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monstruous-pictures-present-blog · 1 year ago

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📆 June 2017 📰 Determination of a Key Antigen for Immunological Intervention To Target the Latent Stage of Toxoplasma gondii 🗞 The Journal of Immunology

Toxoplasma gondii is one of the pathogens that can establish a chronic infection in the brain. Acute infection with the parasite is characterized by proliferation of tachyzoites in various organs, and it can cause various diseases, including lymphadenitis and congenital infection of fetuses (1). Although IFN-γ–mediated immune responses and, to a lesser extent, humoral immunity inhibit tachyzoite growth (2–4), the parasite establishes a chronic infection by forming tissue cysts, which can contain hundreds to thousands of bradyzoites, preferentially in the brain. This infection is ubiquitous and is one of the most common parasitic infections in humans worldwide (1).

It is well recognized that chronic T. gondii infection can reactivate and cause life-threatening toxoplasmic encephalitis in immunocompromised individuals, such as those with AIDS and organ transplants (1, 5, 6). Even in immunocompetent individuals, recent epidemiological studies demonstrated that T. gondii infection is associated with a 1.8-fold increase in the risk for brain cancers (7) and that brain cancer mortality increases with the seroprevalence of IgG Abs to T. gondii (8). Therefore, to improve public health, it is important to develop a method to eliminate T. gondii cysts from chronically infected individuals. However, there is currently no drug that can target the cyst stage of the parasite.

Although it had generally been considered that the immune system of infected hosts is unable to recognize or remove T. gondii cysts, our recent studies demonstrated that CD8+ immune T cells of chronically infected BALB/c mice (the H-2d haplotype), which are genetically resistant to the infection, possess a potent activity to initiate the immune process to remove tissue cysts from the brain when these T cells are transferred to infected immunodeficient (athymic nude or SCID) mice that have already developed large numbers of cysts (9). This anticyst activity of CD8+ immune T cells does not require IFN-γ production, which is essential for controlling tachyzoites, as mentioned earlier, but it does require perforin (9). Perforin is critical for cytotoxic activity of CD8+ T cells; therefore, it is most likely that cytotoxic activity of CD8+ T cells initiates the immune process to remove the cysts.

T. gondii cysts are formed within infected host cells (10, 11); however, the mechanisms by which CD8+ T cells recognize the cyst-containing cells are unknown. To develop a novel method to activate CD8+ T cells capable of removing T. gondii cysts, it is crucial to understand the molecular mechanisms by which the T cells recognize the cyst-containing cells. The present study revealed that H-2Ld is the major Ag-presenting molecule required for CD8+ immune T cells to initiate T cell–mediated cyst elimination. The present study also determined that CD8+ immune T cells bearing TCR Vβ8.1, 8.2+ chain have a potent activity to remove the cysts, and this T cell population recognizes the N-terminal region (aa 41–152) of dense granule protein 6 (GRA6Nt) of T. gondii presented by the H-2Ld molecule. Furthermore, CD8+ T cells activated by immunization with GRA6Nt were able to remove T. gondii cysts. These findings provide the foundation required for an immunological intervention targeting the latent stage of T. gondii to eradicate chronic infection with this parasite.

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coordination-disorder-gayorg · 2 years ago

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Here is the 2nd part that's all of the greyhound names because they got put in a separate list by the author.

