wesleyxjames

[castametric]

the highest honor I can bestow upon a work of fiction is “metaphor for the immune system”

[thymodyke]

ideal threesome dynamics

[brosis-medical]

Kochsalz: Ein überraschender Verbündeter im Kampf gegen Krebs?

Es ist allgemein bekannt, dass zu viel Salz ungesund ist. Neue Studien zeigen jedoch, dass Natriumchlorid, also Kochsalz, in der Krebstherapie nützlich sein könnte, nämlich als Kochsalz gegen Krebs. Höhere Natriumkonzentrationen können die Aktivität tumorbekämpfender T-Zellen steigern, was zu effektiveren Krebstherapien führen könnte. Experten raten jedoch davon ab, mehr Salz zu konsumieren, da…

[lotus-tower]

COVID-19's long-term effects on the body: an incomplete list

COVID’s effect on the immune system, specifically on lymphocytes:

NYT article from 2020 (Studies cited: https://www.biorxiv.org/content/10.1101/2020.05.18.101717v1, https://www.biorxiv.org/content/10.1101/2020.05.20.106401v1, https://www.unboundmedicine.com/medline/citation/32405080/Decreased_T_cell_populations_contribute_to_the_increased_severity_of_COVID_19_, https://www.medrxiv.org/content/10.1101/2020.06.08.20125112v1)

 https://www.biorxiv.org/content/10.1101/2022.01.10.475725v1

https://www.science.org/doi/10.1126/science.abc8511 (Published in Science)

 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9057012/

https://www.forbes.com/sites/williamhaseltine/2022/04/14/sars-cov-2-actively-infects-and-kills-lymphoid-cells/

https://www.cleveland.com/news/2022/10/in-cleveland-and-beyond-researchers-begin-to-unravel-the-mystery-of-long-covid-19.html

SARS-CoV-2 infection weakens immune-cell response to vaccination: NIH-funded study suggests need to boost CD8+ T cell response after infection

https://www.merckmanuals.com/professional/hematology-and-oncology/leukopenias/lymphocytopenia

https://thetyee.ca/Analysis/2022/11/07/COVID-Reinfections-And-Immunity/

Dendritic cell deficiencies persist seven months after SARS-CoV-2 infection

https://www.frontiersin.org/articles/10.3389/fimmu.2022.1034159/full

https://www.n-tv.de/politik/Lauterbach-warnt-vor-unheilbarer-Immunschwaeche-durch-Corona-article23860527.html (German Minister of Health)

Anecdotal evidence of COVID’s effects on white blood cells:

 https://twitter.com/DrJohnHhess/status/1661837956875956224

 https://x.com/TristanVeness/status/1661565201345564673

https://twitter.com/TristanVeness/status/1689996298408312832

Much more if you speak to Long Covid patients directly!

Related information of interest:

China approves Genuine Biotech's HIV drug for COVID patients

COVID as a “mass disabling event” and impact on the economy:

https://www.ctvnews.ca/health/report-says-long-covid-could-impact-economy-and-be-mass-disabling-event-in-canada-1.6306608

https://x.com/inkblue01/status/1742183209809453456?s=20

COVID’s impact on the heart:

https://www.dailystar.co.uk/news/world-news/deadly-virus-could-lead-heart-31751263 (Research from: Japan's Riken research institute)

https://www.brisbanetimes.com.au/national/queensland/unlike-flu-covid-19-attacks-dna-in-the-heart-new-research-20220929-p5bm10.html

https://www.mdpi.com/2077-0383/12/1/186

https://medicalxpress.com/news/2023-04-mild-covid-effects-cardiovascular-health.html

https://publichealth.jhu.edu/2022/covid-and-the-heart-it-spares-no-one

https://www.bhf.org.uk/informationsupport/heart-matters-magazine/news/coronavirus-and-your-health/is-coronavirus-a-disease-of-the-blood-vessels (British Heart Foundation)

COVID’s effect on the brain and cognitive function:

https://www.openaccessgovernment.org/article/brain-infection-by-sars-cov-2-lifelong-consequences/171391/

https://www.cidrap.umn.edu/covid-19/study-shows-covid-leaves-brain-injury-markers-blood

https://www.theguardian.com/world/2020/jul/08/warning-of-serious-brain-disorders-in-people-with-mild-covid-symptoms

