loss

“The greatest obstacle in life is the wait for tomorrow and the loss of today”

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Neither war, nor hunger, nor love. Nor hate, friendship or illness. If there is something that has really bothered us humans throughout the centuries, it is the passage of time. We all (from the richest to the most miserable) come into the world with our days scheduled. Sooner or later we run out of rope without anyone being able to prevent it. It’s that simple. In fact (and for cruel ironic as it may sound) that is one of the very few certainties that we can embrace during our existence, be it more or less extensive: there is no life without death. It’s nothing new. Centuries ago philosophers realized that, in a way, as our lives progress so does our death. If time is short must be valuable (just as happens with precious metals or gems) and everything valuable always brings a challenge. How the hell do you manage it? How to get the most out of it? What’s more, why try to get ‘the most out of it’? Are those who insist on making something of their time happier? useful and helpful Who do you see spending your days lying on the beach? Seneca to the rescue A few centuries ago, around the year 55 AD, there was a Latin philosopher (born in Cordubawhat is now Córdoba and then acted as the capital of Hispania Ulterior) who raised these same questions. His name was Lucius Anneeus Seneca and the answers he found were captured in works such as ‘De brevitate vitae’a text dedicated to a certain Paulino (his father-in-law or brother-in-law) in which he outlines a series of advice. One of the most famous can often be seen in the anthologies of aphorisms: “The biggest obstacle in life is the wait for tomorrow and the loss of today“. The phrase connects with the old maxim of tempus fugit (“time flies”), although there is more to it than may seem at first glance. In it, Seneca addresses one of the most complicated challenges for those who have set out to ensure that time does not slip through their fingers: the balance between the present and the future. A present that is our only certain reality and a tomorrow that will in turn be conditioned by what we do today. In other words, do we bet everything on the present or is it wiser to condition it with tomorrow in mind? They were interesting questions in Rome in the first century AD and they remain so today, twenty centuries later, in procrastination times in which the equation becomes even more complicated. At the end of the day, procrastinating is nothing more than setting traps in time management: deferring, postponing, delaying the moment in which we must carry out a task that (usually) will be beneficial for our future. Seneca’s starting point is as suggestive as it is challenging. Our time may be limited, but that doesn’t mean life is necessarily short. If it seems that way, it is because we ourselves favor it by facing it in the wrong way. And that doesn’t just happen by lying on the couch with your cell phone to kill the hours abandoned to the pleasure of the infinite scroll. For Seneca, the outlook is not much better if we obsess over tasks that make us believe that we do not have enough hours in the day, but in reality they are unimportant. “We don’t have a shortage of time, what happens is that we lose a lot. Life is long enough and to do the most important things it has been generously given to us, if all of it is used well.” “But if it is scattered in ostentation and carelessness, where it is not spent on anything good, when at last the inevitable final trance comes upon us, we realize that a life has passed that we did not know was happening.” “It is like this: we do not receive a short life, but rather we make it short“, concludes the Stoic thinker, who died in 65 AD, aged about 70. The complete reflection that Seneca dedicates to Paulinus and from which the phrase we previously cited about “the loss of today” is extracted is more devastating because it warns of how easy it is to give in to the mirage that we are taking advantage of time. Here we reproduce specifically the translation made by Francisco Socas Gavilán for the version of the Virtual Library of Andalusia. “Can there be anything more stupid than the attitude of some, I mean those men who presume to be far-sighted? They are engaged in too many tasks to be able to live better, they equip life by spending life, their thoughts direct them to the distance. But, of course, the greatest waste of life is procrastination: it cancels each day that is presented, it hides the present while promising what lies ahead.” “The greatest hindrance to living is the expectation that depends on tomorrow and loses what is today. You dispose of what is in the hands of luck, you abandon what is in yours. Where do you look? Where do you orient yourself? All future things remain uncertain: live immediately.” Seneca’s work resonates strongly twenty centuries later because, as remember Socasnot only tells us about death and the passage of time, but also about “life as a positive realization within a limited scope.” “Even though men can’t stop complaining about the brevity of lifethey alone are the real culprits of shortening it with their laziness and vices. “We waste time and do not consider it the greatest and only good,” duck. “The solution will be neither hyperactivity nor laziness, because those who are very busy, always thinking about tomorrow, do not take advantage of their time and are soon surprised by old age, while in idleness passions and amusements rob us of our intimate peace,” comments Socas after remembering Seneca’s words. “The idle fear death more. The busy will not be able to … Read more

