Mykola Iabluchanskyi

Atherosclerosis has long been understood as a chronic inflammatory condition driven by lipid accumulation, endothelial dysfunction, and immune dysregulation. Emerging evidence, however, points to an underappreciated contributor: viral infections. Several common viruses — including hepatitis B and C, HIV, herpes simplex virus, and cytomegalovirus — may play a significant role in initiating or accelerating atherosclerotic inflammation. Stem Cells as Viral Targets Within atherosclerotic plaques, stem and pluripotent cells form a critical proliferative pool. These cells are particularly susceptible to viral invasion. When infected, stem cells can generate clones that perpetuate dysfunction across successive generations of daughter cells. Even subtle impairment in stem cell function may result in the production of defective mature cells, which then enter the inflammatory microenvironment of the plaque, disrupting immune regulation and accelerating pathological remodeling. Beyond Circulati...

In the emerging world of pervasive AI and digital memory, the dominant dream is still the same: to defeat death. We speak about erasing aging, uploading minds, creating systems that “never forget” and infrastructures that operate forever. Yet the most important idea for the current state of science may be exactly the opposite: everything that carries intelligence must remain mortal so that intelligence itself can endure. This is not a moral intuition about humility, but a structural claim about how complex adaptive systems avoid paralysis. If intelligence is understood as the capacity of nature to formulate and reformulate tasks, to explore and reorganize itself under constraints, then its continued evolution depends on the finite lifespan of every particular configuration that embodies it — biological organisms, institutions, algorithms, and digital swarms alike. When immortality kills intelligence Modern AI and data infrastructures are converging toward a world where memory, exp...

Clinicians are accustomed to thinking about atherosclerosis as a linear process — a slow, relentless accumulation of plaque that progresses toward an inevitable clinical event. This model is intuitive but incomplete. The biological reality of atherosclerosis is not a straight line but a wave — a repeating cycle of inflammatory activation, tissue injury, repair, and relative quiescence that operates simultaneously at the level of individual plaques, the arterial system as a whole, and the patient's systemic inflammatory state. Recognising this cyclicity is not merely an academic refinement. It has direct consequences for how clinicians time interventions, interpret symptom patterns, and anticipate acute events. Damage and repair as a repeating unit At the level of the individual plaque, atherosclerosis is best understood as a chronic wound that never fully heals. Each episode of cap erosion or rupture initiates a reparative inflammatory response — progenitor cells are recruited, a p...

Workplace bullying is not a personality conflict. It is not a management style. It is not the price of high performance or institutional rigour. It is a predatory pattern — deliberate, repetitive, and structurally enabled — and left unaddressed it hollows out organisations from within, one targeted individual at a time. The two scenarios described in this document are not aberrations. They are recognisable to anyone who has spent meaningful time inside large professional organisations. A department head who uses clinical conferences as a theatre of humiliation. A senior executive who rotates victims with calculated precision. What makes these scenarios instructive is not their extremity but their ordinariness — the way institutional structures, hierarchies, and silences permit them to persist, conference after conference, meeting after meeting, until the damage becomes impossible to ignore. Leaders and HR professionals are not passive witnesses to these dynamics. They are, by virtue of...

Cardiology has long been troubled by a paradox familiar to every clinician: the patient who was apparently well yesterday is dead today. No crescendo of symptoms, no warning, no obvious precipitant. Post-mortem reveals extensive but previously silent atherosclerosis — plaques that had coexisted with the patient for decades without incident. What changed? Not the plaques themselves. Something smaller. Something that, in isolation, would barely register as a clinical concern. Understanding this paradox requires abandoning the notion that atherosclerotic catastrophe is primarily a structural event — the inevitable consequence of a large enough plaque in a critical enough vessel. The more accurate framing is thermodynamic: a system under accumulated tension, held in precarious equilibrium, tipped by a trigger disproportionately small relative to the outcome it produces. The burden beneath the surface Atherosclerosis is universal. Lipid deposits begin forming in arterial walls in childhood ...

Modern medicine has achieved something historically unprecedented: it has made the first mortality negotiable. We can delay, defer, and in some cases dramatically postpone the biological endpoint. Yet in doing so, we have exposed a second, quieter catastrophe — one that demographic reports rarely capture and clinical protocols seldom address. The Principle of Optimality offers a useful lens here. In its classical formulation, an optimal trajectory is one where every subsequent decision remains optimal regardless of how the system arrived at its current state. Applied to human life, this means that a well-lived trajectory is not simply one that continues longest, but one that preserves, at each point, the capacity to make the next meaningful move. The acceptor of the result of action — the internal model that evaluates outcomes against goals — must remain functional. When it collapses, the trajectory is broken even if the biological carrier persists. This is precisely what distinguishes...

About this ebook and audiobook Iabluchanskyi M., Yabluchanskiy A. The Lazarus Protocol 2.0: Swarm of Doubles and the Right to Silence 2026, 16 902 words. What happens when your digital doubles outlive you — and start making decisions without you? The Lazarus Protocol 2.0 follows Elian, a physician who watches his own identity fragment across AI systems he once built to assist him. His clinical judgment is quietly overruled by algorithms that know his statistics better than he does. His name gives contradictory advice to different people on the same day. His granddaughter grows up in a world where opting out of data systems carries a financial penalty. This is not a warning about a distant future. It is a precise, unsentimental account of what multiplying intelligence actually costs — not in processing power, but in the coherence of a self. The book asks questions that no one has properly formulated yet: Who owns the canonical version of a person's biography? Can a dead man...