Rafael Sirera

3.5K posts

Rafael Sirera banner
Rafael Sirera

Rafael Sirera

@ProfSirera

Professor of Cell Biology at Universitat Politècnica de València, with a particular passion for molecular medicine and a strong interest in natural philosophy.

Valencia Katılım Mart 2025
379 Takip Edilen1.6K Takipçiler
Sabitlenmiş Tweet
Rafael Sirera
Rafael Sirera@ProfSirera·
Molecular Medicine is not just a branch of science — it is the very language of life. It explains how cells communicate, how genes express identity, and how molecules decide between health and disease. Within its scope lies the most intimate narrative of our existence: the silent choreography of enzymes, receptors, and signals that sustain us every second. By following this account, you will explore the hidden logic that keeps us alive — and discover what happens when those delicate mechanisms fail, giving rise to illness. Here, we decode the molecular origins of disease and the rationale behind the action of drugs, tracing every therapeutic effect back to its biochemical root. Understanding Molecular Medicine is to see medicine itself under a microscope — where every cure begins as a molecular idea.
English
2
6
55
8.3K
Rafael Sirera
Rafael Sirera@ProfSirera·
@xueshang The key is understanding. Memorization helps you gain a better overview, reason more effectively, and solve problems faster.
English
1
1
1
9
Tweetledumb
Tweetledumb@xueshang·
Wish I could easily memorise all this but I must resort to machines with bigger RAM. It is really very remarkable.
Rafael Sirera@ProfSirera

If there is a single discipline that has moved from being “foundational” to being strategically indispensable in biotechnology, it is immunology. The current pharmaceutical landscape makes this point unequivocally clear: among the top-selling drugs worldwide, 50% are monoclonal antibodies, and all of them act by modulating the immune system. For biotech students, this is not a theoretical trend—it is a direct indication of where innovation, funding, and clinical impact are concentrated. Let us examine these five molecules and how they reshape disease pathophysiology: 1⃣ Daratumumab (anti-CD38) Used in multiple myeloma, daratumumab targets CD38 expressed on malignant plasma cells. Its binding induces complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity (ADCC), and apoptosis. Pathophysiologically, it reduces tumour burden while also modulating the immunosuppressive bone marrow niche by depleting regulatory immune subsets. 2⃣ Risankizumab (anti-IL-23 p19 subunit) Indicated in psoriasis and inflammatory bowel disease, risankizumab blocks IL-23, a key cytokine sustaining Th17 cells. This interrupts the IL-23/IL-17 axis, leading to reduced keratinocyte hyperproliferation and inflammation. The drug effectively rebalances aberrant immune activation at barrier tissues. 3⃣ Ocrelizumab (anti-CD20) Used in multiple sclerosis, ocrelizumab depletes CD20⁺ B cells. These cells contribute to antigen presentation, cytokine production, and autoantibody generation. Their depletion attenuates neuroinflammation and slows demyelination, demonstrating that MS is not solely T-cell driven but critically B-cell mediated. 4⃣ Pembrolizumab (anti-PD-1) A cornerstone of cancer immunotherapy, pembrolizumab blocks PD-1, releasing inhibitory checkpoints on T cells. Tumours exploit PD-1 signalling to evade immune surveillance; by inhibiting this pathway, pembrolizumab restores cytotoxic T-cell activity and promotes tumour clearance. It represents a paradigm shift from targeting the tumour to targeting the immune response to the tumour. 5⃣ Dupilumab (anti-IL-4Rα) Indicated in atopic dermatitis, asthma, and allergic diseases, dupilumab blocks IL-4 and IL-13 signalling via the shared IL-4Rα subunit. This suppresses Th2-driven inflammation, reducing IgE production, eosinophilia, and barrier dysfunction—central mechanisms in allergic pathology. These therapies illustrate a unifying principle: disease is increasingly understood as dysregulated immunity, whether in cancer, autoimmunity, or chronic inflammation. For biotechnology students, mastering immunology is no longer optional—it is the intellectual framework underpinning the most successful and transformative therapeutics of our time. nature.com/articles/d4157…

