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Which component of blood consists of cell fragments and is the main contributor to healing cuts?
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Components of blood (article) | Khan Academy – Main content. Components of blood. This is the currently selected item. The different components that make up blood. Plasma, white blood cells, red blood cells, platelets.The Main Components of Blood. COMPONENTS OF BLOOD: Plasma Formed elements Red blood cells White Blood cells Platelets. PLATELETS(THROMBOCYTES) Are minute fragments of cells, each consisting of a small amount of cytoplasm surrounded by a cell membrane.Blood consists of plasma, red blood cells, white blood cells, and platelets. Also, the digestive system works with the circulatory system to provide the Blood vessels are the body's highways that allow blood to flow quickly and efficiently from the heart to every region of the body and back again.
m Is a type of connective tissue, consisting of cells and cell… – Blood is composed of plasma and the corpuscular elements which are called red corpuscles or erythrocytes, white corpuscles or leucocytes and blood platelets or thrombocytes. It is generally considered that no sex differences exist in the count of white corpuscles or leucocytes.White blood cells are made in the bone marrow. They are stored in your blood and lymph tissues. Neutrophils. They kill and digest bacteria and fungi. They are the most numerous type of white blood cell and your first line of defense when infection strikes.It consists of the following components Thrombocytes – These are cell fragments that are produced from the specialized cells of the bone marrow. Q: What are the major components of blood? Ans: Blood is made up of two main components – Plasma and Blood cells.
Blood Circulatory System | Cardiovascular System |Types of Blood… – Blood is a body fluid in humans and other animals that delivers necessary substances such as nutrients and oxygen to the cells and transports metabolic waste products away from those same cells.The cellular components of blood are erythrocytes (red blood cells, or RBCs), leukocytes (white blood RBCs, endothelial vessel cells, and other blood cells are also marked by glycoproteins that define These membrane-bound cell fragments lack nuclei and are responsible for blood clotting…Blood cells are the cells which are produced during hematopoiesis and found mainly in the blood. Leukocytosis is a high white blood cell count that can be caused by a number of conditions, including various types of infections, inflammatory disease in the body. There are five main types of WBCs.
Human Body Facts : Blood | Human Body Parts and Functions | Human Anatomy 3d – .
Nanotechnology and Advanced Material [Future Medicine Module Exam Essay] nostalgic memories of uni^^ – Hi everyone, today I would like to recall
my favourite module, that was Future Medicines in my MPharm final year.
I liked this module
because I could prepare my essay before hand and regurgitate it in the exam hall. It was
relatively less stressful since I knew the exam topic before I saw the question paper.
I memorized my essay in a few hours and loved the time I spent reciting it while jogging
in parks and bathing in toilets. The question was to choose one technology,
from 3 options of nanotechnology and advanced materials, gene therapy and RNA therapeutics
or proteins and immunology. After deciding on one technology, I was required to describe
3 issues. They are what are the unmet clinical needs in at least 2 clinical areas? how my
chosen technology address these needs and what are the barriers to clinical adoption?
I chose nanotechnology and advanced materials because pharmaceutics attract me more than
biology. Without further ado, let�s start listening to the essay crafted by me.
The technology which fascinates me the most is nanotechnology and advanced materials in
two clinical areas, i.e. gastrointestinal and central nervous systems to tackle unmet
clinical needs in replacing damaged livers with 3D-printed organs, delivering insulin
with microneedles as well as drugs to the brain with nanoparticles (dendrimers) and
advanced material (hydrogel). The first clinical areas is gastrointestinal
system which include liver and pancreas. Let�s focus on damage or cirrhotic liver.
Liver can be damaged acutely by drugs and severe infections. Otherwise, excess fat in
body or alcohol consumption damages liver cells over a long time and leads to prolonged
hepatitis and ultimately cirrhosis. Even if the liver can regenerate, once cirrhosis has
taken place, its course is often irreversible except in selected cases like treated hepatitis
B virus. In addition, cirrhosis can remain asymptomatic for considerable amount of time.
No extracorporeal support devices have been approved for liver diseases. Transplantation
is the only treatment for patients with end-stage liver diseases currently. However, the supply
from live and deceased donors cannot meet the overwhelming demands. Only about a third
of patients on the waiting list receive transplants each year. The situation is worsened by increased
incidence of liver conditions such as hepatitis C infection, alcohol-driven and obesity-driven
fatty liver diseases nowadays, further reducing the number of eligible donor organs.
Whole liver engineering seeks to reproduce the macro- and microstructural complexity.