In 1845, John Franklin’s expedition set sail in search of the Northwest Passage. 180 years later his loss remains a mystery

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On the morning of May 19, 1845, Captain John Franklin and his expedition weighed anchor from the Greenhithe Harboralmost at the mouth of the Thames. They were looking for the Northwest Passagethe (at that time theoretical) maritime route that would link the Atlantic and the Pacific through northern Canada. They never came home. 129 men who never returned and who, for 170 years, have been one of the great questions of scientific and naval exploration. We now know why the men of John Franklin’s lost exploration died. There are those who insinuate that the trip started badly from the beginning. It should never have been in the first place. John Franklin. The first option William Edward Parryone of the great English explorers, but he had already traveled to the Arctic five times and “was tired.” So he declined the offer. Secondly, they thought about James Clark Ross. Ross has just arrived from Antarctica where he had explored the Ross Sea and Island. In fact, the ships on that expedition were the same as those that would be used on this mission (two of Ross Island volcanoes They are called Erebus and Terror in honor of the ships). But upon returning to England, he became engaged to his future wife and decided that great explorations were no longer for him. He was followed by James Fitzjames (discarded due to inexperience), George Back (considered too controversial) and Francis Crozier (who, well, was Irish and that was more than enough reason to rule him out). Seeing the yard, John Barrow, second secretary of the Admiralty, called John Franklin. To this day no one knows why Franklin, who was already a legend at the time and was almost 60 years old, he said yes. But the fact is that, as I said, they left the vicinity of London that day in 1845. They stopped in Orkney and the convoy formed by the two main ships (HMS Erebus and HMS Terror), the HMS Rattler (the first English warship with steam propulsion) and a transport headed to Greenland. There they sacrificed ten oxen and the expedition began its solo journey. The search for the Northwest Passage The travels of Marco Polo are a peculiar book. Not only does it remain a very interesting precedent for current anthropology, but it served as an inspiration for many during the era of great exploration. The image you can see above is precisely the annotated copy of ‘The Voyages’ that Christopher Columbus had. In one of its versions, the Italian one from 1559, a Chinese province called Anian. We assume that it was from there that the geographers and explorers who discussed whether America was a new continent or, on the contrary, an Asian peninsula, got the name of the Strait of Anian, the separation between Asia and America that would give access to the Northwest Passage. It is what we know today as the Bering Strait and for years it was pure mythology. But, first, Ferdinand Magellan and his crew turned around Cape Espiritu Santo and found themselves face to face with the southeastern passage; and, second, a Dane in the service of Russia, Vitus Beringrediscovered for the West the strait through which Semyon Dezhniov had already traveled sixty years before. The rest was geopolitics: the quick passage to the Pacific without having to pass near the Spanish territories in America was too juicy. In 1745, an English law promised 20,000 pounds to whoever discovered the pass and the boom began. I have tried to convert the amount to a current currency and I have not been able to do it accurately, but I have drawn one conclusion: it was a lot of money. Favorable weather In early August 1845, two whalers, the Prince of Wales and the Enterprise, encountered Franklin’s ships in Baffin Bay. They were waiting for favorable weather to enter the Strait of Lancaster. That was the last time they were seen. Two years passed. And, little by little, Lady Jane Franklin, some members of Parliament, and the fledgling British press began to ask the Admiralty to send someone to search for the heroes of Franklin’s expedition. The Government sent three expeditions: one by land and two by sea, one through the Atlantic and another through the Pacific. They failed. Fearing that they would be forgotten, Lady Jane Franklin composed her lament, the song you can hear just above. And, although I don’t know if it was for that reason, the truth is that was not forgotten. In fact, the search for the lost expedition “became nothing less than a crusade.” In 1850 alone, eleven British and two American ships tried to locate them. It was then that the first tombs were found. Over the years, the different expeditions found fragments, Inuit stories and objects from the expedition. In 1855, following the indications of some Inuit tribes, pieces of wood were found with the name of Erebus. In 59 two messages were found. The first, dated May 28, 1847, was from Franklin himself and read “Sir John Franklin, Commander of the Expedition: All Well.” It is the document on the right. It was a common practice at the time, documents were left in different places so that, in case of problems, they could be reconstruct the details of the trip. But in this case, something curious happened: on the edges there was another message, dated April 25, 1848, explaining that the ships had been trapped in the ice. Franklin and twenty-three other crew members were dead. And the rest, the survivors, had abandoned the ships looking for an exit to the south. In the next few years some objects, some rumors and some tombs appeared. Nothing else. The ships never appeared and we never, in 150 years, discovered what had really happened to Captain John Franklin’s lost expedition. One hundred and fifty years without news In the 1980s, the University of Alberta launched a project to track the expedition. The different possible routes were traveled … Read more