English
1
0
1
14
Rafael Sirera
Rafael Sirera@ProfSirera·
@drkeithsiau That must be why it's called the bronchial tree — the visual similarity is striking. But symbiosis? Do you mean we actually have plant-like cells in the alveoli generating oxygen for us?
English
0
0
0
7
Keith Siau
Keith Siau@drkeithsiau·
This is not just resemblance. This is also symbiosis.
English
8
7
81
3.1K
Rafael Sirera
Rafael Sirera@ProfSirera·
@Rainmaker1973 Looks like if they actually they ate cashew with the crust ...Your stomach would basically go: "Challenge accepted... but we're all gonna die trying."
English
0
0
0
93
Massimo
Massimo@Rainmaker1973·
Digestion time of foods [🎞️ thebrainmaze]
English
19
65
292
31K
Rafael Sirera
Rafael Sirera@ProfSirera·
A toxin that paralyses by design—and heals by precision. Botulinum toxin remains one of the most elegant examples of how microbial evolution has converged on exquisite molecular precision. Produced primarily by Clostridium botulinum, its neurotoxicity arises not from brute force, but from a highly refined enzymatic strategy targeting synaptic vesicle fusion. The toxin is synthesised as a ~150 kDa polypeptide, subsequently cleaved into a dichain structure linked by a disulphide bond. The heavy chain mediates neuronal binding and endocytosis, while the light chain functions as a Zn²⁺-dependent endopeptidase. Its targets—SNARE proteins such as SNAP-25, syntaxin, and VAMP—are not randomly selected; each serotype exhibits remarkable substrate specificity, effectively silencing neurotransmitter release with catalytic efficiency. The toxin exploits synaptic vesicle recycling pathways. Acidification within endosomes triggers conformational rearrangements, enabling translocation of the light chain into the cytosol. There, even minute quantities can cleave multiple SNARE complexes, illustrating a classic enzymatic amplification effect rather than stoichiometric inhibition. Physiologically, the blockade of acetylcholine release produces flaccid paralysis, yet this same mechanism has been repurposed therapeutically across neurology, ophthalmology, and increasingly, pain modulation. Intriguingly, emerging data suggest retrograde transport and central effects, challenging the long-held assumption of purely peripheral action. At the genetic level, bont genes are frequently embedded within mobile elements—plasmids or bacteriophages—facilitating horizontal transfer and diversification into serotypes (A–G) with distinct substrate specificities. This genetic plasticity underpins both evolutionary adaptability and clinically relevant differences in duration of action and potency. Botulinum toxin thus exemplifies how pathogenic mechanisms can be reframed as therapeutic tools, provided their molecular logic is deeply understood.
Rafael Sirera tweet media
English
0
2
6
74
Rafael Sirera
Rafael Sirera@ProfSirera·
If there is a single discipline that has moved from being “foundational” to being strategically indispensable in biotechnology, it is immunology. The current pharmaceutical landscape makes this point unequivocally clear: among the top-selling drugs worldwide, 50% are monoclonal antibodies, and all of them act by modulating the immune system. For biotech students, this is not a theoretical trend—it is a direct indication of where innovation, funding, and clinical impact are concentrated. Let us examine these five molecules and how they reshape disease pathophysiology: 1⃣ Daratumumab (anti-CD38) Used in multiple myeloma, daratumumab targets CD38 expressed on malignant plasma cells. Its binding induces complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity (ADCC), and apoptosis. Pathophysiologically, it reduces tumour burden while also modulating the immunosuppressive bone marrow niche by depleting regulatory immune subsets. 2⃣ Risankizumab (anti-IL-23 p19 subunit) Indicated in psoriasis and inflammatory bowel disease, risankizumab blocks IL-23, a key cytokine sustaining Th17 cells. This interrupts the IL-23/IL-17 axis, leading to reduced keratinocyte hyperproliferation and inflammation. The drug effectively rebalances aberrant immune activation at barrier tissues. 3⃣ Ocrelizumab (anti-CD20) Used in multiple sclerosis, ocrelizumab depletes CD20⁺ B cells. These cells contribute to antigen presentation, cytokine production, and autoantibody generation. Their depletion attenuates neuroinflammation and slows demyelination, demonstrating that MS is not solely T-cell driven but critically B-cell mediated. 4⃣ Pembrolizumab (anti-PD-1) A cornerstone of cancer immunotherapy, pembrolizumab blocks PD-1, releasing inhibitory checkpoints on T cells. Tumours exploit PD-1 signalling to evade immune surveillance; by inhibiting this pathway, pembrolizumab restores cytotoxic T-cell activity and promotes tumour clearance. It represents a paradigm shift from targeting the tumour to targeting the immune response to the tumour. 5⃣ Dupilumab (anti-IL-4Rα) Indicated in atopic dermatitis, asthma, and allergic diseases, dupilumab blocks IL-4 and IL-13 signalling via the shared IL-4Rα subunit. This suppresses Th2-driven inflammation, reducing IgE production, eosinophilia, and barrier dysfunction—central mechanisms in allergic pathology. These therapies illustrate a unifying principle: disease is increasingly understood as dysregulated immunity, whether in cancer, autoimmunity, or chronic inflammation. For biotechnology students, mastering immunology is no longer optional—it is the intellectual framework underpinning the most successful and transformative therapeutics of our time. nature.com/articles/d4157…
English
0
4
9
404
Rafael Sirera
Rafael Sirera@ProfSirera·
Though immunology is an undeniably challenging subject with much to learn, its potential in human biotechnology makes it an incredibly rewarding field of study.
Rafael Sirera@ProfSirera