Greyhoundis names

Arture

Achilles

Andymay

Albertyne

Ampoyne

Athym

Ameaws

Abbotte

Annore

Arsyte

Alberte

Amys

Armetrewe

Amelon

Averus

Asgudde

Annewell

Awntrus

Baby

Boteler

Bribur

Bragger

Blackberde

Brym

Barefote

Blankette

Blameles

Badde

Brente

Brecheles

Brewte

Brynge-yne

Bryngehome

Bere-awey

Boste

Boster

Bowchere

Balle

Ballarde

Bordere

Berdere

Brayneles

Brayne

Braselette

Bryan

Care

Coke

Careles

Colyn

Colyer

Childe

Cayface

Cayme

Cachefaste

Curteise

Charlis

Clubbe

Cacche

Cachepoll

Cacchecurse

Cormerawnte

Compere

Conquerour

Chorle

Champyn

Crakeboste

Cruell

Calis

Corage

Chekke

Cuffe

Cappe

Dragon

Dowȝty

Derlynge

Drawlacche

Derdo

Daschelake

Doglas

Drynkall

Ector

Eglamowre

Elmys

Ercules

Engeste

Frere

Fawkon

Filbagge

Fole

Foly

Farewell

Fretherike

Fliȝt

Feris

Filpott

Foremoste

Gal‹aw›nte

Gaweyne

Galias

Gripe

Gye

Gowere

Goby

Grimbolde

Go-bifore

Go-byhynde

Gentile

Gentilcors

Go-byȝende

Garter

Hurle

Holdefaste

Hardeware

Holy

Harlet

Hentele

Hawkyn

Harde-ynowgh

Honyball

Hiefaste

Hasilwayte

Havegoodday

Happy

Holdere

Horne

Hardeyberde

Hotome

Helpeles

Harmeles

Holande

Harper

Hancaster

Jewe

Japer

J[e]rownde

Jetter

Igo

Iwoll

Javell

Itogo

Jolyvette

Ido

Keuse

Keules

Kempe

Kilbucke

Kailewey

Liȝtfote

Lamprey

Lurdeyne

Lyon

Lybarde

Lyarde

Larwn

Laweles

Leper

Lanchefaste

Luske

Lumpe

Loby

Leydon

Liȝt

Luste

Lusty

Lubike

Makeles

Mullynge

Muskette

Merlyon

Meyntenawnse

Makeboste

Mediller

Marchawnt

Moleyne

Molyneux

Makehitgood

Marmyn

Mouse

Monke

Menele

Myne

Mirthe

Mychere

Nobull

Nameles

Nigarde

Nymhiswed

Noforse

Nowthow

Newget

Neymys

Nede

Negir

Nowell

Nosuche

Nowthus

Olyuere

Ouyrthwart

Orpidde

Okle

Offa

Ofterige

Olyfawnte

Otewell

Pander

Plente

Pereles

Panter

Pusse

Partener

Plunket

Persyvale

Plucke

Parre

Penyboy

Palmere

Pardonere

Pengowȝe

Pawle

Prymsawnte

Prentise

Purveyowre

Parte

Priowre

Pensefe

Pultere

Purchase

Pleyare

Pompeye

Quycke

Quyte

Queynte

Quysedon

Ragge

Russe

Ruffyn

Rumbilowe

Recheles

Rowlande

Ruffe

Romayne

Ragor

Regarde

Raggeman

Rusteler

Romwlus

Rakette

Riȝt

Rowte

Rumbolde

Reuell

Rechemenere

Rifeler

Rabbissche

Redeles

Souerayne

Swepestake

Stancheboste

Stewarde

Sawmpere

Sprynge

Sparenot

Slugge

Selde-ysey

Soneforgete

Sclaueyne

Sloveyne

Sirisson

Saresyn

Swifte

Snacke

Smylfeste

Spilparke

Snappe

Sigood

Synewle

Stopfawte

Soleyne

Stepfaste

Stedefaste

Strecche

Sage

Swetynge

Sterte

Streccheforthe

Stele-awey

Sterte-awey

Stowte

Strikelawnde

Syre

Suget

Schakbagge

Stykefaste

Tullymully

Triaunte

Troye

Trwnket

Tukke

Tiraunte

Turnetripe

Tresowre

Tancarde

Trinket

Tynker

Tarynot

Trewante

Tredefaste

Tumbelere

Treserere

Truste

Takehym

Tuleras

Towche

Thought

Thrifte

Tartir

Turnebukke

Tripe

Tripper

Tredeweye

Troilus

Thlewe

Volante

Vngayne

Vengeabull

Wype

Wellyfownde

Welcome

Wilby

Wastell

Whiteberde

Wellawnde

Wantone

Wynde-aweye

Wo‹n›ell

Wynfelde

Wynall

Wolfe

Wynlonde

Wyse

Wise-ynowȝe

Wilde

Whanne

Yevan

Yowthe

Yorke

Yonkir

Greybicches names

Antigo

Belle

Chapelet

Chiche

Chise

Clenche

Cusse

Dawnse

Eglentyne

Fluse

Frowe

Galentyne

Galyette

Gente

Gentillot

Gygge

Gigelot

Gil

Hille

Kerchefe

Kyra

Lamprwn

Lemman

Letego

Matebrewne

Mirrygo

Mose

Nonne

Pynche

Pynchere

Polasene

Prynkow

Prynkelet

Rollere

Sare

Sysotte

Snekar

Snygge

Spynne

Swalow

Teysarre

Totte

Trille

Trise

Truse

Tapister

Trippe

Wenche

Whirre

Wrecche

The Names of All Manner of Hound

So I have found that there doesn't seem to be a plain text list of that list of "appropriate" 15th century dog names, so I have distilled (almost all of) them down here (there are over 1000 of them so they're going under a cut)

There is a separate category devoted to male and female greyhounds, that will have to go in a sequel post because of the text limits

Huge thank you to David Scott-Macnab for writing a paper on this manuscript that includes the entirety of the list and is where I got the text from.

THE NAMES OF ALL MANNER OF HOUNDS

Here begynnyth the names of all maner of houndis after the a.b.c. Firste to begynne with .a. for houndis names.