Cognitive post-acute sequelae of SARS-CoV-2 (PASC) can occur after mild COVID-19 

Neurologic Effects of SARS-CoV-2 Transmitted among Dogs

https://journals.lww.com/nsan/fulltext/2022/39030/neurological_manifestations_and_mortality_in.4.aspx

https://www.salon.com/2023/06/17/new-evidence-suggests-alters-the-brain--but-the-extent-of-changes-is-unclear/

https://www.scientificamerican.com/article/covid-virus-may-tunnel-through-nanotubes-from-nose-to-brain/

https://neurosciencenews.com/post-covid-brain-21904/

https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(22)00260-7/fulltext

https://medicalxpress.com/news/2022-08-covid-infection-crucial-brain-regions.html

https://news.ecu.edu/2022/08/04/covid-parkinsons-link/

Covid as a vascular/blood vessel disease:

https://www.salon.com/2020/06/01/coronavirus-is-a-blood-vessel-disease-study-says-and-its-mysteries-finally-make-sense/

https://www.salon.com/2023/12/27/brain-damage-caused-by-19-may-not-show-up-on-routine-tests-study-finds/

https://www.nih.gov/news-events/news-releases/sars-cov-2-infects-coronary-arteries-increases-plaque-inflammation

https://www.mdpi.com/2077-0383/12/6/2123

https://www.sciencedaily.com/releases/2021/10/211004104134.htm (microclots)

Long Covid:

Post-COVID-19 Condition in Canada: What we know, what we don’t know, and a framework for action

 https://www.ctvnews.ca/health/coronavirus/more-than-two-years-of-long-covid-research-hasn-t-yielded-many-answers-scientific-review-1.6235227

 https://www.cbc.ca/news/canada/london/cause-of-long-covid-symptoms-revealed-by-lung-imaging-research-at-western-university-1.6504318

 https://www.cbc.ca/news/canada/montreal/long-covid-study-montreal-1.6521131

https://news.yale.edu/2023/12/19/study-helps-explain-post-covid-exercise-intolerance

Other:

- Viruses and mutation: https://typingmonkeys.substack.com/p/monkeys-on-typewriters

Measures taken by the rich and world leaders

Heightened risk of diabetes

https://jamanetwork.com/journals/jama/fullarticle/2805461

https://www.nature.com/articles/d41586-022-00912-y

Liver damage:

https://timesofindia.indiatimes.com/city/mumbai/46-of-covid-patients-have-liver-damage-study/articleshow/97809200.cms?from=mdr

tl;dr: covid is a vascular disease, not a respiratory illness. it can affect your blood and every organ in your body. every time you're reinfected, your chances of getting long covid increase.

avoid being infected. reduce the amount of viral load you're exposed to.

the gap between what the scientific community knows and ordinary people know is massive. collective action is needed.

[garadinervi]

Djane Ki, M​é​canique des Fluides, from Turba & Turbo E​.​P., LBA-KI-CD8, (Digital album), La Bande Adhésive, 2024

Written, produced and mixed by Vanessa Jeantrelle aka Dj Ki Artwork & mastering by Nicolaiev Boutovitch at LBA studio

@dj-ki

[worldsandemanations]

Djane Ki, M​é​canique des Fluides, from Turba & Turbo E​.​P., LBA-KI-CD8, (Digital album)

[tadayoedoshizumazu]

Yashiro teleported perfectly into Doumeki's body

🤨

😏

😠

🍓

*extra - drama cd8 - "WE SWITCHED BODIES?!"

[w3t-c4t]

I hate to do this but its getting bad and she needs help.

This is my grandma and she has skin cancer and is struggling to get the funds she needs so im gonna do what i can to help, i am offering a 30% discount to all my commissions and all proceeds will go towards my grandmother's treatment.

you don't have to donate or do anything just please share around so i can help her.

[willowreader]

COVID-19 and Its Impact on the Immune System: Increased Vulnerability to Future Pathogens

Introduction

The COVID-19 pandemic, caused by the SARS-CoV-2 virus, has had profound effects on global health. Beyond the immediate respiratory symptoms, emerging evidence suggests that COVID-19 can cause long-term alterations to the immune system, potentially making individuals more susceptible to future infections. This article explores how COVID-19 affects immune cells, particularly CD4+ and CD8+ T cells, and draws comparisons with the immunological impacts of HIV.

To listen click on View on Twitter.

[humancelltournament]

Human Cell Tournament Round 1

Propaganda!

