#tdb nicolas

[danieyells]

Are you able to do height comparisons between the characters? I doubt their canon heights were released but one can infer from their models. I'm pretty sure Zenji is the tallest out of all them (besides the octopus).

I mean. Kind of? It seems like they're all set to the same idk plane/image size so they mostly look aligned.

Tumblr's probably not gonna like me using an image that's wider than they allow so idk i can try putting it somewhere else? I tried imgur but it won't open the folder for me after i uploaded it. in fact none of my imgur posts or folders are opening. cool. functional website.

Alan and Hyde are the tallest ones after Moby though, I can tell you that. Zenji is just barely below Hyde.

everyone else is under the cut

[str8upjorkinit]

don't be shy.... yap about the staff?

Besides the obvious blaring issues with the lack of responsibility they have as adults and authority figures (which I won't yap about bc everyone has already talked about this) they are SO DAMN ANNOYING

Summary: I hate their voices

Issue 1

The fucking chancellor. He's SO ANNOYING. HIS VOICE IS SO GRATING. like you're a grown ass adult man running an educational facility but he pronounces the U in desu, normal people don't pronounce the u. That's something kids do or some voice actors will do to sound cute. Why are you trying to sound cute. You're a grown ass adult man, act like it. I will never take someone who says "deeesu~! owo" seriously, like you are not in the position to be using that type of language. It's one thing to look like a kid, it's another thing to act like one.

Issue 2

Moby.... ugh. UGH. he literally pushes work onto us just to fund his stupid idol addiction, gross. He talks like a creep too. I don't like his voice. That is not the voice of a trustworthy adult that we're supposed to look up to.

Issue 3

Hyde... he's really suspicious, I don't hate him as much as the other two but I fs don't trust him. Same issue with his damn voice, why does he gotta talk like a creep? He always sounds like he's hiding something or there's a catch. Not to mention the thing with him and romeo? Sus

Issue 4

The guy working at the convenience store, I don't see the appeal. Not at all. He's not even cute like he's so average I don't see how anyone can simp for him. Also when we first met him he was literally looking at magazines of girls in swimsuits(?) I don't remember exactly but it was definitely girls in revealing "clothes". And that. Is. So. Fucking. Creepy. Like at work?? In front of students??? No. Ew. Like do that at home in the privacy of your room what the hell is wrong with you??? I think he should be fired. He grosses me out sm like why are you looking at that shit at work.

They have like 0 female staff and the reason is prolly bc the men are creeps /hj

Nicolas Dante and the Janitor are fine tho. That's like 4:3 which means most the staff fucking suck

[catboy-beckett]

What better way to begin Tokyo Debunker posting than with a tierlist of the ghouls! I usually don't bother putting them in order within the tiers, but with this one I did! So the leftmost boy on each row is the one I liked most.

Obscuary really had no misses huh.

I know Ritsu has fans and I'm happy for you!!!! I am happy that you get joy out of him. Personally I think he has a pretty face but every time he speaks I desire strongly to kill him with a rock. I also know Leo has dedicated haters and yeah honestly fair.

Click "keep reading" if you wanna see my tierlist of specifically which characters I would fuck vvvv

This one includes the staff members (whom I thought it would be unfair to include in the original tierlist due to lack of screentime) and I threw in the little creatures since I had already made a "cute critter" tier for Lyca.

The Chancellor is not included.

Jin would be higher if they didn't make him a smoker. Wild that they put so much effort into positioning him as THE romance option and then added "by the way he smells absolutely fucking awful" lmao

[istharoth]

Happy Pocky Day! (and Single's Day) Here's the TDB boys + staff on Pocky day!

