The mystery of orange cats decoded — with some help from cat parents
Anyone who has been called a 'crazy cat lady' or asked why they like animals that 'don't even show affection' now stands vindicated. Thanks to ailurophiles, a few weeks ago, science catwalked three steps ahead. Recent research by teams at Stanford University in the US and Japan's Kyushu University has found what gives orange cats their distinct colour — with the help of cat owners.
Despite knowing for over a century that the inheritance of the ginger colour in Felis catus is different from other mammals, cracking the code has not been easy because cats have been characteristically uncooperative, refusing to let researchers stick a cotton swab in their mouths to retrieve samples. As anyone with a cat will attest, it is nearly impossible to make the rebels of the animal kingdom do anything they don't want to. So researchers enlisted the help of the pets' human guardians. Their cooperation has helped uncover what makes Garfield and his fellow gingers possible: A small piece of missing DNA near the gene ARHGAP36. This unique mutation could hold the key to how mutations work in general, potentially deepening the understanding of genetic disorders in humans. These studies have also made apparent the value of engaging with the public in the pursuit of scientific progress .
Studies on cats have taken science far — a previous study found them to have 'perfect' genetic form, staying true to the ancestral animal despite centuries of breeding. That an active collaboration between science and society was made possible because of the affection cats share with their humans ought to shut down any debate on the subject. To all those who ask, 'Why cats?', the answer is now clear: For science.
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
NDTV
2 days ago
- NDTV
Researchers Eyeing Options Beyond US Can Look To This Country
With former US President Donald Trump back in power, the American research community is facing renewed uncertainty. Visa cancellations, abrupt funding cuts, and restrictive policies are pushing scientists and researchers to seek opportunities elsewhere. Amid this exodus, Germany has stepped in as a welcoming alternative-especially through its Max Planck Society. The Max Planck Society, one of the world's leading research networks, has seen a huge surge in applications from US-based researchers for its Spring 2025 intake. Notably, 81 women scientists from the US have applied this year, up from just 25 last year. The rise in applications from the US contrasts with stable numbers from other parts of the world, signalling a significant shift in researcher sentiment. Max Planck Society President Patrick Cramer revealed that nearly half of these new applicants are affiliated with leading US institutions such as Harvard University, Stanford University, MIT, the National Institutes of Health (NIH), and the University of California system. Funded by the German government, the society comprises 84 research institutes and operates on an annual budget of 2 billion euros. It currently hosts 39 Nobel laureates, and 20 new researcher positions are now open. The exodus of researchers is largely linked to the Trump administration's crackdown on international scholars. A controversial directive sought to ban institutions like Harvard from admitting foreign students. Although a federal court has temporarily blocked this move, the uncertainty has already triggered panic in academic circles. The broader global education and research community has taken notice. High-profile scholars such as Yale historian Timothy Snyder have resigned in protest and relocated to institutions abroad. Anticipating this wave of displaced researchers, Germany has launched a national initiative called "1000 Brains" to expand its research infrastructure and absorb global talent.
Time of India
5 days ago
- Time of India
Stanford longevity expert reverses his age by 10 years with one radical lifestyle shift
What would you do if your body was ageing faster than your birth certificate suggested? For Stanford University 's Dr. David Furman , a leading voice in the science of longevity , the answer lay not in pharmaceuticals or high-tech gadgets, but in nature — and a radical family experiment that turned their lives upside down. According to a report from The Mirror; in 2016, Furman found himself battling chronic migraines and the creeping toll of a stressful lifestyle in urban California. A pioneer of the 1000 Immunomes Project and an associate professor at Stanford, Furman decided to take a cellular deep dive into his own health. The revelations were troubling: though he was chronologically 39, his inflammatory age — a biomarker linked to disease and degeneration — clocked in at 42. As a scientist, he knew what that meant: a heightened risk of early ageing, cognitive decline, and chronic illnesses. As a father, he knew something had to change. by Taboola by Taboola Sponsored Links Sponsored Links Promoted Links Promoted Links You May Like Buy Brass Idols - Handmade Brass Statues for Home & Gifting Luxeartisanship Buy Now Undo Life in the Woods: From Headaches to Healing Furman packed up his life, wife, and two children and moved into a minimalist two-bedroom cabin nestled in Northern California's wilderness. Chairs were banned, industrial cleaners were out, and electricity usage was pared back to the bare minimum. By 7:30 every evening, all overhead lights were turned off and the family lived by candlelight, eschewing screens and devices in favour of analog living. Their daily routine included foraging, organic eating , and fitness rooted in nature. Furman, for instance, began each day with 10 to 15 pull-ups, caught fresh fish from a nearby creek, and snacked on hand-picked berries. Meals featured nutrient-dense, unprocessed foods — raspberries, broccoli, and wild greens became the norm. The lifestyle wasn't just a retreat — it was a rigorous biological experiment, and Furman was both subject and