions, such as oxidation. If, for example, your medicine that is normally white has now changed into a different colour, this suggests that a reaction has taken place within your drug and will not be effective when administered. 2) Change in texture – Similar to change in colour, if a normally solid, oral tablet has become soft then this also suggests that the medication will not be as effective when consumed. How you can prevent your medicine from degrading To make sure you do not contribute to wasting medicine, you should do the following: 1) Check storage information – for any medication that you take, this will let you know how to store them correctly. 2) Travel with care – do not pack prescription drugs into your luggage, as it will almost always become very warm due to the surrounding environment. Instead, carry your medicine with you with the labels still on. 3) Do not leave medicine in any vehicle – everyday vehicles such as cars tend to get warm after a period , which can affect the colour and texture of your medicine. 4) Careful deliveries – for those who have their medicine delivered to them, you can request for your local pharmacy to deliver your medicine in temperature-controlled packages. Summary As discussed, chemicals in the majority of over-the-counter prescription drugs are heat sensitive and should therefore be handled with care, to prevent degradation of the drug. Changes in colour and texture are signs of degradation, which result in loss of efficacy, absorption, and potency. However, many other pharmacological factors interfere, so scientists especially involved in drug synthesis should (or continue to) take great precautions with the manufacturing process. Drugs are costly to make and require a lot of time, so the takeaway is to store them correctly! You should contact your pharmacist if you are still unsure about your prescription(s). Written by Harsimran Kaur Sarai Project Gallery

A new theory suggests intelligence develops through reciprocal interactions between abilities Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link A primer on the Mutualism theory of general intelligence 11/12/25, 14:15 Last updated: Published: 10/10/24, 14:19 A new theory suggests intelligence develops through reciprocal interactions between abilities Introduction One of the most replicated findings in psychology is that if a sufficiently large and diverse battery of cognitive tests is administered to a representative sample of people, an all-positive correlation matrix will be produced. For a century, psychometricians have explained this occurrence by proposing the existence of g, a latent biological variable that links all abilities. G is statistically represented by the first factor derived from a correlation matrix using a method called factor analysis, which reduces the dimensionality of data into clusters of covariance between tests called factors. Early critics of g pointed out that nothing about the statistical g-factor required the existence of a real biological factor and that the overlap of uncorrelated mental processes sampled by subtests was sufficient. While the strength of correlations between subtests does generally correspond to intuitive beliefs about processes shared between them, this is not universally the case, and for this reason, sampling theory has never seen widespread acceptance. A new theory called mutualism has been proposed that explains the positive manifold without positing the existence of g. In mutualism the growth of abilities is coupled, meaning improvement in one domain causes growth in another, inducing correlations between abilities over time. The authors of the introductory paper demonstrated in a simulation that when growth in abilities is coupled the interaction between baseline ability, growth speed and limited developmental resources is sufficient to create a statistical general factor from abilities that are initially uncorrelated, offering a novel explanation for why abilities like vocabulary that are ‘inexpensive’ in terms of developmental resources explain the most variance in other abilities. Empirical evidence In the field of intelligence, mutualism has been tested twice among neurotypical children in the lab and once in a naturalistic setting with data from a gamified maths revision platform. Alongside these, a lone study exists comparing coupling in children with a language disorder and neurotypical children, however methodological issues related to attrition preclude it from discussion here. All studies used latent change score modelling (LCSM) to compare competing models of how intelligence develops over time. LCSM is a subset of structural equation modelling in which researchers compare the discrepancy between models of proposed causal connections between variables and their values in the real data using model fit indices. Three parameters resembling those used in the introductory paper’s simulations were used to represent causal connections