Does the Pocky Challenge, but breaks the Pocky stick intentionally. MC, Romeo, Rui, Jiro, Sho

Is a little shit about it, when their lips almost touch, he backs away. Tohma, Leo, Romeo (here too), Haku, Ed, Elias

Is doing the pocky challenge by himself using his reflection in the mirror. Kaito, Moby

Throws away the pocky stick, just kisses the person. Jin (in his case, lover), Towa, Taiga, Hyde, Cornelius

Doesn't know what is going on, accepts the pocky stick and moves on. Luca, Mido, Haru, Ritsu, Zenji, Dante

Shys away from the challenge. Subaru, Nicolas, Benkei Yuri (considers it indecent. How could you before marriage?!), Ren (yells 'sexual harassment' from the top of his lungs) Lyca (cannot eat chocolate, thinks the person wants to poison him)

[bioadvisers]

Bioadvisers shared on Biotech Advisers

The Src family kinase Fgr is a transforming oncoprotein that functions independently of SH3-SH2 domain regulation

Content introduction:

A dysbiotic microbiome triggers TH17 cells to mediate oral mucosal immunopathology in mice and humans

In utero priming of highly functional effector T cell responses to human malaria

Avidity-based binding to HER2 results in selective killing of HER2-overexpressing cells by anti-HER2/CD3

Sphingosine 1-phosphate stimulates eyelid closure in the developing rat by stimulating EGFR signaling

The Src family kinase Fgr is a transforming oncoprotein that functions independently of SH3-SH2 domain regulation

1. A dysbiotic microbiome triggers TH17 cells to mediate oral mucosal immunopathology in mice and humans

Periodontitis is one of the most common human inflammatory diseases, yet the mechanisms that drive immunopathology and could be therapeutically targeted are not well defined. Here, Nicolas Dutzan at NIH in Bethesda, USA and his colleagues demonstrate an expansion of resident memory T helper 17 (TH17) cells in human periodontitis. Phenocopying humans, TH17 cells expanded in murine experimental periodontitis through local proliferation. Unlike homeostatic oral TH17 cells, which accumulate in a commensal-independent and interleukin-6 (IL-6)–dependent manner, periodontitis-associated expansion of TH17 cells was dependent on the local dysbiotic microbiome and required both IL-6 and IL-23. TH17 cells and associated neutrophil accumulation were necessary for inflammatory tissue destruction in experimental periodontitis. Genetic or pharmacological inhibition of TH17 cell differentiation conferred protection from immunopathology. Studies in a unique patient population with a genetic defect in TH17 cell differentiation established human relevance for our murine experimental studies. In the oral cavity, human TH17 cell defects were associated with diminished periodontal inflammation and bone loss, despite increased prevalence of recurrent oral fungal infections. Their study highlights distinct functions of TH17 cells in oral immunity and inflammation and paves the way to a new targeted therapeutic approach for the treatment of periodontitis.

Read more, please click http://stm.sciencemag.org/content/10/463/eaat0797

2. In utero priming of highly functional effector T cell responses to human malaria

Malaria remains a significant cause of morbidity and mortality worldwide, particularly in infants and children. Some studies have reported that exposure to malaria antigens in utero results in the development of tolerance, which could contribute to poor immunity to malaria in early life. However, the effector T cell response to pathogen-derived antigens encountered in utero, including malaria, has not been well characterized. Here, Pamela M. Odorizzi at University of California in San Francisco, USA and his colleagues assessed the frequency, phenotype, and function of cord blood T cells from Ugandan infants born to mothers with and without placental malaria. They found that infants born to mothers with active placental malaria had elevated frequencies of proliferating effector memory fetal CD4+ T cells and higher frequencies of CD4+ and CD8+ T cells that produced inflammatory cytokines. Fetal CD4+ and CD8+ T cells from placental malaria–exposed infants exhibited greater in vitro proliferation to malaria antigens. Malaria-specific CD4+ T cell proliferation correlated with prospective protection from malaria during childhood. These data demonstrate that placental malaria is associated with the generation of proinflammatory malaria-responsive fetal T cells. These findings add to our current understanding of fetal immunity and indicate that a functional and protective pathogen-specific T cell response can be generated in utero.