If there is a single discipline that has moved from being “foundational” to being strategically indispensable in biotechnology, it is immunology. The current pharmaceutical landscape makes this point unequivocally clear: among the top-selling drugs worldwide, 50% are monoclonal antibodies, and all of them act by modulating the immune system. For biotech students, this is not a theoretical trend—it is a direct indication of where innovation, funding, and clinical impact are concentrated. Let us examine these five molecules and how they reshape disease pathophysiology: 1⃣ Daratumumab (anti-CD38) Used in multiple myeloma, daratumumab targets CD38 expressed on malignant plasma cells. Its binding induces complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity (ADCC), and apoptosis. Pathophysiologically, it reduces tumour burden while also modulating the immunosuppressive bone marrow niche by depleting regulatory immune subsets. 2⃣ Risankizumab (anti-IL-23 p19 subunit) Indicated in psoriasis and inflammatory bowel disease, risankizumab blocks IL-23, a key cytokine sustaining Th17 cells. This interrupts the IL-23/IL-17 axis, leading to reduced keratinocyte hyperproliferation and inflammation. The drug effectively rebalances aberrant immune activation at barrier tissues. 3⃣ Ocrelizumab (anti-CD20) Used in multiple sclerosis, ocrelizumab depletes CD20⁺ B cells. These cells contribute to antigen presentation, cytokine production, and autoantibody generation. Their depletion attenuates neuroinflammation and slows demyelination, demonstrating that MS is not solely T-cell driven but critically B-cell mediated. 4⃣ Pembrolizumab (anti-PD-1) A cornerstone of cancer immunotherapy, pembrolizumab blocks PD-1, releasing inhibitory checkpoints on T cells. Tumours exploit PD-1 signalling to evade immune surveillance; by inhibiting this pathway, pembrolizumab restores cytotoxic T-cell activity and promotes tumour clearance. It represents a paradigm shift from targeting the tumour to targeting the immune response to the tumour. 5⃣ Dupilumab (anti-IL-4Rα) Indicated in atopic dermatitis, asthma, and allergic diseases, dupilumab blocks IL-4 and IL-13 signalling via the shared IL-4Rα subunit. This suppresses Th2-driven inflammation, reducing IgE production, eosinophilia, and barrier dysfunction—central mechanisms in allergic pathology. These therapies illustrate a unifying principle: disease is increasingly understood as dysregulated immunity, whether in cancer, autoimmunity, or chronic inflammation. For biotechnology students, mastering immunology is no longer optional—it is the intellectual framework underpinning the most successful and transformative therapeutics of our time. nature.com/articles/d4157…