In molecular biology, CD4 (cluster of differentiation 4) is a glycoprotein that serves as a co-receptor for the T-cell receptor (TCR). CD4 is found on the surface of immune cells such as helper T cells, monocytes, macrophages, and dendritic cells. CD4+ T helper cells are white blood cells that are an essential part of the human immune system. They are often referred to as CD4 cells, T helper cells or T4 cells. They are called helper cells because one of their main roles is to send signals to other types of immune cells, including CD8 killer cells, which then destroy the infectious particle. If CD4 cells become depleted, for example in untreated HIV infection, or following immune suppression prior to a transplant, the body is left vulnerable to a wide range of infections that it would otherwise have been able to fight.

In cell biology, a vesicle is a structure within or outside a cell, consisting of liquid or cytoplasm enclosed by a lipid bilayer. Vesicles form naturally during the processes of secretion (exocytosis), uptake (endocytosis), and the transport of materials within the plasma membrane. Vesicles perform a variety of functions. Because it is separated from the cytosol, the inside of the vesicle can be made to be different from the cytosolic environment. For this reason, vesicles are a basic tool used by the cell for organizing cellular substances. Vesicles are involved in metabolism, transport, buoyancy control,[2] and temporary storage of food and enzymes. They can also act as chemical reaction chambers.

[covid-safer-hotties]

Arthritis medications could reverse COVID lung damage - Published Sept 6, 2024

Arthritis drugs already available for prescription have the potential to halt lingering lung problems that can last months or years after COVID-19 infections, new research from the University of Virginia School of Medicine and Cedars-Sinai suggests.

By examining damaged human lungs and developing an innovative new lab model, the scientists identified faulty immune processes responsible for the ongoing lung issues that plague an increasing number of people after they've otherwise recovered from COVID-19. These lasting harms of COVID infection, known as "post-infection lung fibrosis," have no good treatments. The new research, however, suggests that existing drugs such as baricitinib and anakinra can disrupt the malfunctioning immune response and finally allow damaged lungs to heal.

"Using advanced technologies like spatial transcriptomics and sophisticated microscopy, we compared lung tissues from patients and animal models we developed in the lab. We found that malfunctioning immune cells disrupt the proper healing process in the lungs after viral damage. Importantly, we also identified the molecules responsible for this issue and potential therapeutic options for patients with ongoing lung damage."

"'Spatial-omics' are state-of-the-arts technologies that can measure the molecular features with spatial location information within a sample," explained researcher Chongzhi Zang, PhD, of UVA's Department of Genome Sciences. "This work demonstrates the power of spatial transcriptomics combined with data science approaches in unraveling the molecular etiology of long COVID."

The researchers note that the findings could prove beneficial not just for lung scarring from COVID but for lung fibrosis stemming from other sources as well.

"This study shows that treatments used for the acute COVID-19 disease may also reduce the development of chronic sequelae, including lung scarring," said Peter Chen, MD, the Medallion Chair in Molecular Medicine and interim chair of the Department of Medicine at Cedars-Sinai. "Our work will be foundational in developing therapies for lung fibrosis caused by viruses or other conditions."

Understanding COVID-19 lung damage The researchers – led by Sun, Chen and Zang – wanted to better understand the cellular and molecular causes of the lingering lung problems that can follow COVID infections. These problems can include ongoing lung damage and harmful inflammation that persists well after the COVID-19 virus has been cleared from the body.

The researchers began by examining severely damaged lungs from transplant patients at both UVA and Cedars-Sinai. None of the patients had a lung disease that would have required a transplant prior to contracting COVID-19, so the scientists were hopeful that the lungs would provide vital clues as to why the patients suffered such severe lung damage and persistent fibrosis. Using the insights they obtained, the scientists then developed a new mouse model to understand how normally beneficial immune responses were going awry.

The researchers found that immune cells known as CD8+ T cells were having faulty interactions with another type of immune cell, macrophages. These interactions were causing the macrophages to drive damaging inflammation even after the initial COVID-19 infection had resolved, when the immune system would normally stand down.

The scientists remain uncertain about the underlying trigger for the immune malfunction – the immune system may be responding to lingering remnants of the COVID-19 virus, for example, or there could be some other cause, they say.

The new research suggests that this harmful cycle of inflammation, injury and fibrosis can be broken using drugs such as baricitinib and anakinra, both of which have already been approved by the federal Food and Drug Administration to treat the harmful inflammation seen in rheumatoid arthritis and alopecia, a form of hair loss.

While more study is needed to verify the drugs' effectiveness for this new purpose, the researchers hope their findings will eventually offer patients with persistent post-COVID lung problems much-needed treatment options.

