They may be responding to consumer preference in that market. Plenty of people buy Teslas without instrument clusters. Adding the cluster does cost money. This isnâ(TM)t like putting in seat heaters and then charging to have them functional. This is an additional component.

Should we complain that there is an up charge for fog lamps? There is the space for them on some cars, but theyâ(TM)re not always installed.

And think of how many car models are out there where one trim level has a tachometer and another doesnâ(TM)t. They are giving the consumer choice. Get extra displays or not.

You have this entirely backwards. People in Florida's gated communities love their security. Every gated neighborhood I've ever been has security cameras pointed at the entrances and exits, and some even have an actual human making copies of the driver's licenses of everyone who enters. The residents with transponders or barcodes to enter? Yep, that activity is automatically logged, too.

Most of the people physically protesting Flock cameras are college (age) kids and this retired guy with a pool pole. They're generally not wealthy.

Kalshi: builds a platform specifically designed to encourage and profit from insider trading
Santos: engages in insider tradiing
Kalshi: no, not like that

We all know that politicians like any other human being are often out of their depth when society gets into a critical situation. They have blind spots, ignore trends with the regular people and fumble. And talk trash about people issues without even noticing.

But this Trump thing you USians have going on seems to be an entirely new level of malignant corruption. I mean, like some satire of a corrupt government with some man-child in charge asking for rockets to be more pointy because pointy is more dangerous.

Is anybody taking this seriously anymore over there? Wouldn't impeachment of this President be overdue by now?

An inquisitive European is curious to know, please enlighten me. Seriously.

Like most companies, Apple has been ethical when it suited their interests. There's always been a slimy side there - Jobs cheated Woz before Apple even existed.

No, What Apple lost was taste.

They used to profit from producing products they'd want to use. Now they make profit-maximizing devices.

I'd argue that the OSes are starting to suffer, too. I mean, bugs are up again, but that's always been cyclic. But I feel like they're losing coherence, too. And a lot of subsystems more technical users like are rotting or being made much more difficult to work with (Gatekeeper and shell scripts, for instance). (I also find it ugly now, but that's subjective and it has has ugly iterations before, too.)

Anyway, yeah, Apple will make a ton of money for a long time to come. But I'm pretty sure it is losing its sense of taste. It might make the most popular and most profitable phone, but they aren't trying to make the phone people want anymore.

Except that Motorola sells a huge range of phones with costs varying by more than a factor of 5, all with identical Android images and unlocked. The only difference is the hardware specs. The only possible way these phones are subsidized in a way the flagships aren't is if Motorola thinks of the entry-levels as a way to get customers "hooked" on the brand and start paying for the more expensive (and presumably higher-margin) flagships.

Finally, recalcitrant peptides are depleted in cytoplasmic and mitochondrial domains and strongly enrichedby up to 16-foldin calcium-dependent phospholipid-binding C2 domains. C2 domains mediate Ca2+-regulated binding of proteins to anionic phospholipids on membrane surfaces, (58) and their enrichment indicates that peptide persistence is disproportionately associated with proteins stabilized at membranes, rather than within freely soluble intracellular compartments. Loss of ionic homeostasis and rising intracellular Ca2+ during post-mortem decay (6) would be expected to further promote sustained membrane association of such proteins. Membrane-adjacent microenvironments are structurally constrained, concentrating redox-active substrates and catalysts (such as lipids and metals) while restricting diffusion and oxygen availability relative to the cytosol. In this context, radical oxidation is less likely to proceed via chain propagation, which requires continuous access to molecular oxygen, (59) and more likely to locally terminate via cross-linking. Such cross-linking would be expected to reduce molecular mobility and solubility, sterically hinder enzymatic and hydrolytic attack, and promote the formation of insoluble aggregates resistant to degradation. (60)

A further factor likely reinforcing this taphonomic trajectory is the brain’s unusually large and heterogeneous reservoir of redox-active iron. (61) Nervous tissue contains high iron concentrations relative to most other soft tissues, distributed across multiple pools such as heme proteins, ferritin-bound stores, and iron-rich compartments associated with mitochondria, myelin, and oligodendrocytes. (62) In life, these pools are tightly regulated to support oxidative metabolism while limiting collateral damage. (63) After death, however, progressive membrane failure and loss of regulatory control are expected to alter iron speciation and availability, increasing the likelihood of local metal-catalyzed radical generation. Importantly, such chemistry need not produce uniform oxidative destruction: when redox reactions involving iron occur within membrane-adjacent or diffusion-limited microenvironments, they may favor the formation of short-lived aromatic radicals that terminate by covalent cross-linking rather than by chain-propagating oxidation (Table S22). The enrichment of peroxidaseswhich often involve heme iron or metal cofactors (64)among recalcitrant peptides is compatible with localized, metal-associated redox chemistry, in which iron-containing cofactors may contribute to peroxide-driven radical formation without sustaining chain-propagating oxidation.

The brain is particularly predisposed to follow this trajectory. In life, it is among the most oxidatively stressed organs: it consumes a disproportionate share of oxygen, is rich in redox-active metals, and relies heavily on antioxidant and repair systems to maintain protein integrity. (65) Additionally, the brain combines extreme membrane density, (66) an abundance of structurally stable, long-lived proteins that accumulate heterogeneous oxidative modifications during life, (67) and anatomical sequestration within the cranial vault. Together, these features establish a post-mortem environment characterized by pre-existing chemical and structural heterogeneity, limited molecular mobility, and restricted oxygen exchange: conditions that favor local, diffusion-limited radical reactions and termination by cross-linking rather than runaway, chain-propagating oxidation. Notably, the molecular features that define this post-mortem pathway closely parallel those that stabilize aggregation-prone protein assemblies in neurodegenerative disease: enrichment of -sheet and structurally ordered fragments, (68) redox-active residue modifications, (69) and oxidative cross-links (70) are hallmarks of pathological protein aggregation in vivo. While the biological contexts differ fundamentally, these parallels indicate that common chemical processes govern protein persistence across clinical and geological time scales.