Read more, please click http://stm.sciencemag.org/content/10/463/eaat6176

3. Avidity-based binding to HER2 results in selective killing of HER2-overexpressing cells by anti-HER2/CD3

A primary barrier to the success of T cell–recruiting bispecific antibodies in the treatment of solid tumors is the lack of tumor-specific targets, resulting in on-target off-tumor adverse effects from T cell autoreactivity to target-expressing organs. To overcome this, Dionysos Slaga at Genentech Inc in South San Francisco, USA and his colleagues developed an anti-HER2/CD3 T cell–dependent bispecific (TDB) antibody that selectively targets HER2-overexpressing tumor cells with high potency, while sparing cells that express low amounts of HER2 found in normal human tissues. Selectivity is based on the avidity of two low-affinity anti-HER2 Fab arms to high target density on HER2-overexpressing cells. The increased selectivity to HER2-overexpressing cells is expected to mitigate the risk of adverse effects and increase the therapeutic index. Results included in this manuscript not only support the clinical development of anti-HER2/CD3 1Fab–immunoglobulin G TDB but also introduce a potentially widely applicable strategy for other T cell–directed therapies. The potential of this discovery has broad applications to further enable consideration of solid tumor targets that were previously limited by on-target, but off-tumor, autoimmunity.

Read more, please click http://stm.sciencemag.org/content/10/463/eaat5775

4. Sphingosine 1-phosphate stimulates eyelid closure in the developing rat by stimulating EGFR signaling

In many mammals, the eyelids migrate over the eye and fuse during embryogenesis to protect the cornea from damage during birth and early life. Loss-of-function mutations affecting the epidermal growth factor receptor (EGFR) signaling pathway cause an eyes-open-at-birth (EOB) phenotype in rodents. Ganlan Bian at Fourth Military Medical University in Xi’an, China and his colleagues identified an insertional mutation in Spinster homolog 2 (Spns2) in a strain of transgenic rats exhibiting the EOB phenotype. Spns2, a sphingosine 1-phosphate (S1P) transporter that releases S1P from cells, was enriched at the tip of developing eyelids in wild-type rat embryos. Spns2 expression or treatment with S1P or any one of several EGFR ligands rescued the EOB Spns2 mutant phenotype in vivo and in tissue explants in vitro and rescued the formation of stress fibers in primary keratinocytes from mutants. S1P signaled through the receptors S1PR1, S1PR2, and S1PR3 to activate extracellular signal–regulated kinase (ERK) and EGFR-dependent mitogen-activated protein kinase kinase kinase 1 (MEKK1)–c-Jun signaling. S1P also induced the nuclear translocation of the transcription factor MAL in a manner dependent on EGFR signaling. MAL and c-Jun stimulated the expression of the microRNAs miR-21 and miR-222, both of which target the metalloprotease inhibitor TIMP3, thus promoting metalloprotease activity. The metalloproteases ADAM10 and ADAM17 stimulated EGFR signaling by cleaving a membrane-anchored form of EGF to release the ligand. Their results outline a network by which S1P transactivates EGFR signaling through a complex mechanism involving feedback between several intra- and extracellular molecules to promote eyelid fusion in the developing rat.

Read more, please click http://stke.sciencemag.org/content/11/553/eaat1470

5. The Src family kinase Fgr is a transforming oncoprotein that functions independently of SH3-SH2 domain regulation

Fgr is a member of the Src family of nonreceptor tyrosine kinases, which are overexpressed and constitutively active in many human cancers. Fgr expression is restricted to myeloid hematopoietic cells and is markedly increased in a subset of bone marrow samples from patients with acute myeloid leukemia (AML). Here, Kexin Shen at University of Pittsburgh School of Medicine in Pittsburgh, USA and his colleagues investigated the oncogenic potential of Fgr using Rat-2 fibroblasts that do not express the kinase. Expression of either wild-type or regulatory tail-mutant constructs of Fgr promoted cellular transformation (inferred from colony formation in soft agar), which was accompanied by phosphorylation of the Fgr activation loop, suggesting that the kinase domain of Fgr functions independently of regulation by its noncatalytic SH3-SH2 region. Unlike other family members, recombinant Fgr was not activated by SH3-SH2 domain ligands. However, hydrogen-deuterium exchange mass spectrometry data suggested that the regulatory SH3 and SH2 domains packed against the back of the kinase domain in a Src-like manner. Sequence alignment showed that the activation loop of Fgr was distinct from that of all other Src family members, with proline rather than alanine at the +2 position relative to the activation loop tyrosine. Substitution of the activation loop of Fgr with the sequence from Src partially inhibited kinase activity and suppressed colony formation. Last, Fgr expression enhanced the sensitivity of human myeloid progenitor cells to the cytokine GM-CSF. Because its kinase domain is not sensitive to SH3-SH2–mediated control, simple overexpression of Fgr without mutation may contribute to oncogenic transformation in AML and other blood cancers.