The buzzword in the world of sports and weight loss is “autophagy.” Sounds good, the only problem is that it’s bullshit

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On December 7, 2016, Yoshinori Ohsumi He stood on the stage of the Medical Classroom of the Karolinska Institute in Stockholm and began to explainin detail, “the discoveries of the mechanisms of autophagy.” Three days later, in front of a completely packed auditorium, won the Nobel Prize in Medicine and Physiology. Now, dozens of people are dedicated to using these mechanisms to lose weight. Isn’t it a beautiful example of the value of basic science? It would be, in fact, if it weren’t for the fact that it’s all a hoax. Autophagy exists. Of course yes: as I say, the 2016 Nobel Prize went to its discoverer. It is a cellular mechanism that recycles damaged components. We know that when nutrients are lacking or there is stress, the cell wraps parts of itself (damaged proteins, old organelles like mitochondria) in double-membrane vesicles called autophagosomes, which fuse with lysosomes to degrade and reuse those components. It is something essential in cellular life. Basic, essential: essential to preserve the functionality of tissues throughout life. This maintains internal well-being, obtains extra energy or materials and contributes to cellular defense. It reaches such a point that a few days ago, the journal Nature Immunology explained in detail how all this is a fundamental piece in longevity. What’s the problem then? Measuring its effect on humans is complex. After all, direct markers They are difficult to grasp outside of biopsies or highly controlled laboratory conditions. Indirect markers abound, yes; but they are not very specific. This makes us know that prolonged fasting activates the mechanisms of autophagy, yes; but we don’t know anything about anything like intermittent fasting or any type of diet doing that. In fact, even when we can see increases in autophagy gene expression, we cannot make the leap to clinical benefits. So… Can it be used, then, to lose weight? Well no. The truth is that selling it as a “trick” to lose weight is going too far: weight is lost due to a caloric deficit, not by “eating yourself.” Ultimately, all the examples given are nothing more than the extrapolation of isolated cellular models. There is no no kind of scientific evidence that endorses any of that. The only thing we know about autophagy at a clinical level is that, well, it sounds good: it sells. And, really, that’s enough. Saving the distance, ‘autophagy’ is the new ‘quantum diet’: something that sounds scientific, that has the endorsement of the community of experts and that means absolutely nothing. A perfect breeding ground for charlatans. Is it a scam then? I wouldn’t say that much. What’s more, we may find out in the next few years that autophagy mechanisms do indeed do things in normal diets. The important thing is that, along the way, all those who want to take advantage do not destroy the credit that Oshumi achieved with his revolutionary work. Image | Marco Vitiello In Xataka | The lies of the nutritional pyramid: from pedagogical tool to corporate battleground

We have discovered the “button” that activates our hunger. And it is the next revolution in weight loss medications

