Think Knicks and Rangers (let’s go Isles) have to be ahead bc of the absurd title droughts both teams went through prior to winning it all. However, b on sheer improbability, 2007 Giants have to be #1. I will be talking about that run on my death bed.

I agree the Giants is it because of the improbability. Where they were seeded, who they beat, then taking down an undefeated team.

Absolutely YES! The statistical improbability of the mail-in votes for Raman defy statistical reliability. An audit must be done.

Here;s a little more to chew on while I drive. ERVs, Syncytin, and the Stacked Improbability Problem ERVs, endogenous retroviruses, are often presented as one of the strongest arguments for common ancestry. The common explanation is that ancient retroviruses infected the germline of animals, inserted their DNA, and those viral sequences were then passed down through generations. For years, many ERV sequences were treated as leftover junk, genetic debris from ancient infections. But that framing has become much harder to maintain. We now know that some ERV-derived sequences are functional, regulatory, and in some cases tied to extremely important biological systems. The clearest example is syncytin. Syncytins are involved in placental development. They help form fused trophoblast layers at the maternal-fetal interface. In mice, syncytin-A is so important that knockout embryos die in utero. Syncytin-B knockout disrupts placental layer formation. In humans and other primates, syncytin-1 and syncytin-2 are involved in trophoblast fusion and placental function. So this is not a trivial case of junk DNA doing something minor. This is about reproduction, embryonic survival, and placental development, one of the most mission-critical systems in mammalian biology. The Popular Story Sounds Simple The usual explanation goes something like this: A retrovirus infected an ancestor, inserted an envelope gene into the genome, and that viral gene was later co-opted for placental development. At first, that sounds neat. Retroviral envelope proteins can mediate membrane fusion, and placentas need controlled cell fusion. But that summary leaves out most of the actual difficulty. Because this did not supposedly happen once. Primates have syncytin-1 and syncytin-2. Mice and related rodents have syncytin-A and syncytin-B. Other mammal groups, including rabbits, carnivores, ruminants, and marsupials, have their own distinct syncytin-like genes. These are generally treated as separate viral capture events, not as one inherited syncytin gene from a common mammalian ancestor. So the real claim is not: One viral gene entered the genome and became useful. The real claim is closer to this: Different retroviruses independently infected different mammalian lineages, inserted envelope genes into the germline, avoided harmful effects, escaped silencing, acquired placental expression, became regulated by the host, produced controlled cell fusion, improved reproduction, spread through populations, became fixed, and in several cases became essential to embryonic survival. That is a very different claim. This Is Not Just Incredulity. It Is a Stacked Probability Problem. People often dismiss this objection as mere incredulity. But that misses the point. The issue is not that one step sounds unlikely in isolation. The issue is that the syncytin story requires a long chain of conditional events, where each step must succeed before the next one matters. For the viral-origin story to work, all of the following must happen: A retrovirus must infect the germline or an early embryo in a heritable way. The insertion must land somewhere that does not destroy fertility or development. The viral envelope gene must remain intact enough to function. The host must not silence or degrade it. The gene must become expressed in the right tissue, the placenta. It must be expressed at the right developmental stage. Its fusogenic activity must be controlled, not chaotic or harmful. It must coordinate with existing placental gene networks. It must improve reproductive success enough to spread. It must become fixed in the population. It must eventually become integrated deeply enough that removal disrupts placental development or causes embryonic death. That is a compounding probability problem. Even if each individual step were assigned a modest probability, the combined probability drops quickly because the requirements are sequential and dependent. And then the problem gets much worse: the model requires this same general chain to occur repeatedly across different mammalian lineages, involving different viral genes, but producing similar functional outcomes in placental biology. That is the core issue. Multiple Different Viruses, Similar Biological Outcome This is where the syncytin case becomes especially difficult. The standard model says primate syncytins and mouse syncytins came from different viral captures after the primate-rodent split. Other mammalian syncytins are also generally interpreted as separate captures. So we are not being asked to accept one lucky viral insertion. We are being asked to accept multiple independent viral insertions, from different retroviral sources, in different animal lineages, all somehow ending up tied to the same basic biological function: placental development. That is not merely convergence. That is repeated convergence inside one of the most sensitive and indispensable systems in mammalian life. A generic fusogenic protein is not enough. Placental development does not merely need fusion. It needs fusion in the right cells, in the right tissue, at the right time, under tight regulatory control, without killing the embryo, damaging the mother, wrecking maternal-fetal exchange, or triggering the wrong immune response. A viral envelope protein can fuse membranes. Fine. But a placental system requires controlled, coordinated, developmentally integrated fusion. Those are not the same thing. The Mission-Critical Problem This matters because the placenta is not an optional feature. In