scientist. The Stunning Results: Turning Back the Clock Three years later, Furman ran the same cellular test that once gave him a wake-up call. The results were staggering: his inflammatory age had dropped to 32. In other words, he had turned back the clock by a full decade. Gone were the migraines, replaced by sharper focus, sustained energy, and what Furman describes as 'a lot of productivity.' His academic output surged — he published three research papers in a single year, and felt, in his own words, 'better than ever.' Science Says: Nature Really Does Heal Furman's forest-bound lifestyle wasn't just a personal success story; it echoed a growing body of global research. A 2019 study on 'forest bathing' revealed that time spent in green spaces significantly improves health outcomes and mental wellbeing — even for those with chronic diseases or disabilities. The magic number? Just two hours a week in nature, according to researchers from the University of Exeter. These sessions didn't need to be in remote woodlands — urban parks and beaches had similar effects. What mattered was immersion and consistency. Dr. Mathew White, a wellness researcher at Exeter, underscored the findings: 'It didn't matter where in nature you went... 60 or 90 minutes didn't seem to have the same benefits. It really needed to be at least two hours a week.' Furman's journey is both inspiring and instructive — a testament to the power of nature, simplicity, and conscious living. While not everyone can relocate to the woods, his story invites us to rethink the architecture of our daily routines. Could reversing ageing be as simple as switching off your phone, walking in a park, and eating what the earth gives you? For Dr. David Furman, it wasn't a theory — it was his life. And it changed everything.
The Hindu
29-05-2025
- The Hindu
Major study says malaria reinfection creates special immune cells
In a groundbreaking discovery that could reshape our understanding of the immune system and pave the way for revolutionary new vaccines and drugs, scientists have characterised a previously less-understood immune cell with powerful regulatory functions. They have found that immune cells called T R 1 cells play a dominant role in mounting an immune response to malaria. The implications of the study, published in the journal Science Immunologyon April 25, are far-reaching, potentially opening new pathways to conquer not only malaria but many other 'difficult' infections for which we currently lack effective vaccines. Lines of defence The human immune system has a complex multi-layered defence against infections. Its arsenal of weapons includes numerous components and subcomponents with precisely defined tasks to execute. They must also coordinate with each other to ensure the response is effective and minimises self-harm. When an infectious agent breaches the first layers of defence (skin and mucosae), specialised arms of the immune system respond. The first among them is innate immunity: it acts against any threat non-specifically, while activating other arms of the system, which are collectively called adaptive immunity. In addition to acting against a threat, adaptive immunity stores a record of the molecular signature of the threat, or antigen, with help from the memory cells. Every antigen has specific memory cells. When they recognise an antigen they've encountered before, they accelerate and enhance the immune response. This adaptive immunity has two important subcomponents. Antibody-mediated humoral immunity is mediated chiefly by B-cells while cell-mediated immunity involves the T-cells. The real heroes The new study, led by Jason Nideffer of Stanford University, focused on a subtype of T-cells called CD4+ cells. They are also called helper cells because they help activate B-cells, T-cells, and immune cells like macrophages during an immune response. The team examined helper cells in children and adults who have suffered malaria multiple times. One subset of helper cells are the type-1 regulatory T-cells, or T R 1 cells. Another subset of helper cells are the T H 1 cells. The study was conducted in eastern Uganda, where the malaria parasite Plasmodium falciparum (Pf for short) is perennially transmitted. Ugandan children under 5 years of age often suffer three to five episodes of malaria every year. After multiple episodes, they become clinically immune by about 10 years of age: i.e., they don't develop symptoms despite getting infected by Pf again. The researchers have surmised that Pf-specific helper cells play a crucial role in developing this clinical immunity. Specifically, for many years, malaria textbooks said that the human body responded to a Pf infection by mounting a 'classic' immune response mediated by CD4+ T H 1 cells. But by sequencing more than 500,000 single CD4⁺ T-cells and tracking their genetic barcodes, the researchers found that T R 1 cells are the real heroes. While they make up only around 3% of resting CD4⁺ cells, they account for almost 90 % of all Pf-specific helper cells. This forces us to rethink what an effective anti-malarial T-cell response looks like. Technique that turned tables The research team took advantage of an ongoing three-year study called Malaria in Uganda Systems Biology and Computational Approaches study (MUSICAL). The study is trying to understand malaria in Uganda using advanced systems biology and computational approaches. Investigators follow the participants with regular surveillance, including blood smear, quantitative PCR tests, peripheral blood mononuclear cell sampling. In the new study, the researchers tracked helper-cell clones through multiple infections in humans to assess their long-term stability and the efficiency with which they could facilitate an immune response inside the body over hundreds of days. (Helper cells that respond to the same antigen are said to be clones of each other.) The first unique feature of the study was its longitudinal nature. All previous studies on the subject