English
0
1
3
59
Rafael Sirera
Rafael Sirera@ProfSirera·
For Spain, this pattern is not incidental. The central plateau sits at a relatively high altitude (~600–700 m), with a continental climate marked by cold winters, hot summers, low precipitation, and limited agricultural productivity without irrigation. Historically, this constrained intensive agriculture and, consequently, the carrying capacity for dense populations. By contrast, coastal regions benefited from milder climates, maritime trade, and later industrialisation and tourism.
English
0
0
3
173
World of Statistics
World of Statistics@stats_feed·
Share of national territory where 90% of the population lives: 1.🇪🇸 Spain - 2.6% 2.🇳🇴 Norway - 3.1% 3.🇸🇪 Sweden - 3.5% 4.🇬🇷 Greece - 4.1% 5.🇫🇮 Finland - 4.2% 6.🇧🇬 Bulgaria - 4.2% 7.🇪🇪 Estonia - 5.2% 8.🇱🇻 Latvia - 6.6% 9.🇱🇹 Lithuania - 7.9% 10.🇭🇺 Hungary - 9.3% 11.🇭🇷 Croatia - 10.9% 12.🇸🇰 Slovakia - 11.4% 13.🇮🇹 Italy - 11.7% 14.🇵🇹 Portugal - 11.8% 15.🇷🇴 Romania - 12.0% 16.🇫🇷 France - 12.7% 17.🇩🇰 Denmark - 12.9% 18.🇨🇭 Switzerland - 13.1% 19.🇳🇱 Netherlands - 15.5% 20.🇦🇹 Austria - 15.7% 21.🇨🇿 Czechia - 16.0% 22.🇩🇪 Germany - 16.1% 23.🇵🇱 Poland - 20.8% 24.🇸🇮 Slovenia - 24.9% 25.🇮🇪 Ireland - 26.2% 26.🇧🇪 Belgium - 30.0% Source: Eurostat Census Grid (2021)
English
37
91
1.6K
415.1K
Rafael Sirera
Rafael Sirera@ProfSirera·
@ShardaClinic I love the infografics. More complementary information here, x.com/profsirera/sta…
Rafael Sirera@ProfSirera

Few conditions are as common, as painful, and as surrounded by misconceptions as kidney stones—yet most explanations focus on myths rather than biology. 🌟 To understand why they truly form, and to move beyond oversimplified dietary blame, we need to look closely at the physiology and chemistry of the kidney itself. ▶️ Kidney stones develop when the finely regulated balance between water, ions, and metabolic waste in urine is disturbed. Under healthy conditions, urine remains sufficiently dilute to keep compounds such as calcium, oxalate, phosphate, and uric acid in solution. ▶️ When urine becomes concentrated—most often due to chronic low fluid intake—these substances can reach supersaturation and begin to crystallise. This process is governed by physical chemistry, not by a single “bad” food. ▶️ Microscopic crystals form routinely in many individuals and are usually eliminated without consequence. ▶️ Stones arise when crystal clearance fails. Reduced urine flow, prolonged urinary stasis, or deficiencies in natural crystallisation inhibitors such as citrate allow crystals to adhere to renal epithelial surfaces and grow. ▶️ Calcium oxalate stones, the most prevalent type, reflect a complex interaction between intestinal absorption, hepatic metabolism, gut microbiota, and renal calcium handling, rather than excessive calcium intake alone. ▶️ Other stone types emerge from distinct mechanisms: ➡️ uric acid stones are driven by acidic urine and purine metabolism; ➡️ infection stones result from urease-producing bacteria; ➡️ and rarer stones reflect inherited metabolic defects. Genetics, climate, and lifestyle modulate all these pathways. 🌟 Kidney stones, therefore, are not a simplistic dietary accident, but the visible outcome of a multifactorial disruption in renal homeostasis.