Argente

Aldirman

Archere

Archebawde

Absolon

Awgere

Braches names

Argentyne

Armonye

Amyable

Amatiste

Tereris

Arguere

Argument

Awfyne

Houndis names

Beawmonde

Bowman

Balfrymownde

Bangore

Burgoyne

Bliot

Beawyew

Blamer

Bragger

Braynesike

Bobagh

Brigawnte

Beggerre

Burgenon

Boleyne

Bonyoure

Blewet

Bowreman

Beste-of-all

Bokette

Baldre

Blawmbere

Besaunte

Bailemownd

Bendebowe

Bonyfaunte

Beawchefe

Breydan

Blodeman

Boynarde

Beawchere

Berdeles

Birdismowthe

Bultyngebrake

Bresawde

Boye

Blawncharde

Bonere

Brakette

Bawderese

Bawdewyn

Braches names

Blawnche

Burnette

Burmay

Blabbe

Beele

Bellore

Bleise

Belamy

Bwnne

Besoyne

Belotte

Blawmbele

Blawndese

Beawte

Besye

Tereris nam‹e›s

Beawfronte

Berde

Burlette

Bemoll

Bekere

Beawfise

Beawkane

Brawlere

Houndis names

Cleremownde

Cantor

Colle

Careaway

Chauntir

Cloider

Colier

Colman

Crampette

Clibawde

Crochette

Chawnte

Chefteyne

Chider

Chawndose

Chamfray

Chawmpir-n‹o›wne

Clikette

Clymber

Caluyrleye

Cryere

Coydur

Clynker

Chapeleyne

Chawnseler

Chepman

Chopper

Croyle

Crapawde

Carbonette

Cutte

Curteyne

Curtawnde

Cunnynge

Curteise

Ca‹mi›ot

Cannone

Cradokke

Charlemayne

Creseyte

Comforte

Clowdisleye

Chastelyn

Cosynette

Cheueteyne

Capteyne

Compaynowne

Chol‹s›ey

Curlewe

Clanygere

Chambirleyne

Cofenette

Cademan

Clowder

Braches names

Claris

Cowntese

Clere

Coose

Clare

Chawnteres

Colynette

Chowne

Cowntirfette

Chalenge

Chawngeabull

Chawnteclere

Clarense

Crowde

Clowde

Cherefull

Chamelette

Chalawndir

Clybbe

Chyȝemyne

Chamberere

Cere-ȝyne

Tereris names

Crabbe

Crykette

Crakestone

Creper

Houndis names

Druggeman

Denebawde

Derby

Downdyuale

Dygre

Dere-ybowȝt

Dolfyn

Dudman

Ducheman

Dene

Dowell

Dawngere

Dewdenere

Dollynge

Dawnmerse

Dyademe

Drewxȝ

Dewyn

Dornykke

Dawnsere

‹Dyamound›

Dredefull

Draynewhey

Braches names

Duchesse

Daliawnce

Dyane

Dowble

Downe

Dowse-amye

Dowse

Dyuerse

Damysene

Damysell

Dytayne

Tereris names

Dasyberde

Dedde

Dygger

Dybenman

Dyamawnde

Dappir

Doore

Dyngill

Houndis names

Elemente

Emerawde

Ewgeny

Elfyn

Elewyn

Errawnte

Eferose

Ewyn

Br[a]ches names

Elebre

Emelyn

Emelotte

Esperawnse

Tereris names

Ergo

Ermyne

Enmye

Ernyste

Envye

Eggetene

Howndis names

Forboise

Forster

Flynger

Fynder

Fredom

Freman

Frebodye

Fynore

Fryse

Fynke

Florentyne

Frankeleyne

Foy

Flaterere

Fleire

Forgere

Fyndewell

Frowmwnde

Braches names

Flowre

Flore

Fonne

Freresse

Foliette

Flame

Fynche

Florense

Foyse

Felise

Felette

Tereris names

Felowe

Foxe

Fill

Figge

Feete

Filthe

Frigun

Houndis names

Greynder

Gowere

Gormownde

Galeise

Gybon

Gaale

Gaylarde

German

Gilbarde

Goodynowȝe

Gyon

Gwette

Gyamownde

Gebage

Gwndir

Braches names

Genypre

Gelofre

Gwnne

Gille

Gilmote

Gawntelette

Gwnnore

Tereris names

Goyon

Garlik

Houndis names

Herawde

Hawtemownde

Hawdyfer

Huwet

Hilder

Harbeger

Hurlebucke

Halymote

Heuealowe

Halydaye

Halibred

Haywarde

Hernye

Hwdell

Halibutte

Braches names

Honysoke

Hewlette

Honydewe

Hosewife

Tereris names

Hurnette

Hardye

Hygon

Hakette

Howchyn

Houndis names

Juffo

Juvynell

Jakeman

Jangelor

Judde

Justyne

Jurdan

Jayberde

Jolye

Jeester

Joskyn

Jolybronde

Jongkade

Braches names

Joyou[s]

Junosse

Jakemyn

Tereris names

Jacke

Juell

Jakette

Joliboye

Jogeler

Izawde

Justyne

Jentill

Houndis names

Knave

Knewliche

Kenewale

Kynnysman

Kowghan

Kendale

Braches names

Kolette

Kote

Tereris names

Knotte

Knyvet

Kalot

Houndis names

Louell

Labour

Lyuette

Lurke

Lynke

Lorell

Ludman

Lymnore

Lyuyrmore

Lyncolne

Lutere

Lotomere

Liberall

Labell

Lodisman

Ludmer

Litillwitte

Lowrere

Leyne

Loyere

Braches names

Lyawnse

Lynore

Lawreall

Liberte

Lewte

Loreyne

Letewse

Lewde

Loyre

Louette

Tereris names

Litilman

Lapeyse

Lepar

Lwfkyn

Litilboye

Houndis names

Moraunt

Moreman

Mo‹r›gan

Merymowthe

Mordaunt

Meryuale

Mownamy

Millefoile

Malifawnte

Misavisid

Mervaile

Mafoy

Martynet

Makamete

Musike

Marrok

Mackowe

Muntayne

Mercurye

Marynere

Meruaylus

Merboise

Mownferaunt

Mailarde

Braches names

Mabbe

Madir

Misago

Maniye

Murre

Morles

Mery

Muriell

Mynerue

Merawde

Mellore

Merable

Malagun

Tereris names

Malaperte

Meryman

Mynor

Mustarde

Mistirman

Mynstrell

Houndis names

Nosewise

Newgurte

Nikole

Nason

Nero

Nedy

Norman

Braches names

Nyȝtyngale

Notemye

Nurture

Tereris names

Notemyge

Nise

Nody

Houndis names

Organ

Oravante

Orgaile

Orpyn

Oliferne

Ogan

Orebien

Overte

Orenge

Ordynall

Orlage

Braches names

Orage

Oribull

Olife

Ordynawnse

Tereris names

Oriell

Okirre

Houndis names

Pyarde

Pyoll

Polaynere

Perrye

Pagente

Plwmstede

Pykemownde

Profite

Petipase

Pipar

Pwffyne

Plentivous

Parfite

Poleyne

Poynter

Picarde

Plodder

Pawlyn

Parkere

Prowte

Poraile

Penawnte

Pilate

Braches names

Plesaunce

Peritory

Philomene

Perwynke

Plubele

Pyany

Tereris names

Pretyman

Pretiboy

Perkyn

Pursyvawnte

Pastey

Perte

Petite

Pratte

Perle

Proppe

Paris

Houndis names

Quester

Querister

Quynteyne

Braches names

Quonyam

Quyppe

Queyntaunse

Tereris names

Quarell

Quylette

Houndis names

Ryngedale

Richemownde

Reynere

Rabelle

R‹e›lefe

Rugemownde

Ribawde

Ryngeborne

Ruskyn

Ryngere

Rowdale

Rypette

Rybschawe

Robette

Rokell

Richere

Roweberde

Remownde

Rowterre

Rowtynge

Radissche

Riderre

Rowte-owte

Rossyngdale

Rangere

Reuerence

Regende

Rude-ynowgh

Reporte

Ryngewode

Rage

Braches names

Riall

Reynes

Riches

Rude

Reise

Ramet

Rainell

Russette

Roose

Ribibe

Rasyne

Reuerse

Ri‹s›chawde

Tereris names

Redy

Robynette

Redyman

Rube

Roset

Houndis names

Soylarde

Seyntamownde

Stalkere

Somnor

Syngerre

Seymore

Sowdiowre

Schakeschaw

Sergeaunt

Scheparde

Symbale

Sykamore

Staunchere

Salmon

Sibbisman

Sowdan

Stileman

Screveyne

Surisbye

Stacynere

Staynesmore

Sel‹w›de

Synfull

Sojorne

Seuerawnse

Sexteyne

Scathelok

Braches names

Solace

Symfonye

Spowse

Strawnge

Sufferawnse

Solible

Soyowruaunte

Seruysable

Tereris names

Sturdy

Sable

Safere

Symple

Sloote

Syte

Houndis names

Tawndur

Talbot

Tremayne

Turbeise

Tigale

Trailer

Tegon

Traileboise

Taileboise

Towkere

Turke

Traueile

Troile

Tabaryn

Trentaile

Talkerre

Tidan

Thrifti

Turkeise

Trauers

Torkoplere

Trusty

Torve

Tryare

Braches names

Tamaret

Trefoile

Truwde

Trewe

Trebille

Tawne

Tedewale

Tereris names

Tidore

Terry

Toppe

Terpyn

Talewise

Trifill

Tarde

V/W

Houndis names

Vagrawnte

Valamownte

Vailaunt

Veleyne

Vapuruawnt

Vertwe

Volantyne

Wakedale

Walker

Wodelefe

Wisedome

Wodewarde

Wyender

Wodewale

Woderofe

Wodeman

Watirman

Wynbawde

Wrawe

Wynbucke

Wyseman

Warnere

Wellyfedde

Warrokke

Braches names

Vyoll

Vyolette

Valis

Visemente

Valeise

Tereris names

Vrry

Wappis

Wilmot

Wellytawȝt

Wastepayne

Christ?

