Tomasz Jetka

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Tomasz Jetka

Tomasz Jetka

@TJetka

Maths x Bio x Bioinf x Drug Development, PhD. Building AI x Bio in Poland.

Szczecin Se unió Ağustos 2019
211 Siguiendo139 Seguidores
Tomasz Jetka
Tomasz Jetka@TJetka·
@Jakub_moscicki Filozoficznie, to my w sumie opisywaliśmy życie. Wszyscy najbardziej lubili zawsze zadania tego typu 🤣🤣🤣
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Remek Kinas
Remek Kinas@KinasRemek·
@prywatnik NeurIPS - Sydney, Paryż, Atlanta. Tak - wysyłamy 3 publikacje z firmy Ingenix.ai 👍 No i deadline na abstract za 2h a na publikacje za 2 dni.
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Łukasz Olejnik
Łukasz Olejnik@prywatnik·
Właśnie zauważyłem, że NeurIPS 2026 w tym roku w Paryżu, a deadline na abstrakty za dwie godziny. Wysyłacie coś?
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Tomasz Jetka
Tomasz Jetka@TJetka·
Starting our scientific year at Ingenix.AI at the #ICLR2026 MLGenX Workshop with @rpowalski & @KinasRemek . If you’re at ICLR, connect with them on-site! We’re presenting Funomics T0, a first step to train a transcriptomics model across biological scales.
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Tomasz Jetka
Tomasz Jetka@TJetka·
@PiotrRMilos This is not a good example :) for drugs, esp. novel, everything is ood. (Although I probably agree that there is a lot of room for in-domain in science and even biomed).
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Piotr Miłoś
Piotr Miłoś@PiotrRMilos·
I agree and disagree :). I do agree that our goal, true dream, should be OOD. At the same time, even in domain is hugely useful. In science, there is a lot to be discovered simply by interpolation. E.g. I could easily imagine inventing novel drugs by by stitching up the existing knowledge.
François Chollet@fchollet

Simply retrieving a reasoning trace looks a lot like human reasoning, until it's time to navigate uncharted territory. If you memorized all reasoning traces of humans from 10,000 BC, you could automate their lives but you could not invent modern civilization.

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Dmitry Penzar
Dmitry Penzar@dmitrypenzar·
Not cool at all. My colleagues and I checked several well-known pathogenic variants, and they were predicted as VUS. Certain variants are simply missing (e.g, there is no information for rs879254374). I like the idea, I don’t see any reason to use Evo2. Garbage in, garbage out.
owl@owl_posting

very cool work. more dna language model pilled than i was an hour ago when i wrote my Evo 2 article a long time ago (owlposting.com/p/a-socratic-d…) the question was always 'how do you interpret the outputs of these models if it just spits out log-likelihoods?' and increasingly the answer is 'use probes to annotate embeddings, and ask the LLMs to interpret those'. in feb 2025, when i wrote my article, i didnt really trust the models to do that well. now i do, and perhaps there is an immense amount of greenspace for really crazy things to be done but one of the big failure modes of LLM-for-science approaches is that the models try really hard to be consistent with the data instead of reality. theres no experimental validation here, so who knows whether that's happening here id be extremely curious for someone to cross-reference the annotated VUS's here with, e.g. the UK Biobank 500k~ exomes with linked phenotype data. maybe Claude one-shot human variant function annotation, or maybe the annotations are slop, or maybe its in between

