Chick fil a near i 95

I happened upon a pile of CRT monitors at my university that were destined for scrap. The left is a Dell M991(BIG!) and the right is a Sony G220
The Sony seems damned near perfect, while the Dell needs some minor color adjustments. Hopefully I can get it dialed in this weekend :D

https://www.pnas.org/doi/full/10.1073/pnas.2200960119
TL;DR in last paragraph.
“In line with the potential neurotropic properties of SARS-CoV-2, recent evidence indicated the presence of viral proteins in brain regions of COVID-19 patients (21, 22) as well as in the brains of K18-ACE2 transgenic mice (22, 23) and Syrian hamsters (24) infected with SARS-CoV-2. The presence of SARS-CoV-2 in the human brain has been associated with marked astrogliosis, microgliosis, and immune cell accumulation (21). Further indicating the ability of SARS-CoV-2 to infect cells of the CNS, SARS-CoV-2 has also been shown to infect human brain organoid cells in culture (22, 25–27). Recently, SARS-CoV-2 has been found to cross the blood–brain barrier (BBB) in mice (28–30) and in two-dimensional static and three-dimensional microfluidic in vitro models (31, 32), therefore potentially reducing the integrity of the BBB.
We performed a cortical surface–based morphometry analysis (using a high-resolution 3T MRI) on 81 subjects diagnosed with mild COVID-19 infection (62 self-reported anosmia or dysgeusia) who did not require oxygen support. The analysis was performed within an average (SD) interval of 57 (26) d after SARS-CoV-2 detection by qRT-PCR, and the subjects were compared with 81 healthy volunteers (without neuropsychiatric comorbidities) scanned during the COVID-19 pandemic (balanced for age [P = 0.97] and sex [P = 0.3]). The COVID-19 group presented higher levels of anxiety and depression symptoms, fatigue, and excessive daytime sleepiness (SI Appendix, Table S1 shows epidemiological and clinical data). An analysis of cortical thickness (adjusted for multiple comparisons using the Holm–Bonferroni method) revealed areas of reduced cortical thickness exclusively in the left hemisphere, including the left gyrus rectus (P = 0.01), superior temporal gyrus (P = 0.036), inferior temporal sulcus (P = 0.02), and posterior transverse collateral sulcus (P = 0.003) (Fig. 1A). There was no observed increase in cortical thickness.
A subgroup of 61 participants of the COVID-19 group also underwent neuropsychological evaluation, which assessed episodic verbal memory (logical memory subtest, immediate and delayed recall, Wechsler Memory Scale), sustained attention (Color Trails A), and alternating attention and cognitive flexibility (Color Trails B). The tests were performed a median of 59 d (range between 21 and 120 d) after diagnosis; we observed fatigue in ∼70% of individuals and daytime sleepiness in 36%. Despite the high level of education of the participant subgroup (median of 16 y), the comparisons with Brazilian normative data (z scores were adjusted for age, sex, and education) showed that nearly 28% of participants presented impairments (z scores ≤ −1) in immediate episodic verbal memory (immediate recall, including mild, moderate, and severe impairments), and ∼34 and 56% underperformed (z scores ≤ −1) on Color Trails A (sustained attention) and B (alternating attention and cognitive flexibility), respectively (SI Appendix, Fig. S1 and Table S2). Interestingly, 77% of these COVID-19 patients also presented acute anosmia or dysgeusia, which may be related to the observed changes in cortical thickness (19). The high proportions of anosmia and dysgeusia support the idea of the virus entering the nervous system, more specifically the orbitofrontal region (due to the proximity and communication with the nasal cavity).
We observed a negative correlation between BAI (Beck Anxiety Inventory) scores and the cortical thickness of orbitofrontal regions (adjusted for fatigue scores) (Fig. 1B and SI Appendix, Table S3). We also identified a positive correlation between immediate episodic verbal memory and cortical thickness of regions associated with language (adjusted for fatigue scores) (Fig. 1C and SI Appendix, Table S3). There was a likely correlation between Color Trail B and the thickness of the gyrus rectus after adjusting for fatigue (r = 0.2, P = 0.13). Our findings indicate that cortical thickness atrophy is associated with neuropsychiatric symptoms and cognitive impairment in COVID-19 patients with mild or no respiratory symptoms.