Christall

Christabell

Yolante

Yockyn

Yeman

Yolman

Yolyn

Zachelle

Zedewale

Zepryne

Etwyn

Etkyn

Contackte

Converse

#the names of all manner of hound #greyhound edition #dogs #meme #names #for the record #feel free to reblog this version especially #because it is the actual complete one

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salt-and-vynegar · 2 years ago

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Labyrinth Pavilion Notes

The rooms in the Labyrinth are a harder version than the ones in the Bright Pavilion, in my opinion.

The basic mechanic is: Don’t get spotted, and reach the exit within the time limit.

In theory, it seems simple enough, but in practice, it gets really hard, really quick. It gets especially hard if you try to collect everything in one go.

But the good news is, there is more than one way to finish each of these rooms. There’s no right answer, but it’s being able to get the collectibles and escape. That’s what counts.

Additional ideas for routes: @vynegar’s write up here, Athyme’s guide here, and Youtube video links from Sara and Yang (1, 2, 3, 4)

Once you complete and gather the collectibles from the Way of Adversity and the Way of Truth rooms, the final challenge for the Ink Study room is unlocked. Once you complete and gather the collectibles from the Way of Mystery and the Way of choices, the final challenge for the Bright Pavilion is unlocked.

There doesn’t seem to be any Easter Eggs for this pavilion either, but the little banter in the opening is still fun to see with each suitor.

I’ll link the routes I took for the different rooms under the cut, since it is spoilers, but there are a couple of things I’ve noticed while doing the rooms.

For certain rooms, you’re not always safe where you start or at the exits. Figuring out where your safe places are to wait out/hide out are a must. This is very important in rooms where the exits are being patrolled as well.

Watch the patrols on both ends carefully. Sometimes a space that was safe on one go around will not become safe later on. Just because you’re not controlling a character doesn’t mean they can’t get caught.

If you bang into any of the people on patrol, you will get caught and the game will end. However, if you walk near them while their light is not on you, you can sneak by them. This also works for distance - you may be able to sneak by a guard if you’re pretty far away from their line of sight/flashlight.

I recommend not being too adventurous, unless you have a way out or a way to come back and try again. Hiding behind screens and looping around people to get around them are some of the best maneuvers, if you can manage them. It can be really nerve-wracking though.

Even when it looks like there’s no way through, make sure to check the patrol routes carefully. You may find out that a guard’s range is narrower than you think.

Also, things can change as the clock counts down - what was inaccessible can become accessible. As the time winds down, you may find an opening, even when backed into a corner. So keep a close eye on your surroundings.

Be very careful when choosing what mechanisms you activate and when. Sometimes, you don’t need to activate everything to get all the collectibles and complete the room.

Breathe and stay calm. There is enough time to get everything. Since this sneaking game relies a lot on the touchscreen control, if you’re able to keep your hands steady as you go through the rooms and make your maneuvers, it will help you out in the long run.

To unlock the final challenge for the Labyrinth Pavilion, you need to obtain all of the collectibles from the First Try, Second Try, and Third Try areas from the Vault Section.

SPOILERS: The routes I took to get the collectibles

(If you’re using the app, highlight and copy the link, then paste it in an internet browser. The video should pop up.)

Way of Adversity

Way of Truth

Way of Mystery

Way of Choices

To see the answer to The Insatiable Journey (The Labyrinth Pavilion Challenge), I’ve made a post on it here.

#Tears of Themis #ToT: Blizzardous Threads of Red Event #My Analysis

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xinxiaogato · 2 years ago

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hello everyone.... i'm back groveling on my knees to any tears of themis returners who could use my returner code (WDF7L67KNN) in the “returner gifts” event so that i can try to get luke's ssr card: dreamlike drama (◞‸◟；) 🤲

LONG HAIR ML??? ✓ TRADITIONAL CHINESE CLOTHING??? ✓ LUKE PEARCE??? ✓ MATCHING HIGH PONYTAILS??? ✓ FIREWORKS??? ✓ LOVING GAZE??? ✓ IT'S THE WHOLE SHEBANG

ALSO ❗ for anyone who is struggling with the main event, Athyme on Reddit has everything you need! this person is an absolute archonsend oml my brain is too smooth for these puzzles

&& feel free to share ur returner code in the replies if need be! :>

#stella rants — !#tears of themis #tot #blizzardous threads of red #returner code

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kramlabs · 5 years ago

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Peter’s current thoughts on stearic acid, ketones, ROS, etc