"Tens of millions of people around the world are dealing with complications from long COVID or other post-infection syndromes," Sun said. "We are just beginning to understand the long-term health effects caused by acute infections. There is a strong need for more basic, translational and clinical research, along with multi-disciplinary collaborations, to address these unmet needs of patients.

Journal reference: Narasimhan, H., et al. (2024). An aberrant immune–epithelial progenitor niche drives viral lung sequelae. Nature. doi.org/10.1038/s41586-024-07926-8 www.nature.com/articles/s41586-024-07926-8

[heartinarosebud]

My Cutest Wobbledogs

Rose: 0E:B1tB9F0Fo:cDA3PF:cF::30c::ccFcB^:9c0cccE:c^c:^1^:Cot883B:ec0cB40:017E00aFDEtctEtE^ctFF3t2EFlF3E03t8t::^0EeF3Ac^FUtP:Ftt:ttE1=:Ectt^h10cc:tF sL6::ctR6m:::l1BFFiPDYc:Dc^98F02tEt1F0A^Ec0^:EBt:cFFF:i0F07t

Ringo: F2:D8bb9088EE000:E00c0s:;06FFcc60F:BcF00t452t:^BFDEt8<FF8t0it:att1t:4oc=c::9^:8cF^chcccc9B:n74FF:3:BRC69Ecic6^:c0c^pFa:3^0Ym3lFD5040FEE33FC4FEF:4FBF280:EB0FtcP0c.011t80:^F08^Bg0ABa:011:1D207g0a:01^aB05^0ccB0040A9:^a8aF1E:83c0c:02UBP0F552c;cc:0AP

Amethyst: b4C3bCA30FC0B685cFAF:62.<^b9040501YE077^0CC600;F1dE182C0^yj8Dmc5P00E1AEC8c64=0B6269BC6=C8F^5BE<B7tdtbA884<2=C:DE0:<4:hh31C3:cd8;A091cF;F<00=08FF53:8E=0C770C5bFcD=bCaDEFgF^0b6c:P0:0F3m7F196:9c1C13B34D<P^ebsB^4F0aB8044^^U323c38814FC^B750:3015B18C08E8A24:C0FeF1DC5d=^:DF5E0F18Eb8D:FAaF0FEFa34FaF3CC00aFEF2a10

Wayne: F1t^Cb00Fb10c=a01a000F8F0FF8<^dB8001c:F483:=F8277P051jFcP2b^0408Ea892u0tAf8lD=34g460t2a00500t:5aF2:873FFFF<=Ccc3CF=C<3<F:0;BFC;b;=DcC6FC10hE^65c3F2BFa3<D^Db=t=;34;B94cDF5DmEFKF9:f80FF21B:FC0Fc0F33ron8^10-PF21FF:AF.3^^aF3:C550:cD1a040^^01810F00i0FC8<46F^B37FDE40FCEa48F4C7fFE0AA50FF3U709C0E2F8FaYF50

Big Devil: =8B3FF16cFCCbFC1AB16:AFh^E7B32FF^7F112F1=B372DEADBC7CiD10AE159ae9D2DDF45ECBB0DF:FD7F8c:A9aFBFe0F935FFD711F945aa^D3FFC::FA0cFFFcF=<7F3DF2jaD:Fc:A:CFEF3a60;4=FF6F::449=;9:Faaa645F;::B3F3FFAbCm;Eb=^DCFFBFDB14BrFAlFFCFFA^PBPU=^820F1Y18E000cB^02gv1EFi:801C20^a32 2D06A35B^c9^bFDa0054FED610031B^F=64a<baPBD20c05DDFFFFEC=

[gaysie]

at this conference and someone introduced a keynote by being like “he was one of the first guys to really—put a mouse in a blender and get all them [tissue resident cd8 t cells] out” but all i heard was rodent and blender and there is armand everywhere for those with eyes to see

[kon-igi]

COVID = AIDS?

@heresiae mi ha chiesto di commentare QUESTO POST (commentare non del tipo 'Maestro, illuminaci!' ma più tipo '???????') e mi tocca dire che nonostante alcuni punti siano meritevoli di approfondimento (perché, di massima, corretti) le informazioni vengono sparate in stecca con un tono allarmistico e, a mio avviso, esagerato.

In sintesi, nel post linkato si paragona il covid all'aids perché sono venute fuori evidenze (come leggerete, comuni ad altre infezioni virali) che la malattia da Sars-CoV2 abbia un effetto indebolente sul sistema immunitario... senza scendere in spiegazioni dettagliate su cosa siano i Linfociti T (T Cells nell'originale), in sostanza si correla l'infezione con un'aumentata APOPTOSI (morte cellulare programmata, utile al rinnovo) di queste cellule del nostro sistema immunitario, col risultato che dopo la malattia quest'ultimo diventerebbe più 'debole' e quindi più suscettibile ad altre infezioni nonché tumori.