have been cross-sectional, i.e. studying a population at one point in time. Longitudinal studies are more challenging since they require repeated biological sampling, active case-finding, and long-term follow-ups of participants. The researchers used an advanced technique called single-cell RNA and T-cell receptor (TCR) sequencing to track the relative proliferation of different CD4+ T-cell clonotypes (clones derived from the same ancestor cell), their changes afterwards, and whether they multiplied in the same ways after every infection. Together, these data connote the cells' memory potential (how well they remember) and clonal fidelity (how well they make copies of themselves). This was the second unique feature of this study. Previous studies on the CD4+ T-cell response to malaria were based on characterising them using enzyme-linked immunosorbent spot assays or flow cytometry-based approaches, which have many inherent limitations. As a result, researchers have thus far had trouble confirming whether the T R 1 cells induced by malaria were a bona fide class of helper cells distinct from other T H 1 cells. Follow the barcode By sequencing memory CD4+ T-cells before, during, and multiple times after repeated episodes of malaria, the researchers acquired an unbiased picture of CD4+ T-cells' memory in the body. To perform its specific functions, each cell needs specific proteins. The sequencing technique reveals which proteins a cell is making. Call it a genetic barcode that the sequencing reads to reveal the cell's current state. The team found that nearly all clonotypes displayed a strong preference for one of seven subsets of CD4+ T-cells. This finding was made possible by the team's use of single-cell genomics in vivo. Perhaps the biggest finding was that the T R 1 cells also displayed high average clonal fidelity. The study also identified T R 1 cells as the dominant CD4+ T-cell subset induced after paediatric malaria and that they are capable of long-term memory with clonal fidelity upon reinfection. Sequence samples in the same individuals also revealed many clonotypes at multiple time points that retained their fidelity for hundreds of days. The researchers used each T-cell's barcode TCR sequence to keep track of 'who was who' as the cells went from a calm, resting state to a revved-up, activated state. The technique let them see — without any guess-work — which genes flipped on universally and which flipped on only in, say, T R 1 cells. It revealed the presence of fresh subset-specific genes. It also showed that while helper cells 'shouted' by expressing the TNF and IL-2 genes, regulator cells hit the brakes by expressing the FAS gene. The researchers also conducted another test that likened the seven CD4⁺ T-cells subsets to an army with seven regiments. When they blew a loud horn, every soldier charged forward. But when they waved a specific enemy flag — in this case, Pf-infected red blood cells — only one regiment, the T R 1 peacekeepers, stepped forward. These T R 1 troops are normally a small minority yet almost all malaria-recognising T-cell badges belonged to them. In other words, people who have never fought malaria don't have that regiment, so nothing much happens when their cells see the specific flag. In sum., the researchers were able to verify that T R 1 cells mounted a focused, antigen-specific response to blood-stage malaria and not a broad, nonspecific reaction. With longitudinal follow-ups, researchers found that T R 1 cells' abundance increased with every infection — even when the second infection occurred hundreds of days from the first — and more than tripled after a few infections. The abundance also correlated with the frequency of Pf parasites in the blood, suggesting that the T R 1 cell response depends on the antigen load. Although the abundance also dropped a bit from the peak once an individual recovered from an infection, it still maintained higher baseline levels in clinically immune individuals. In fact, even though a subset of helper cells called T H 1 cells also clonally expanded after a symptomatic infection, they didn't expand upon reinfection — whereas the T R 1 helper cells did. This suggested that the T H 1 cells are likely not Pf-specific and that their expansion after the first infection was unrelated to the infection being malaria. The finding is important because it almost completely negates a suggestion from previous studies that malaria primarily induces a T H 1 response. The researchers also found some preliminary evidence to suggest that the T R 1 cell response is encoded epigenetically, meaning the response is controlled in a way that is independent of the genes. Gene-expression studies of T R 1 cells showed that there are distinct subgroups of these cells: naïve-like T R 1 cells, effector T R 1 cells and memory T R 1 cells. The expansion and contraction of these subpopulations during and after symptomatic infections proved that these are functionally distinct entities and validated the memory potential of individual Pf-specific T R 1 clones. Tuning the immune system These insights into the immune response against malaria are likely to be game-changers: in approaches to prevent or manage malaria infections as well as in terms of opening new avenues to interrogate certain diseases and how our bodies respond to them. For example, by proving that T R 1 cells are the ones to follow during a malaria reinfection, the study offers new ways to develop effective vaccines against malaria. If T R 1 cells take centrestage, and given how they work, they may be helping the body carry Pf parasites without falling severely ill. Their specific role also opens the door to host-directed therapies, i.e. improving treatment outcomes by 'tuning' the immune system rather than targeting the pathogen itself. The findings may also open new avenues of research into the immunology of other infectious diseases and new ways to conquer them. Puneet Kumar is a clinician, Kumar Child Clinic, New Delhi.