Read more, please click http://stke.sciencemag.org/content/11/553/eaat5916

[abbkine]

BioAdvisers said on Biotech Advisers

The Src family kinase Fgr is a transforming oncoprotein that functions independently of SH3-SH2 domain regulation

Content introduction:

A dysbiotic microbiome triggers TH17 cells to mediate oral mucosal immunopathology in mice and humans

In utero priming of highly functional effector T cell responses to human malaria

Avidity-based binding to HER2 results in selective killing of HER2-overexpressing cells by anti-HER2/CD3

Sphingosine 1-phosphate stimulates eyelid closure in the developing rat by stimulating EGFR signaling

The Src family kinase Fgr is a transforming oncoprotein that functions independently of SH3-SH2 domain regulation

1. A dysbiotic microbiome triggers TH17 cells to mediate oral mucosal immunopathology in mice and humans

Periodontitis is one of the most common human inflammatory diseases, yet the mechanisms that drive immunopathology and could be therapeutically targeted are not well defined. Here, Nicolas Dutzan at NIH in Bethesda, USA and his colleagues demonstrate an expansion of resident memory T helper 17 (TH17) cells in human periodontitis. Phenocopying humans, TH17 cells expanded in murine experimental periodontitis through local proliferation. Unlike homeostatic oral TH17 cells, which accumulate in a commensal-independent and interleukin-6 (IL-6)–dependent manner, periodontitis-associated expansion of TH17 cells was dependent on the local dysbiotic microbiome and required both IL-6 and IL-23. TH17 cells and associated neutrophil accumulation were necessary for inflammatory tissue destruction in experimental periodontitis. Genetic or pharmacological inhibition of TH17 cell differentiation conferred protection from immunopathology. Studies in a unique patient population with a genetic defect in TH17 cell differentiation established human relevance for our murine experimental studies. In the oral cavity, human TH17 cell defects were associated with diminished periodontal inflammation and bone loss, despite increased prevalence of recurrent oral fungal infections. Their study highlights distinct functions of TH17 cells in oral immunity and inflammation and paves the way to a new targeted therapeutic approach for the treatment of periodontitis.

Read more, please click http://stm.sciencemag.org/content/10/463/eaat0797

2. In utero priming of highly functional effector T cell responses to human malaria

Malaria remains a significant cause of morbidity and mortality worldwide, particularly in infants and children. Some studies have reported that exposure to malaria antigens in utero results in the development of tolerance, which could contribute to poor immunity to malaria in early life. However, the effector T cell response to pathogen-derived antigens encountered in utero, including malaria, has not been well characterized. Here, Pamela M. Odorizzi at University of California in San Francisco, USA and his colleagues assessed the frequency, phenotype, and function of cord blood T cells from Ugandan infants born to mothers with and without placental malaria. They found that infants born to mothers with active placental malaria had elevated frequencies of proliferating effector memory fetal CD4+ T cells and higher frequencies of CD4+ and CD8+ T cells that produced inflammatory cytokines. Fetal CD4+ and CD8+ T cells from placental malaria–exposed infants exhibited greater in vitro proliferation to malaria antigens. Malaria-specific CD4+ T cell proliferation correlated with prospective protection from malaria during childhood. These data demonstrate that placental malaria is associated with the generation of proinflammatory malaria-responsive fetal T cells. These findings add to our current understanding of fetal immunity and indicate that a functional and protective pathogen-specific T cell response can be generated in utero.

