#α1

[coffeenuts]

[dphotoworld]

Sony A1 получит функцию фокусировки в видео по глазам животных

Sony выпустит важное обновление прошивки для св... Читать дальше »

[deltaphoto3]

風で散る雪の夜 #wind #snow #night #sonya1 #α1 https://www.instagram.com/p/Cml7ncRPuzH/?igshid=NGJjMDIxMWI=

[johnnyslittleanimalblog]

A Pair of Brown Bears - DSC07573a by Ronald Todd Via Flickr: Grizzly (Alaska Brown Bear) female nonchalantly walking right in front of me!!! Shortly, she got too big fit in my frame. All she was interested in was fishing. I was just another part of the scenery.

[agnickradio]

Κέντρο διά βίου μάθησης Δήμου Αγίου Νικολάου, νέα τμήματα

Από το Κέντρο Διά Βίου Μάθησης – Νέα Φάση του Δήμου Αγίου Νικολάου γνωστοποιείται ότι πρόκειται να ξεκινήσει άμεσα την λειτουργία του το τμήμα «Βασικά  Γερμανικά Α1» διάρκειας 50 ωρών. Continue reading Untitled

[thisworld1]

by Japanese photographer 岡本幸太郎 SONY α1 @c9_tereko

[sunovermordor]

α1

Με δάχτυλα βαθιά μπηγμένα στα πλευρά, η ελπίδα χορεύει στη ζεστασιά που αναζητώ. Και τότε, αυτά ξυπνάν, ελευθερώνοντας δαιμόνια και κακό.

[meopi]

✧*。About my oc✧*｡

Hestaert

Compassionater 【Hestaert】 born in a chaotic sea of stars,nurtured by the concept of shadows and colors, she represents the star is the Southern Cross.You can call her HEL/ Hestaert/Meopi/Compassionater…whatever, it's not important.

Creation：Schuiefena

Living in the nebula within the body of Hestaert or in the constellation of the Southern Cross α1. The collective belief of the entire ethnic group is Hestaert.

[kawatooo]

Anima

α1

[shoesofthefishermanswife]

In med school and also preparing for my exam. I have to learn a whole course about antidepressants so here it goes I guess !

Hi! I'm sure that the majority of this will be pretty basic review but let's talk about it!

The first generation of antidepressants were monoamine oxidase inhibitors (MAOIs). They were originally invented to treat tuberculosis but in 1953 Iproniazid was developed and patients taking it showed improvements in their depression symptoms. As their name suggests, they function by inhibiting the breakdown of monoamine neurotransmitters (serotonin, dopamine, norepinephrine, ect) by the enzyme monoamine oxidase, and this leaves more neurotransmitters available for synapse. The problem with this method is that there are monoamines in our food. Patients taking MAOIs have to be careful eating foods that contain lots of tyramine because it can't be broken down. High levels of tyramine can cause sudden increases in blood pressure and even cerebral hemorrhage! Understandably, MAOIs aren't prescribed very often anymore.

The next generation of antidepressants, known as tricyclic antidepressants, was developed in the late 50s. These work by inhibiting both serotonin and norepinephrine reuptake. They are also antagonists for postsynaptic adrenergic α1 and α2 receptors, muscarinic receptors, and histamine H1 receptors. Reuptake inhibition is the mechanism found in a lot of our current antidepressants, but they're a little bit more focused.

In the late 80s, Fluoxetine was finally approved by the FDA and SSRIs continue to dominate the antidepressant landscape. SSRI stands for Selective Serotonin Reuptake Inhibitors, and they do what their name suggests, inhibiting the serotonin transporter (SERT) at the presynaptic axon terminal. This leaves more serotonin (5-HT) available for synapse. Additionally, SSRIs target the 5-HT1A autoreceptors. This seems counter productive at first, because the autoreceptor activation slows 5-HT production and release. But over time, this builds autoreceptor tolerance. Generally, autoreceptors can shut off signaling when there's too much and is a main contributor to building drug tolerance. But since the autoreceptor is now being activated, that shut off function loses efficacy and the extra 5-HT in the synapse from SERT inhibition doesn't cause tolerance to be built up (as much). This is why it takes SSRIs weeks to kick in because the two processes do cancel each other out until the autoreceptors have gotten tolerant. There is variety within SSRIs. Fluoxetine (Prozac) has a half life much longer than Sertraline (Zoloft) and takes longer to get peak plasma concentration.

