Senior Bal-Vigyan 2022-23

Theme: TECHNOLOGY AND TOYS

Sub theme: Innovations
Topic: ‘Sickled innovations for Life’

Guided By:
Ms. PRATIBHA NAIR
Ms. Deepankshi Saxena

Team:
Harshita Nair
Anuja Sachan
Tanvi Herwani
Anvesha Hardiya

CERTIFICATE
 This is to certify that the Project Report entitled “Sickled innovations for
Life’” has been accomplished by Harshita Nair, Anuja Sachan, Tanvi
Herwani and Anvesha Hardiya under our guidance and supervision.

The project is submitted by them in fulfilment of all the requirements.

To the best of my knowledge and belief, this work has not been submitted by
the students anywhere else and is a satisfactory account.

Principal’s Signature

Teachers’ Signatures

Date: Seal of the Institution

 Acknowledgements

A project is never a unilateral effort; there is always a team of other people who
contribute in different ways. The credit for the successful completion of this
project goes to a number of people who helped us to do justice to this project
therefore; we would like to take the opportunity to express our gratitude towards
them.

We would like to express our indebtedness towards Ms. Geetha

Somashekhran our Principal for her words of inspiration.

It is indeed a great pride for us to express deep gratitude towards Ms. Pratibha
Nair and Ms. Deepankshi Saxena for the valuable and magnanimous guidance
and generous assistance extended us by our teachers whose vigilant supervision
helped us shape our work.

We are equally thankful to our parents, all our friends and well-wishers who
extended all possible support and encouraged us throughout this project.
 Declaration

We hereby declare that the project work entitled “Sickled innovations for life”
is a record of an original work done by us under the guidance Ms. Pratibha
Nair and Ms. Deepankshi Saxena of Queens’ College, Indore. The result
embodied in this project has not been submitted to any other institute.

Signatures:

Harshita Nair
Anuja Sachan
Tanvi Herwani
Anvesha
Hardiya

Date:

Work Plan
DATE ACTIVITY RESULT
October 20, 2022 Discussion and group meeting Few topics got selected
for topic selection
October 25, 2022 Finalization of topic and Topic was clear to the
selection of students, briefing students and motivation for
was done to the students further work was achieved
October 30, 2022 Searching of information on Students and teachers co-
internet and from the books. operated in the process.
November 05, 2022 Sorting out important points for Active participation of all
the project and presentation. students/ teachers.
November 15, 2022 Had a telephonic conversation Active participation
with Dr .F .Hussain, ICAR,
Indore
November 17, 2022 Spoke to resource persons in MY Gathered major data for
Hospital and Anand Hospital. survey.
November 18, 2022 Had an interview and discussion Gave us information on the
with Mr. P. Joshi, who briefed uslatest farming technologies
about mulching. applied in his farm.
An awareness rally in school. Students participated
actively.
November 23, 2022 Data was compiled, project file Work successfully done.
was ready. Working on the
PowerPoint presentation
November 29, 2022 Report and presentation Report and Presentation
completed. completed.
November 30, 2022 Submission of file. File was submitted.

