#ImageJ

[wolframcarbide]

[filmvis]

Furiosa: A Mad Max Saga, George Miller, 2024

[vividotg]

ImageJ 1.53 Java 7 Di Exagear Windows Emulator

[halfslashmoon]

im not sure about risky horsewater

[unopenablebox]

sweater WIP in question. this sleeve is way closer to done than i remember it being, thanks to my 2019 self for your many mitzvot

[tenfluenza]

no one was proud of me for getting this done and they're wrong what matters is IM proud of me for today

[lixenn]

sorting out all those pictures is such a pain

I found pictures of dermis on my laptop but those are different ones than what i have on my presentation? i think my supervisor added the presentation ones and i don't have them saved.

well i saved them now and they are definitely better looking than the ones i had (because the qualtiy of those pictures... fucking horrible)

but i made lots of folders so hopefully i can sort this out and edit them a lil bit to make them look less god ugly

*stares at microscopy pictures on my new laptop*

HOly shit! I need to adjust them they look fucking horrible a few of them have this green undertone? the fuck?

Downloading ImageJ it is...

Fuck... how the hell do I open them in imagej when the pictures are on a power point

ummm

oh thank god i can save them from the powerpoint 🫡

[covid-safer-hotties]

Also preserved in our archive

By Dr. Sushama R. Chaphalkar, PhD.

In a recent research paper posted to the bioRxiv preprint* server, researchers in the United States investigated the potential effect of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on cholesterol metabolism, focusing on the role of the viral protein open reading frame 3a (ORF3a).

They found that SARS-CoV-2 causes cholesterol sequestration in lysosomes via the ORF3a protein, which disrupts protein trafficking and reduces the levels of bis(monoacylglycero)phosphate (BMP) in the cell, enhancing viral survival.

Background Coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, disrupts lipid metabolism, particularly cholesterol homeostasis, which can persist during and after infection. This is linked to disease severity and long-term complications like dyslipidemia and cardiovascular diseases.

Cholesterol is crucial for cellular function and is primarily transported through lysosomes, where proteins like Niemann-Pick C1 and C2 (NPC1 and NPC2) facilitate its release. SARS-CoV-2 may exploit plasma membrane cholesterol to enhance infectivity.

Disruptions in the lysosomal cholesterol pathway can cause cholesterol buildup, impairing cellular functions, and viruses like Ebola are known to hijack this mechanism. Notably, BMP plays a dual role: it aids in cholesterol transport and contributes to viral infection by promoting viral fusion with lysosomal membranes.

In the present study, researchers investigated the potential impact of SARS-CoV-2 infection on cholesterol transport in cells, focusing on the role of the viral protein ORF3a.

About the Study A variety of experimental techniques were employed, including culturing A549, HeLa, and Vero E6 cells, followed by SARS-CoV-2 infection at different multiplicities of infection. SARS-CoV-2 ORF3a-VPS39 interaction was studied using mutations at key residues (notably W193 and Y184, which were identified as critical for this interaction). Immunofluorescence, filipin staining, and confocal microscopy were used to assess cholesterol localization and vesicular dynamics, while high-content imaging quantified cell-specific responses.

Cholesterol levels were measured using gas chromatography-mass spectrometry (GC-MS), and lipid species were analyzed through shotgun lipidomics. For further protein analysis, western blotting was performed to detect secreted NPC2 and cathepsin D, along with cell lysates. Data were analyzed using ImageJ and Prism 9, and statistical significance was determined by t-tests or analysis of variance.

Results and Discussion SARS-CoV-2 infection was found to increase filipin-positive puncta in lysosomes of A549-hACE2 and Vero E6 cells, indicating altered cholesterol distribution, especially in lysosomes, without affecting total cholesterol levels. Among the 28 viral proteins tested, ORF3a showed the strongest increase in filipin puncta, suggesting significant lysosomal cholesterol sequestration.

Notably, SARS-CoV-2 ORF3a localized to lysosomes and caused them to swell, whereas SARS-CoV ORF3a did not induce such effects, highlighting a distinct pathogenic strategy unique to SARS-CoV-2.