placental mammals, proper placental development is necessary for embryonic survival. If the system fails, the organism does not reproduce. In mice, disruption of syncytin-A is embryonic lethal. That means the proposed viral acquisition did not merely add a side benefit. It allegedly became part of a system without which the organism cannot continue. That creates a serious explanatory problem. If the placental system required syncytin-like function, then how did it operate before that function existed? If it did not require syncytin-like function, then how did a viral insertion become so deeply integrated that later removal breaks the system? Either way, the model has to explain not just origin, but transition. It has to explain how a reproductive system survived before the viral gene, how the viral gene entered without damaging that system, and how the gene later became essential. That is not a small detail. That is the heart of the problem. Fixation Makes the Problem Harder It is also not enough for a viral insertion to happen in one animal. For the syncytin story to work, the insertion must become heritable and then fixed in a population. That means it must spread until it is carried broadly across the lineage. Modern humans do show some polymorphic HERV-K insertions, meaning certain ERV-like insertions are present in some people and absent in others. But that is not the same thing as directly observing a new viral envelope gene become fixed in the entire human population because it generated an essential developmental function. That distinction matters. The syncytin model depends on rare insertions becoming inherited, useful, regulated, fixed, and eventually indispensable. One such event would already require explanation. Several such events, independently producing similar placental functions, require much more. The Missing Parent Virus Problem There is also no exact ancestral virus sitting in a freezer that can be compared directly to syncytin-1, syncytin-A, syncytin-B, syncytin-Car1, syncytin-Rum1, or the others. The viral-origin claim is inferred from sequence similarity, retroviral envelope-like structure, LTRs, and phylogenetic analysis. That evidence may show that syncytins resemble retroviral envelope genes. But resemblance is not the same as demonstrating the full causal pathway. It does not directly show the infection event. It does not show the intermediate stages. It does not show how the host survived the transition. It does not show how the gene became properly regulated. It does not show how separate events repeatedly produced similar placental outcomes. So the real burden is much larger than simply saying these genes look viral. The real burden is explaining how viral-looking genes became mission-critical components of mammalian reproduction, multiple times. Why the Junk-DNA Story Should Make People More Cautious The syncytin case should also make people cautious about the old junk-DNA assumptions. Sequences once dismissed as viral leftovers are now known to be involved in major biological functions. Some are regulatory. Some are tissue-specific. Some are tied to development. Syncytin is not just active; it is involved in reproduction and embryonic survival. That should at least raise a serious question: Were these sequences really accidental viral debris later patched into useful roles, or are we looking at functional genomic components that were too quickly interpreted through an evolutionary lens? The standard answer assumes viral origin first and then explains function later. But the more function we discover, especially in critical systems, the less satisfying the ancient viral accident framing becomes. The Better Explanation: Common Design From a design perspective, the pattern is not surprising. Different mammalian groups need to solve similar biological problems: controlled cell fusion, maternal-fetal exchange, immune modulation, trophoblast-layer formation, and placental development. It makes sense that similar functional modules would appear in different mammalian systems. The standard viral-origin model says this pattern was produced by multiple independent viral accidents, filtered by selection, and gradually integrated into reproduction. The design model says similar biological problems are solved with similar engineered tools. The first explanation depends on stacked, repeated, historically unobserved events producing mission-critical outcomes. The second explanation treats the pattern as intentional reuse of functional design principles. At minimum, syncytin should not be presented as a simple victory for the viral-origin story. It is far more complicated than that. The evidence may show viral-like features. But the explanation still has to account for the compounding improbability of multiple independent infections, heritable germline insertions, beneficial regulation, population fixation, and repeated integration into one of the most essential systems in mammalian biology. That is the syncytin problem. It is not just that it sounds unlikely. It is a legitimate cumulative-probability problem hiding inside one of the most popular ERV arguments. References for Further Reading Mi et al., 2000: identification of syncytin-1 as a retroviral-envelope-derived gene involved in human placental morphogenesis. Dupressoir et al., 2005: identification of syncytin-A and syncytin-B in mice as placenta-specific fusogenic genes. Dupressoir et al., 2009: syncytin-A knockout causes embryonic death and placental defects. Dupressoir et al., 2011: syncytin-B knockout disrupts syncytiotrophoblast layer formation. Cornelis et al., 2015: review of retroviral envelope gene captures and syncytin exaptation across mammals, including marsupials. Vernochet et al., 2014: review of mouse syncytin-A/B and multiple independent syncytin captures in mammalian lineages. Grandi and Tramontano, 2018: overview of HERVs as roughly 8% of the human genome and discussion of HERV domestication. Kahyo et al., 2017; Belshaw et al., 2005: HERV-K insertional polymorphism in humans.