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Michael Shafrir
Michael Shafrir@michaelshafrir·
@LocasaleLab My wife was on this trial. Stage 4 panc cancer, 40 years old. She was in this trial and lived 18 months after chemo stopped working. We took trips to Spain, Disney, Jersey Shore. She got two more birthdays with our kids. Shove your hype and misrepresentation up your ass.
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Tomasz Jetka
Tomasz Jetka@TJetka·
@jarokrolewski O, Gratulacje! :) Pamietam, ze pierwsze wersje Cleory faktycznie dobrze radzily sobie z PPI'ami. Ciekawe jak zadziala na naszych benchmarkach, co nie @KinasRemek ;)?
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Jarosław Królewski
Jarosław Królewski@jarokrolewski·
Tabela benchmarkowa z wynikami #Cleora, w tym na datasecie PPI (Protein-Protein Interaction) - jednym ze standardowych benchmarków w graph #ML, używanym do oceny algorytmów embeddingów grafowych. cleora.ai/benchmarks Dataset PPI to graf interakcji białko-białko: 3 890 węzłów (białek), 76 584 krawędzi, z zadaniem klasyfikacji wieloetykietowej do 50 klas funkcjonalnych. Wyniki mówią same za siebie - Cleora osiąga idealną dokładność (1.000) zarówno w Accuracy jak i Macro F1, przy najniższym zużyciu pamięci (21 MB). Z ośmiu porównywanych algorytmów tylko trzy w ogóle dały wynik (RandNE i ProNE z tragicznymi score'ami), a pięć - HOPE, NetMF, GraRep, DeepWalk i Node2Vec - albo wyczerpało pamięć (OOM), albo przekroczyło limit czasu. Kosmos 🔥 #synerise #ai #bigdata
Jarosław Królewski tweet mediaJarosław Królewski tweet mediaJarosław Królewski tweet media
Jarosław Królewski@jarokrolewski

Prawie 7 lat temu, gdy hype na #ai był zdecydowanie mniejszy niż dziś, open-source’owaliśmy część naszego IP w obszarze #AI. Wówczas pokazaliśmy, jak wiele można osiągnąć dzięki doskonałości algorytmicznej. Dziś robimy kolejny krok. Publikujemy Cleora 3.2: Algorytm, który nie powinien istnieć ✨ Maksymalna dokładność. Polska 🇵🇱 technologia. cleora.ai Embedding grafu o 2 milionach węzłów w 31 sekund. Na jednym rdzeniu CPU. Za mniej niż $0.02. Bez GPU. Bez random walks. Bez negative sampling. 100% open source. Suwerenne AI to kontrola nad kodem, kosztami obliczeń oraz możliwość pełnej inspekcji i wdrożenia. Od zastosowań biomedycznych po analizę złożonych sieci - Cleora pozwala iterować w tempie, które wcześniej było nieosiągalne. Bravo @Synerise Research Team! #science #bigdata

