goals were: a) to detect viral load in indoor air in different areas and floors of a separate COVID building in a hospital [...], b) to evaluate the effect of an air-cleaner in the reduction of viral load in the presence of patients, and c) to examine the correlation between viral presence in the air and particle matter burden.
their methodology is making me happy!
Their system separated aerosols into > 2.5 μm, 1.0 to 2.5 μm, 0.5 to 1.0 μm, 0.25 to 0.50 μm, and < 0.25 μm, and found
SARS-CoV-2 was detected in all different fractions and the highest viral loads were detected at stages A (> 2.5 μm) and B (1 - 2.5 μm).
however this was in open-window conditions, ie. low CO2 and higher airflow; sampling with the same equipment in households, they found
the highest amount was detected in Stage 4 (0.25 - 0.5 μm)
The data is mostly PCR but they did do some sequencing, and positively confirmed the dominant variants were stable through the study, and not confounding.
Note the air cleaner was a "Airocide (APS GCS-25 model) air purifier" which uses "photocatalytic oxidation technology" as well as 254nm UV, with no HEPA or other mechanical filter.
Also, this is vindicating for those of us pleading with folks to not immediately de-mask in the hallway:
the highest concentration was detected in COVID clinic rooms displaying a high peak of 1123 copies/m3, whereas at the corridor area showed 481 copies/m3
Also highly of note, they could not detect any virus in the areas that were upstream of negative-pressure COVID-19 care. So yes, home isolation protocols that emphasize negative pressure zones absolutely are well founded!
These findings support the “Broken Bridge Syndrome” hypothesis, positing that structural disconnections between the brainstem and cerebellum contribute to PCS [Long COVID] symptomatology. Furthermore, we propose that chronic activation of the Extended Autonomic System (EAS), encompassing the hypothalamic-pituitary-adrenal (HPA) axis and autonomic nervous system, may perpetuate these symptoms
In this high quality brain volume data,
Significant volume loss was observed in the superior cerebellar peduncle (SCP) in LC patients compared to healthy controls (LC: 219.74 mm³ vs. controls: 347.03 mm³, p < .001, Hedges’ g = 3.31). Furthermore, reduced volumes were evident in the dorsal raphe (DR) and midbrain reticular formation (mRt) (p < .001)
It was not metabolism-marker scanning, but volumentric, so they were able to capture:
Three-dimensional reconstructions revealed deformities in the 4th ventricle and cerebellar peduncles, suggesting impaired cerebrospinal fluid dynamics [...] Importantly, these volume reductions and FA changes correlated with motor deficits, proprioceptive dysfunction, and autonomic dysregulation
TLDR?
Our findings reveal significant structural and functional alterations in the brainstem and cerebellar peduncles of LC patients
Most interesting detail: "we detected the virus passing from one sinus at the peak of infection to the other a few days later"
Model animals: "cynomolgus macaques"
They also evaluated "two convalescent animals [...] exposed to the SARS-CoV-2 Delta variant three months prior" and found "no major uptake by the nasal cavity" but "detection of the PET signal for SARS-CoV-2 spike antigen up to three months post initial infection in the lungs and brains"
"local accumulation [...] in areas of the brain [...] consistent with previous findings of neuroinflammation in humans infected with SARS-CoV-2 and in rhesus macaques up to six weeks after SARS-CoV-2 infection. The localized crossing of the blood-brain barrier (BBB) by the radiotracer in convalescent animals can be explained by thrombo-inflammation previously reported in patients with active long-COVID."
pregnant than if they are 