Dottore has always been rejected by the world and by people; Pantalone is basically a ridiculous improbability in his life, someone who understands him, understands his hatred for fate, and supports his cruelest actions to the end because he sees the reason and gain from them.

The improbability of the Pico Lopes story is summed up by the fact he is now even redeeming LinkedIn

Judging by your profile picture, I find that statement to be a statistical improbability.

Basic Physical Constants And “Goldilocks Zones” The idea that basic physical constants lie within "Goldilocks Zones" refers to the fine-tuning argument in cosmology, which suggests that certain fundamental physical constants have values that fall within a narrow range, enabling the existence of life as we know it. These constants govern the fundamental forces and properties of the universe, and even slight deviations from their observed values could render the universe inhospitable to life. What Are Physical Constants and the Goldilocks Zone? Physical constants are universal values that govern the behavior of physical systems, such as the speed of light, the gravitational constant, or the strength of fundamental forces. The "Goldilocks Zone" in this context means that these constants have values that are "just right" for the formation of stable galaxies, stars, planets, and ultimately life. If these constants were slightly different, the universe might be too chaotic, too uniform, or otherwise incapable of supporting complex structures or life. The fine-tuning argument posits that the precise values of these constants are unlikely to occur by chance, as the range of life-permitting values is extremely narrow compared to the theoretically possible range. Examples of Physical Constants in Goldilocks Zones Here are some key physical constants and how their values appear finely tuned for a life-permitting universe: 1. Gravitational Constant (G): · Role: Determines the strength of gravity, which governs the formation of stars, galaxies, and planets. · Goldilocks Zone: If G were slightly stronger, stars would collapse too quickly, burning out before life could evolve. If weaker, stars and planets wouldn’t form, as matter wouldn’t clump together effectively. For example, physicist Brandon Carter estimated that a change in G by more than a factor of ~2 could prevent star formation or make stars burn too rapidly. 2. Electromagnetic Fine-Structure Constant (α ≈ 1/137): · Role: Governs the strength of the electromagnetic force, which holds atoms together and drives chemical reactions essential for life. · Goldilocks Zone: If α were slightly larger (e.g., >0.1), atoms would become unstable, and fusion in stars would be disrupted. If smaller (e.g., <0.005), chemical bonding would be too weak to form complex molecules. The observed value allows stable atoms and molecules like DNA. 3. Strong Nuclear Force Constant: · Role: Determines the strength of the force that binds protons and neutrons in atomic nuclei. · Goldilocks Zone: A ~2% increase would prevent proton formation in the early universe, leaving no atoms. A ~2% decrease would make nuclei unstable, preventing the formation of heavy elements like carbon and oxygen, which are essential for life. 4. Cosmological Constant (Λ): · Role: Governs the rate of the universe’s expansion, driven by dark energy. · Goldilocks Zone: The observed value is incredibly small (~10⁻¹²² in Planck units). If Λ were slightly larger, the universe would expand too rapidly for galaxies to form. If negative or too small, the universe could collapse before life emerges. The viable range is estimated to be within 1 part in 10¹²⁰ of its observed value. 5. Ratio of Electromagnetic to Gravitational Forces (N ≈ 10³⁶): · Role: Sets the relative strength of electromagnetic and gravitational forces between particles like protons. · Goldilocks Zone: If this ratio were much smaller, stars would be too small and short-lived to support planetary systems. If much larger, stars would be too massive and unstable. The balance allows for stable, long-lived stars like our Sun. 6. Mass Ratio of Fundamental Particles (e.g., Electron to Proton Mass): · Role: Affects the stability of atoms and the chemistry of life. · Goldilocks Zone: The electron’s mass is about 1/1836 that of the proton. A significant change could disrupt atomic stability or prevent the formation of stable chemical bonds, making complex chemistry impossible. Why Are These Considered "Goldilocks Zones"? The term "Goldilocks Zone" is borrowed from the concept of planetary habitability, where conditions are "just right" for liquid water. For physical constants, the analogy holds because: Narrow Range: Calculations show that life-permitting values occupy a tiny fraction of the possible range. For example, physicist Roger Penrose noted that the entropy of the early universe (related to cosmological parameters) is fine-tuned to 1 part in 10¹⁰^¹²³, an almost unimaginable precision. Sensitivity to Change: Small deviations in these constants lead to catastrophic outcomes, like a universe with no stars, no atoms, or no stable chemistry. For instance, a 1% change in the strong force could prevent carbon-based life. Interdependence: Many constants are interconnected, so altering one (e.g., the strong force) affects others (e.g., nuclear fusion rates), amplifying the need for precise balance. Explanations for Fine-TuningThe fine-tuning of physical constants has sparked debate, with several proposed explanations: 1. Anthropic Principle: We observe these constants because only a life-permitting universe allows observers to exist. This is often tied to the multiverse hypothesis, where many universes exist with different constants, and we happen to be in one that supports life. 2. Design Hypothesis: Some argue that the precise values suggest a purposeful intelligent design, though this is a philosophical rather than scientific claim. 3. Undiscovered Physics: The constants might be determined by a deeper, yet-undiscovered theory (e.g., string theory), where their values are not arbitrary but fixed by fundamental principles. 4. Chance: The constants could simply be a lucky coincidence, though the extreme improbability makes this less satisfying to some. Challenges and Context Theoretical Ranges: The "possible" range of constants is often based on theoretical assumptions, as we don’t fully know the constraints on these values in a complete theory of physics. Life’s Definition: The fine-tuning argument often assumes carbon-based life as the standard. Other forms of life might be possible under different conditions, though this is speculative. Scientific Limits: While the fine-tuning is well-documented, explanations like the multiverse or design remain speculative, as they are difficult to test empirically. Conclusion The basic physical constants, such as the gravitational constant, electromagnetic fine-structure constant, and cosmological constant, appear to lie within extraordinarily narrow "Goldilocks Zones" that allow for a universe capable of supporting stars, planets, and life. Small changes in these values could lead to a universe without atoms, stars, or chemistry, making the observed values seem remarkably precise. While this fine-tuning is a fascinating feature of our universe, its ultimate explanation—whether due to a multiverse, deeper physics, or another mechanism—remains an open question in cosmology.