between variables: the change score - wave #2 score minus wave #1 score of the same ability, the self-feedback parameter – the regression coefficient of baseline ability on the change score of the same ability and the coupling effect parameter – the regression coefficient of one ability at wave #1 on the change score of the other ability. The following models were compared: the g-factor model defined by the absence of coupling and growth driven by change in the g-factor, the investment model defined by coupling from matrix reasoning to vocabulary and the mutualism model defined by bidirectional coupling. Mutualism in the lab The first two lab studies investigated coupling between vocabulary and matrix reasoning in samples of 14-25 year olds and 6-8 year olds respectively. The mutualism model showed the best model fit in both studies albeit less decisively in the three wave younger sample, suggesting the stronger model fit of the first study may have been an artefact of regression to the mean. I think it’s problematic to interpret this as empirical support for mutualism due to issues that follow from only using two abilities. A g-factor extracted from two abilities may reflect specific non-g variance shared between tests as much as it does common variance caused by g. Adding to this ambiguity is the fact that the correlations between the change scores of the two tests after controlling for coupling and self-feedback effects were positive, reflecting the influence of an unmodelled third variable, be that g or unmeasured coupling. Another problematic feature of the studies comes from their model specification of the g-factor as being without coupling. This is despite the fact no latent change score modelling study of childhood development has ruled out that g may develop in a coupled or partially coupled manner. Studies using the methodology to study cognitive ageing have shown that some abilities are coupled whereas others are not suggesting that only sampling abilities that do show coupling may lead to a biassed comparison. Mutualism in the classroom Mutualism showed a marginally better fit than the investment model in explaining the development of counting, addition, multiplication and division over three years in a study featuring a sample of 12,000 Dutch 6-10 year olds using the revision platform Mathgarden. The change scores of each ability showed strong correlations after controlling for coupling and self-feedback effects. When considered in relation to the good model fit of the investment model, I believe this may reflect the standardised effect of the curriculum on the development of abilities independent of coupling and baseline ability. A finding with negative implications for mutualism from this study is the fact that the number of games played was not associated with any greater strength in coupling. This could reflect that coupling is a passive mechanism of development with little environmental input but it could equally reflect sorting of high ability students into a niche combined with self-feedback effects of their baseline ability impeding coupling. To observe the causal effect of effort on coupling after controlling for cognitive aging and the tendency of high ability people to train harder a randomised control trial of cognitive training is needed. Cognitive training Unfortunately, no cognitive training study has used latent change score modelling, meaning coupling must be inferred from the presence of far transfer (gains on untrained abilities), rather than directly estimated. COGITO’s youth sample resembled the first lab study to test mutualism in its age range and choice of fluid reasoning as a far transfer measure. Participants underwent 100 days of hour-long training sessions of working memory, processing speed and episodic memory. The authors found no near or far transfer gains for working memory and processing speed, possibly indicating developmental limits on their improvement. However, moderate effect sizes were found for fluid reasoning and episodic memory. The study’s results are lacklustre and developmentally bound but they offer an example of experimentally induced far transfer in a literature – in which it is a rarity – leaving open the possibility that the coupling effects observed in the lab studies were not mere passive effects of development. In contrast to COGITO which targeted young people at the tail end of their cognitive development, the Abecedarian Project started almost as soon as the subjects were born. Conceived of as a pre-school intervention to improve the educational outcomes of African Americans in North Carolina, the Abecedarian Project consisted of an experimental group that received regular guided educational play for infants aimed at building early language and a control condition which only received nutritional supplementation. At the entry of primary school, the experimental group showed a 7 point difference in IQ, which persisted in a diminished