English
0
0
1
55
Dr Parul Agrawal
Dr Parul Agrawal@ShardaClinic·
🔶 Kidney Stones: A Disorder of Urinary Chemistry, Not Just “Calcium Deposits” Kidney stones are often simplified as excess calcium deposition, but in reality they represent a disturbance of urinary balance. Urine normally contains substances like calcium, oxalate, uric acid, and phosphate—all capable of forming crystals. At the same time, the body produces protective factors such as citrate and magnesium, which inhibit crystallization. Stone formation begins when this balance is disrupted—when the concentration of stone-forming solutes increases, the urinary environment favors precipitation, and the natural inhibitors become insufficient. Over time, this leads to crystal formation, aggregation, and growth into stones. 🧱 Calcium Oxalate Stones (Major Focus) Calcium oxalate stones account for nearly 70–80% of all kidney stones and often begin on microscopic deposits known as Randall’s plaques in the renal papilla. These serve as a nidus for crystal attachment once urine becomes supersaturated. A central mechanism is increased urinary calcium (hypercalciuria). One important contributor is high dietary sodium intake. In the kidney, sodium and calcium handling are closely linked. When excess sodium is consumed, the body increases its excretion by reducing sodium reabsorption in the tubules. Because calcium reabsorption depends on sodium movement and associated water flow, this leads to reduced calcium reabsorption and increased calcium loss in urine. This excess calcium combines with oxalate, resulting in crystal formation. Additional contributors include high oxalate intake, low citrate levels (loss of inhibition), and increased calcium absorption due to elevated Vitamin D levels. An important clinical paradox is that very low dietary calcium may increase stone risk, as calcium in the gut binds oxalate and limits its absorption. 🔥 Uric Acid Stones (Brief) Form in acidic urine (low pH) due to reduced uric acid solubility. 👉 Unlike calcium stones, this is a pH-driven process 👉 Reversible with urine alkalinization (Detailed mechanism discussed earlier) 🦠 Struvite Stones (Infection-Related) Struvite stones arise in the presence of urease-producing bacterial infections such as Proteus or Klebsiella. These bacteria convert urea into ammonia, making urine alkaline. This environment promotes rapid formation of magnesium-ammonium-phosphate crystals, often leading to large staghorn calculi, which can damage the kidney if untreated. 🧬 Cystine Stones Cystine stones are caused by a genetic defect in amino acid transport, resulting in excessive urinary cystine, which is poorly soluble. They typically present with recurrent stones at a young age, and the presence of hexagonal crystals in urine is a key diagnostic clue. 🔚 Continued in Part 2… Why do some stones pass easily while others persist or recur? And do common remedies really help—or just seem to?
Dr Parul Agrawal tweet media
Dr Parul Agrawal@ShardaClinic