ORF3a was found to interact with VPS39, a key component of the HOPS complex involved in cholesterol egress from lysosomes. Key residues W193 and Y184 were shown to form a hydrophobic binding interface critical for this interaction, distinguishing SARS-CoV-2 ORF3a from its SARS-CoV counterpart. Mutations at W193 and Y184 disrupted this interaction, while S171 and H182 had no significant effect.

SARS-CoV-2 ORF3a expression was shown to cause cholesterol accumulation in lysosomes, which was reduced by the W193A mutation. It also led to the mislocalization of NPC2 and increased its secretion, indicating disrupted NPC2 trafficking, likely due to interference with TGN-to-endosome transport. Additionally, BMP levels were significantly reduced in infected cells, which likely exacerbates lysosomal cholesterol sequestration.

In SARS-CoV-2-infected Vero E6 cells, BMP levels were found to decrease at 12 hours post-infection, coinciding with increased cholesterol at 18 hours. In HeLa-Flp-In cells, SARS-CoV-2 ORF3a was found to reduce BMP levels by 20%, with partial rescue in the W193A mutant. Lipidomics confirmed this reduction, correlating BMP loss with cholesterol accumulation and suggesting BMP reduction may contribute to cholesterol sequestration.

SARS-CoV-2 may reduce plasma membrane cholesterol to limit secondary infections, as shown by decreased SARS-CoV-2 infection in NPC1 inhibitor-treated cells. This supports the hypothesis that the virus manipulates cholesterol distribution to optimize replication conditions. Interestingly, the virus also appears to reduce its own infectivity within a single cell, suggesting a self-regulating mechanism to prevent viral overload and ensure broader host-level spread.

Conclusion In conclusion, a novel mechanism by which SARS-CoV-2 disrupts host cell lipid metabolism, specifically through cholesterol sequestration in lysosomes, has been elucidated. By uncovering the specific interaction between the viral protein ORF3a and host protein VPS39, the study highlights a critical role of lysosomal cholesterol trafficking disruption in SARS-CoV-2 pathogenesis.

This discovery opens potential therapeutic avenues to target lipid dysregulation in COVID-19, which could help mitigate both the disease's immediate and long-term metabolic consequences, including dyslipidemia and cardiovascular complications.

Journal reference: Preliminary scientific report. Manipulation of Host Cholesterol by SARS-CoV-2. Aliza Doyle et al., bioRxiv, 2024.11.13.623299 (2024), DOI: 10.1101/2024.11.13.623299,

Study Link: www.biorxiv.org/content/10.1101/2024.11.13.623299v1

[animacion-marina]

How to resize image without losing quality

Supervised Learning: KNN is a supervised learning algorithm, meaning it learns from labeled data to make predictions. Instance-Based Learning: KNN is also considered an instance-based or lazy learning algorithm because it stores the entire training dataset and performs computations only when making predictions. 

Use Java Maven Project For Image Resize

media stands out as the best tool for resizing pictures. With its user-friendly interface and advanced resizing capabilities, Shrink. media allows you to adjust your pictures' dimensions and file sizes while maintaining excellent visual quality.

Boof CV for Java Image Processing

Java CV for Java Image Processing

ImageJ for Java Image Processing

Boof CV is a comprehensive library designed for real-time computer vision and image processing applications. It focuses on providing simple and efficient algorithms for tasks such as image enhancement, feature detection, and object tracking.

[danrealxd]

Awful thing I drew💔

Based on this stupid ass imagej

[wolframcarbide]

[kunosoura]

I know for sure now I'm not ever going to be happy doing some super analytical and instrumentation heavy analysis. i'm just a potion monkey put me in an organic synthesis lab and I'll make whatever you want till the skies fall and have a great day every time. don't ever make boot up imagej ever again kthx

[filmvis]

Oppenheimer, Christopher Nolan, 2023

[cherenkovs]

casting a spell of IMAGEJ WORKS TODAY

[halfslashmoon]

kind of more limited ability to upload videos (fair) so im breaking off into a separate post but this is a more active ijm script from last year that lets you watch a virtual slime fight for its life and eventually deplete its resources, toxify its environment and die so hard that future molds struggle to survive on top of its remains. Hooray!!!!

[unopenablebox]

apparently, by happening to know that you need to preallocate arrays in matlab, i've saved my labmate like five days of simulation time

the shock of having had useful programming-related knowledge not already known to all of mankind was so enormous that i may need to lie down