Per amor di precisione, il paragone con l'aids è stato estrapolato da un'osservazione specifica che è stata posta fuori contesto, infatti HIV e il Sars-CoV2 sono due virus COMPLETAMENTE differenti e il Sars-CoV2 NON SI COMPORTA COME L'HIV che invece si aggancia e gemma all'interno dei linfociti CD4, inattivandone completamente la capacità immunitaria; inoltre sono stati riportati solo articoli scientifici che parlano dell'aumentata apoptosi cellulare senza specificare che:

SI TRATTA DI UN FENOMENO TEMPORANEO

E' PROPORZIONALE ALLA GRAVITA' DELL'INFEZIONE

Risultati: L’estesa linfopenia delle cellule T osservata in particolare nei pazienti con COVID-19 grave durante l’infezione acuta si era ripresa 6 mesi dopo l’infezione, accompagnata da una normalizzazione delle risposte funzionali delle cellule T agli antigeni virali comuni. Abbiamo rilevato un’attivazione persistente delle cellule T CD4+ e CD8+ fino a 12 mesi dopo l’infezione, in pazienti con COVID-19 lieve e grave, misurata dall’aumento dell’espressione di HLA-DR e CD38 su queste cellule. L’attivazione persistente delle cellule T dopo COVID-19 era indipendente dalla somministrazione di un vaccino COVID-19 post-infezione. Inoltre, abbiamo identificato un sottogruppo di pazienti con COVID-19 grave che presentava una conta di cellule T CD8+ persistentemente bassa al follow-up e mostrava un fenotipo distinto durante l’infezione acuta costituito da una risposta disfunzionale delle cellule T e segni di eccessivo processo pro-infiammatorio. produzione di citochine. Conclusione: il nostro studio suggerisce che il numero e la funzione delle cellule T si riprendono nella maggior parte dei pazienti dopo COVID-19. Tuttavia, troviamo prove di attivazione persistente delle cellule T fino a 12 mesi dopo l’infezione e descriviamo un sottogruppo di pazienti affetti da COVID-19 grave con conteggi di cellule T CD8+ persistentemente bassi che mostrano una risposta immunitaria disregolata durante l’infezione acuta.

Fonte: [X]

Questi fenomeni non sono dicotomici e irreparabili come nell'infezione da HIV e nell'AIDS (che ricordo essere due cose diverse: si può essere positivi all'HIV e non sviluppare l'aids) e anche se nessuno (che abbia un QI perlomeno a due cifre) nega che ci possano essere queste complicazioni, esse NON SONO LA NORMA e condensare molteplici studi e osservazioni ancora in fieri in un unico post dandogli un taglio così netto e allarmistico a me pare controproducente ed esagerato.

Come avevo accennato all'inizio, sono parecchie le infezioni - spesso ritenute 'innocue' - che nel breve e nel lungo periodo possono potenzialmente dare GROSSI problemi al nostro sistema immunitario e all'organismo più in genere, però non ve le dico tanto non ci potete fare nulla e vivreste in un costante stato di paura che davvero non merita.

[firewalker]

Tanto per non farci mancare niente, ora ci mettiamo pure le malattie autoimmuni letali. Prima di tutto però voglio dire che è una condizione rara, quindi non andate subito in panico. Detto questo, spieghiamo - per come l'ho capita io - che cacchio hanno trovato. La prendo larga.

Esistono diversi meccanismi di difesa contro i patogeni, il più famoso è il sistema immunitario. Esiste anche un sistema di difesa sviluppato dalle singole cellule e quasi esclusivo della lotta contro i virus: l'interferone. Senza entrare nei dettagli dei vari tipi di interferone e di come agisca, il punto saliente è che viene stimolato dalla presenza di un doppio filamento di RNA nel citoplasma. Non è normale avere un doppio filamento di RNA nel citoplasma, generalmente è un filamento singolo che viene riconosciuto dai ribosomi e viene degradato subito dopo aver fatto da modello per la traduzione delle proteine. Molti virus - tra cui SARS-CoV-2 - nel loro ciclo vitale hanno un momento in cui producono un RNA a doppio filamento, e questo fa da trigger per la sintesi di interferone.

