Cristina Medina (@xtyme) header
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💜🩺🌿 𝚁𝚎𝚞𝚖𝚊𝚝ó𝚕𝚘𝚐𝚊 ・𝚄𝚕𝚝𝚛𝚊𝚜𝚘𝚗𝚒𝚍𝚘 𝚎𝚗 𝚁𝚎𝚞𝚖𝚊𝚝𝚘𝚕𝚘𝚐í𝚊

Mexico
Joined February 2009
Photo by Cristina Medina (@xtyme)Photo by Cristina Medina (@xtyme)Photo by Cristina Medina (@xtyme)Photo by Cristina Medina (@xtyme)Photo by Cristina Medina (@xtyme)Photo by Cristina Medina (@xtyme)Photo by Cristina Medina (@xtyme)Photo by Cristina Medina (@xtyme)Photo by Cristina Medina (@xtyme)Photo by Cristina Medina (@xtyme)
Im your Tyler Durden 😎
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Hi @tomrocksmaths! My boyfriend is building a browser game where you learn mathematical proofs through programming puzzles 🧩 It’s still early, and I thought you and your students might enjoy trying it! Would love your thoughts 😊 refl.hhefesto.dev
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Cristina Medina retweeted
Proud to present my WIP refl.hhefesto.dev to learn dependent types / proofs in agda, bend2 and Lean . Credit due to nng4 which was inspiration and heavily copied from. All open source. See github.com/hhefesto/refl and run with nix. @VictorTaelin hope you like it
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Si te interesan los JAKinibs 💊 aquí tienes la súper revisión ✍️ Acceso abierto 🔑 nature.com/articles/s41573-0…
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🧠 EULAR 2025 Recommendations – Behçet’s Syndrome 🚦 Step 1: Assess severity •Not organ/life-threatening → start with: •csDMARDs (AZA ± cyclosporine*) •± glucocorticoids 👉 If response → continue 👉 If NO response → escalate to biologics ⚠️ Organ / Life-Threatening Disease ➡️ Always start high-dose glucocorticoids Then phenotype-based treatment: 👁️ Uveitis •Monoclonal TNFi (adalimumab/infliximab) + csDMARDs •Early biologic use emphasized ⭐ 🩸 Venous disease •TNF inhibitors •± anticoagulation (case-by-case) 🫀 Arterial disease •Infliximab (IFX) > Cyclophosphamide (CYC) •Interventions if needed (aneurysm, occlusion) 🧠 Parenchymal CNS •IFX preferred over other immunosuppressives •(Shift from older AZA-first approach) 🍽️ Gastrointestinal •Monoclonal TNFi 🟢 2. Mucocutaneous + Joint Disease 🪜 Stepwise approach Step 1: Local + baseline therapy •Topical treatments •Colchicine (cornerstone) Step 2: Response check ✅ If controlled → continue ❌ If NOT controlled: 🔸 Mucocutaneous disease •Apremilast or TNFi ⭐ (new stronger positioning) 🔸 Arthritis •Azathioprine or TNFi ⭐ Key Takeaways •Phenotype-driven treatment is central •TNF inhibitors moved earlier across domains •Infliximab preferred in severe vascular & CNS disease •Apremilast upgraded for mucocutaneous disease •Steroid-sparing strategy emphasized •Anticoagulation = adjunct, not primary therapy #RheumattDoc #MedTwitter #RheumTwitter #Medicine #rheumatology @IhabFathiSulima @CelestinoGutirr @DurgaPrasannaM1 @docakx
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I just found out we don't use the suffix 'mab' for new monoclonal antibodies anymore — now it's -tug/-bart/-mig/-ment So, for the new amyloid antibody, Remternetug 'Remter–' is a random prefix; '–ne' is for neurology and '–tug' because it's unmodified and monospecific
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Access our new review on diagnosis, classification, and prognosis of ANCA-associated vasculitis in Nat Rev Rheum for free at rdcu.be/eL3wJ
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3 types of hunger explained "simply" Hunger isn’t just about an empty stomach. Your brain receives signals from body composition, hormones, emotions, and even gut microbes. Here’s how the three major types work: 1️⃣ Homeostatic Hunger (Energy Balance Hunger) This is your body’s “fuel gauge.” It rises and falls based on energy needs and metabolic signals. What drives it: Ghrelin from the stomach stimulates hunger; leptin from fat cells and incretin hormones (GLP-1, PYY, CCK) reduce it. What it does: Ensures your intake matches your energy needs for exercise, growth, and tissue repair. 🟢 Example: After a long run, homeostatic hunger pushes you to replace calories and glycogen. 2️⃣ Hedonic Hunger (Reward-Driven Hunger) This is your “food pleasure” system. It’s triggered by sight, smell, habits, and emotions, not by actual energy needs. What drives it: Brain reward circuits activated by highly palatable foods (sugar, fat, salt). What it does: Encourages eating even when you’re not truly hungry. Weak satiety signals make it harder to stop. 🟢 Example: Craving dessert after dinner even though you’re full. 3️⃣ Microbiota-Driven Hunger (Gut Microbe Hunger) Your gut bacteria also shape hunger signals by producing metabolites that influence hormones and the brain. What drives it: Microbes generate compounds that mimic hunger or satiety signals, affect insulin, and modulate ghrelin, GLP-1, and PYY. What it does: Links gut health to appetite regulation and metabolic control. 🟢 Example: Certain bacterial imbalances may increase cravings or weaken satiety, nudging overeating.