INDEX
 SL.N TOPIC PAGE NO
O

1 Introduction

2 Why did we choose this topic?

3 Inheritance of sickle cell anaemia

4 Mutation and its effects

5 Signs and symptoms

6 Methodology -interview, case study and survey

7 Traditional diagnosis

8 Traditional treatment methods

9 Innovative methods

10 Toys for awareness

11 Conclusion

12 Bibliograph

Introduction
Cells in tissues need a steady supply of oxygen to work well. Normally,
haemoglobin in red blood cells takes up oxygen in the lungs and carries it to all
the tissues of the body. Red blood cells that contain normal haemoglobin are
disc shaped. This shape allows the cells to be flexible so that they can move
through large and small blood vessels to deliver oxygen. Sickle haemoglobin is
not like normal haemoglobin. It can form stiff rods within the red cell, changing
it into a crescent, or sickle shape.
The term sickle cell disease (SCD) describes a group of inherited red blood cell
disorders. People with SCD have abnormal haemoglobin, called haemoglobin S
or sickle haemoglobin, in their red blood cells. (Haemoglobin is a iron
containing cytochrome pigment in red blood corpuscles that carries oxygen
throughout the body) .“Inherited” means that the disease is passed by genes
from parents to their children. SCD is not contagious. People who have SCD,
inherit two abnormal haemoglobin genes, one from each parent. In all forms of
SCD, at least one of the two abnormal genes causes a person’s body to make
haemoglobin S. When a person has two haemoglobin S genes, Haemoglobin SS,
the disease is called sickle cell anaemia. This is the most common and often
most severe kind of SCD.

Figure A shows
normal red
blood cells
flowing freely
in a blood
vessel. The
inset image
shows a cross-
section of a
normal red
blood cell with
normal
haemoglobin.
 Figure B shows
abnormal, sickled red
blood cells blocking
blood flow in a blood
vessel. The inset image shows a cross-section of a sickle cell with abnormal
(sickle) haemoglobin forming abnormal stiff rods.

Each red blood cell contains about 280 million hemoglobin molecules.
Hemoglobin is the most important component of red blood cells. It is composed
of protein (globulin) and a molecule (heme), which binds to iron.
● In the lungs, the heme component takes up oxygen and releases carbon dioxide.
The red blood cells carry the oxygen to the body's tissues, where the
hemoglobin releases the oxygen in exchange for carbon dioxide, and the cycle
repeats. The oxygen is essential for all cells in the body to function.
● Sickle cell disease reduces or denies adequate oxygen to many parts of the
body. This contributes to the severe pain experienced as a sickle cell crisis and
both short- and long-term organ damage.

WHY DID WE CHOOSE THIS TOPIC?

The main purpose of this research is to develop a system that could measure the
complex rheological properties of sickle blood as it passes through small blood
vessels with decreasing oxygen levels. People of all age groups lose their lives
due to lack in early diagnostic procedures.

It is estimated that:

● SCD affects 90,000 to 100,000 Americans.

● SCD occurs among about 1 out of every 500 Black or African-American
births.
● SCD occurs among about 1 out of every 36,000 Hispanic-American
births.
● SCT occurs among about 1 in 12 Blacks or African Americans.

MORTALITY
Sickle cell-related death among Black or African-American children younger
than 4 years of age fell by 42% from 1999 through 2002. This drop coincided
with the introduction in 2000 of a vaccine that protects against invasive
pneumococcal disease.
RELATIVE TO THE RATE FOR THE PERIOD 1983 THROUGH 1986,
THE SCD MORTALITY RATE FOR THE PERIOD 1999 THROUGH
2002 DECREASED BY:
● 68% at age 0 through 3 years;
● 39% at age 4 through 9 years; and
● 24% at age 10 through 14 years.

MORTALITY AMONG CHILDREN WITH SICKLE CELL DISEASE:

Among the children with Hb SS disease, 1% died as a result of SCD-related
causes during the first 3 years of life. In California and Illinois, by the end of
1995, the cumulative mortality rate was 1.5 per 100 Black or African-American
children with SCD. The equivalent cumulative mortality rate for all Black or
African-American infants born during this period in California and Illinois was
2.0 per 100 Black or African-American newborns.

ECONOMIC COSTS:
During 2005, medical expenditures for children with SCD averaged $11,702 for
children with Medicaid coverage and $14,772 for children with employer-
sponsored insurance. About 40% of both groups had at least one hospital stay.
SCD is a major public health concern. From 1989 through 1993, an average of
75,000 hospitalizations due to SCD occurred in the United States, costing
approximately $475 million.

THE CASE IN INDIA:

The state Lokayukta had directed the public health department to conduct
primary population survey to determine the prevalence of sickle cell disease.
Though the department did not conduct the survey, it helped a non-
governmental organization with a similar survey. The report says 10.5% of the
tribal population, approximately 9,45,000 persons, are affected by the disease in
Maharashtra.

HOW IS SICKLE CELL DISEASE INHERITED?