Three-dimensional (3D) bioprinting deposits cells or cells aggregates as tissue constructs
directly. This method involves less steps and the conditions are milder than 3D printing
where the acellular 3D scaffolds are seeded with cells after fabrication. Larger structures
like venous, arterial and ductular vasculature with large diameters can be made by these
technologies with relative ease. Lobules are functional units of liver and
they consist of multiple cell types such as cholangiocytes, endothelial cells, fibroblasts,
Kupffer cells, liver sinusoidal endothelial cells (LSECs), mesenchymal stem cells, natural
killer cells and stellate cells. Small biomaterial volumes and individual cells can be spatially
patterned in 3D with precise geometries. With advances in 3D bioprinting, researchers
successfully fabricated sinusoids which are tiny blood vessels of the lobules. They are
crucial especially in printing liver to prevent the densely populated cells from developing
a necrotic core. Unlike typical capillaries found in other tissues, sinusoids are lined
by fenestrated undiaphragmed endothelial cells which are discontinuous with each other to
allow exposure of blood onto hepatocyte surfaces. They do not have basement membrane.
To fabricate sinusoids, researchers cast sacrificial substances around the bulk cell-laden material.
Next, the printed sacrificial substances are removed leaving a hollow network. Finally,
the network is seeded with endothelial cells like endothelial progenitor cells (EPCs) or
human umbilical vein endothelial cells (HUVECs). Two examples of sacrificial substances are
Pluronic F127 ink which liquefies at lower temperatures and carbohydrate glass sacrificial
ink which dissolved with water. The best way of assembling these different
parts to produce fully functional liver remain unknown. Poor scalability and extended build
time are limiting clinical adoption of 3D bioprinting. Further work may be done to shorten
the time from 3 days using a 200�m nozzle to one hour using 64-multinozzle array to
print 1L adult liver. Besides, more thorough assessment methods beyond hepatocyte viability
need to be developed to provide robust measurement of tissue functionalities in vitro and in
vivo in line with various functions of liver. The ability of EPCs or HUVECs to differentiate
into LSECs has to be confirmed. Further barrier to bioengineer whole liver with intact biliary
tract is the lack of advance in regeneration of biliary epithelium.
Another unmet need was in diabetes management. Current treatment for type I diabetes and
type II diabetes uncontrolled by lifestyle modifications and oral agents depends heavily
on insulin subcutaneous injections which can be painful.1 Some patients refused to comply
with their prescribed insulin regimens because of the pain from insulin injections or finger
prick tests, hypoglycaemic experiences, complex instructions with insulin SC injections, unsure
of how to adjust doses based on finger prick test results, inconvenient to carry around
and complex storage instruction for used and unused pens. The latter becomes bothersome
during travel. Adequate control of blood glucose level is
difficult to maintain even with tireless self-monitoring and injecting the correct dose of insulin.
This is because patients� immediate physiological needs change invariably with daily activities,
driving, weather and so on. Uncontrolled blood glucose leads to serious macrovascular and
microvascular complications like leg amputations, blindness, cardiovascular diseases and kidney
problems in the long run. More recent invention i.e. continuous glucose
monitors (CGMs) may help patients to stay in their target blood glucose level most of
the time. Main disadvantages is the reading shown reflects the true blood glucose levels
in the previous 5-15 minutes because it takes time for glucose to diffuse from blood into
the interstitial fluid in abdomen when it is being measured by CGM. This is problematic
when dosing of insulin depends on blood glucose levels instead of interstitial glucose levels.
Other disadvantages of CGMs are frequent calibration, maintenance, replacement, inconvenience of
bringing the machine (size of pagers) around, high cost and infection risk.
Yu and colleagues designed �Smart insulin patch� which is a 11 by 11 (a total of 121)
microneedles (MNs) on a square patch (6mm by 6mm). They are basically insulin encapsulated
microneedles where insulin is being delivered via hypoxia sensitive nanoparticles (NPs).
These microneedles are fabricated by first loading the nanoparticles solution into silicone
moulds and centrifuging them. Next, drops of methacrylated hyaluronic acids are added
dropwise with binder and photoinitiator. After centrifugation, they are exposed to UV to
enable crosslinks formation resulting in stiffer microneedles and better entrapment of nanoparticles
in microneedles. Microneedles penetrate the stratum corneum
and then into the viable epidermis. NPs are exposed to glucose in interstitial fluid.
Then, glucose is being consumed by glucose oxidase in the core of nanoparticles creating
hypoxia microenvironment. Consequently, 2-nitroimidazole (found in the outer layer of nanoparticles)
was being reduced to 2-aminoimidazole. This increased hydrophilicity ruptures the outer
layer and releases insulin from the core of nanoparticles. Insulin is being released at
basal rate in normoglycemia and increased accordingly in hyperglycemia depending on
the extent of bioreduction. This allows rapid response to subtle changes in glucose levels.