Protons (52): A correction and a few thoughts on satiety

There has never been a completed concept of the Protons thread. Logic and data have allowed it to emerge and I still have no idea where it will end, but there have been a few mis-steps on the way. A reader recently pointed my incorrect post from 2013 where I was looking to see how fasting or ketogenic diets might blunt insulin signalling. Nowadays my feeling is that it is high physiological ROS generation which achieves this. At the time I clearly got it wrong with: "We appear to have two basic states of the electron transport chain. There is the situation under fasting or ketogenic dieting conditions. Here delta psi is low, complex I throughput is low and there is plenty of FADH2 input through electron transporting flavoprotein dehydrogenase coming from the first step of beta oxidation of real fats, like palmitic acid. With a low delta psi it is near impossible to generate reverse electron flow through complex I so activation of insulin signalling is rapidly aborted by the continuing action of tyrosine phosphatase". That does not appear to be the case and, having thought about it, my email reply went like this. We had been chatting about ketones, delta psi, RET and insulin resistance from ketones vs from saturated fats. I may as well copy/paste some of it here, slightly edited for clarity, and place a link within the 2013 post: "My thinking currently is that ketones do not induce insulin resistance unless, like glucose, there is enough input via complex II to do this. So RET is possible but will only occur when the cell has adequate caloric supply. If you combined ketones with stearic or palmitic acid the long chain fatty acid would undoubtedly input at ETFdh and drive RET, rather than it being the ketones. Incidentally, this probably also represents "cellular satiety". Clearly under physiological conditions ketones will normally be associated with elevated FFAs. The differential effects of FFAs vs ketones would be that FFAs would then drive insulin resistance in cells which can metabolise them, muscle etc, but ketones would drive far less RET in cells which require some small amount of glucose in excess of the energy supplied by the ketones themselves, ie neurones… On the adipocytes things look more complex. Undoubtedly both ketones and FFAs exert a negative feedback on lipolysis in addition to any effect of their driving/not driving RET during oxidation. But some degree of insulin signalling is essential to physiology in addition to this negative feedback, otherwise we get diabetic ketoacidosis due to failure of insulin availability to oppose glucagon. Once you start to think about stearic acid plus glucose you have to differentiate between cellular levels and dietary levels. Simply treating isolated adipocytes with elevated glucose and elevated long chain FFAs will result in ROS. If you set your experiment up correctly (no MUFA, no PUFA, high glucose) the resulting RET will result in apoptosis or necrosis. There is an infinite supply of papers doing this to almost any cell type. In the whole animal things are different. If physiology is functional the stearic acid will provoke a prompt first phase insulin response and will effectively augment insulin delivery via the portal vein to the liver. Insulin acting in the liver will limit glucose release to the systemic circulation and so limit the need for systemic hyperinsulinaemia to deal with the glucose. Then the animal stays slim as there is minimal systemic hyperinsulinaemia. If physiology is non functional we are talking DM T2 which is largely the aftermath of chronic PUFA ingestion and things then become even more complex. The low carb approach side steps the problems of failure of correct insulin secretion/hepatic signalling by simply reducing the reliance on any sort of insulin signalling beyond the most minimal needed. Then stearic acid becomes problem free. When (or if) physiology normalises then some degree of glucose consumption by mouth might be acceptable along side saturated fats but by then anyone with any sense will be fat adapted and unwilling to go back to a mixed diet". This set of thoughts is currently relevant as Brad Marshall has taken the concept of stearic acid as the best physiological generator of adipocyte physiological insulin resistance and converted it in to a moderate carb, highly saturated fat diet with interesting results. You can read about his croissant diet on his blog Fire in a Bottle: Introducing The Croissant Diet. This experiment is based on the PhD of Valerie Reeves where a mixed macro diet based around stearic acid markedly limited weight gain in db/db mice. The db/db mouse is an extremely severe obesity model as it lacks functional leptin receptors. So a complete lack of leptin signalling can be side-stepped, still in the presence of starch, by supplying roughly 40% of calories as predominantly stearic acid. Not low carb. Not ketogenic. It works (from my point of view) by directly manipulating ROS generation (ie increasing it) at the electron transport chain level to signal "cellular" satiety, with appropriate ability to resist insulin's fat storage signal. This will be recapitulated in the brainstem neural circuits which control whole body satiety. Signalling from the ETC is core. It works by generating physiological insulin resistance and clearly over-rides any effect from leptin signalling. Also in the comments of the last post came this gem from ctviggen, worth a post in its own right. Interesting paper. Limited insights within the discussion but great data! Dietary Stearic Acid Leads to a Reduction of Visceral Adipose Tissue in Athymic Nude Mice While all of these ideas were kicking around the concept of fasting as a state of caloric excess emerged. Obviously, not eating makes you hungry. Initially. There comes a point where, when insulin is low enough and FFAs rise to levels approaching over 2000micromol/l (plus ketones), when hunger decreases. Prolonged fasting does not invariably generate ravenous hunger. This is because FFAs (and ketones) represent an energy glut beyond any single cell's imagination and it does not require insulin signalling to access it (there do appear to be other controls on ATP generation). So cells which can metabolise FFAs should behave as it they have more than enough calories so that they should resist insulin. Access to excess metabolic substrate must result in ROS and the appropriate disabling of insulin signalling. Starvation as generator of a caloric excess signal... An interesting concept. And PUFA, failing to generate adequate ROS, might well lead to glucose "wastage" in to cells such as myocytes which might well result in profound and symptomatic hypoglycaemia, essentially a failure of satiety signalling. Another interesting idea. Which clearly would not happen if metabolism was based around stearic acid... Peter

POSTED BY PETER AT SATURDAY, DECEMBER 14, 2019

#peter #stearic acid #hyperlipid #IF #fasting #satiety

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vynegar · 2 years ago

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TT someone tell me if you find a really good labyrinth pavilion guide. like, literally showing the entire route + good hiding spots

otherwise i’ll wait for the wiki to release maps of each area

(oh and also athyme’s guide links to a video at the end. but really i need the hiding spots TT)

here’s a video guide for level 4 (i still haven’t passed it yet though)

here’s another one! it’s the one i used and i really recommend it!!!

my written guide for level 3 below

(gonna use vyn as the ML)

as far as i can tell, MC doesn’t have a safe hiding spot for most of the level so keep an eye on her even when you’re exploring with vyn. in the area she starts in, there’s only one guard who moves in a loop so just occasionally move MC around

move vyn to the upper left and pull the lever; can hide in the horizontal space between the bookshelves if needed

with vyn, go down the narrow hallway that has a guard (wait until the flashlight is aimed away from the path). go toward the left and up, there should be some black paper screens with a silk pouch behind them. (this will be vyn’s hiding spot later)

leave the paper screens and go right a bit and down, there should be two levers that you can reach from behind the bookcases. pull both, then go back to hide where the silk pouch was (vyn is safe here and his exit is just to the left)

switch to MC, go down to the area that vyn unlocked with the two levers. go to the right side first for the silk pouch. hide until it’s safe to head to the left side, then grab the item from there. you have all the items now.

MC will probably need to first duck into the right side, wait and hide, and then be able to leave (exit is to the upper right from the items area)

switch to vyn, his exit is to the left after exiting the paper screens hiding place

#TOT liveblog #having to explore w one character while avoiding patrollers with the other is just too much

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biomedres · 2 years ago

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Uses of the Novel Small Peptide, KTH-222, in Treating Human Pancreatic Cancer: Evaluation of Different Treatment Regimens using a Mouse Xenograft Model

Uses of the Novel Small Peptide, KTH-222, in Treating Human Pancreatic Cancer: Evaluation of Different Treatment Regimens using a Mouse Xenograft Model Biomedical Journal of Scientific & Technical Research

https://biomedres.us/fulltexts/BJSTR.MS.ID.005798.php

KTH-222 is a novel, 8-amino acid length peptide derived from atrial natriuretic peptide and a group of related peptides that reduce cancer cell growth. It was previously reported that KTH-222 reduces the rate of tumor growth and prolongs survival in mice implanted with MIA PaCa-2 human pancreatic cancer cells more effectively than gemcitabine when used as primary therapy. The goal of the present study is to explore the effectiveness of KTH-222 for treating pancreatic cancer when used in two other roles: combination primary therapy and salvage therapy. Female athymic nude mice were inoculated subcutaneously in the right flank with MIA-PaCa-2 tumor cells. KTH-222 was administered as part of a combination primary therapy together with gemcitabine and paclitaxel or as a salvage therapy. When used in combination with gemcitabine and paclitaxel as primary therapy, KTH-222 further reduced tumor volume, although it did not extend the interval until terminal tumor volume was reached. When used a salvage therapy, KTH-222 did extend the interval until terminal tumor volume was reached and, in one case, produced a sustained regression in tumor growth. The results of this study, together with earlier results, suggest that KTH-222 could be used in several different ways in the treatment of pancreatic cancer.