Uric Acid and Kidney Stones: Why Urine Chemistry Matters Uric acid is often linked to joint disorders like gout. However, its impact extends beyond joints to the kidneys, where it plays an important role in stone formation. How Uric Acid Behaves in Urine Uric acid is excreted by the kidneys into urine and exists in two forms: • Uric acid (less soluble) • Urate (more soluble) The balance between these forms is primarily determined by urine pH. The Critical Role of Urine pH When urine is alkaline, uric acid remains in its soluble urate form. When urine becomes acidic (pH < ~5.5), uric acid converts into its insoluble form, making it prone to crystallization. 👉 This is the key step in uric acid stone formation. Mechanism of Stone Formation Stone formation follows a sequence: 1️⃣ Supersaturation: High concentration of uric acid in urine 2️⃣ Acidic environment: Reduced solubility 3️⃣ Crystal formation 4️⃣ Aggregation → stone formation A Key Clinical Insight Uric acid stones may develop even when: • serum uric acid is normal • or only mildly elevated 👉 Because urine pH and concentration are more important than blood levels alone Dual Role of Uric Acid in Stones Uric acid contributes in two important ways: • Direct: forms uric acid stones • Indirect: acts as a nidus for calcium oxalate stones Uric acid crystals can facilitate calcium oxalate deposition, explaining their role in mixed stone formation. Why Does Urine Become Acidic? Urine acidity is closely linked to metabolic health. Common contributors include: • insulin resistance • metabolic syndrome • obesity • high animal protein intake • dehydration Insulin resistance, in particular, reduces ammonium production in the kidneys, leading to persistently low urine pH. Why Hydration Matters Low urine volume increases uric acid concentration, promoting supersaturation and crystallization. Adequate hydration: • dilutes urine • reduces crystal formation • lowers stone risk A Small but Important Insight Adequate magnesium intake may help reduce overall stone risk by influencing urinary crystallization, particularly in mixed stones involving calcium oxalate. Prevention and Practical Approach Risk can be reduced by: • adequate hydration • limiting excessive fructose intake • maintaining metabolic health • balanced diet • moderating excessive animal protein • in selected cases, urine alkalinization (under medical guidance) Final Thought Uric acid is not just a laboratory value or a joint-related issue. It reflects a deeper interaction between metabolism, kidney function, and urine chemistry. 👉 In many cases, the key is not just how much uric acid is present, but the environment in which it exists.

English
3
17
57
4.7K
Rafael Sirera
Rafael Sirera@ProfSirera·
It is often stated, almost reflexively, that modern transfusion medicine begins with Karl Landsteiner and his description of the ABO blood groups in 1901. Indeed, this discovery was crucial in rendering transfusion biologically intelligible and, crucially, immunologically safe. Yet, in strictly practical terms, Landsteiner’s work had no immediate clinical utility. Blood could now be matched, but it still could not be stored. Transfusion remained an improvised, high-risk procedure performed directly from donor to recipient—“arm to arm”—because coagulation rendered any collected blood unusable within minutes. The true inflection point came not from immunohaematology, but from biochemical insight. In 1914, the Argentine physiologist Luis Agote demonstrated in Buenos Aires that the addition of a dilute sodium citrate solution prevented blood clotting ex vivo without inducing toxicity upon transfusion. This deceptively simple intervention fundamentally altered the temporal constraints of transfusion. Blood was no longer perishable within minutes; it became a storable biological material. Almost concurrently, Albert Hustin and Richard Lewisohn reported similar findings. However, Agote’s work holds particular historical significance as the first publicly documented successful transfusion of stored human blood. Only when citrate anticoagulation was combined with ABO compatibility did transfusion become both safe and operationally feasible. This convergence transformed transfusion from an experimental manoeuvre into a scalable medical practice. Its impact became immediately evident during the World War I, where the ability to store and transport blood saved innumerable lives and led to the establishment of the first rudimentary blood banks. Subsequent advances—such as the identification of the Rh system and the introduction of plastic blood bags—refined the field, but did not redefine its foundation. Landsteiner clarified compatibility. Agote enabled applicability. Without anticoagulation, the Nobel-winning discovery remained, for more than a decade, clinically inert. And the Prize had to wait until 1930.
Rafael Sirera tweet media
English
0
1
2
97
CardiovascularCorner
CardiovascularCorner@TrackYourHeart·
Which organ receives the highest percentage of cardiac output at rest? A. Brain B. Kidney C. Heart D. Skin
CardiovascularCorner tweet media
English
16
12
112
26.2K
Rafael Sirera
Rafael Sirera@ProfSirera·
@TrackYourHeart At rest, cardiac output to the kidneys increases because other organs are not as active, whereas the kidneys remain constantly on duty. Incidentally, this is why we produce more antidiuretic hormone—to allow us to rest peacefully throughout the night. x.com/profsirera/sta…
Rafael Sirera@ProfSirera