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Tomasz Jetka
Tomasz Jetka@TJetka·
@RuxandraTeslo It has already happened in Medieval Ages as well. After the initial 'cathedral period', there were times of 'medicore' architecture when builder-profession become more common, hence less master-level. Large shift in Demand-Supply. Then, it bounced back, fortunately.
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Tomasz Jetka
Tomasz Jetka@TJetka·
@kosik_md @kawecki_maciej Gdyby tylko ;) to jeszcze nawet nie myśli o żadnych próbach zastosowania. Od aktywności do czegoś drug-like to rollercoaster. W Polsce prawie nikt nie wie, jak to robić, choć to już w miarę standardowy proces w branży. To dobry hit, ale nawet nie lead compound.
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Jakub Kosikowski
Jakub Kosikowski@kosik_md·
@kawecki_maciej Nie chce wyjść na niszczyciela zabawy, ale od znaleźli do zastosowania jest jeszcze daleka droga, sami badacze studzą entuzjazm w opublikowanym na stronie UJ stanowisku
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Maciej Kawecki - This Is IT
Maciej Kawecki - This Is IT@kawecki_maciej·
Incredible news: Polish scientists find a way to "unplug" cancer’s immortality. Wonderful news! A team of researchers from the Jagiellonian University has discovered a molecule that effectively disrupts DNA replication and repair processes by blocking the function of PCNA—a protein that plays a critical role in these mechanisms. This fundamental discovery paves the way for innovative cancer therapies. Following the necessary clinical trials, this molecule (or its derivatives) could be delivered as a drug using nanoparticle carriers directly to cancer cells, effectively halting their division. At the heart of every cancer cell lies the PCNA protein. Think of it as a "construction manager" that ensures the cancer’s DNA is copied without errors and repairs any damage. This protein is what makes cancer feel nearly indestructible. The team led by Dr. hab. Wojciech Strzałka has discovered a molecule that acts as a precision brake, stripping the cancer of its ability to survive and multiply. The Team Behind the Breakthrough Pictured are the innovators from the JU Faculty of Biochemistry, Biophysics, and Biotechnology (from left): Dr. Arkadiusz Borek, Dr. Ewa Kowalska, Dr. hab. Wojciech Strzałka, and Dr. hab. Monika Bzowska. This is a massive achievement! Congratulations to the entire team!
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Tomasz Jetka
Tomasz Jetka@TJetka·
@PiotrStec2 @ScimagoIR Jeśli się nie mylę, to dla PL instytucji można spróbować machnąć coś prostszego całkowicie open-source'owo, bo OPI udostępnia dane, a OpenAlexa podstawowe metryki. Z Claudem pewnie tydzień pracy lub 3-4 weekendy. Kończe coś w tym stylu dla NCNu
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Piotr Stec
Piotr Stec@PiotrStec2·
Podczas gdy my próbujemy wymyślić narzędzia korygujące wątpliwe praktyki publikacyjne w ewaluacji załoga @ScimagoIR wyszła z propozycją wskaźników w zasadzie do skopiowania w rozporządzeniu. Starczy zerknąć na scimagoiris.com i skopiować co trzeba.
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Sprawne Państwo
Sprawne Państwo@SprawnePanstwo·
Dziś świetny tekst @annawitten i @MarcinDarmas o biurokratycznej inercji przy budowie polskiego pomnika w Paryżu. Kilka dni temu @AlexObuchowski też pięknie opisał patologiczne zasady podziału kasy z #KPO na cyfryzację ochrony zdrowia. W obu przypadkach winna #silosowość i niska jakość instytucji publicznych. Temat mało znany, a kluczowy dla zrozumienia dlaczego nasze państwo działa, jak działa. Czy #urzędnicy rozumieją sens swojej pracy, czy może kurczowo trzymają się procedur, żeby skutecznie udowadniać, że "się nie da"? W każdym razie, @portalzeropl - dobra robota👍 #służbacywilna🇵🇱
Patryk Słowik@PatrykSlowik

Polska chciała postawić w Paryżu pomnik Józefa Poniatowskiego. Projekt był tak ważny, że rozmawiali o nim Donald Tusk, Andrzej Duda i francuski prezydent Emmanuel Macron. Rok później rzeźby wciąż nie ma, bo trzy polskie ministerstwa nie potrafiły ustalić, kto powinien zapłacić za jego budowę. A ambasador, który prowadził projekt, został odwołany z placówki w związku z aferą Collegium Humanum. zero.pl/news/nie-bedzi…

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Tomasz Jetka
Tomasz Jetka@TJetka·
@RuxandraTeslo From many “industry experts” I usually hear how complex everything is, then zooming into a narrow slice, (losing the “why”) and answering criticism with non-relevant edge cases. Recently, the only person with real clarity on the goal was a parent of a child in a clinical trial.
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Ruxandra Teslo 🧬
Ruxandra Teslo 🧬@RuxandraTeslo·
This is the reaction of a researcher in the space responding to skeptics. It's annoying that many biologists appear more focused on proving how knowledgeable they are than addressing the core issue, which is that the system used to test and evaluate these treatments is broken.
Ruxandra Teslo 🧬 tweet media
Ruxandra Teslo 🧬@RuxandraTeslo