Read more, please click http://stm.sciencemag.org/content/10/463/eaat6176

3. Avidity-based binding to HER2 results in selective killing of HER2-overexpressing cells by anti-HER2/CD3

A primary barrier to the success of T cell–recruiting bispecific antibodies in the treatment of solid tumors is the lack of tumor-specific targets, resulting in on-target off-tumor adverse effects from T cell autoreactivity to target-expressing organs. To overcome this, Dionysos Slaga at Genentech Inc in South San Francisco, USA and his colleagues developed an anti-HER2/CD3 T cell–dependent bispecific (TDB) antibody that selectively targets HER2-overexpressing tumor cells with high potency, while sparing cells that express low amounts of HER2 found in normal human tissues. Selectivity is based on the avidity of two low-affinity anti-HER2 Fab arms to high target density on HER2-overexpressing cells. The increased selectivity to HER2-overexpressing cells is expected to mitigate the risk of adverse effects and increase the therapeutic index. Results included in this manuscript not only support the clinical development of anti-HER2/CD3 1Fab–immunoglobulin G TDB but also introduce a potentially widely applicable strategy for other T cell–directed therapies. The potential of this discovery has broad applications to further enable consideration of solid tumor targets that were previously limited by on-target, but off-tumor, autoimmunity.

Read more, please click http://stm.sciencemag.org/content/10/463/eaat5775

4. Sphingosine 1-phosphate stimulates eyelid closure in the developing rat by stimulating EGFR signaling

In many mammals, the eyelids migrate over the eye and fuse during embryogenesis to protect the cornea from damage during birth and early life. Loss-of-function mutations affecting the epidermal growth factor receptor (EGFR) signaling pathway cause an eyes-open-at-birth (EOB) phenotype in rodents. Ganlan Bian at Fourth Military Medical University in Xi’an, China and his colleagues identified an insertional mutation in Spinster homolog 2 (Spns2) in a strain of transgenic rats exhibiting the EOB phenotype. Spns2, a sphingosine 1-phosphate (S1P) transporter that releases S1P from cells, was enriched at the tip of developing eyelids in wild-type rat embryos. Spns2 expression or treatment with S1P or any one of several EGFR ligands rescued the EOB Spns2 mutant phenotype in vivo and in tissue explants in vitro and rescued the formation of stress fibers in primary keratinocytes from mutants. S1P signaled through the receptors S1PR1, S1PR2, and S1PR3 to activate extracellular signal–regulated kinase (ERK) and EGFR-dependent mitogen-activated protein kinase kinase kinase 1 (MEKK1)–c-Jun signaling. S1P also induced the nuclear translocation of the transcription factor MAL in a manner dependent on EGFR signaling. MAL and c-Jun stimulated the expression of the microRNAs miR-21 and miR-222, both of which target the metalloprotease inhibitor TIMP3, thus promoting metalloprotease activity. The metalloproteases ADAM10 and ADAM17 stimulated EGFR signaling by cleaving a membrane-anchored form of EGF to release the ligand. Their results outline a network by which S1P transactivates EGFR signaling through a complex mechanism involving feedback between several intra- and extracellular molecules to promote eyelid fusion in the developing rat.

Read more, please click http://stke.sciencemag.org/content/11/553/eaat1470

5. The Src family kinase Fgr is a transforming oncoprotein that functions independently of SH3-SH2 domain regulation

Fgr is a member of the Src family of nonreceptor tyrosine kinases, which are overexpressed and constitutively active in many human cancers. Fgr expression is restricted to myeloid hematopoietic cells and is markedly increased in a subset of bone marrow samples from patients with acute myeloid leukemia (AML). Here, Kexin Shen at University of Pittsburgh School of Medicine in Pittsburgh, USA and his colleagues investigated the oncogenic potential of Fgr using Rat-2 fibroblasts that do not express the kinase. Expression of either wild-type or regulatory tail-mutant constructs of Fgr promoted cellular transformation (inferred from colony formation in soft agar), which was accompanied by phosphorylation of the Fgr activation loop, suggesting that the kinase domain of Fgr functions independently of regulation by its noncatalytic SH3-SH2 region. Unlike other family members, recombinant Fgr was not activated by SH3-SH2 domain ligands. However, hydrogen-deuterium exchange mass spectrometry data suggested that the regulatory SH3 and SH2 domains packed against the back of the kinase domain in a Src-like manner. Sequence alignment showed that the activation loop of Fgr was distinct from that of all other Src family members, with proline rather than alanine at the +2 position relative to the activation loop tyrosine. Substitution of the activation loop of Fgr with the sequence from Src partially inhibited kinase activity and suppressed colony formation. Last, Fgr expression enhanced the sensitivity of human myeloid progenitor cells to the cytokine GM-CSF. Because its kinase domain is not sensitive to SH3-SH2–mediated control, simple overexpression of Fgr without mutation may contribute to oncogenic transformation in AML and other blood cancers.