For more articles in Journals on Biomedical Sciences click here

bjstr

Follow on Twitter : https://twitter.com/Biomedres01 Follow on Blogger :https://biomedres01.blogspot.com/ Like Our Pins On : https://www.pinterest.com/biomedres/

#Journals on Medical Informatics #Journals on Biomedical Imaging #Journals on Biomedical Intervention #Journals on Medical Microbiology #Journals on Medical Casereports

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asokan-blog · 2 years ago

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They think they have everything under control!

Maybe the nihilistic part of me cannot stomach all these. My athymic insides cannot stomach the idea that someone can be so cocksure about everything. I have come to understand that Time and Tide wait for no man and that Time is the greatest killer of Man. Time flies; Man’s hopes go! No Man has yet to win over Time; Shiva, a wandering seeker, is the exception and was conferred the title ‘Kala…

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vivekbajaj-grs · 3 years ago

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Global Patient Derived Xenograft/PDX Models Market Size, Status and Forecast 2021-2027

Patient derived xenografts (PDX) are models of cancer where the tissue or cells from a patient's tumor are implanted into an immunodeficient or humanized mouse. PDX models are used to create an environment that allows for the natural growth of cancer, its monitoring, and corresponding treatment evaluations for the original patient.

Several types of immunodeficient mice can be used to establish PDX models: athymic nude mice, severely compromised immune deficient (SCID) mice, NOD-SCID mice, and recombination-activating gene 2 (Rag2)-knockout mice. The mice used must be immunocompromised to prevent transplant rejection. The NOD-SCID mouse is considered more immunodeficient than the nude mouse, and therefore is more commonly used for PDX models because the NOD-SCID mouse does not produce natural killer cells.

Download FREE Sample of this Report @ https://www.grandresearchstore.com/report-sample/global-patient-derived-xenograftpdx-models-2021-2027-752

Market Analysis and Insights: Global Patient Derived Xenograft/PDX Models Market

The global Patient Derived Xenograft/PDX Models market size is projected to reach US$ 178.5 million by 2027, from US$ 92 million in 2020, at a CAGR of 9.5% during 2021-2027.

With industry-standard accuracy in analysis and high data integrity, the report makes a brilliant attempt to unveil key opportunities available in the global Patient Derived Xenograft/PDX Models market to help players in achieving a strong market position. Buyers of the report can access verified and reliable market forecasts, including those for the overall size of the global Patient Derived Xenograft/PDX Models market in terms of revenue.

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Global Patient Derived Xenograft/PDX Models Scope and Market Size

Patient Derived Xenograft/PDX Models market is segmented by company, region (country), by Type, and by Application. Players, stakeholders, and other participants in the global Patient Derived Xenograft/PDX Models market will be able to gain the upper hand as they use the report as a powerful resource. The segmental analysis focuses on revenue and forecast by Type and by Application in terms of revenue and forecast for the period 2016-2027.

Segment by Type

Mice Models

Rat Models

Segment by Application

Pre-clinical Drug Development and Basic Cancer Research

Biomarker Analysis

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U.S.

Canada

Europe

Germany

France

U.K.

Italy

Russia

Nordic

Rest of Europe

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China

Japan

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India

Australia

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Mexico

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Turkey

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Rest of MEA

By Company

Crown Bioscience

The Jackson Laboratory

Champions Oncology

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Oncodesign

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EPO Berlin-Buch

Xentech

Urolead

Get the Complete Report & TOC @ https://www.grandresearchstore.com/life-sciences/global-patient-derived-xenograftpdx-models-2021-2027-752

Table of content

1 Report Overview 1.1 Study Scope 1.2 Market Analysis by Type 1.2.1 Global Patient Derived Xenograft/PDX Models Market Size Growth Rate by Type: 2016 VS 2021 VS 2027 1.2.2 Mice Models 1.2.3 Rat Models 1.3 Market by Application 1.3.1 Global Patient Derived Xenograft/PDX Models Market Share by Application: 2016 VS 2021 VS 2027 1.3.2 Pre-clinical Drug Development and Basic Cancer Research 1.3.3 Biomarker Analysis 1.4 Study Objectives 1.5 Years Considered 2 Global Growth Trends 2.1 Global Patient Derived Xenograft/PDX Models Market Perspective (2016-2027) 2.2 Patient Derived Xenograft/PDX Models Growth Trends by Regions 2.2.1 Patient Derived Xenograft/PDX Models Market Size by Regions: 2016 VS 2021 VS 2027 2.2.2 Patient Derived Xenograft/PDX Models Historic Market Share by Regions (2016-2021) 2.2.3 Patient Derived Xenograft/PDX Models Forecasted Market Size by Regions (2022-2027) 2.3 Patient Derived Xenograft/PDX Models Industry Dynamic 2.3.1 Patient Derived Xenograft/PDX Models Market Trends 2.3.2 Patient Derived Xenograft/PDX Models Market Drivers 2.3.3 Patient Derived Xenograft/PDX Models Market Challenges 2.3.4 Patient Derived Xenograft/PDX Models Market Restraints 3 Competition Landscape by Key Players 3.1 Global Top Patient Derived Xenograft/PDX Models Players by Revenue 3.1.1 Global Top Patient Deri

CONTACT US: 276 5th Avenue, New York , NY 10001,United States International: (+1) 646 781 7170 / +91 8087042414 Follow Us On linkedin :- https://www.linkedin.com/company/grand-research-store/

#PatientDerivedXenograftPDXModelsMarket

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digigrimoire · 7 years ago

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My personal altar. I need to buy some more tea candles and I ran out of salt packets (I usually grab some when I go out to eat). At the moment it has an amethyst wand, a coin, a pendulum and chart, an onyx arrowhead I use as an athyme, and an altar cloth. I don't keep matches with me because I always have a lighter or two in my purse. Altoids tins and other all containers make excellent pocket altars and can hold quite a bit. They may look like just a pack of mints but to they are completely different on the inside and can provide a look into who each witch is as both a person and a practitioner. If you live in a small or shared space or are constantly on the go I highly recommend one of these, especially if you have nosy or chaotic roommates or family members.

#pocket altar #mini altar #Altoids tin #bigger on the inside

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abbkine · 5 years ago

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New Post has been published on Abbkine - Antibodies, proteins, biochemicals, assay kits for life science research

Hard work, Do not forget your initiative mind- Abbkine Added 210 Citations in April

In April 2020, Abbkine collected 210 English articles published using Abbkine products, and some of them sent us good news on their own initiative. The joy was beyond words. In this collection of articles, the highest impact factor (IF) is 13.05, with articles with IF>7 accounting for 10.4% and articles with IF>4 accounting for 43%.