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In the molecular complexity that reigns in our body with the aim of controlling all its processes, Weight and appetite are undoubtedly one of the most complicated to keep under control.. Now, an international team of scientists has shed light about a molecular mechanism that acts as a master modulator, changing the way our brain processes hunger and satiety signals. Something that can give rise to new medications such as the famous Ozempic. The study. Published in the journal Nature, this research focuses on a key player in our metabolism: the melanocortin-4 receptor or MCR4. In this way, you can think that MCR4 is the “guardian of appetite” because it is nothing more than a protein present in our neurons that, when activated, tells us that we are satiated and that it is time to burn energy and reduce food intake. However, the operation is not as simple as the switch that turns the light on or off in our house. This is where its lesser-known, but crucial, partner comes into play: the MRAP2 accessory protein. The big change. Until now, it was known that the MRAP2 protein interacts with MC4R, but the consequences of this relationship were not fully understood. The new research reveals that MRAP2 has a drastic effect on the behavior of the appetite guardian and this is where the role it may have as a therapeutic target comes into play. What was known until now is that MC4R receptors tend to clump together on the surface of cells, forming “oligomers” or, to simplify, working in pairs or groups. Now the study shows that when MRAP2 enters the scene, it breaks these bonds and forces the MC4R receptors to act as “monomers”, that is, alone. A priori, the fact of going from being paired to acting alone may be insignificant, but the consequences it has are enormous and completely modify the recipient’s response to stimuli. Boosts the main signal. This is one of the effects caused by the MRAP2 interaction in this equation. Specifically, it has been seen that when it is in a monomeric state, MC4R becomes much more efficient in activating signaling pathways mediated by the G protein. This means that, with the same amount of stimulus (the α-MSH hormonewhich makes us feel satiated), the cell’s response is considerably stronger. Cancels stop signal. Normally, after activation, the receptors recruit a protein called β-arrestin2, which acts as a brake: it stops signaling and causes the receptor to be internalized, removing it from the cell surface to “reset” the system. Surprisingly, MRAP2 impairs this process. It hinders the recruitment of β-arrestin2, which in turn reduces the internalization of the receptor, so its ligands can bind to it in a much simpler way. The receiver on the front line. By preventing the receptor from entering the cell, MRAP2 allows MC4R to remain on the cell surface longer, ready to continue receiving signals. It’s like keeping a soldier on the front lines of battle instead of sending him to rest. In summary, MRAP2 acts as a “tuner” that modifies the MC4R receptor, biasing its function toward more potent and sustained G protein-mediated effects, while disabling its own braking system. The importance. Once this process has been understood, we move on to its importance in the clinic. The first thing that has been seen is that mutations in the MRAP2 gene are associated with cases of severe obesity in humans. This study provides for the first time the detailed molecular mechanism that explains why. Bottom line, if MRAP2 isn’t working properly, the MC4R “appetite keeper” doesn’t get that extra boost, becoming less efficient and contributing to an energy imbalance. These findings open a new avenue for drug development. Instead of looking for molecules that simply activate or deactivate MC4R, one could now think of therapies that modulate the interaction between MC4R and MRAP2. We could design treatments that mimic the effect of MRAP2 to enhance the satiety signal in people with obesity, offering a much more sophisticated approach tailored to the biology of our body. More drugs. Right now on the market we have different treatments that are focused on those people who have the most problems losing weight. We talk especially about GLP-1 agonists such as Ozempic or Mounjaro, which have given good results. But on the horizon we can see that they will not be alone and many others will arrive. Images | i yunmai Drew Hays In Xataka | Solving one of the great myths of losing weight: if “walking quickly” works by itself to lose weight