Figure 1: Cortical thickness atrophy after mild COVID-19 infection. Surface-based morphometry by high-resolution 3T MRI (A). Results from the analysis of 81 subjects with confirmed SARS-CoV-2 diagnosis (who had mild respiratory symptoms and did not require hospitalization or oxygen support) compared with 81 healthy volunteers (without a diagnosis of COVID-19). The analysis was performed within an average (SD) of 57.23 (25.91) d after diagnosis. (B) Correlation between anxiety scores (BAI) and right orbital gyrus thickness. (C) Correlation between Color Trail B test (Z-TRAILB: z-scores were based on Brazilian normative data) and left gyrus rectus thickness. Data depict partial correlation coefficients (adjusted for fatigue).
[...] To investigate proteome-level changes caused by SARS-CoV-2 infection, we conducted a liquid chromatography–mass spectrometry (LC/MS) proteomic analysis with a separate set of samples consisting of 12 postmortem brain samples from COVID-19 patients vs. 8 SARS-CoV-2–negative controls (SI Appendix, Tables S6 and S7). We identified 656 differentially expressed proteins: 117 down-regulated and 539 up-regulated. Pathways associated with neurodegenerative diseases, carbon metabolism, and oxidative phosphorylation were enriched among the differentially expressed proteins (SI Appendix, Fig. S6). Notably, proteins expressed in astrocytes were enriched among the differentially expressed proteins, consistent with the higher frequency of infected astrocytes observed in COVID-19 postmortem brains (Fig. 2F).
To gather further evidence of the susceptibility of human astrocytes to SARS-CoV-2 infection, neural stem cell–derived human astrocytes (BR-1 cell line) (35) were exposed to the virus, and the viral load was determined at 24 hpi (Fig. 3A). Confirming what was seen in the postmortem brain samples, viral genetic material (Fig. 3B), dsRNA, and spike protein (Fig. 3 C and D) were detected in infected cells with significant overlap (Fig. 3 C and E). SARS-CoV-2 infection reduces cell viability by over 25% at 72 hpi (Fig. 3F). To confirm the ability of SARS-CoV-2 to infect human astrocytes, we used a replication-competent eGFP reporter–pseudotyped vesicular stomatitis virus (VSV) in which the glycoprotein gene (G) of VSV was replaced by the full-length SARS-CoV-2 spike (S; VSV-eGFP-SARS-CoV-2) (36). The human astrocyte culture was also infected by VSV-eGFP-SARS-CoV-2 (Fig. 3 G and H). Altogether, these results provide strong evidence that human astrocytes are permissive to SARS-CoV-2 infection and also represent a site for viral replication in the CNS.
[...] …we started by using a publicly available, single-nucleus RNA-sequencing (snRNA-seq) dataset from brain samples of patients with COVID-19 (37) to analyze the mRNA expression of the classical SARS-CoV-2 receptor ACE2 as well as the alternative receptors NRP1 and BSG (38–40). These analyses revealed that ACE2 mRNA was undetected in astrocytes (21, 37); however, astrocytes did express detectable levels of NRP1 and BSG mRNA (Fig. 4 A and B). We also found that the levels of expression and percentage of astrocytes expressing NRP1 and BSG mRNA were increased in astrocytes from COVID-19 patients compared with controls (Fig. 4 A and B). [...] …we performed western blotting using cultured neural stem cell–derived astrocyte extracts to evaluate if the data from snRNA-seq matched proteome-level data from our in vitro model with ACE2-transduced A549 cells as the positive control. The human astrocytes used in this study did not express ACE2, whereas they did express NRP1 (Fig. 4 C–E and SI Appendix, Fig. S7). To determine whether NRP1 was the receptor permitting SARS-CoV-2 infection in astrocytes, we preincubated these cells with a neutralizing anti-NRP1 antibody. Neutralization of NRP1 inhibited the infection of cultured astrocytes by SARS-CoV-2 (Fig. 4D) as well as the infection of cultured astrocytes by VSV-eGFP-SARS-CoV-2 (Fig. 4 E and F). These results confirm that SARS-CoV-2 infects human astrocytes via the NRP1 receptor.
[...] …we analyzed the proteome of SARS-CoV-2–infected human astrocytes. LC/MS-based shotgun proteomics revealed 170 differentially expressed proteins in SARS-CoV-2–infected astrocytes compared with mock controls… [...] …pathway enrichment and interactome analyses predicted a wide range of biological processes and regulatory networks affected by SARS-CoV-2 infection (Fig. 5A). Pathways involved in carbon/glucose metabolism were among the most enriched (Fig. 5B). More specifically, proteins found differentially expressed in SARS-CoV-2–infected astrocytes and in COVID-19 postmortem brain tissue samples belonged to glycolysis/gluconeogenesis, carbon metabolism, and the pentose phosphate pathway (Fig. 5C). Collectively, these data reinforce that SARS-CoV-2 infects astrocytes in the CNS, possibly affecting energy metabolism pathways and modulating proteins associated with neurodegeneration.