capacity at 4.4 IQ points by age 21. In contrast to previous early life interventions, in cognitive training studies and studies on the cognitive outcomes of adoption the gains were domain general rather than improvements on specific abilities. This provides causal evidence that if interventions are sufficiently early and target highly g-loaded abilities such as vocabulary they can induce cascades of domain-general improvement, a finding in line with the predictions of mutualism. It would be unfair to end this segment without mentioning perhaps the most standardised cognitive training regime there is: schooling. The causal effect of a year of schooling on IQ can be teased apart from the developmental effects of ageing by using a method called regression discontinuity analysis. In this method, the distance of a student’s birthday from the year cutoff for two year groups is used as a predictor variable alongside the school year in a multiple regression predicting IQ. A recent paper reanalysing data from a study using this method found that the subtest gains from a year of schooling showed a moderate negative correlation with their g loading. As mutualism states that g develops through coupling, this would lend credence to the view that coupling effects are passive mechanisms of g’s development rather than being inseparable from experience. Conclusion I believe that it’s more accurate to say there is evidence for coupling effects than it is to say there is evidence for mutualism. There is convergent evidence from a year of schooling effect, coupling effects not rising with the amount of maths games played and the COGITO intervention’s results that the environment has little causal role in coupling effects and their strength. Opposing evidence comes from the Abecedarian Project, however this is not an environmental stimulus to which most people will be exposed to. Therefore, more weight should be placed on the effects of a year of schooling because it is generalisable. To reconcile this conflicting evidence, future authors should seek to replicate the COGITO intervention in an early adolescent identical twin sample with co-twin controls. This would allow researchers to observe coupling effects while executive functions are still in development and give them a more concrete understanding of the self-feedback parameter grounded in developmental cascades of gene expression. A more readily available alternative would be to apply latent change score modelling to the Abecedarian Project dataset. I will end with a quote from a critic of mutualism, Gilles Gignac: I conclude with the suggestion that belief in the plausibility of the g factor (or mutualism) may be impacted significantly by individual differences in personality, attitudes, and worldviews, rather than rely strictly upon logical and/or empirical evidence. As the current evidence stands, this may be true, but with the availability of new developmental studies such as the Adolescent Brain Cognitive Development study and old ones like the Louisville twin study there’s less of an excuse than ever. Written by James Howarth Related articles: Nature vs nurture in childhood intelligence / Does being bilingual make you smarter? REFERENCES Carroll, J. B. (1993). Human cognitive abilities: A Survey of Factor-Analytic Studies . Cambridge University Press Rindermann, H., Becker, D., & Coyle, T. R. (2020). Survey of expert opinion on intelligence: Intelligence research, experts’ background, controversial issues, and the media. Intelligence , 78 , 101406. https://doi.org/10.1016/j.intell.2019.101406 Spearman, C. (1904). “General intelligence,” objectively determined and measured. The American Journal of Psychology , 15 (2), 201. https://doi.org/10.2307/1412107 Thomson, G. H. (1916). A hierarchy without a general factor. British Journal of Psychology 1904-1920 , 8 (3), 271–281. https://doi.org/10.1111/j.2044-8295.1916.tb00133.x Jensen, A. R. (1998). The g factor: The science of mental ability. Praeger Publishers/Greenwood Publishing Group Van Der Maas, H. L. J., Dolan, C. V., Grasman, R. P. P. P., Wicherts, J. M., Huizenga, H. M., & Raijmakers, M. E. J. (2006). A dynamical model of general intelligence: The positive manifold of intelligence by mutualism. Psychological Review, 113 (4), 842–861. https://doi.org/10.1037/0033-295X.113.4.842 Johnson, W., Nijenhuis, J. T., & Bouchard, T. J. (2008). Still just 1 g: Consistent results from five test batteries. Intelligence , 36 (1), 81–95. https://doi.org/10.1016/j.intell.2007.06.001 Project Gallery