● When the hemoglobin S gene is inherited from only one parent and a normal
hemoglobin gene is inherited from the other, a person will have sickle cell
trait. 
● People with sickle cell trait are generally healthy. Only rarely do people with
sickle cell trait have complications similar to those seen in people with
SCD. 
● But people with sickle cell trait are carriers of a defective hemoglobin S
gene. So, they can pass it on when they have a child. If the child’s other
parent also has sickle cell trait or another abnormal hemoglobin gene (like
thalassemia, hemoglobin C, hemoglobin D, hemoglobin E), that child has a
chance of having SCD.
● If only one parent passes the sickle cell gene to the child, that child will have
the sickle cell trait. With one normal hemoglobin gene and one defective
form of the gene, people with the sickle cell trait make both normal
hemoglobin and sickle cell hemoglobin. Their blood may contain some
sickle cells, but they generally don't experience symptoms. However, they
 are carriers of the disease, which means they can pass the defective gene on
to their children.
The image shows how sickle hemoglobin genes are inherited. A person inherits
two hemoglobin genes—one from each parent. A normal gene will make
normal hemoglobin (A). A sickle hemoglobin gene will make abnormal
hemoglobin (S).
In the image below, each parent has one hemoglobin A gene and one
hemoglobin S gene, and each of their children has:

TYPE OF MUTATION OBSERVED:

Type of mutation observed in SCD is substitution.
A substitution is a mutation that exchanges one base for another (i.e., a change
in a single "chemical letter" such as switching an A to a G). Such a substitution
could:
● Change a codon to one that encodes a different amino acid and cause a
small change in the protein produced. For example, sickle cell anaemia is
caused by a substitution in the beta-haemoglobin gene, which alters a
single amino acid in the protein produced.
● Change a codon to one that encodes the same amino acid and causes no
change in the protein produced. These are called silent mutations.
 ● Change an amino-acid-coding codon to a single "stop" codon and cause
an incomplete protein. This can have serious effects since the incomplete
protein probably won't function.

EFFECTS OF MUTATION: SICKLE CELL ANAEMIA 

The mutations that cause sickle cell anaemia have been extensively studied and
demonstrate how the effects of mutations can be traced from the DNA level up
to the level of the whole organism. Consider someone carrying only one copy of
the gene. She does not have the disease, but the gene that she carries still affects
her, her cells, and her proteins: 

1. There are effects at the DNA level 

1. There are effects at the protein level 

Normal hemoglobin and hemoglobin in sickled red blood cells look different;
the mutation in the DNA slightly changes the shape of the hemoglobin
molecule, allowing it to clump together.

Signs and symptoms of sickle cell anAemia

Often don't appear until an infant is at least 4 months old and may include:
● ANAEMIA: Sickle cells are fragile. They break apart easily and die, leaving
you without a good supply of red blood cells. Red blood cells usually live for
about 120 days before they die and need to be replaced. But sickle cells die
after an average of less than 20 days. This results in a lasting shortage of red
blood cells (anemia). Without enough red blood cells in circulation, your
body can't get the oxygen it needs to feel energized. That's why anemia
causes fatigue.
● EPISODES OF PAIN: Periodic episodes of pain, called crises, are a major
symptom of sickle cell anemia. Pain develops when sickle-shaped red blood
cells block blood flow through tiny blood vessels to your chest, abdomen
and joints. Pain can also occur in your bones.
● HAND FOOT SYNDROME: Swollen hands and feet may be the first signs
of sickle cell anemia in babies. The swelling is caused by sickle-shaped red
blood cells blocking blood flow out of their hands and feet
● VISION PROBLEMS:  Some people with sickle cell anemia experience
vision problems. Tiny blood vessels that supply your eyes may become
plugged with sickle cells. This can damage the retina — the portion of the
eye that processes visual images.
● GENERAL SYMPTOMS IN CHILDREN: Pain is the most common
complaint. It can be acute and severe or chronic, usually from orthopedic
problems in the legs and low back. Other symptoms include:
● Fatigue and shortness of breath (signs of anemia)
● Irritability
● Jaundice (yellowish discoloration of the skin and eyes)
● delayed puberty (in young teenagers)
● severe joint pain
● progressive anemia
● leg sores
● gum disease