[...] Astrocytes are essential to brain homeostasis not only because they are the main energy reservoirs of the brain (42) but also, due to their important role in protective responses to cell damage triggered by infection or sterile inflammation (43, 44). There is evidence that astrocytes may secrete yet undetermined neurotoxic factors (43–45) and are also involved in the uptake, synthesis, and distribution of brain metabolites (46, 47). Thus, we investigated if neuronal viability could be affected by exposure to media conditioned by SARS-CoV-2–infected astrocytes. To test this hypothesis, we cultured NSC-derived neurons or differentiated SH-SY5Y neurons for 24 h in a control or conditioned medium in which SARS-CoV-2–infected astrocytes were grown (Fig. 6A). The conditioned medium increased the rates of apoptosis by 45.5 and 22.7% in NSC-derived neurons and SH-SY5Y neurons, respectively (Fig. 6 B–E and SI Appendix, Fig. S10 A and B). The possibility of neuronal infection was ruled out as viral RNA was not detected in either cell type after exposure to the conditioned medium (SI Appendix, Fig. S10 E and F), and direct exposure to SARS-CoV-2 did not reduce the viability of NSC-derived neurons or SH-SY5Y neurons after 24 (Fig. 6 D and E), 48, or 72 h (SI Appendix, Fig. S10 C and D). These results suggest that SARS-CoV-2–infected astrocytes release soluble factors, which reduce neuronal viability.
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Figure 6 (cropped): Percentage of living or nonliving (D) NSC-derived neurons and (E) SH-SY5Y cells. Cells were classified as living (gray bars; double negative), in early apoptosis (purple bars; apotracker+/FVS−), in late apoptosis (pink bars; double positive), or necrotic (green bars; apotracker−/FVS+). (F) Differentiated SH-SY5Y cells were cultured for 24 h in the presence of medium conditioned by SARS-CoV-2–infected astrocytes (ACM CoV-2) or uninfected astrocytes (ACM CTL). The viability of SH-SY5Y cells was assessed using an ATP (adenosine triphosphate) -quantifying, luminescence-based cell viability assay (CellTiter-Glo) at 24 h postinfection. P values were determined by one-way ANOVA followed by Tukey’s post hoc test. **P < 0.01 compared with the mock group; ***P < 0.001 compared with the mock group; ****P < 0.0001 compared with the mock group
[...] ...we found that SARS-CoV-2 infection elicits a neurotoxic secretory phenotype in astrocytes that results in increased neuronal death. A similar phenomenon has been observed when astrocytes are activated by inflammatory factors (43, 86, 87). The alterations in cortical thickness we observed in COVID-19 patients could be explained by this neuronal death, at least partially, as well as by other mechanisms, including reactive astrogliosis and alterations in astrocyte specification and morphogenesis, as previously described in Alzheimer's disease, autism, and schizophrenia (88–90), as well as epilepsy, autism, and self-injury (91–94). Matschke et al. (21) reported astrogliosis in 86% of individuals who died following a diagnosis of SARS-CoV-2 infection. In agreement, snRNA-seq data show that the main markers of reactive astrocytes (95) are enriched in samples from the medial frontal cortex of patients with COVID-19 compared with noninfected patients, supporting the hypothesis that reactive astrogliosis is a feature of COVID-19 (SI Appendix, Fig. S11). Astrocytes are also relevant in the regulation of synapses (and neural networks) and have been linked to the manifestation of depression (96), anxiety symptoms (97), and memory impairment (98), all of which have been observed in our post-COVID infection cohort.
In summary, our findings are consistent with a model in which SARS-CoV-2 is able to reach the CNS of COVID-19 patients, infect astrocytes via NRP1 interaction, and secondarily impair neuronal function and viability. These changes may contribute to the alterations of brain structure observed here and elsewhere, thereby resulting in the neurocognitive and neuropsychiatric dysfunctions manifested by some patients with COVID-19. Our study comes as a cautionary note that mechanisms of neuroinvasion in fatal COVID-19 could also be operative in mild COVID-19. However, it is important to note that the study was limited in that neuroimaging and cognitive testing were obtained from a different cohort than fatal COVID-19, in which only a minority of individuals showed evidence of astrocytic invasion.”