How to activate spotify Hifi and configure loss -free quality

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Let’s explain How to configure losses without losses in spotifyso that you can make the most Spotify Hifi. This service is already beginning to be available in Spain, and if you are a premium user of the service you will soon begin to receive the notification that warns you. Remember that the quality of Spotify Hifi is the so -called improved CD quality or Lossless. Is 24-bit/48 kHz compared to 16-bit/44.1 kHz, although It is a lower quality to the hi-re lossless offered by others competition services. Even so, for most users it should be more than enough. It should also be remembered that You will not enjoy the HIFI if you use bluetooth headphonessince this technology is not able to transport the amount of data offered by this audio quality. You will need a device compatible with spotify Connect or quality headphones and wired connection, and even in many cases it will cost to notice the difference. How to activate and configure Spotify Hifi To configure spotify Hifi at any timeyou have to enter the application configuration, either on the mobile or desk. Click on your profile image to see the options, and in them click on Configuration. Once inside, click on the option Multimedia content quality That will appear inside. This will take you to options where you have three adjustments where you can configure the lossless audio as sound quality. You will be able to do it when playing music with Wifi, when playing music with your data rate, and when you download music. Keep in mind that the sound quality is almost 10 times better than until now, which means that the songs music files are also almost ten times larger. My recommendation is that you consider not using the HIFI with your data rate. First for data spending, but also because surely when you leave home you listen to music through Bluetooth, and because even if you do not do it, between external noise and others you can not perceive the difference so much. Therefore, I recommend activating this quality for when you play music with the WiFi, because you will not spend so many data. AND Also in downloadsalthough if you are going to do it, I recommend that you disable the option to download songs using the data rate, to only be able to do it with WiFi. In the Apra Desktop application everything is exactly the same, only that you only have to Configure the section of Audio quality. Here, you can open the options of Streaming quality and Dischargeand in them choose the option of Loss without loss. But When you activate spotify HIFI for the first time Everything will be easier, because you will appear a full -screen message warning you. And then you just have to press on the button Access quality without lossand advance until reaching the sound quality configuration of the service. In Xataka Basics | 14 apps and services to discover new music in Spotify, Apple Music and other streaming services

The loss of the Broadcom chips factory is a malazo for Spain. Now you have to trust everything to your plan B