The story about bureaucracy almost stopping a man from treating his dog’s cancer with an mRNA vaccine went viral. The problem transfers to humans: we’ve made these clinical trials unnecessarily hard, denying hope to patients. New article on this. writingruxandrabio.com/p/the-bureaucr… Excerpts: "A story about Paul Conyngham, an AI entrepreneur from Sydney who treated his dog Rosie’s cancer with a personalized mRNA vaccine, has been circulating on X since yesterday. What makes the story inspiring is the initiative the owner showed: he used AI to teach himself about how a personalized vaccine could work, designed much of the process himself and approached top researchers to take it forward. Whether the treatment itself was fully curative and how much of an improvement it is over state-of-the art is not the main focus of this essay. Others have already debated that question at length, and I recommend following their discussions. What interests me instead is the bureaucratic absurdity the dog’s owner encountered while trying to pursue the treatment. He described the long and frustrating process required simply to test the drug in his dog: “The red tape was actually harder than the vaccine creation, and I was trying to get an Australian ethics approval and run a dog trial on Rosie. It took me three months, putting two hours aside every single night, just typing the 100 page document.” Even in a small and urgent case, where the owner was fully willing to fund the treatment himself, the effort was slowed by layers of procedure. Of course, this kind of red tape is not confined to Australia, nor to veterinary medicine. In fact, in the US, the red tape is even worse, at least for in-human trials. In a previous post, I recommended the Australian model for early stage In the United States, GitLab co-founder Sid Sijbrandij found himself in a similar position after the relapse of his osteosarcoma. When the ordinary doors of medicine closed, he entered what he called “founder mode on his cancer.” Like many entrepreneurs confronted with a difficult problem, he began trying to build his own path forward by self-funding his exploration of experimental therapies. Even then, he ran into the same maze of regulatory and institutional barriers that not only delayed him, but also unnecessarily raised the price of his experimental therapies. These are obstacles that only someone with extraordinary resources could hope to navigate, often by assembling an entire team to deal with them and navigate the opacity. In the end, Sijbrandij prevailed: he has been relapse free since 2025, after doctors had told me he was at the end of his options. Around the same time, writer Jake Seliger faced a similar situation while battling advanced throat cancer. Like Sid Sijbrandij, he was willing to try anything that might help. The difference was that Seliger was not a billionaire. He could not hire a team to navigate the system on his behalf, and he struggled even to enroll in the clinical trials that might have offered him a chance. A system originally conceived to safeguard patients has gradually produced a strange and troubling outcome: the mere chance of survival is effectively reserved for the very few who possess the means to assemble an army of experts capable of navigating its labyrinthine procedures. What makes these stories particularly frustrating is that we already know clinical trials — especially small, early-stage ones like the ones Sijbrandij enrolled in for himself— can be conducted far more cheaply and with far less bureaucracy than is currently required. Ironically, the original article cites Australia as a bad example, yet clinical trials there are conducted 2.5–3× cheaper and faster than in the U.S., at least for human trials, without any increase in safety events—a genuine free lunch. Removing unnecessary barriers has long been important. That is why I co-founded the Clinical Trial Abundance initiative in 2024, a policy effort aimed at increasing both the number and efficiency of in-human drug trials and have consistently argued about the importance of making this crucial but often neglected part of the drug discovery process more efficient. Since then, the issue has only become more urgent with the rise of AI. One of the central promises of the AI revolution is that it will accelerate medical progress. Organizations such as the OpenAI Foundation list curing disease as a core goal, and researchers like Dario Amodei of Anthropic have argued that AI could dramatically speed up biomedical innovation. But, as I have written before in response to an interview between Dario and Dwarkesh Patel, AI will not automatically accelerate a key bottleneck in making these dreams a reality: clinical trials. Conyngham’s observation that navigating the red tape to start a trial for his dog took longer than designing the drug itself only underscores the point. Clinical trials themselves vary widely. At one end are small, bespoke trials involving one or a few patients testing highly experimental therapies—like the treatment in the Australian dog story or the experimental therapy Sijbrandij pursued. At the other end are large-scale trials involving thousands of participants, designed to confirm earlier findings and support regulatory approval. Different types of trials require different reforms. In this essay, I will focus on the former: small, exploratory trials, which will be called early-stage small n trials for the purpose of this essay. These are often the fastest way to test promising ideas in humans and learn from them. They represent our best chance at a meaningful “right-to-try,” form the top of the funnel that generates proof-of-concept evidence, and may be the only viable path for personalized medicine