Adaptation is what has been shown. Small variations based on existing information and minute tweaks. It's interesting and quite important, but evolution has not actually explained or shown how complexity arises. The mechanism offered are actually illogical. The bulk of the theory relies on piles of assumptions and at some point they become absurd. Identical systems arising in separate/disconnect species. The improbability of such is immeasurable and requires twisting logic and science into a mutant pretzel to try to make sense of it. ERV's are another and some are so absurd I'm actually shocked any reasonable person can believe it. Much harder to believe than anything in scripture.

Yet, even with billions of years at play, the sheer improbability of life emerging in the first place can’t be ignored. The chance of non-living matter spontaneously organizing into a living cell is compared to throwing all the pieces of a pocket watch into a turbulent ocean,

Agnostic just means nobody knows. Every other concept is ridiculed if one doesn't know anything about it. Now when one question the improbability of the random formation of current reality from nothing, that's something off? 🙄

Just because you don’t like it doesn’t make it any less true—calling it “horseshit” is an emotional reaction, not a rebuttal to the improbability of the bullet’s path and the outcome.

stand by this assessment. hats off to knicks as nyc native was very happy to see it believe me. the improbability of the knicks win still hasn't been reckoned.

More fine tuning of the universe: if initial explosion had differed in strength by 1 part followed by 60 zeroes the universe would have collapsed or expanded too quickly making life impossible. Improbability below:

He is a scientist with a huge savior complex who rebelled against the self-proclaimed god-director Phobos to save Nevada. His Aerola is an improbability device that modifies the reality around him; Christoff is nothing without it.

Well i would like to see just 1 person keep their word on here. That is a improbability. Havent met 1 yet lets see if you are my first.

It’s a thought experiment to show the improbability of their wins. If it doesn’t resonate with you, it’s okay to just keep scrolling.

Peak Improbability Debates, ESPN Future Ratings, & The Absolute Weakness... youtu.be/l_o-OIR8f8c?is=ePtO… via @YouTube