METHODOLOGY
1.INTERVIEW:
DR.RAJKUMAR AGRAWAL and DR.A SABARWAL:

We had an elaborated interview with both the specialized dr. who gave us
several information about sickle cell anaemia. According to them sickle cell
anaemia is a severe disease which is inherited from parents to offspring’s. 
People at risk for inheriting the gene for sickle cell descend from people who
are or were originally from Africa and parts of India and the Mediterranean.
Sickle cell disease changes normal, round red blood cells into cells that can
be shaped like crescent moons. Because of this disease many people are
dying worldwide. This disease needs to be diagnosed otherwise this may
affect our population very badly. They told us about unawareness of people
regarding this disease. They gave us several traditional method upon which
this disease can be taken care of. Not only this they both seemed very happy
after looking our enthusiasm towards this severe disease and the way are we
trying to absolve it.

PICS OF INTERVIEW
2.CASE STUDIES:
a.Here is a case study taken from worldwide about the people who are suffering
from SICKE CELL ANAEMIA and their experience which was shared by his
parents.
On the morning of admission, our patient, a 19-year-old African-American man
with sickle cell anaemia, felt himself to be in his usual state of health, although
he had just been discharged the previous day from a hospitalization for acute
chest syndrome.. However, at approximately 5:45 p.m., he noticed that he could
not pull up his trousers due to weakness in his left arm. As he walked out , he
noted that he was having difficulty walking because of weakness in his right
and left leg. These events transpired rapidly, within about six minutes, at which
point his family called Emergency Medical Services (EMS) and our patient was
transported to hospital. 
On arrival at our hospital, he was alert and oriented and cranial nerves II to XII
were intact. He had flaccid paralysis of the bilateral upper extremities and the
left lower extremity.. The results of the rest of his physical examination were
normal. 
Relevant medical history included asthma, recurrent acute chest syndrome and
intermittent attempts at Hydroxyurea. He was treated for the three years with
exchange transfusions to maintain hemoglobin S < 30 percent; during this time
he did very well. At 10 days prior to presentation, he was hospitalized with an
acute chest syndrome.. He was treated with antibiotics and a transfusion. His
discharge hemoglobin was 6.6 and oxygen saturation 96 percent. He was
without symptoms at the time of discharge. 
 The results of peripheral blood and urine cultures were negative. A chest X-ray
showed patchy consolidation in the right upper lobe suspicious for pneumonia.
The results of computed tomography (CT) angiography of the head and neck
were unremarkable. 
Later the initial MRI was read to also show swelling of the cord in the same
area. He was admitted to the neurologic intensive care unit where he received an
exchange transfusion with no significant improvement in his symptoms
andsubsequent hemoglobin electrophoresis. While in the intensive care unit
(ICU) he experienced episodes of hypotension that were initially managed with
vasopressors. His erythrocyte sedimentation rate (ESR) and C-reactive protein
(CRP) levels were both elevated, and proteins C and S were found to be low but
within the expected range for someone with sickle cell disease. He was anti-
coagulated with a heparin drip during his stay in the acute care facility, but this
was discontinued on discharge. A monthly exchange transfusion regimen was
instituted with the goal of keeping his haemoglobin S level. Currently, at 20
months post-spinal cord infarction, his condition is unchanged. 
b.A 25-year-old woman with a history of sickle cell disease (SCD) presents to
the clinic for follow-up after a hospitalization for a vaso-occlusive pain crisis
complicated by influenza A. She has a history of an acute ischemic stroke at age
5 years and has received monthly, simple red cell transfusions since the stroke.
Her last transfusion was approximately four months prior. She is taking
deferasirox 20 mg/kg daily but occasionally misses doses.Laboratory results
show the following:

Hemoglobin 7.5 g/dL

Hematocrit 24%

Leukocyte count 9,300/mm3

Platelet count 202,000/m3

Mean corpuscular volume 105 fL

Hemoglobin electrophoresis 92% HbS, 6% HbF, 2%

HbA2

Aspartate aminotransferase 24 U/L

Alanine aminotransferase 45 U/L

Ferritin 1,300 ng/mL

3.SURVEYS:
Here is a survey done by our queens. Our queens surveyed three people Palak
Dubey, Avantika Joshi and Sharad Agrawal who are been suffering through this
disease. They shared their experience with us.