Read more, please click http://stke.sciencemag.org/content/11/553/eaat5916

[cancersfakianakis1]

Membrane-Proximal Epitope Facilitates Efficient T Cell Synapse Formation by Anti-FcRH5/CD3 and Is a Requirement for Myeloma Cell Killing

Publication date: Available online 2 March 2017 Source:Cancer Cell Author(s): Ji Li, Nicola J. Stagg, Jennifer Johnston, Michael J. Harris, Sam A. Menzies, Danielle DiCara, Vanessa Clark, Maria Hristopoulos, Ryan Cook, Dionysos Slaga, Rin Nakamura, Luke McCarty, Siddharth Sukumaran, Elizabeth Luis, Zhengmao Ye, Thomas D. Wu, Teiko Sumiyoshi, Dimitry Danilenko, Genee Y. Lee, Klara Totpal, Diego Ellerman, Isidro Hötzel, John R. James, Teemu T. Junttila The anti-FcRH5/CD3 T cell-dependent bispecific antibody (TDB) targets the B cell lineage marker FcRH5 expressed in multiple myeloma (MM) tumor cells. We demonstrate that TDBs trigger T cell receptor activation by inducing target clustering and exclusion of CD45 phosphatase from the synapse. The dimensions of the target molecule play a key role in the efficiency of the synapse formation. The anti-FcRH5/CD3 TDB kills human plasma cells and patient-derived myeloma cells at picomolar concentrations and results in complete depletion of B cells and bone marrow plasma cells in cynomolgus monkeys. These data demonstrate the potential for the anti-FcRH5/CD3 TDB, alone or in combination with inhibition of PD-1/PD-L1 signaling, in the treatment of MM and other B cell malignancies.

Teaser

Li et al. report that the size and epitope location of the target play a key role in the efficiency of T cell activation induced by T cell-dependent bispecific antibodies (TDBs). They develop a TDB targeting FcRH5 expressed in all multiple myeloma tumor cells and show its potential in treating this disease. http://ift.tt/2lFGgS1

[str8upjorkinit]

You should put whoever you think deserves it into a jello cube prison!!!

moby should get fired

[danieyells]

so I'm back on a TD brainrot and was thinking of Rui when I got slapped with a memory of when I read a Vash x reader fic. it's called Its the Thought that Counts by Jelly_Doughnut on Ao3 and basically, Vash is, unknowingly, gifted a dildo so he can give it to reader. and Vash is given a bracelet that the person attuned to him. anyways reader does end up using the dildo and it turns out that bracelet connected what reader was doing to the dildo to Vash's cock. and now all I can think of is smth similar going on with Rui ,,,

Belated(and probably too late haha) welcome back to TDB brainrot for however long you stick/stuck around!

And. . .HONESTLY THAT'S A GOOD IDEA. . .like lbr sex has advanced technology for ages, if there aren't anomalous sex toys I WOULD BE SHOCKED. Something as simple as a cockring that actually doesn't let you cum(shout out to @nsftdb 's leo x sho [x alan] fic--) and even as complicated as like. Portal underwear or a dildo or strap-on that lets you feel through it. . .LIKE YOU'D JUST HAVE TO FIND WHOEVER'S RESEARCHING THAT STUFF AND MAKE AN ORDER SURELY. . . . THE ANOMALOUS INVESTIGATION INSTITUTE HAS PARTNERED WITH LOVESENSE TO BRING YOU--

But with Rui and the reader I can see it being intentional, a deliberate introduction of a workaround. . .it's not the same but the sensation is there. That's important! Idk why I'm imagining Hyde being the one to bring it up--somehow this is relevant to his field of study, anomalous biology applies to people's intimate lives as well! Nicolas is too much of a prude to explore this area.

Anomalies can be constructed(hence why he has Romeo testing out explosives he made for him) and he and. A team he works with on these things. Have a prototype and, honor student, I think this would be perfect for you and your relationship and circumstances you know~?