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For Spain lose the packaging plant Integrated circuits that Broadcom was going to build on Spanish soil is a real maza. And it is for several reasons of weight. The most obvious is that the presence of a factory of this American company would place the country on the European map of The production of advanced substrates. And, in addition, presumably would generate high qualification jobs, would develop the technological ecosystem of the area in which new investment would finally be installed and attracted. As we explain yesterday, this project finally It will not come to fruition. The leaks ensure that the negotiation held by the Spanish government and the Broadcom directive since July 2023 entered a man -dead point several months ago. There is no doubt that it was a very interesting plan for Spain, but, fortunately, it is not the only project that seeks to develop the local semiconductor industry and increase the relevance of Spanish companies in the global market of integrated circuits. These projects give Spain the opportunity to grow in the chips industry The installation that we can see in the cover photography of this article is the authentic protagonist of one of the most important projects that Spain is developing in the sector that concerns us: INNOFAB. The image building is the Alba synestron, which is housed in the Catalan town of Cerdanyola del Vallès, just 6 km from the center of Barcelona. And his role in the Innofab project will be crucial. An note before moving forward: a syncrotron is an electrons of circular electrons used to analyze atomic level the properties of matter, such as various types of materials, or even proteins. The Spanish institution that is involved in this Plan is the Barcelona Microelectronics Institute belonging to the CSIC (IMB-CNM-CSIC), a center that has a lot of experience in both microelectronics and in advanced techniques for integrated circuit manufacturing. INNOFAB will be a state -of -the -art semiconductor factory which will be housed next to the Alba syrrtron. It will cost approximately 392 million euros and will be financed with funds from the Next Generation Plan of the European Union, as well as with capital contributed by the governments of Spain and the Generalitat. Innofab’s construction works will begin soon with the purpose of the plant starting chips production in 2028 Construction works will begin soon with the purpose of the plant starting chips in 2028. This project is led by the Catalan Institute of Nanoscience and Nanotechnology, and will reside very close to the Autonomous University of Barcelona. Its purpose is to develop, as I have mentioned a few lines above, next -generation integrated circuits, but it will not be conventional chips; They will be semiconductors in which advanced materials, such as graphene, will be used to unmark silicon semiconductors whose production It is controlled by Asia and the USA. When the INNOFAB factory is ready, the ALBA particle accelerator will allow to analyze the candidate materials to be used in the production of semiconductors atomic. And also the properties of integrated avant -garde circuits. An important note is that Innofab will not produce chips in large quantities; Your role will be to develop advanced technologies which will then be commercially exploited in other plants. This role in a way justifies that its cost is somewhat less than 400 million euros. In any case, Innofab is not the only project dedicated to the chips that Spain is developing. The Godic plan It seeks to develop the necessary technologies to make possible the large -scale manufacture of polyristaline silicon carbide. This initiative is framed within the belonging of microelectronics and semiconductors (popularly known as the chip) and has a budget of 3.3 million euros to which the State contributes by assuming 68% of the total cost. It sounds good, but there is more than we should not overlook: the reason why this project is so important to Europe and Spain. The Godic plan seeks to develop the necessary technologies to make possible the large -scale manufacture of polyristaline silicon carbide The current situation of tension in geopolitical and geostrategic fields That they support the US and Europe on one side, and China to the other, it is promoting that the old continent is doing everything in its hand to reinforce its supply chain linked to the integrated circuit industry. Its purpose is put an end to its deep dependence of Asian suppliers in general, and of China in particular, so having a manufacturing plant of their own silicon carbide is crucial on the road to this objective. It is for Spain and also for Europe because it currently lacks this resource. The Diosic project began its journey at the end of 2023 and will last 26 months, so presumably the Spanish companies involved in it will conclude the development of innovations that are necessary to carry it forward in early 2026. Or, perhaps, if everything goes like silk, at the end of 2025. Anyway it is important that we do not overlook that beyond consolidating the independence of Spain and Europe Cost of the production of integrated circuits by 30%, and, at the same time, increase their yield by 35%. Before concluding this article, it is worth not overlooking another project that is also very important for Spain: the set -up The new European pilot line that pursues Lead the integration and encapsulation of components and electronic systems. The Spanish institution that is involved in this plan is the CSIC Barcelona Microelectronics Institute (IMB-CNM-CSIC), a center that has a lot of experience in both microelectronics and in advanced techniques for manufacturing integrated circuits. Any initiative that increases the competitiveness of Europe in a strategic industry such as semiconductors must be welcome “We intend to work on two approaches depending on whether the evacuation of high heat densities is required, as in the case of the ASIC, or if what is sought is a homogeneous distribution of temperature, more applicable to … Read more

Reducing weight loss carbohydrates seemed a perfect plan. We have just discovered that it comes with unforeseen risks

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Carbohydrates or carbohydrates are a fundamental macronutrient in our diet. They represent, together with the fats, the main energy contribution to our body. Carbohydrates are also protagonists in some diets destined for weight loss, diets based on the fact that, in the absence of these nutrients, our body will resort to the energy stored in their fatty tissue. A plan that is not infallible. DNA damage. A new study has found a mechanism that could link low carbohydrate diets with a Risk increase of suffering from colorectal cancer. The union link would be in the microorganisms that reside in our digestive system, our intestinal microbiome. In a study conducted with mice, the team responsible for the analysis observed that these types of diets could worsen the deterioration of DNA caused by some of the microbes that usually inhabit our digestive tract. This facilitates the appearance of polyps that in turn increase the risk of appearance of this type of tumors. “Colorectal cancer has always been seen as the consequence of a number of diverse factors, including diet, intestinal microbioma, environment and genetic,” explained in a press release Alberto Martin, co -author of the study. “Our question was, does the diet affect the ability of specific bacteria to cause cancer?” Three diets under study. In his study, the team tested three types of diet: a “normal”, a carbohydrates, and a “western” rich in fat and sugar. He did it by combining these diets with different types of usual bacteria between our intestinal microbiota and suspects of keeping some kind of relationship with the risk of colorectal cancer. They found a combination of diet and microorganism with potential to trigger adverse relationships, that of the low carbohydrate diet and a variety of bacteria of the species Escherichia coli (E. coli). They observed that this diet encouraged production by the bacterium of the colibactin, a compound with the ability to damage the DNA and with it of producing cancer. The key I could be in the fiberthe team points out. This type of diets facilitates inflammation, altering the microbial community of its interior, which in turn creates an ideal environment for the propagation of the E. coli. A fallen barrier. The team also observed that the mucous barrier that separates epithelia cells (the outermost cells of the intestine) of bacteria was reduced, which could also facilitate that colibactin reaches intestine cells. This would increase the harmful potential of the compound. The details of the study have been published In an article In the magazine Nature Microbiology. And what about humans? Studies with mice have an obvious limitation, and it is that extrapolating what is observed in these rodents to our own species is not always possible. The team He stood out for it The need to confirm their findings in people, although they were also optimistic about the possibility that their study could be applied in cancer prevention. The microbioma in the spotlight. This is not the only recent study that has put in the spotlight to the bacteria of the species E. coli already the colibactin in regards to colorectal cancer. A few days ago We had the news of A study Made with patients from 11 countries who found exposure tests at an early age to this toxin could be linked to an increased risk of these types of tumors. In Xataka | During millennia, humanity has eaten what it played. Now he has started eating what he wants and that has consequences Image | Pixabay