They do not cause hypoglycaemia unlike insulin subcutaneous injections and some oral agents
like sulphonylureas. This makes patches safer as patients are less worried about experiencing
a hypoglycaemic episode and gives prescribers greater peace of mind during prescribing.
These patches appeal to many patients because they are painless. Short microneedles avoid
contact with pain nerve fibres in deeper dermis. Their small sizes make them easy to be carried
around. Some barriers include these patches are tested
on mice but not yet in human. Their next plan is to test in pigs whose skin is more similar
to human and to understand systemic insulin-release kinetics in larger animals. Besides, patients
may have immune reactions due to repeated exposure to the numerous components of these
patches. UV irradiation during fabrication may affect insulin stability and subsequently
its safety and efficacy. Another barrier is beta cells can release insulin in anticipation
of food while smart insulin patch will only release insulin after a rise of glucose level
is detected in the interstitial fluid. Demands for these patches diminish if pancreatic beta
cells can be replaced. Next, we move on to the second clinical area,
the central nervous system, the brain. The first disease is cerebral palsy. �CP�
is an umbrella term including a group of disorders of varying degrees of motor, sensory and cognitive
impairment due to an injury to the developing fetal brain. It is associated with focal necrosis
around the ventricles as well as diffuse ongoing activation of microglial and astrocyte in
the immature white mater. Microglia are immune cells found in the brain. Once activated,
they trigger release of free radicals, proinflammatory cytokines and excitotoxic metabolites. These
exaggerate inflammatory response leading to brain injury. When inflammation becomes severe,
astrocytes can no longer protect the neurons from oxidative injury.
Currently, there are no cure for this condition. CP can be so difficult to treat because different
types of brain cells (astrocyte, microglia, oligodendrocyte, neuron) or their connections
(myelin sheath) can become damaged. Various strategies are being investigated such as
stem cell therapies but a complete cure is unlikely to emerge in near future. Scientists
expect future treatments aim at protecting or repairing the damaged brain cells before
their deaths. Hence, I will not address stem cell therapies any further but focus on attenuating
sustained neuroinflammation in CP in this essay. Moreover, CP is only diagnosed some
time after birth. This makes postnatal treatment of a prenatal insult to brain very difficult.
Furthermore, the diffuse nature of injury or inflammation makes local brain delivery
impossible. Blood-brain barrier (BBB) poses a challenge for drugs to get across to reach
the ventricles and the white matter. Kannan and the team used nanoparticles i.e.
polyamidoamine (PAMAM) dendrimers as vehicles to deliver N-acetyl-L-cysteine (NAC) intravenously
into rabbits with �CP� phenotypes. Dendrimers are synthesised to mimic natural globular
proteins to facilitate transport across �BBB� to diffuse target sites. �NAC� is an antioxidant
or anti-inflammatory agent. Rabbits which received single IV treatment of �D-NAC�
conjugates with �NAC� at 10mg/kg within 6 hours of birth showed marked improvement
in motor function while taking steps and hopping after 5 days when peak myelination occurred.
�D-NAC� outperformed free �NAC� even with 10-fold greater free �NAC� concentration
than �D-NAC�. They found �D-NAC� selectively accumulated
in activated microglia and astrocytes in white matter of rabbits with �CP� phenotypes
but not in age-matched healthy controls. This is due to impaired �BBB� integrity in
diseased brains or effective vehicles as described above. Conjugation also improves bioavailability
and reduces the toxicity of free NAC to the immature brain. This is because free �NAC�
produces excess L-cysteine which is harmful to oligodendrocytes and neurons. Besides,
�D-NAC� helps to replenish glutathione especially in astrocytes more effectively
than free �NAC�. Consequently, astrocytes can resume their neuroprotective roles against
oxidative stress. Effective passive targeting with nanoparticles
to deliver therapeutics during postnatal period to treat a prenatal injury opens up a new
window of opportunity for treatment to begin at the very early stages of life. Hopefully,
with other non-invasive, in vivo imaging technologies like �PET� and �MRI �scans to detect
neuroinflammation, �CP� patients develop less motor and cognitive deficits.
One of the barriers to clinical adoption is that even closest animal models (in this case
rabbits in terms of white matter development, microglial presence, oxidative insult, impaired
myelination, neuronal loss, hindlimb involvement) still do not match human conditions exactly.