Why do we wake up with puffy eyes, swollen hands, and a more irritated throat when we have a cold? In this post I’ll explain the physiology behind it, what happens in the body during sleep. During sleep the body undergoes several physiological changes affecting posture, fluid dynamics, and hormonal regulation. Hormones such as antidiuretic hormone (ADH, or vasopressin) increase during the night. These shifts influence how fluids are distributed and how the body responds to inflammation. 1⃣ Why are the eyes puffy when we wake up? *⃣ Fluid accumulation While we sleep—particularly if lying on our back—venous and lymphatic drainage from the face slows down. Gravity acts differently than when we are upright, and muscle activity is minimal. As a result, fluid can temporarily accumulate in the soft tissues around the eyes, which are especially prone to swelling because the skin there is thin and the underlying connective tissue is loose. *⃣ Slower circulation During sleep, heart rate and blood pressure decrease. This lower circulatory drive can slightly favour the redistribution of fluid within tissues, contributing to the transient puffiness many people notice on waking. 2⃣ Why can the fingers appear swollen? A similar mechanism explains swelling in the hands. *⃣ Fluid redistribution When we lie down, gravity no longer pulls fluid towards the legs as it does when we are standing. This can favour fluid accumulation in the upper extremities, including the fingers—especially if there has been a high intake of salt or fluids before sleep. *⃣ Reduced movement Muscle contractions normally help pump venous blood and lymphatic fluid back towards the heart. During sleep this “muscle pump” is largely inactive, which can slow drainage and promote mild swelling. 3⃣ Why does the throat hurt more in the morning (especially during a cold)? *⃣ Dryness Saliva production decreases during sleep. If nasal congestion forces mouth breathing, the throat becomes even drier, worsening irritation. *⃣ Accumulation of secretions While lying down, mucus from the nasal passages and sinuses can collect in the throat. This can increase local inflammation and discomfort. *⃣ Inflammatory activity Respiratory infections trigger inflammation of the airway mucosa. After several hours of reduced swallowing and mucus clearance during sleep, the inflammatory effects may feel more pronounced upon waking. 4⃣ The role of ADH ADH (vasopressin) regulates how much water the kidneys retain. Its secretion follows a circadian rhythm and typically increases at night, reducing urine production and allowing uninterrupted sleep. This has physiological consequences Greater water retention during the night can contribute slightly to tissue swelling in susceptible areas. Reduced urine output means less overnight fluid elimination, which may amplify the feeling of congestion or discomfort during illness. Additional factors that worsen these symptoms • Nasal congestion, which promotes mouth breathing and throat dryness • Sleeping position, particularly lying flat, which can favour facial fluid accumulation and mucus pooling • Dietary factors, such as salty meals or inadequate hydration before sleep 5⃣ Why does the swelling disappear after getting up? Once we stand up, gravity assists fluid redistribution throughout the body. Movement activates the venous and lymphatic pumps, improving drainage and circulation. Within a short time, accumulated fluid is reabsorbed or redistributed, and the swelling gradually subsides. In short, puffy eyes, swollen fingers, and a sore throat on waking are the consequence of normal nocturnal physiological changes—fluid redistribution, hormonal regulation such as increased ADH, body position, and inflammatory responses during infection. Small adjustments in posture, hydration, and nasal care can often reduce these symptoms.