This is what we know about the new generation of drugs for weight loss

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Many pharmaceuticals and laboratories have spent months to work seeking to replicate the success of drugs such as Ozempic, Wegovy or Zepbound. Based on compounds originally devised as diabetes treatments (semaglutida and tirzepatida) that ended up triumphing as a method to lose weight. Pharmaceuticals responsible for these have not stopped working. New generation. Novo Nordisk, the Danish company responsible for the development of Ozempic and its active compound Semaglutida, announced a few days ago New advances In Cagrisema clinical trials, a drug that combines semaglutida with another similar compound, Cagrilintida. Now the pharmacist has announced another novelty in the development of the new generation of drugs capable of fighting diabetes and helping to reduce our weight, an exclusive license agreement for UBT251, a triple agonist associated with three different receptors. Danish is not the only pharmaceutical in this race. Cagrisema A few months ago, Novo Nordisk gave us new details Cagrisema. This is a drug based on Cagrilintida, in turn a compound that emulates amiline (and also calcitonin), similar to how the semagglutide emulates the peptide similar to type 1 glucagon (LPG-1). Redefine 2. In Your last announcementNovo Nordisk realized some results of the redefine 2 trials, the third phase of the clinical trials with which the safety and effectiveness of the new combined drug has been tested. The essay studied these factors over 68 weeks in more than 1,200 participants. The trial showed that the average weight loss of the group under treatment was 15.7%, considerably higher than the weight loss of the group to which a placebo was administered, which was 3.1%. The detailed results of the clinical trials of the Redfine program (Redefine 1 and Redefine 2), will be presented later this year, while the date the company manages for the approval of these treatments by the regulatory agencies is the first quarter of 2026. Triple agonist. But perhaps the main course is yet to come. This same week, the Danish pharmacist He also announced An exclusive license agreement for a new compound, now known as UBT251. Until now we already had double agonist drugs, such as the tirzepatid Zepbound and Mounjaro of the American pharmacist Eli Lilly. These drugs function as analogues of the GLP-1 and GIP hormones, but not the glucagon. New agreement. The agreement has been signed between Novo Nordisk and Chinese Laboratory United Biotechnology. By virtue of the contract, the latter will maintain the rights for the development, manufacture and marketing of the drug in continental China, Hong Kong, Macao and Taiwan; while the European will be responsible for these activities in the rest of the world. To the race. Novo Nordisk was the pharmacist who opened the melon of drugs against diabetes converted to treatments for weight loss but may not be the leader in the race to achieve the triple agonist drug, the new generation of medications of the Ozempic family. And is that the American Lilly advances in the development of the Festatrutidawhich is already found In phase III of their clinical trials. In Xataka | “I lost 55 kilos, but I recovered 30 when leaving it”: we talked to the Spaniards who have tried the roller coaster of Ozempic Image | HAVEREDAS / I Yunmai

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