Nanoparticles have unique properties Facebook X (Twitter) WhatsApp LinkedIn Pinterest Copy link Nanoparticles: the future of diabetes treatment? 17/07/25, 10:52 Last updated: Published: 06/05/24, 13:20 Nanoparticles have unique properties Diabetes mellitus is a chronic metabolic disorder affecting millions worldwide. Given its myriad challenges, there is a substantial demand for innovative therapeutic strategies in its treatment. The global diabetic population is expected to increase to 439 million by 2030, which will impose a significant burden on healthcare systems. Diabetes occurs when the body cannot produce enough insulin, a hormone crucial for regulating glucose levels in the blood. This deficiency leads to increased glucose levels, causing long-term damage to organs such as the eyes, kidneys, heart, and nervous system, due to defects in insulin function and secretion. Nanoparticles have unique properties making them versatile in their applications and are promising to help revolutionise the future of the treatment of diabetes. This article will explore the potential of this emerging technology in medicine and will address the complexities and issues that arise with the management of diabetes. Nanoparticles have distinct advantages: biocompatibility, bioavailability, targeting efficiency and minimal toxicity, making them ideal for antidiabetic treatment. The drug delivery is targeted, making the delivery precise and efficient, avoiding off-target effects. Modifying nanoparticle surfaces enhances therapeutic efficacy, enabling targeted delivery to specific tissues and cells, while reducing systemic side effects. Another currently researched key benefit is real-time glucose sensing and monitoring, which addresses a critical aspect in managing diabetes, as nanoparticle-based glucose sensors can detect glucose levels with high sensitivity and selectivity. This avoids the use of invasive blood sampling and allows for continuous monitoring of glucose levels. These can be functionalised and integrated into wearable devices, or implanted sensors, making it convenient and reliable to monitor and to be able to optimum insulin therapy. Moreover, nanoparticle-based approaches show potential in tissue regeneration, aiding insulin production restoration. For example, in particular, nanomedicine is a promising tool in theranostics of chronic kidney disease (CKD), where one radioactive drug can diagnose and a second delivers the therapy. The conventional procedure to assess renal fibrosis is by taking a kidney biopsy, which is then followed by a histopathological assessment. This method is risky, invasive, and subjective, and less than 0.01 % of kidney tissue is examined which results in diagnostic errors, limiting the accuracy of the current screening method. The standard use of pharmaceuticals has been promising but can cause hypoglycaemia, diuresis, and malnutrition because of the low caloric intake. Nanoparticles offer a new approach to both diagnosis and treatment and are an attractive candidate for managing CKD as they can carry drugs and enhance image contrast, controlling the rate and location of drug release. In the treatment of this multifaceted disease, nanoparticle delivery systems seem to be a promising and innovative therapeutic strategy, with the variety in the methods of delivery. The range of solutions that are currently being developed are promising, from enhancing the drug delivery to monitoring the glucose level, to direct tissue regeneration. There is immense potential for the advancement of nanomedicines, helping improve patient outcomes, the treatment efficacy, and allowing the alleviation of the burden and side effects of the disorder. With ongoing efforts and innovation, the future treatment of diabetes can be greatly helped with the use of nanoparticles, and these advancements will improve strategies for the management and future treatment of diabetes. Written by Saanchi Agarwal Related articles: Pre-diabetes / Can diabetes mellitus become an epidemic? / Nanomedicine / Nanoparticles on gut health / Nanogels / Nanocarriers REFERENCES Lemmerman LR, Das D, Higuita-Castro N, Mirmira RG, Gallego-Perez D. Nanomedicine-Based Strategies for Diabetes: Diagnostics, Monitoring, and Treatment. Trends Endocrinol Metab. 2020 Jun;31(6):448-458. doi: 10.1016/j.tem.2020.02.001. Epub 2020 Mar 4. PMID: 32396845; PMCID: PMC7987328. Dehghani P, Rad ME, Zarepour A, Sivakumar PM, Zarrabi A. An Insight into the Polymeric Nanoparticles Applications in Diabetes Diagnosis and Treatment. Mini Rev Med Chem. 2023;23(2):192-216. doi: 10.2174/1389557521666211116123002. PMID: 34784864. Luo XM, Yan C, Feng YM. Nanomedicine for the treatment of diabetes-associated cardiovascular diseases and fibrosis. Adv Drug Deliv Rev. 2021 May;172:234-248. doi: 10.1016/j.addr.2021.01.004. Epub 2021 Jan 5. PMID: 33417981. L. Tillman, T. A. Tabish, N. Kamaly, A. El-Briri F, C. Thiemermann, Z. I. Pranjol and M. M. Yaqoob, Review Advancements in nanomedicines for the detection and treatment of diabetic kidney disease, Biomaterials and Biosystems, 2022, 6, 100047. J. I. Cutler, E. Auyeung and C. A. Mirkin, Spherical nucleic acids, J Am Chem Soc, 2012, 134, 1376–1391. Veiseh, O., Tang, B., Whitehead, K. et al. Managing diabetes with nanomedicine: challenges and opportunities. Nat Rev Drug Discov 14, 45–57 (2015). https://doi.org/10.1038/nrd4477 Project Gallery