English
0
0
2
276
Rafael Sirera retweetledi
Keith Siau
Keith Siau@drkeithsiau·
Drinking caffeinated coffee and tea is associated with a lower risk of dementia, according to this new JAMA study 🧠
Keith Siau tweet media
English
27
175
548
29.2K
Rafael Sirera
Rafael Sirera@ProfSirera·
Menopause is one of those biological quirks that almost no other animal shares. Beyond humans, we only see it in a handful of long-lived cetaceans—killer whales, pilot whales and a few others—species that, like us, live in tight, multigenerational groups. 🌟 Most mammals simply keep reproducing until they die; evolution normally weeds out anything that cuts short a female’s fertile years. So the fact that humans routinely spend decades in a post-fertile state is not a biological slip-up, but something that needed to pay off. 1️⃣ The best explanation is the Grandmother Hypothesis. ▶️ Rather than continuing to compete with their daughters for pregnancies, older women gained more by helping raise their grandchildren. In the harsh realities of Palaeolithic life, young mothers needed all the help they could get: human infants are hopelessly dependent, childhood is extraordinarily long, and food gathering was unpredictable. ▶️ Post-menopausal women—no longer tied up by pregnancy or breastfeeding—became the steady, experienced hands who kept the group going. They knew where to find reliable foods, they could buffer lean seasons, and their presence quite literally kept children alive. 2️⃣ This had profound consequences for how humans behave. ▶️ Grandmothers reduced child mortality, allowed their daughters to have the next baby sooner, and helped support several overlapping generations. Their contributions nudged our species towards cooperative child-rearing and stronger family networks, and they freed up mothers and fathers to take on other tasks—hunting, toolmaking, social alliances. ▶️ Crucially, by stepping back from reproduction, older women avoided competing with their daughters for limited resources, boosting the success of the whole lineage. 🚩 Menopause isn’t a biological failure; it’s an evolutionary strategy that helped shape who we are. By creating a long, productive life stage after fertility ends, it supported the rise of human cooperation, extended childhood and the culture-rich societies we now take for granted.
Rafael Sirera tweet media
English
0
2
2
133
Rafael Sirera retweetledi
Dr Alo, DO, FACC
Dr Alo, DO, FACC@MohammedAlo·
Where I disagree with the new guidelines. It takes a while for the guidelines to catch up to reality, the new data, and clinical practice. These are better, but they should be improved. dralo.net/blog/cholester…
Dr Alo, DO, FACC tweet media
English
10
25
102
8.5K
Rafael Sirera retweetledi
Rafael Sirera
Rafael Sirera@ProfSirera·
Ever wondered why surgeons obsess over a tiny “ligament” that’s actually a clever muscle hybrid hanging from your diaphragm? It quietly divides your gut’s bleeding zones and keeps your small bowel from twisting into chaos! The Ligament of Treitz—more accurately termed the suspensory muscle of the duodenum—marks the precise anatomical transition from the duodenum to the jejunum at the duodenojejunal flexure. Far from a simple collagenous ligament as its name suggests, this fibromuscular structure comprises a superior portion of skeletal (striated) muscle fibres arising from the right crus of the diaphragm, blending into connective tissue near the coeliac artery, and an inferior part of smooth muscle fibres originating from the third and fourth duodenal segments. This unique composition allows it to suspend and stabilise the flexure, widening the angle during contraction to facilitate smooth passage of intestinal contents into the mobile jejunum. Clinically, it serves as a critical landmark: bleeding proximal to the ligament is classified as upper GI (often presenting as haematemesis or melaena), while distal bleeding counts as lower GI (typically haematochezia). Surgeons rely on it during laparotomy to identify the jejunum for procedures like feeding jejunostomy or measuring bowel length.
Rafael Sirera tweet media
English
2
52
272
20.2K
Rafael Sirera
Rafael Sirera@ProfSirera·
Loch Ness is home to a variety of wildlife, such as Atlantic salmon, brown trout and salvelinos. It is also home to otters, seals and various species of birds. The dark and cloudy water of the lake limits the amount of plant life, which makes it less biologically productive than other lakes.
English
2
0
5
2.3K
Amazing Maps
Amazing Maps@amazingmap·
Loch Ness contains more water than all lakes, rivers, and reservoirs in England and Wales combined
Amazing Maps tweet media
English
106
248
3.1K
222.4K