Jette is Mataray 😊

Monbusho scholar. Oral pathologist. Mol biol. Cancer research-Tumor suppressors & oncogenes. Dent. Oral Immunol. Cranio genetics.

[Jette is Mataray 😊 @white_bite]

@DavosSafety Yes. Thank you for asking. Am based in Manila so we’re all good. This is down south so we didn’t feel anything here.

[Jette is Mataray 😊 @white_bite]

@27Hutch27 Have you ever won one?

[Jumel Bornilla, M.D. @jvbornillamd]

An Open Letter to the Philippine Orthopedic Association, Philippine Heart Association, and Philippine College of Physicians

[Jette is Mataray 😊 @white_bite]

@DavosSafety Just like any therapeutic under development, it’s all good news until we talk about affordability.

[Jette is Mataray 😊 @white_bite]

Pft. Bakit ba ang mga tao umaasa na may hiya pa mga yan?

[DZRH NEWS @dzrhnews]

‘KUNG MERON PA SIYANG HIYA’

Halos 400 raliyista ang sumugod sa labas ng Senado para ipanawagan ang pagbibitiw ni Senate President Alan Peter Cayetano.

Bitbit ang mga placard at tarpaulin, iginiit ng mga miyembro ng Sandugo na kung may kaunti pang hiya si Cayetano, bumaba na siya sa pwesto.

Kasabay nito ang pagsaludo nila kay Senador Chiz Escudero na siyang dahilan ng quorum kahapon.

Nananawagan din ang mga tagasuporta ni Pang. @bongbongmarcos ng agarang impeachment trial laban kay VP @indaysara Duterte, at pag-aresto kay Senador Bato dela Rosa.

Bukod sa paghilera sa southbound ng Diokno Blvd., idinaan ng mga ito sa pag-indak ang kanilang panawagan sa Senado’t suporta sa administrasyon. | RH 15 @JecelleRicafort, DZRH News

[Harry Spoelstra @HarrySpoelstra]

Impact of SARS-CoV-2 infection on subclinical myocardial injury in the general population: the Trøndelag Health Study

🚨NORWEGIAN CONFIRMATION BOMBSHELL:
COVID infection leaves lasting, hidden scars on the heart muscle, even years later.

"An elevated cardiac troponin I (cTnI) level indicates the presence of heart damage!"

➡️Study:
- This was a prospective longitudinal cohort study within the Trøndelag Health Study (HUNT), a large population-based survey in Norway,
- Researchers measured high-sensitivity cardiac troponin I (hs-cTnI), a sensitive blood marker of subclinical myocardial (heart muscle) injury, at baseline before the COVID-19 pandemic (2017–2019) in 37,823 general-population adults,
- The same marker was then re-measured after the pandemic wave (2021–2023) in the 19,550 participants who returned for follow-up,
- SARSCoV2 infection status was rigorously determined at follow-up via spike and nucleocapsid IgG antibody tests in blood, combined with self-reported infection history and any available laboratory confirmation of prior infection,
- Infection was defined using nucleocapsid IgG (specific to natural infection, not vaccination) plus spike IgG, self-report, and lab confirmation, precisely to capture true infections regardless of vaccination,

➡️Pre-infection result:
- Higher baseline hs-cTnI was associated with a lower risk of subsequent SARSCoV2 infection,

➡️Post-infection result:
- Confirmed SARSCoV2 infection (any definition) was independently linked to higher post-pandemic hs-cTnI concentrations and a significantly greater probability of an increase in hs-cTnI from pre- to post-pandemic levels, after full adjustment for confounders and baseline troponin,

➡️Vaccination:
- Study reports that 98.9% of participants were vaccinated and explain(in Methods) why they used nucleocapsid IgG (not spike) to avoid vaccine confounding,

➡️Limitations:
- Correctly sited and commented,
- No data on symptoms, asymptomatic/mild/severe cases, or hospitalization, but one may rightfully assume that the majority were mild SarsCoV2 cases,

➡️Conclusion:
“SARSCoV2 infection is associated with increased risk of developing chronic subclinical myocardial injury in the general population, but pre-existing chronic subclinical myocardial injury is not associated with increased risk of contracting SARS-CoV-2.”