Serotonin-Noradrenaline reuptake inhibitors work very similarly, they just also inhibit norepinephrine reuptake. (Say what you will about anti-depressants, at least they're named straightforwardly lol). Some patients respond better to SSRIs, some respond better to SNRIs. Unfortunately, a lot of patients don't respond well to either and they can come with difficult side effects.

Moving on from depression, let's talk a little about anxiety and anxiolytics. One of the key brain changes in general anxiety is reduced PFC inhibitory control, associated with reduced GABA(A) receptors. This is coupled with amygdala overactivity. Benzodiazepines help regulate anxiety by increasing GABA control. They do so without nearly as many side effects as the previous barbiturates, and took off in the 1960s. But because they act on GABA, mixing benzodiazepines with alchohol (also acts on GABA) creates lots of abuse potential (think of the Valium + martini housewife). The positive side to this is that benzodiazepines can be used to help someone with alcohol withdrawal, which is otherwise very dangerous. Second generation anxiolytics are partial agonists for 5-HT1A receptors. Moving away from GABA reduces the abuse potential, but also makea the drugs less effective. Generally, SSRIs are prescribed for anxiety before other classes of drugs.

Hope that was a good basic review!

[wwwwwwwwwwww123]

岡本幸太郎 SONY α1さんはTwitterを使っています: 「これ以上水面に近いカワセミはもう撮れないと思います😁 超貴重写真😊👍 12月07日撮影 📷 α1 SEL600F40GM #カワセミ https://t.co/KXiUL3kQtB」 / Twitter

[kazukoba]

SEKAI NO OWARI DOME TOUR 2022 「DuGaraDiDu」　 2022.09.15 ＠東京ドーム

撮影機材 α1 / FE 70-200mm F2.8 GM OSS II

[longhaulerbear]

Pathway analysis identified the strongest network interactions particularly for proteins involved in thrombogenicity and enhanced platelet activity, but also inflammation, cardiac contractility and hypertrophy, and increased adrenergic activity. Our observations generated by the first use a label-free unbiased quantification reveal the proteomic footprint of POTS in terms of a hypercoagulable state, proinflammatory state, enhanced cardiac contractility and hypertrophy, skeletal muscle expression, and adrenergic activity. These findings support the hypothesis that POTS may be an autoimmune, inflammatory and hyperadrenergic disorder.

Growing evidence points toward POTS being an autoimmune disease, oftentimes triggered by a viral or bacterial infection, Lumican (LUM) interacts with CD14 and CD18 on macrophage and neutrophils to promote innate immune response, and normally helps to restrict autoimmunity, antiviral, bacterial and inflammatory responses.

Increased expression of skeletal muscle myosin in POTS

We observed significantly increased expression of myosin light chain 1/3, skeletal muscle isoform (MYL1) expressed only in fast skeletal muscles in adults and required for proper formation and maintenance of myofibers, and muscle function.

POTS, differences in sympathetic nerve discharge and fiber loss from skeletal muscles is observed which could putatively explain muscle fatiguability and deconditioning associated with POTS.

Upregulated alpha-adrenergic activity in POTS

We noted significant upregulation of myosin regulatory light chain 12B (MYL12B) protein in POTS, which triggers polymerization of vascular smooth muscle.

Vascular smooth muscle cells are predominantly innervated by the sympathetic α1 adrenergic receptors and play an important role in maintaining cardiovascular homeostasis by regulating vascular tone, blood flow and blood pressure. In POTS, increased sympathetic activation causes activation of the adrenergic receptors and a surge in norepinephrine levels, and approximately 89% of patients with POTS exhibit elevated levels of autoantibodies against the adrenergic α1 receptor.

[johnnyslittleanimalblog]

Brown Bear cub fishing - DSC00408 by Ronald Todd Via Flickr: Grizzly (Alaska Brown Bear) cub tries its hand at salmon fishing.