In the current evaluation of scientific research, scientific research papers, as the systematic summary and theoretical crystallization of scientific research carried out by scientific researchers, are still the main objects for measuring innovative activities, especially basic research activities. Science, Nature and Cell are internationally recognized journals with the highest academic reputation. According to the statistical results of Chinese scientific papers in 2018, the number of Chinese papers published in the above three journals in 2017 was 309, an increase of 11 articles over the previous year, ranking fourth in the world. China's scientific research strength should not be underestimated!

Let's take a look at some of the research workers in China who are studying some topics.

Title: MST4 kinase suppresses gastric tumorigenesis by limiting YAP activation via a non-canonical pathway

Magazine: Journal of Experimental Medicine

Impact factor: 9.83

University: Tongji University

Abstract: Hyperactivation of YAP has been commonly associated with tumorigenesis, and emerging evidence hints at multilayered Hippo-independent regulations of YAP. In this study, we identified a new MST4–YAP axis, which acts as a noncanonical Hippo signaling pathway that limits stress-induced YAP activation. MST4 kinase directly phosphorylated YAP at Thr83 to block its binding with importin α, therefore leading to YAP cytoplasmic retention and inactivation. Due to a consequential interplay between MST4-mediated YAP phospho-Thr83 signaling and the classical YAP phospho-Ser127 signaling, the phosphorylation level of YAP at Thr83 was correlated to that at Ser127. Mutation of T83E mimicking MST4-mediated alternative signaling restrained the activity of both wild-type YAP and its S127A mutant mimicking loss of classical Hippo signal. Depletion of MST4 in mice promoted gastric tumorigenesis with diminished Thr83 phosphorylation and hyperactivation of YAP. Moreover, loss of MST4–YAP signaling was associated with poor prognosis of human gastric cancer. Collectively, our study uncovered a noncanonical MST4–YAP signaling axis essential for suppressing gastric tumorigenesis.

Article link: https://rupress.org/jem/article/217/6/e20191817/151647

Products using from Abbkine:

IPKine™ HRP, Goat Anti-Mouse IgG LCS (CAT#A25012)

IPKine™ HRP, Mouse Anti-Rabbit IgG LCS (CAT#A25022)

Title: TRIM32/USP11 Balances ARID1A Stability and the Oncogenic/Tumor-Suppressive Status of Squamous Cell Carcinoma

Magazine: Cell Reports

Impact factor: 8.04

University: Chinese Academy of Medical Sciences and Peking Union Medical College

Abstract: Squamous cell carcinoma (SCC) is an aggressive epithelial malignancy, yet the molecular mechanisms underlying SCC development are elusive. ARID1A is frequently mutated in various cancer types, but both mutation rates and expression levels of ARID1A are ubiquitously low in SCCs. Here, we reveal that excessive protein degradation mediated by the ubiquitin-proteasome system (UPS) contributes to the loss of ARID1A expression in SCC. We identify that the E3 ligase TRIM32 and the deubiquitinase USP11 play key roles in controlling ARID1A stability. TRIM32 depletion inhibits SCC cell proliferation, metastasis, and chemoresistance by stabilizing ARID1A, while USP11 depletion promotes SCC development by promoting ARID1A degradation. We show that syndecan-2 (SDC2) is the downstream target of both ARID1A and USP11 and that SDC2 depletion abolishes the oncogenic function of ARID1A loss. In summary, our data reveal UPS-mediated protein degradation as a mechanism underlying ARID1A loss and propose an important role for the TRIM32/USP11-ARID1A-SDC2 axis in SCC.

Article link: https://www.sciencedirect.com/science/article/pii/S2211124719316675

Products using from Abbkine:

ExKineTM Nuclear and Cytoplasmic Protein Extraction Kit (CAT#KTP3001)

Title: Microneedle drug eluting balloon for enhanced drug delivery to vascular tissue

Magazine: Journal of Controlled Release

Impact factor: 7.82

University: Yonsei University, Seoul

Abstract: High rates of restenosis and neointimal formation have driven increasing interest in the application of drug eluting balloons (DEB) as counteractive measures for intraluminal drug delivery. The use of DEBs eliminates the need for stents so that serious side effects including in-stent restenosis and stent thrombosis can be avoided and long-term medication of antiplatelet agent is not needed. Despite their benefits, DEBs have poor drug delivery efficiency due to short balloon inflation times (30~60 seconds) that limit the passive drug diffusion from the balloon surface to the luminal lesion. To increase drug delivery efficiency, a microneedle DEB (MNDEB) was developed by a conformal transfer molding process using a thin polydimethylsiloxane mold bearing a negative array of MNs of 200 μm in height. A MN array composed of UV curable resin was formed onto the surface of DEB, and drugs were coated onto the structure. The mechanical properties of the MN array were investigated and MN

penetration into luminal vasculature was confirmed in vivo. An increase in drug delivery efficiency compared to a standard DEB was demonstrated in an in vivo test in a rabbit aorta. Finally, the superior therapeutic efficacy of MNDEBs was evaluated using an atherosclerosis rabbit model.

Article link: https://www.sciencedirect.com/science/article/abs/pii/S0168365920300894

Products using from Abbkine:

EliKine™ Mouse IL-1β ELISA Kit (CAT#KET7005)

EliKine™ Mouse TNF-α ELISA Kit (CAT#KET7015)

Title: Polyphyllin VI Induces Caspase-1-Mediated Pyroptosis via the Induction of ROS/NF-κB/NLRP3/GSDMD Signal Axis in Non-Small Cell Lung Cancer