Come lo fa? Nella cellula esiste una famiglia di molecole chiamata RLRs che lega l'RNA estraneo (doppio filamento o singolo con alcune caratteristiche precise). Il legame di queste molecole con l'RNA estraneo scatena una cascata di segnale (una serie di reazioni chimiche) che porta alla sintesi di interferone.

Una delle RLRs è la MDA5, che è la protagonista della nostra storia. Esiste infatti una malattia rara, chiamata dermatomiosite, che è una malattia autoimmune in cui gli anticorpi del corpo se la prendono contro la MDA5. Il risultato è una malattia che può manifestarsi in diversi distretti corporei: spesso è cutanea, ma a volte può portare disturbi anche più fastidiosi come fatica e spossatezza ma senza danneggiamento dei muscoli: ecco perché si chiama anche dermatomiosite amiopatica.

Ecco, il punto è che si è scoperto che l'infezione da SARS-CoV-2 può portare, in rari casi, allo sviluppo di una malattia analoga alla dermatomiosite, ma che colpisce i polmoni e risulta essere quindi spesso fatale. L'hanno chiamata MIP-C: MDA5-autoimmunity and Interstitial Pneumonitis Contemporaneous with COVID-19 ovvero: una malattia autoimmune contro MDA5, la dermatomiosite di prima, localizzata nei polmoni e causata dalla CoViD-19.

SARS-CoV-2 stimola, con il suo RNA, MDA5, ma per qualche motivo stimola anche la creazione di anticorpi contro quella molecola. Non è una cosa nuova in generale, si chiama cross-reazione, e a volte succede di vedere che un patogeno stimola una risposta immunitaria contro di sé ma anche contro molecole simili ai suoi bersagli molecolari ma del tutto innocue, anzi utili all'organismo. È una delle cause dell'artrite reumatoide.

Perché? Nelle discussioni dell'articolo (qui il pdf) si fa riferimento al fatto che nei linfonodi l'attivazione di MDA5 può portare anche all'attivazione di alcuni tipi di linfociti, e questo può portare a reazioni autoimmuni. Dato che questi ricercatori hanno dimostrato che questa cosa è causata dall'RNA del virus, non possono escludere che sia anche un possibile - e finora sconosciuto - effetto collaterale anche dei vaccini.

Our finding incriminate MDA5 protein activation, whether linked to natural infection, or vaccination or potentially both as a trigger for MIP-C and that MDA5-mediated sensing (and mounting of an immunophenotype that is comprised of type 1 interferonopathy and antigen-specific CD8+ T cell responses; elaborated below) is a distinct trigger in MIP-C.

Staremo a vedere come si evolve la situazione. Al momento, non ci sono allarmi riguardanti la MIP-C legati alle vaccinazioni, anche perché - a logica - direi che è molto più facile trovare il virus nei linfonodi piuttosto che il vaccino inoculato per via intramuscolare.

Rimaniamo con le antenne dritte.

[baconcolacan]

Important question about Stay AU

Can and do Tom and AK loaf in their full forms

(I’ve imagined several scenarios now in which whenever Tom doesn’t want to do anything in full form he just goes loaf mode)

They can! And heres a lil doodle of AK in his monster form <3 loafy and happy. Just note, AK is a pup, Hellhound pups look very different from fully grown Hellhounds.

CLASSIFIED DOCUMENTATION

It is a well known fact that the fur, pelt, scales, and other organic materials of Lymphocanis CD8 pups are highly valuable and sought after. Products synthesized vary; attire, weapons, armor, ä̸͔́͐n̶̼͑d��̧̻̆ ̷̯̟̇̌r̴͇͕͝á̶̡͒r̷̹͙̐͋ẹ̶̛̮̽ľ̴̳̘ỹ̷͠ͅ ̷̰͙̔̃e̵̮̽̈́v̸͎̖̆̎e̵͓͒̇n̶̍̒͜ ̷̲̀̐m̴̜͋́e̷̫̊̾a̸̫̐̌t̵̘̑. These produced are always of high quality, and due to the nature of Lymphocanie adolescence wherein most fur will be lost and scales no longer shed, there is a great scarcity and rarity to them. Mature Lymphocanis are known to secret highly poisonous oils from their glands, making most materials harvested virtually unusable. It is only with the young that useful materials can be synthesized. Although it was once a norm for Lymphocanie parents to donate the shed fur and scales of their young, thus leading to production of needed materials during the rapture, it is now highly illegal to be in possession of Lymphocanis materials due to the risk of demand, and the highly probable outcome of Lymphocanie young being hunted for materials.