[schlauemaus]

Sedativa

Benzodiazepine

Antagonist: Flumazenil (sehr teuer, Verwendung nur im Notfall)

von allen Sedativa die wenigsten Nebenwirkungen

oft verwendet zur Anästhesieeinleitung gemeinsam mit Ketamin

Grundsätzliche Wirkungen (variabel nach Individuum):

zentrales Muskelrelaxanz

antikonvulsiv

Sedierung bei alten/ schwachen Tieren und Neonaten (bei gesunden Tieren nicht)

wirken auf gesunde Tiere aufputschend

schneller Wirkungseintritt; Wirkungsdauer: 45 min

Nebenwirkungen

dämpft Atmung leicht -> kann Atemdämpfung des Anästhetikums verstärken (zB Ketamin)

Diazepam: i.v., löst sich in Plastik! Midazolam: i.v., s.c. oder i.m.

Neuroleptika

KEIN ANTAGONIST VERFÜGBAR

wirkt verstärkt auf Boxer -> niedrig dosieren

bewirkt Penisprolaps beim Pferd -> nicht bei Hengsten anwenden!

wirkt leicht sedierend/hypnotisch ohne Ataxie (nicht muskelrelaxierend) -> "Wurschtigkeitsspritze"

schützt Herz vor arrythmogener Wirkung anderer Medis

antiemetisch

selbst nicht analgetisch (potenziert aber Wirkung anderer Analgetika)

langsamer Wirkungseintritt: 20-30 min; sehr lange Wirkungsdauer: 6 Std

Nebenwirkungen

periphere Vasodilatation -> Blutdruckabfall (wg. Blockade v. α1-Rez.)

!Kann zu starken Blutdruckabfall bei Tieren im Schock/aufgeregten Tieren mit hohen Adrenalinspiegel führen, weil Adrenalin auch vasodilatatorisch wirkt!

Hämatokritabfall (wg. Ery-Sequestration in der Milz)

Hypothermie (wg. Ausfall der Thermoregulation und Vasodilatation)

Phenodiazine

Azepromazin

Butyrophenone

Azaperon: nur mehr beim Schw gebräuchlich

Alpha 2 Agonisten

Antagonisten: Atipamezol, Yohimbin, Tolazolin

starke Sedation

(viszerale) Analgesie

muskelrelaxierend

schneller Wirkungseintritt, Wirkungsdauer dosisabhängig

Nebenwirkungen

peripher: Vasokonstriktion (wg. Aktivierung v. α2-Rez.) -> Hypertension (-> je nach Agonist, kann daraufhin eine hypotensive Phase folgen od. Rückkehr zur ursprünglichen Druck)

zentral: Bradykardie (=Reaktion auf Hypertension), Bradyarrythmie (AV-Block)

ev. Atemdepression u. Bronchokonstriktion

Hypothermie

reduzierte Magendarmmotilität

Erbrechen bei i.m. Gabe v.a. bei Ktz

Xylazin: starke Atemdepression und sehr emetisch beim Kleintier; Verwendung va beim KolikerPfd (wg. kurzer Wirkdauer: 20-30min)aber Achtung: plötzliches "Aufwachen" durch schmerzhaften Reiz möglich! Detomidin: zugelassen f. Pfd, Rd u. Hd; Vergleich Xylazin: leichtere Administration da geringeres Volumen benötigt, wirkt weniger muskelrelaxierend (Eingriffe im Stehen), längere Wirkung (Achtung bei KolikPferd! Verschleiert Kolik!): bis 120min Medetomidin: f. Kleintiere; KEINE hypotensive Phase! Dexmedetomidin: f. Kleintiere; Vergleich Medetomidin: doppelt so starke Analgesie aber schwächere Sedierung Romifidin: zugelassen nur f. Pfd.; Analgesie verschwindet vor Sedation! + wenig muskelrelaxierend! -> Achtung vor Ausschlagen! Verwendung meist f. Feldsedation; starker Blutdruckanstieg, hypotensive Phase selten