Magazine: Cancers

Impact factor: 5.87

University: Southwest Medical University

Abstract: Trillium tschonoskii Maxim (TTM), a traditional Chinese medicine, has been demonstrated to have a potent anti-tumor effect. Recently, polyphyllin VI (PPVI), a main saponin isolated from TTM, was reported by us to significantly suppress the proliferation of non-small cell lung cancer (NSCLC) via the induction of apoptosis and autophagy in vitro and in vivo. In this study, we further found that the NLRP3 inflammasome was activated in PPVI administrated A549-bearing athymic nude mice. As is known to us, pyroptosis is an inflammatory form of caspase-1-dependent programmed cell death that plays an important role in cancer. By using A549 and H1299 cells, the in vitro effect and action mechanism by which PPVI induces activation of the NLRP3 inflammasome in NSCLC were investigated. The anti-proliferative effect of PPVI in A549 and H1299 cells was firstly measured and validated by MTT assay. The activation of the NLRP3 inflammasome was detected by using Hoechst33324/PI staining, flow cytometry analysis and real-time live cell imaging methods. We found that PPVI significantly increased the percentage of cells with PI signal in A549 and H1299, and the dynamic change in cell morphology and the process of cell death of A549 cells indicated that PPVI induced an apoptosis-to-pyroptosis switch, and, ultimately, lytic cell death. In addition, belnacasan (VX-765), an inhibitor of caspase-1, could remarkably decrease the pyroptotic cell death of PPVI-treated A549 and H1299 cells. Moreover, by detecting the expression of NLRP3, ASC, caspase-1, IL-1β, IL-18 and GSDMD in A549 and h1299 cells using Western blotting, immunofluorescence imaging and flow cytometric analysis, measuring the caspase-1 activity using colorimetric assay, and quantifying the cytokines level of IL-1β and IL-18 using ELISA, the NLRP3 inflammasome was found to be activated in a dose manner, while VX-765 and necrosulfonamide (NSA), an inhibitor of GSDMD, could inhibit PPVI-induced activation of the NLRP3 inflammasome. Furthermore, the mechanism study found that PPVI could activate the NF-κB signaling pathway via increasing reactive oxygen species (ROS) levels in A549 and H1299 cells, and N-acetyl-L-cysteine (NAC), a scavenger of ROS, remarkably inhibited the cell death, and the activation of NF-κB and the NLRP3 inflammasome in PPVI-treated A549 and H1299 cells. Taken together, these data suggested that PPVI-induced, caspase-1-mediated pyroptosis via the induction of the ROS/NF-κB/NLRP3/GSDMD signal axis in NSCLC, which further clarified the mechanism of PPVI in the inhibition of NSCLC, and thereby provided a possibility for PPVI to serve as a novel therapeutic agent for NSCLC in the future

Article link: https://www.mdpi.com/2072-6694/12/1/193

Products using from Abbkine:

Caspase-1 Assay Kit (Colorimetric) (CAT#KTA3020)

Title: Integrin β3 promotes cardiomyocyte proliferation and attenuates hypoxia-induced apoptosis via regulating the PTEN/Akt/mTOR and ERK1/2 pathways

Magazine: International Journal of Biological Sciences

Impact factor: 4.04

University: Shanghai Jiaotong University

Article link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6990915/

Abstract: Integrin β3 is one of the main integrin heterodimer receptors on the surface of cardiac myocytes. Our previous studies showed that hypoxia induces apoptosis and increases integrin β3 expression in cardiomyocytes. However, the exact mechanism by which integrin β3 protects against apoptosis remains unclear. Hence, the present investigation aimed to explore the mechanism of integrin β3 in cardiomyocyte proliferation and hypoxia-induced cardiomyocyte apoptosis.

Products using from Abbkine:

Annexin V-AbFluor™ 555 Apoptosis Detection kit (CAT#KTA0003)

#Cell #science

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zdravzivotzavas-blog · 8 years ago

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ПЕЧУРКИ: Здравствени придобивки

Шампињони (Agaricus bisporus fam. Agaricaceae)

Шампињоните се најчесто користени печурки. Тие содржат фитохемиски супстанции корисни за превенција од рак на простатата.

Во научни студии спроведени на стаорци, забеле��ано е дека шампињоните имаат и хипогликемиска и хиполипемична активност, т.е. ја намалуваат концентрацијата на гликоза, холестерол и триглицеридите во крвта.

Буковка (Pleurotus ostreatus fam. Pleurotaceae)

Според една научна студија, како најпотентна за супресија на пролиферација на ракот на дојката и ракот на дебелото црево ја издвоиле буковката.

Вргањ (Boletus edulis fam. Boletaceae)

Студиите покажуваат дека вргањот има антипролиферативен ефект на ракот на дебелото црево.

Полисахаридите на вргањот имаат антиинфламаторен ефект и биле тестирани кај глувци со асма, при што е забележан позитивен ефект.

Шитаке (Lentinula edodes fam. Marasmiaceae)

Студиите покажуваат дека при користење на шитаке во исхраната се зголемува имунитетот и се намалува инфламацијата.

Магистар по фармација Тања Велјановска

*Содржината на текстот е од информативен карактер и не е наменета за дијагностицирање или лекување. За вашата здравствена состојба консултирајте се со вашиот лекар.

Референци:

1. Adams LS, Phung S, Wu X, Ki L, Chen S., White button mushroom (Agaricus bisporus) exhibits antiproliferative and proapoptotic properties and inhibits prostate tumor growth in athymic mice, National Center for Biotechnology Information, https://www.ncbi.nlm.nih.gov/pubmed/19005974

2. Jeong SC, Jeong YT, Yang BK, Islam R, Koyyalamudi SR, Pang G, Cho KY, Song CH., White button mushroom (Agaricus bisporus) lowers blood glucose and cholesterol levels in diabetic and hypercholesterolemic rats, National Center for Biotechnology Information, https://www.ncbi.nlm.nih.gov/pubmed/20116660

3. Jedinak A, Sliva D., Pleurotus ostreatus inhibits proliferation of human breast and colon cancer cells through p53-dependent as well as p53-independent pathway, National Center for Biotechnology Information, https://www.ncbi.nlm.nih.gov/pubmed/19020765

4. Gu YH1, Sivam G., Cytotoxic effect of oyster mushroom Pleurotus ostreatus on human androgen-independent prostate cancer PC-3 cells, National Center for Biotechnology Information, https://www.ncbi.nlm.nih.gov/pubmed/16822205

5. Lemieszek MK, Ribeiro M, Guichard Alves H, Marques G, Nunes FM, Rzeski W., Boletus edulis ribonucleic acid - a potent apoptosis inducer in human colon adenocarcinoma cells, National Center for Biotechnology Information, https://www.ncbi.nlm.nih.gov/pubmed/27302173

6. Songquan Wu, Guangli Wang, Ruhui Yang, and Yubao Cui, Anti-inflammatory effects of Boletus edulis polysaccharide on asthma pathology, National Center for Biotechnology Information, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5095342/

7. Dai X, Stanilka JM, Rowe CA, Esteves EA, Nieves C Jr, Spaiser SJ, Christman MC, Langkamp-Henken B, Percival SS, Consuming Lentinula edodes (Shiitake) Mushrooms Daily Improves Human Immunity: A Randomized Dietary Intervention in Healthy Young Adults, National Center for Biotechnology Information, https://www.ncbi.nlm.nih.gov/pubmed/25866155

8. D. Handayani, J. Chen, B. J. Meyer, and X. F. Huang , Dietary Shiitake Mushroom (Lentinus edodes) Prevents Fat Deposition and Lowers Triglyceride in Rats Fed a High-Fat Diet, National Center for Biotechnology Information, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199106/

#шампињони #буковка #вргањ #шитаке #имунитет #рак #инфламација

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