‼️To all minimiser still shrugging off SARS-CoV-2 as “just a cold” or “over”: this Norwegian study proves every infection silently scars hearts across the general public with lasting subclinical damage, and with the now-established cumulative cardiac injury from reinfections, your denial is quietly killing many! WAKE-UP!
#AvoidSars2 #AvoidReinfections
https://t.co/7CwdsPsslD

[Prof. Akiko Iwasaki @VirusesImmunity]

Is there an association between human herpesviruses (HHVs) reactivation and Long COVID? We analyzed HHV DNA shedding in saliva and found that HHV-6 correlates with Long COVID severity. Claire Laxton, @S_Tabachnikova, Lily Cooke, Kexin Wang et al.

https://t.co/jsZznyXiGq (1/)

[Jette is Mataray 😊 @white_bite]

@RobbieMeriales Hay naku. They’re trained differently now. My kids didn’t have those theme writing books anymore and they’re from private schools.

[Danielle Beckman @DaniBeckman]

Not all organs respond equally to #COVID infection. DISCO-seq, a new technique led by my talented friend @HarsharanBhatia, combines 3D imaging and single-cell analysis to map Spike Protein tropism and found mostly in the liver, lungs, intestine & kidneys. https://t.co/9dA0axeUbU

[Prof. Akiko Iwasaki @VirusesImmunity]

Open-access link of our study is found here 👇🏼https://t.co/PT2EEI3iYj

[Prof. Akiko Iwasaki @VirusesImmunity]

Excited to share our study by @keylas3 et al. on pathological autoantibodies in people with Long COVID. We asked whether IgG in patients with Long COVID bind to human tissues/antigens and cause pathologies when transferred into mice. With @PutrinoLab

https://t.co/tcowCufWyf

[Harry Spoelstra @HarrySpoelstra]

Exosomal ORF3a mediates lung-liver axis to dysregulate hepatic lipid metabolism in mild COVID-19

🚨Mild COVID doesn’t “just go away.”

This new and very interesting Chinees study illustrates:

SARS-CoV-2 turns your lungs into a factory that ships ORF3a protein via exosomes straight to your liver.
No virus in the liver, yet it triggers massive fat buildup, inflammation, and early fibrosis.

Is this why so many people gain stubborn weight after even “mild” infection? SEMAGLUTIDE?

Study:
➡️ Mild COVID-19 causes liver dysfunction in 52.6% of patients (elevated ALT, AST, GGT) without direct viral infection of the liver,

➡️SARS-CoV-2 accessory protein ORF3a is packaged into exosomes by infected lung cells and systemically delivered to the liver,

➡️In hepatocytes, ORF3a binds Vps39 (HOPS complex), blocking autophagosome-lysosome fusion and causing massive lipid-droplet accumulation, steatosis, inflammation (↑IL-6, TNFα, IL-1β), macrophage polarization, and HSC-driven mild fibrosis,

➡️Findings confirmed in mouse mild-infection and lung-specific ORF3a models, plus human pluripotent stem cell-derived liver organoids,

➡️Exosome inhibitor GW4869 abolishes hepatic ORF3a delivery and damage,

(GW4869 is commercially available, but only as a laboratory research chemical. It is not yet an approved drug for human use or consumption)

➡️SARS-CoV-2 ORF3a is more potent than SARS-CoV ORF3a, and the effect is lost in the Beta variant (S171L mutation).

➡️Mild COVID-19 silently weaponizes lung-derived exosomal ORF3a to reprogram the liver into a lipid-storing, inflamed, fibrotic organ, proving AGAIN, that “mild” infection is never harmless

‼️So, thinking out loud, this may indicate that even mild COVID-19 could induce a Long COVID phenotype, effectively reprogramming the liver into an inflamed, fat-trapping organ.

Remarkably, GLP-1 receptor agonists like semaglutide (Ozempic/Wegovy) address this exact metabolic disruption head-on.

They might even reverse the liver damage, dropping the weight, and slashing inflammation.

This is another reason why they deserve the growing attention as a promising avenue in ongoing trials.