and treatments for ultra-rare diseases. Understanding why these trials have been made unnecessarily difficult—and how we might change that—is essential if medical innovation is to keep pace with our growing ability to design new therapies. When the story first circulated on X, many people interpreted it as evidence that a cure already exists but simply hasn’t been used due to bureaucracy. That isn’t quite true, as I explained. The type of mRNA vaccine that the owner pursued looks promising, but he did not know a priori whether it worked or not, as it had not been tested before. So it was not a cure, but “a chance at a cure”. I hesitate to call it an “experimental treatment”, since this term evokes fears of potential safety issues while we generally can predict safety quite well now. The inaccuracy of whether this was a cure or not, however, does not make the story of the bureaucratic red tape that Conyngham encountered any less infuriating. More and more promising treatments are accumulating in the pipeline, fueled by an explosion of new therapeutic modalities, ranging from mRNA to better peptides and more recently, by AI. Yet we are not taking full advantage of them. To better understand these points, it is helpful to briefly outline the clinical development process—the sequence of in-human trials through which a promising scientific idea is gradually translated into a therapy. Drug development is often described as a funnel: many ideas enter at the top, but only a few become approved treatments. Early human studies, known as Phase I trials, sit at the entrance of this process. They involve small numbers of patients and are designed to quickly test whether a new therapy is safe and shows early signs of effectiveness. If the results look promising, the therapy moves to larger and more complex studies, including Phase III trials that enroll large numbers of patients to confirm whether the treatment truly works. Most people gain access to new therapies only after these large randomized trials are completed. On average, moving from a promising idea to Phase III results takes seven to ten years and costs roughly $1.2 billion. Accelerated approval pathways in areas such as cancer or rare diseases can shorten this timeline by relying on surrogate endpoints, but the process remains slow. As a result, many discoveries that make headlines today will take close to a decade before they become treatments that patients can widely access. Part of this delay is unavoidable. Observing how a drug affects the human body simply takes time. But much of it is not. Layers of unnecessary bureaucracy, regulatory opacity, and rising trial costs add years to the process without clearly improving patient safety, which is why I started Clinical Trial Abundance. Allowing a higher volume of small-n early stage trials, the focus of this essay, is a rare “win-win” for both public health and scientific progress. For patients, it transforms a terminal diagnosis from a closed door into a “chance at a cure,” providing legal, supervised access to cutting-edge medicine that currently sits idle in labs. For researchers and society, it unclogs the drug discovery funnel; by lowering the barrier to entry for new ideas, we ensure that the next generation of mRNA, peptide and AI-driven therapies are tested in humans years sooner, ultimately accelerating the arrival of universal cures for everyone. Next, I will explain why making it easier to run these early stage trials matters. First, from a patient perspective, they often provide the closest practical equivalent to a right-to-try. In theory, right-to-try laws allow patients with serious illnesses to access treatments that have not yet been confirmed in large randomized Phase III trials. In practice, these pathways rarely function as intended. Pharmaceutical companies are often reluctant to provide experimental drugs outside formal trials, and treatments typically must have already passed Phase I testing. As a result, very few patients gain access through these mechanisms. Early-stage trials offer a more workable alternative. They allow experimental therapies to be tested in structured clinical environments—often in academic settings or academia–industry collaborations—where patients can be monitored and meaningful data can be collected. Second, early-stage small-n trials are essential for personalized medicine and the treatment of ultra-rare diseases. Many emerging therapies—such as personalized cancer vaccines, gene therapies, and other individualized interventions—do not fit easily into the traditional model of large randomized trials involving thousands of participants. By their nature, these treatments target very small patient populations and often require flexible, adaptive clinical designs. From a societal perspective, these trials play a crucial learning role. As I argued in my earlier essay Clinic-in-the-Loop, early-stage trials are not simply regulatory checkpoints on the path to approval. They are part of the discovery process itself, creating a feedback loop between laboratory hypotheses and human biology. Later-stage studies, particularly Phase III trials, are designed mainly for validation: they test whether a treatment works under defined conditions and produce the evidence needed for approval. Early-stage trials, by contrast, are oriented toward learning. Conducted with small patient groups and often using exploratory designs, they allow researchers to observe how a therapy behaves in the human body and how the disease responds. In this way, they close the gap between theory and real-world biology. In the Clinic-in-the-Loop essay, I explain how these trials were crucial to the discovery of Kymriah, the first curative cell therapy for blood cancer."