And maybe you're a little uncertain because, hey, that kind of experimentation in the bedroom is kind of dangerous? But he assured you it's totally safe so far! They just need more trials! He can prove how safe it is if you want he could show you--no, you'll take his word for it? Okay, then give it a try and report back!

And it's a. . .sleeve? A cock sleeve. And a dildo of similar design and. . .the instructions are simple. Put the sleeve on the penis(it's tight enough to mold to fit but soft enough material to not be an painful iron grip) and introduce the dildo to the desired hole(right now through insertion) don't forget lube! Unless you're into that much friction. . . .

And you're a little skeptical but. . .you give it a try. Rui puts on the sleeve and. Well it's a weird sensation at first because it. . .doesn't really feel like anything most of the way around? But he can kind of feel the way the dildo sits against the bed as if he's resting his cock on the sheet. It's a little strange but. He's excited too? He can already tell it works??

And you wrap your fingers around it just to pick it up and he jumps because yeah actually he did feel that! Just this. . .sensation of fingers holding him. And it's been a long time since he's had fingers on him at all that weren't his own and you're kind of thinking. . .maybe we should like ease into this more? We haven't hugged or kissed yet. Maybe they have something for that??? Maybe we shouldn't jump straight into. . . .

Well he already put the sleeve on and you're already here so you. . .start testing. At first running your fingers over it and gently squeezing it. And it shudders and jolts and twitches when he does. And he's sensitive because it's really been a long time. And you don't wanna start stroking him without any lube but you're supposed to be testing it so. . . .

You run a stripe from the base to the tip with your tongue and no, no, there's nothing wrong with it it doesn't hurt it's the opposite it's just. A lot all of a sudden. You've been together so long but you're skipping almost everything that would come between now and this moment and there's something exciting for him about that.

You've masturbated together and experimented with toys before but this is. Almost contact. It's as close as he can get without getting there right now. And as you move from teasing licking to experimental sucking and stroking, it's both intimate because it's with his lover, someone he wouldn't hesitate to hold if only he didn't fear killing them, and there's a nostalgic feeling, like before the curse, with flings he barely knew the name of, the fun of pleasure at a sort of distance. . . .

And you can watch him absorbed in the pleasure, gripping the sheets in lieu of holding your head, watching you with his pupils dilated to take in as much of you as he can. You're doing that. You are personally doing that. Not just the sight or thought of you but your actual actions. It feels tight and wet like your mouth, he feels you moving your tongue and hollowing your cheeks and teasing your own throat, and you feel him reacting and hardening and bucking between your lips.

And he grabs hold of the sleeve, moaning your name and thrusts into it--

And then you gag and you both stop because

You felt that actually, it moved on its own. It still needs to be held up in some way, but it thrust into your mouth for him and. Oh dear you have a lot of experimenting to do. . . .

(Obviously you try penetration if you're into that. Thighfucking, titfucking if applicable, he fucks your hands and feet and asscheeks. You try leaving the sleeve on and tease him while he's in the garden. He drops you off at the cathedral and feels you give him a kiss goodbye through it.

Why didn't he think to ask someone for something like this before, something that would transfer tactile sensations, Yuri has a syringe that transfers damage dealt from its target to the person who dealt it, surely the technology for long-distance sensation exists in some anomalous form already, even if he has to wear a whole damn fencing uniform to feel it--

And he's not the only one who's on the receiving end of teasing. You try leaving it in and it doesn't feel like anything at first, oddly enough. You feel the weight but it barely even feels like it's inside. Until you feel wet from lube being dripped into the sleeve during class. Until you feel fingers pushing into you, probing and stretching and thrusting while running an errand. Until you feel vibrations teasing your opening and pushed inside while you're trying to sleep.

He gives you a courtesy text to get permission before he puts his cock in. That may be a bit much to surprise you with.

It's still very distant and it's not the same as actually doing it but. . .you can report to Hyde that it seems to be working well enough and if his. Expert team of researchers have anything similar to trial you might be willing to give it a try.

And he tells you about all the features they're working on and looking into--sharing temperature is the closest on the list to being done. External stimulation is in the works. They'd love to be able to actually transfer fluids rather than just the absent feeling of them, but that's a bit difficult to work with. . .it's a little embarrassing to hear about work like this but it's also exciting to think you could share a more accurate intimate experience, right?)