IMPORTANT REMINDER: “Mild” was never mild!
#AvoidSars2 #AvoidReinfections
https://t.co/WOBUMWqlk3

[Harry Spoelstra @HarrySpoelstra]

Cellular Metabolic Signatures of Long COVID-19

🚨Long COVID = MITOCHONDRIAL COLLAPSE
➡️MECHANISTIC EVIDENCE IS BECOMING OVERWHELMING: LC= CELLULAR ENERGY CRISIS!

➡️Small, but very interesting study from the USA in which they profiled metabolic dysfunction in IMMUNE CELLS of Long COVID (LC-19) patients versus recovered and pre-pandemic controls,

➡️Study:
- Small cohort of 20 volunteers (10 LC-19, 10 post-COVID recovered without symptoms),
- Analysed blood-derived immune cells for disruptions in glucose, galactose, pyruvate, fructose, mannose, and citric-acid-cycle pathways, mitochondrial function, energy utilization, responses to IL-1β/IL-6, and symptom-severity correlations,

➡️Findings:
- LC-19 cells are trapped in prolonged stress, they initially burn energy sources at high rates but rapidly exhaust,
- Energy utilization in recovered (non-LC) individuals is 2–3x higher than in virus-naïve controls, in LC-19 it collapses,
- Mitochondria cannot efficiently process fuel, causing reduced energy output,
- Patients with ≥4 symptoms showed the most dramatic metabolic failure,
- Immune cells also became desensitized to inflammatory signals,

➡️Symptom Link:
- Fatigue, dizziness, memory issues, shortness of breath, muscle pain, and exercise intolerance directly match the cellular “energy crisis,"

➡️Limitations:
- Small sample (n=20), larger validation studies needed.

‼️SO AGAIN, Long COVID is not psychological or vague inflammation , it is a measurable, severe cellular energy crisis driven by mitochondrial collapse and metabolic reprogramming. Human cells are literally running out of power, and current medicine hasn’t got a fix yet!

‼️With the overwhelming mechanistic consensus from 2024–2026 studies (including this study), it’s clear that SarsCoV2 can directly damage mitochondria, suppress OXPHOS genes, trigger structural collapse, and cause persistent ATP collapse, turning cells into an energy blackout, IMMUNE CELLS included. Symptoms follow directly. #LC
#AvoidSars2 #AvoidReinfections #LongCOVID #MitochondrialDysfunction
https://t.co/Xwg2W3ZFOd

[marv @mvn_dn]

TL cleanse: even after a tough loss, listen to this young woman displaying maturity, level-headedness and eloquence on the world stage while representing our country. I wish our leaders here could be the same. Mabuhay ka Alex

[ad @diapolym]

These are strange times. In all my years keeping track of PH politics, I would never imagine myself rooting for a Tito Sotto Senate Presidency, cheering for a Tulfo in the Senate, and agreeing with Migz Zubiri.

but here we are.

[Jette is Mataray 😊 @white_bite]

@RobbieMeriales I volunteer to do the root canal on vital teeth and extractions…WITHOUT ANESTHETICS!

[Eric Topol @EricTopol]

The ramp up of cancer immunotherapy is remarkable. Now we're seeing vaccines achieve some cures or remissions in the most refractory cancers: pancreatic, melanoma, glioblastoma, renal, triple-negative breast cancer.
✓ out the new Ground Truths (link in profile)

[Jette is Mataray 😊 @white_bite]

@RobbieMeriales @pauloMDtweets Napakapal ng konti. Siguro para pumantay ng konti yung baba.

[Arnaud Bertrand @RnaudBertrand]

This is pretty insane: the U.S. just tried to literally re-colonize part of the Philippines.

They did so under the so-called "Pax Silica" initiative, the brainchild of - surprise, surprise - an ex-Palantir guy named Jacob Helberg who now runs U.S. economic "diplomacy" from the State Department.

It's causing a big outcry in the Philippines, which is quite a feat given this is by far the most US-friendly country in Southeast Asia.

If you're the US and you're getting the Marcos administration - of all governments - to push back on sovereignty, you've really overplayed your hand.

What is the "Pax Silica" initiative? In a nutshell it's about the US getting other countries to commit to restructuring their AI tech infrastructure around a US-led stack. It's basically vendor lock-in: you hand over your critical minerals, align your export controls with Washington's, regulate AI the way America wants, and in return you get to be a US "trusted partner," whatever that means these days.