Clinical trials need to be done on human to check whether �D-NAC� works in human.
Another potential barrier is the �promises� of other therapies which may cure �CP�.
This may result in funding being channelled away from this nanotechnology because this
method does not offer a cure but helps to modify the disease course. Despite there is
no subsequent progress in this technology after 2012, I think it is still a promising
strategy given limited progress of other approaches. The second disease is Glioblastoma Multiforme.
GBM is the most aggressive and common brain tumours in adults with very low median survival
(12 to 15 months) after standard treatment (surgical resection and radiotherapy and/or
chemotherapy). Chemotherapy consists of carmustine delivered
locally as BCNU Gliadel wafer or systemically as temozolomide (TMZ). Gliadel wafers are
associated with many complications like cerebrospinal fluid leak, impaired wound healing, intracranial
abscess, meningitis, seizures and tumour cyst formation. Besides, wafers cannot fit the
shape of resection sites exactly and may migrate and end up in unintended sites. Moreover,
carmustine released from the wafer is not long enough (at most one week) and cannot
penetrate deep into surrounding brain tissues. On the other hand, �BBB� is an effective
pharmacological and physiological barrier for oral agents like TMZ, preventing accumulation
of cytotoxics at therapeutic doses at tumour sites without inflicting many side effects.
Furthermore, �GBM� cells have intrinsic or acquired resistance against these alkylating
agents. They upregulate DNA repair pathways (for example mismatch and base excision repairs)
and overexpress epidermal growth factor receptors and O6-methylguanine methyltransferase (MGMT)
to survive. The latter enzyme helps to reverse the cytotoxic action of temozolomide.
Moreover, the recurrences rate after surgeries is very high. 80% to 90% of recurrences are
confined within 2 cm of the original tumour site. The highly malignant cancerous cells
in the primary tumour proliferate and infiltrate nearby healthy brain tissues, forming micrometastases.
They are difficult to be removed completely and safely. In light of this, local drug delivery
during surgeries seems very promising. Bastiancich and colleagues designed a simple
formulation of hydrogel consists of 2 ingredients only, i.e. lipid-nanocapsules (LNCs) and anticancer
prodrug lauroyl-gemcitabine (GemC12). This advanced material can be injected into and
adapt to the shape of tumour resection cavity using 30-G needle syringes. It adheres to
the brain parenchyma and slowly releases the drug to eradicate surrounding micrometastases.
Lipid-nanocapsule is made up of a hydrophobic triglycerides core with an outer layer of
non-ionic surfactants and polyethylene glycol (PEG) molecules. Gemcitabine is an excellent
radio-sensitisor. It is not affected by MGMT. It is conjugated with lauroyl group. The latter
12-carbon alkyl chain is incorporated into the outer layer of lipid-nanocapsules to orientate
the drug towards the water phase to form H-bond crosslinks. This immobilizes surrounding water
phase to form a gel with compatible mechanical properties.
Cumulative drug release in vitro test results suggested sustained release. It was desirable
for drug to be released rapidly for the first two days to kill residual cancerous cells
and then slowly to maintain the cytotoxic activity over a month. As the hydrogel consists
of 2 ingredients only, the rate of gel degradation is proportional to rate of drug release.
For in vivo evaluation, they injected this hydrogel into mice carrying subcutaneous human
glioblastoma tumours. After 8 days, the tumours shrinked significantly or disappeared in mice
receiving GemC12-lipid-nanocapsules compared with mice receiving phosphate-buffered saline,
GemC12 or lipid-nanocapsules only. It is reported to be well tolerated in the short-term.
Before this technique is being tried on human, its anti-tumour efficacy has to be established
in orthotopic and tumour resection animal models of GBM. Besides, lack of long term
safety data might impede its clinical adoption. As the gel is being degraded, smaller fragments
might migrate and kill nearby otherwise healthy tissues. Since gemcitabine release is not
selective against cancerous tissues, more side effects will be experienced with greater
penetration depth of its release from hydrogel. In conclusion, the future therapies favour
the combination of various technologies like immunotherapy, gene therapy and so on. Hence,
we shall all work together for better healthcare of mankind.
Here is the list of references that you can have a look at. This is the end of my exam
essay. Please note that any content of this video
does not substitute professional medical advices. If you have any health issues, please speak
to your doctor and healthcare team. Thank you for watching Lively Life Snippets
and if you like my videos, hit the like and share button. Don�t forget to subscribe
and see you all in the next episode. Comment below on what type of content you would like
to see in the future. .
THE INFLAMMATORY RESPONSE – The inflammatory response is initiated within hours of infection or wounding and is characterized by edema, or swelling, heat, redness, and
pain at the site of an infection or injury.