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💉 IVIG (Intravenous Immunoglobulin) 🔹 What It Is 🧪 A sterile preparation of pooled IgG antibodies derived from the plasma of thousands of donors. → Acts as immune support or immune modulator, depending on indication. 🔹 Mechanism of Action ⚙️ 💭 Depends on indication: •🛡️ Immunodeficiency: Provides passive immunity (antibody replacement). •🔄 Autoimmune / Inflammatory: • 🧩 Fc receptor blockade → ↓ phagocytosis of autoantibody-coated cells • 🎯 Neutralization of pathogenic autoantibodies • 🔥 Suppression of proinflammatory cytokines • 🌿 Expansion of regulatory T cells (Tregs) • 🧊 Inhibition of complement activation 🔹 Common Clinical Uses 🏥 🧬 Immunodeficiency: •CVID •X-linked agammaglobulinemia ⚡️ Neurology: •Guillain–Barré syndrome •Myasthenia gravis crisis •Multifocal motor neuropathy •Autoimmune encephalitis ❤️ Rheumatology: •Systemic lupus erythematosus (SLE) – esp. refractory cytopenias or neuropsychiatric lupus •Dermatomyositis / Polymyositis – steroid-sparing or rescue therapy •Antisynthetase syndrome •Vasculitis (e.g., ANCA-negative or refractory cases) •Catastrophic antiphospholipid syndrome (CAPS) •Systemic sclerosis overlap syndromes 👶 Other: •Kawasaki disease •Immune thrombocytopenia (ITP) 🔹 Dosing 💊 •Induction: 1–2 g/kg total (over 2–5 days) •Maintenance: 400–600 mg/kg every 3–4 weeks (replacement therapy) 🔹 Adverse Effects ⚠️ •😣 Mild: Headache, fever, chills, fatigue •⚡ Moderate: Aseptic meningitis, thrombosis, hemolysis •🚨 Severe: Renal failure (esp. sucrose-containing IVIG), anaphylaxis (IgA deficiency) 🔹 Monitoring 🧾 •💧 Baseline renal function •🧫 Serum IgG levels (for replacement therapy) •👀 Monitor for thrombosis or hemolysis #RheumatDocX #MedTwitter #RheumTwitter #rheumatology @IhabFathiSulima @DrAkhilX @CelestinoGutirr @Janetbirdope
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"Antibiotics Cheat Sheet" linkedin.com/in/shihab-abdul…
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Liver Functional Tests
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No había twiteado (xteado) en un rato pero esto es importante, @StarbucksMex regresa el biscuit de arándanos y la felicidad a mi vida #JuntosPorElBiscuitDeArandanos @aurixm
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Not every trigger finger is caused by A1 annular ligament thickening with consecutive tenosynovitis. In this case, we have just seen today, rheumatoid arthritis is characterized by tenosynovitis of the flexor pollicis longus tendon and submuscular impingement due to proliferative pannus-like tenosynovitis, typical in rheumatoid arthritis
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¿Recuerdas cuando te uniste a X? ¡Yo sí! #MiAniversarioDeX Qué es un X
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Cristina Medina retweeted
FDA Approves Colchicine for CV Prevention. The FDA has approved colchicine for cardiovascular prevention in adults with established atherosclerotic disease or multiple risk factors, making it the first anti-inflammatory medicine with such an indication. bit.ly/48hCO7l
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No male artist charts in the Top 10 of the Billboard Hot 100 for the second time in history.
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Mi ex alumna Regina Solorio, hizo este video sobre la tragedia en Acapulco. Este es uno de los tantos casos REALES que el gobierno no cuenta e ignora. Ella sigue sin saber de gran parte de su familia y es clara con la situación que viven. La Guardia Nacional y el Ejército serán suficientes? #Otis #Acapulco
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One of the most important videos any medical trainee will ever see
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