BUT YEAH EXCELLENT IDEA I'M LOVE. . .I was thinking about portal/penetration-enabling underwear and sensation-transferring straps the other day actually lmao

[danieyells]

I keep thinking of Ed(?) that vampire guy and thinking of mc trying to keep the relationship with him a secret, or at least on the down low, but after like, 2 check ups from Yuri and Jiro, they v quickly realize what's going on when they see their blood level is lower than usual after their first mission with obscuary..

and after the look of just being done with everything yuri is going on a rant about why they need to be more careful or wtv and 'why would you even do that??'

or even a walk of shame to the chancellors office when they get too silly and oops mc is a vampire now(assuming it can be easy to turn into one idk much about them LOL)

I wanna think of him in a hotter way but I just get too many silly thoughts of him lmao

(The vampire in Obscuary is Edward Hart, yes! Mostly just called Ed so far.)

Silly thoughts are the best tho lmao LBR THE GUY ALLEGEDLY CAN'T TIE HIS OWN SHOELACES, DOESN'T CLEAN UP AFTER HIMSELF, FALLS ASLEEP WHEREVER HE WANTS, IS KNOWN BY OTHER CAPTAINS TO BE A SLACKER, AND CARELESSLY TOUCHES RUI KNOWING IT'LL KILL HIM FOR A BIT; HE'S A MAGNET FOR SILLY THOUGHTS.

tbf we don't know how vampire lore is gonna work in tdb yet(Ed does have bitemarks on his neck, so biting is required to spread it presumably), so it's fair to not know how exactly it's spread or anything! I assume it won't be spread without intention to do so or without the target being near death or something(just so we can get that sweet feeding goodness), but it's also fun to imagine that the pc just like. . .offers to feed Ed and ends up a vampire because they just did not consider they'd catch vampirism. Why didn't anyone tell them! What do you mean they thought they knew!!! (on the other hand. . .would vampirism override their curse? Vampirism overrides Rui's curse when Edward touches him, it'd be a reasonable thing to try. . . .)

But lmaoooo going to Mortkranken and they're like. Why are you so anemic???? And the pc hadn't even considered it because hey blood comes back! And then it's even lower the second time. And they just. Figure it out right away like goddamn it your missions have been with Obscuary. And Yuri is so annoyed that they're doing something to jeopardize their wellbeing. Yes, he does need to feed daily if he's going on missions but he does not need to drink that much especially from the same person. Your blood comes back but it's still finite!

Yuri just scolds and fusses over them while Jiro prepares some iron supplements and like a list of food you should eat to help recover faster lolol

Another day they just got fed on by Ed and then get a text from Romeo saying to come to the VIP room and they're like "uh can i wait like. 20 minutes" "No. Come now." "I don't think that's a good idea." "Now."

and the second they step into Sinostra Taiga's sniffing them out because they've still got a partially bleeding wound and oh no he's hungry (and Romeo blames them anyway despite that they very specifically said they didn't think it's a good idea)

They pass out in class from the anemia and now Nicolas is worrying over them too(he's a lot nicer than Yuri at least) and now they're trying to figure out how they'll schedule with Ed to have a talk with him when Moby doesn't even wanna go to Obscuary(or Hotarubi!) despite being the dorm advisor

The pc gets turned and just. . .is Cornelius' office even open late? What do they even do about this!? They could go to Mortkraken, they're always up. . .they could find Hyde, he seems to be awake regardless of the time of day. And Ed is just so freespirited he doesn't even worry about it just pats them like oh don't worry about it you can spend as much time in Obscuary as you'd like!! Maybe this is what you needed! I'll teach you all about being a vampire, it'll be fun!!!

Of course when they eventually have to tell Cornelius or somebody it's a whole damn hassle. And they don't know how it'll effect the curse either. So now it's a mystery and things are up in the air and do they keep searching for a cure for something that may not even affect them anymore???? They aren't a ghoul but you're an anomaly now Obscuary is a ghoul-only dorm but do they place you there???? Do they keep you in containment??? It's just one problem after another!!! And what about keeping them fed!?