These characteristics reflect four changes in local blood vessels. 1. The heat and redness during inflammation is the result of an increase in vascular diameter. The increase in vascular diameter also results in slower blood flow. 2. There is also an increase in vascular permeability.
The endothelial cells that line the blood vessel walls are usually packed tightly together, but during inflammation, they have gaps between them – This results in fluid from the blood exiting and accumulating in the local tissues, and this results in edema and pain. The fluid contains plasma proteins such as complement proteins and mannose binding lectin, which aid in defending against pathogens. 3. Endothelial cells, which line the walls
of blood vessels, are “activated” during inflammation. That is, endothelial cells express cell-adhesion molecules that promote the binding of circulating leukocytes, otherwise known as white blood cells. 4. There is clotting in the microvessels at
the site of infection, which prevents pathogens from spreading via the blood.
The purpose of the inflammatory response is threefold:
1. Allows the body to defend itself from invading microorganisms. The increase in vascular diameter, along with the activated endothelial cells, results in leukocytes being able to attach
to the endothelium, and then migrate into the tissues where they can attack pathogens. This process of leukocytes leaving the bloodstream and entering tissues is called extravasation.
2. Induces local blood clotting, and this creates a physical barrier preventing the
infection from spreading into the bloodstream. 3. Promotes the repair of injured tissue.
But what triggers the inflammatory response?
The state of inflammation is set up when tissues are physically damaged, or when pathogens are recognized by macrophages and later by other white blood cells. These circumstances induces the release of a variety of inflammatory mediators which cause the inflammatory response. Macrophages and neutrophils secrete prostaglandins, leukotrienes, and platelet-activating factor
(PAF), which are lipid mediators of inflammation. These are produced rapidly because they are made from degraded membrane phospholipids. Then, macrophages secrete cytokines, which are substances released by cells of the immune system that affect other cells. One kind of
cytokine are chemokines, which act as chemoattractants. Chemokines cause directed chemotaxis, which is the movement of cells or parts of cells in a direction corresponding to a gradient of increasing or decreasing concentration of a substance. In the case of chemokines, they direct phagocytes to move towards the source of the chemokines, which is where they are needed. Now I'd like to point out two cytokines important to the inflammatory response are C5a and Tumor Necrosis Factor-α , or TNF-α. The complement fragment C5a plays multiple important roles in the inflammatory response. For instance, it stimulates respiratory, or oxidative burst, which is the rapid release of reactive oxygen species. At the same time it attracts neutrophils and monocytes. So it essentially preps them for battle as they arrive. It also increases vascular permeability, increases expression of adhesion molecules on the endothelium, and causes local mast cells to release granules containing the inflammatory molecule histamine, and TNF-α. TNF-α is also an important cytokine, which is produced rapidly by macrophages upon pathogen detection and is a potent activator of endothelial cells. Activation of endothelial cells is central to the inflammatory response. Cytokines produced by macrophages, especially TNF-α, cause endothelial cells to rapidly externalize granules called Weibel-Palade bodies containing P-selectin within minutes of pathogen detection by macrophages. P-selectin now appears on the surfaces of local endothelial cells. Selectins are one of three structural
families of adhesion molecules important for leukocyte recruitment, with the other two
being intercellular adhesion molecules (ICAMs) and leukocyte integrins. Later, within 2 hours of pathogen detection, the endothelial cells express mainly E-selectin. Shortly after P-selectin gets to the cell surface, mRNA encoding E-selectin is synthesized. Both selectins interact with the sulfated sialyl-LewisX that is present on the surface of neutrophils.
Once inflammation has begun, neutrophils make up the first wave of cells that cross the
blood vessel wall to enter an inflamed tissue. After this, monocytes cross the blood vessel wall and differentiate into tissue macrophages. In later stages of inflammation, other leukocytes such as eosinophils and lymphocytes also enter the infected site. Usually, leukocytes travel in the center of small blood vessels, where blood flow is fastest. However, in inflamed tissues, the slower blood flow allows leukocytes to interact in large numbers with the endothelial cells lining the blood vessels. In addition, injury to blood vessels triggers two enzyme cascades – the kinin cascade and the coagulation cascade. The kinin system consists of plasma proteases. The eventual result of this cascade is the production of
several inflammatory mediators, including bradykinin, a vasoactive peptide that increases vascular permeability and causes pain. Pain makes you aware of the problem and causes you to immobilize that part of your body, helping prevent the spread of infection. The coagulation system is another protease cascade whose activation leads to formation of a fibrin clot. .