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Tomasz Jetka retuiteado
Angelica 🌐⚛️🇹🇼🇨🇳🇺🇸
I’ve been thinking about the Polish–Lithuanian Commonwealth lately. It’s really a delightfully idiosyncratic proto-democracy. The nobles of Poland and Lithuania decided to strip the monarchy of its hereditary nature and treat the king almost like a CEO position. After the old dynasty died out they literally talent-searched across Europe for a suitable foreign prince and then treated him more like an employee, complete with a kind of job contract. He couldn’t pass laws without parliament (the Sejm). The whole system was designed to stop the king from turning into a tyrant, especially at a time when most of Europe was absolute monarchy. And for a long time it actually worked. Part of the reason is that politics in the Commonwealth ran on consensus. The sejm had a culture of working together to reach unanimity. That’s where the infamous Liberum veto comes from. Any one noble could veto legislation. On paper that sounds insane, but it mostly worked because ppl almost never used it. The problem came once politics became more factional, the veto turned into the perfect sabotage tool. Foreign powers could simply bribe a single deputy to bring the Sejm to a grinding halt. Catherine the great got very good at this. She also got one of her lovers in as the last king so definitely some foreign interference heh. Aaaaand then she just partitioned it and poor Poland wasn’t a country for a looooong time after that. What makes the story interesting is that the rules themselves didn’t suddenly change. What changed was the political culture around them. The system was built on the assumption that elites would act with a certain level of restraint and shared responsibility. Once that assumption stopped being true, the safeguards became attack surfaces. I sometimes wonder if something similar is happening in the United States. The founders designed the American system with checks and balances to prevent executive overreach. But it was actually dependent heavily on norms that are not written down and are hard to put back after they erode for whatever reason.
Angelica 🌐⚛️🇹🇼🇨🇳🇺🇸 tweet mediaAngelica 🌐⚛️🇹🇼🇨🇳🇺🇸 tweet media
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Tomasz Jetka
Tomasz Jetka@TJetka·
@RiyueSunnyBao Hmm, yes and no. We surely know that there will not be a spectacular correlation at gene level. But surely, both can lead to a much more robust conclusion about what processes are ongoing and what phenotype is active
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Tomasz Jetka
Tomasz Jetka@TJetka·
@KinasRemek Niech pracuje przez weekend! Co jak co, ale z crunch'ami dla AI będziemy bezlitośni ;)
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Remek Kinas
Remek Kinas@KinasRemek·
No cóż … telefon sam postanowił zadziałać … i coś zakomunikować. Zaraz napiszę co tam w automacie do kodowania. Później już praca praca … ciekawe rzeczy. Przetestujemy w naszej firmie Ingenix.ai pewnie GPT-5.4 co @TJetka? 👍😁
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Karol Karpinski
Karol Karpinski@karolkarpinski·
@TJetka As Pradyu said, I don't miss being poor! (But perhaps there are rich funders among my followers who are would like to support a mid-level bureucrat with an economic history hobby!)
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Karol Karpinski
Karol Karpinski@karolkarpinski·
I'll be honest. Thanks to Claude Code and other agentic tools, for the first time in my life I'm feeling pretty bad about not having done a proper PhD. Make of this what you will regarding the near and far future of knowledge work.
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Tomasz Jetka
Tomasz Jetka@TJetka·
@kosik_md Hmm, a ja ciągle wychodze z założenia, że fajnie będzie dopiero, jak dowieziemy tak jeszcze z x10 klas molekuł, które są obecnie 😅 Sorry :)
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Jakub Kosikowski
Jakub Kosikowski@kosik_md·
Onkologia kliniczna doszła już do takiego etapu skomplikowania, że tak właściwie nazwy nowych leków onkologicznych są trudne do odróżnienia od nazw Pokemonów
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