born to make histo:re

the man who named me,

     the man who killed me,

          the man who gave me hope,

CONTINUATION FROM EP 2 PART 1

Hemorrhage [aka Bleeding]: DAMAGED BLOOD VESSEL WALL WILL RESULT IN BLOOD CONTENTS LEAKING OUT 

L-selectin, also known as CD62L, is a cell adhesion molecule found on lymphocytes and the preimplantation embryo.

L-selectin acts as a “homing receptor” for lymphocytes to enter secondary lymphoid tissues via high endothelial venules. Ligands present on endothelial cells will bind to lymphocytes expressing L-selectin, slowing lymphocyte trafficking through the blood, and facilitating entry into a secondary lymphoid organ at that point.

NB: Refer to Ep 1 Part 1 for Endothelial Cells

An abrasion is a wound caused by superficial damage to the skin, no deeper than the epidermis. It is less severe than a laceration, and bleeding, if present, is minimal. 

The epidermis is the outer layer of the three layers that make up the skin, the inner layers being the dermis and hypodermis. 

The epidermis layer provides a barrier to infection from environmental pathogens and regulates the amount of water released from the body into the atmosphere through transepidermal water loss. 

Vasoconstriction is the narrowing of the blood vessels resulting from contraction of the muscular wall of the vessels, in particular the large arteries and small arterioles. The process is particularly important in staunching hemorrhage and acute blood loss. 

INNATE IMMUNE SYSTEM

Microorganisms or toxins that successfully enter an organism encounter the cells and mechanisms of the innate immune system. 

The innate response is usually triggered when microbes are identified by pattern recognition receptors, which recognize components that are conserved among broad groups of microorganisms,or when damaged, injured or stressed cells send out alarm signals, many of which (but not all) are recognized by the same receptors as those that recognize pathogens. 

Innate immune defenses are non-specific, meaning these systems respond to pathogens in a generic way.

This system does not confer long-lasting immunity against a pathogen. The innate immune system is the dominant system of host defense in most organisms.

ADAPTIVE IMMUNE SYSTEM

The adaptive immune system evolved in early vertebrates and allows for a stronger immune response as well as immunological memory, where each pathogen is “remembered” by a signature antigen.

The adaptive immune response is antigen-specific and requires the recognition of specific “non-self” antigens during a process called antigen presentation. 

Antigen specificity allows for the generation of responses that are tailored to specific pathogens or pathogen-infected cells. The ability to mount these tailored responses is maintained in the body by “memory cells”. Should a pathogen infect the body more than once, these specific memory cells are used to quickly eliminate it.

NB: GENERALLY THERE’S A LOT OF MACROPHAGES AROUND SO THEY’RE NOT USUALLY “LATE”. 

THEY PROBABLY TRIED TO SIMPLIFY IT SO THERE’S NOT TOO MANY CELLS AROUND UNTIL THEY HAVE MORE TIME TO EXPLAIN EACH CELL’S FUNCTION

THE INFLAMMATORY PROCESS IS A HUGE CASCADE OF EVENTS SO I WON’T ACTUALLY GO INTO DETAIL FOR NOW [I’M LAZY TO SUMMARIZE] SO MAYBE READ UP ON IT YOURSELF IF YOU WANT TO KNOW MORE

CONTINUING THE SERIES OF BIOLOGY REFERENCES IN CELLS AT WORK!

AKA COPY PASTE FROM WIKIPEDIA. THANK YOU WIKIPEDIA!

PLATELETS

Platelets, also called thrombocytes (from Greek θρόμβος, “clot” and κύτος, “cell”), are a component of blood whose function (along with the coagulation factors) is to react to bleeding from blood vessel injury by clumping, thereby initiating a blood clot.

Coagulation Cascade Overview [AKA Clotting process]

Coagulation (also known as clotting) is the process by which blood changes from a liquid to a gel, forming a blood clot. 

It potentially results in hemostasis (process to stop bleeding), the cessation of blood loss from a damaged vessel, followed by repair. The mechanism of coagulation involves activation, adhesion, and aggregation of platelets along with deposition and maturation of fibrin.

Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium lining the vessel. Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial tissue factor to plasma Factor VII, which ultimately leads to fibrin formation.

Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: Additional coagulation factors or clotting factors beyond Factor VII respond in a complex cascade to form fibrin strands, which strengthen the platelet plug.

Endothelial cells are attached to the subendothelial collagen by von Willebrand factor (VWF) which these cells produce.

When the endothelial layer is disrupted, collagen and VWF anchor platelets to the subendothelium. Platelet GP1b-IX-V receptor binds with VWF; and GPVI receptor and integrin alpha2beta1 bind with collagen.

NB: Recap on Endothelial cells in EP 1 Part 1

Coagulation factors are generally indicated by Roman numerals, with a lowercase a appended to indicate an active form. [See above flow chart]

Fibrin (also called Factor Ia) is a fibrous, non-globular protein involved in the clotting of blood. 

It is formed by the action of the protease thrombin on fibrinogen which causes it to polymerize. The polymerized fibrin together with platelets forms a hemostatic plug or clot over a wound site.

NB: I’M NOT ACTUALLY SURE IF PLATELETS DO ANYTHING TO THE FIBRIN BEFORE USE….But I guess this is adorable AF so why the hell not

CLOT COMPLETE! 

JOB WELL DONE, PLATELET-CHAN!

Bokuto Koutarou / Ch. 327 Bonus:

black as ink.

(it’s a bonus print for my hq inktober zine!)