In essence, let's not kid ourselves, it's all about China: this is the US's initiative to "win the AI race" by getting other countries to contractually commit to keeping China out of their tech supply chains. When you can't preserve your lead through innovation, you seek to lock countries in contractually.

For instance as a country, this would mean telling Huawei they can't sell you AI chips, and telling Chinese firms they can't invest in your data centers - even if they're better and cheaper. It's not about choosing the best technology, it's about choosing the right flag.

But in this instance, the US went much further still: they literally tried to carve out 4,000 acres of Philippine territory (in New Clark City, 60 miles north of Manila) to be governed under US common law with diplomatic immunity - the first arrangement of its kind anywhere in the modern world.

This is according to the WSJ who ran the story last month (https://t.co/kydhIQfo2A) as if it was a done deal (it wasn't).

Heard about the "French concession" or "British concession" in China during the century of humiliation? Same thing: the US basically asked for an "American concession" in the Philippines.

Unsurprisingly, there was quite a bit of backlash in the country with for instance the Peasant Movement of the Philippines (KMP) calling it a “massive sellout” of the country’s land, minerals, and sovereignty (https://t.co/nkXSajH2Q7).

So much so that the Philippines' government - namely Joshua Bingcang, president and chief executive of the Bases Conversion and Development Authority (BCDA) - issued a statement saying that the Philippines had rejected US proposals that would place the project beyond local jurisdiction (https://t.co/ZmNWJB03eH).

Note, by the way, this delicious irony: the BCDA is the government agency that was created in 1992 specifically to convert former US military bases at Clark and Subic Bay after the Philippines spent decades negotiating their closure. New Clark City - where the Pax Silica's hub would go - is built on the old Clark Air Base.

So the agency whose entire reason for existing is to turn former American colonial territory (i.e. US military bases) into sovereign Philippine land is the one now being asked to hand part of that very same land back under US jurisdiction (and, apparently, declined).

Of course though, blocking this specific jurisdiction grab doesn't change the bigger picture. The Philippines is still a Pax Silica signatory, and Pax Silica itself is structurally neocolonial: you supply the cheap labor and raw materials, align your export controls and regulations with Washington's, cut yourself off from the world's rising technological powerhouse - and in exchange you get assembly jobs and the privilege of getting a pat on the head and being called a "trusted partner."

They dropped the most cartoonishly colonial demand - governing Philippine soil under US law - but the underlying architecture is the same: you serve America's supply chain, on America's terms, and you relinquish your sovereign right to trade with whoever offers the best deal.

[Harry Spoelstra @HarrySpoelstra]

L0NG C0VID IS QUIETLY WRECKING HEARTS.

Maybe time for a recap based on 2026 science.

Here’s the comparison for MACE, Stroke, Deadly Clots & overall CV risks:

➡️MACE (heart attack, stroke, heart failure)
• Non-COVID: HR 1.0
• COVID-19: 1.8–3.9x
• Long COVID: ~4.5x

➡️Stroke (ischemic):
• Non-COVID: HR 1.0
• COVID-19: ~2–3x
• Long COVID: ~3.5x

➡️Deadly clots (PE / VTE):
• Non-COVID: HR 1.0
• COVID-19: ~2–4x
• Long COVID: 3.2–4.4x

➡️Overall CV risks:
• Non-COVID: baseline
• COVID-19: ↑1.5–2.5x (arrhythmias, CAD, HF)
• Long COVID: 2–4.5x higher

Long COVID adds extra danger beyond regular post-COVID.

Risks hit even non-hospitalized patients and last for years.

Vax may reduce risks but certainly doesn’t erase it.

Absolute risks lower in young/healthy, but serious if older/comorbid.

‼️Today’s evidence shows that while any COVID-19 infection elevates cardiovascular risks, long COVID dramatically amplifies them, making proactive heart monitoring essential for affected patients.

Bottom line: Get your heart checked post-Covid19/ LongC0vid and #AvoidSars2 #AvoidReinfections!

🚨C0VID-19/L0NG C0VID are serious CV RISK FACTORS!