Common conclusion:
Out of the three surveys that we conducted all the patients had problem in
managing their normal routines. No medicines are there to rectify the error.
They were thrilled to learn about the new painless method of early diagnosis of
the problem. They enquired about the application of this diagnostic chip in
INDIA and its availability.

PICS OF SURVEY

Traditional diagnosis methods

1.HAEMOGLOBIN ELECTROPHORESIS:
Sickle-shaped red blood cells can be seen when a blood sample is examined
under a microscope. But sickle cell disease is diagnosed by a blood test called
hemoglobin electrophoresis, which measures the amount of the abnormal sickle
hemoglobin. The amount of sickle hemoglobin determines whether the person
is a carrier (sickle cell trait) or has sickle cell disease.

2.ADDITIONAL TESTS:
To confirm any diagnosis, a sample of blood is examined under a microscope to
check for large numbers of sickle cells — a marker of the disease. If you or
your child has the disease, a blood test to check for anemia — a low red blood
cell count — will be done. And your doctor may suggest additional tests to
check for possible complications of the disease.
3.TESTS TO DETECT SICKLE CELL GENES BEFORE BIRTH:
Sickle cell disease can be diagnosed in an unborn baby by sampling some of the
fluid surrounding the baby in the mother's womb (amniotic fluid) to look for the
sickle cell gene. If you or your partner has been diagnosed with sickle cell
anemia or sickle cell trait, ask your doctor about whether you should consider
this screening. 

TREATMENT
Treatment goals for sickle cell disease aim to relieve pain, prevent infections,
and manage complications.
There was no cure for sickle cell disease other than experimental transplantation
procedures, but treatments for complications of sickle cell have prolonged the
lives of many patients who are now living into adulthood.

1.BONE MARROW TRANSPLANTATION

Stem cell transplantation is a potential cure for sickle cell disease. Stem

cells can be found in bone marrow. Bone marrow is the substance in the center
of your bones that produces red blood cells. A person with sickle cell disease
has bone marrow that produces red blood cells with defective hemoglobin S.
But if that bone marrow is replaced with healthy bone marrow, a person's body
may start to produce normal hemoglobin. Stem cell transplants require bone
marrow from another person (donor). This is called an allogeneic stem cell
transplant.
Before the transplant, bone marrow stem cells are taken from someone who has
closely matching bone marrow, usually a healthy brother or sister. The child
who has sickle cell disease is then treated with drugs that destroy his or her
bone marrow cells. After that, the donated bone marrow stem cells are injected
into a vein.
After the process is complete, the donor's bone marrow begins to replace the
recipient's bone marrow. These new cells restore the immune system and make
normal red blood cells.

2.TRANSFUSION

Blood transfusions are often critical for treating sickle cell disease. Transfusions
may be used either as treatment for specific episodes or as chronic transfusion
therapy to prevent life-threatening complications Ongoing transfusions can also
help improve height and weight in children with sickle cell disease. Normal
hemoglobin levels for patients with sickle cell disease are around 8 g/dL.
Doctors will try to keep the hemoglobin level no higher than 10 g/dL after
transfusion.

INNOVATIVE METHODS OF DIAGNOSIS

1.MICROFLUIDIC CHIPS
Molecular biomarkers are useful as predictive indicators and can guide
intervention and treatment in many diseases. However, no reliable molecular
markers exist for SCD. A biophysical marker that holds great promise for
helping to determine the severity of sickle cell disease in patients, as well as
developing new treatment methods has been developed.
A micro fluidic device called SICKLE CELL CHIPS that mimics physiological
conditions in blood cells could aid the study of sickle cell anemia. The device
can characterize the dynamics of vaso-occlusion by measuring a biophysical
parameter that quantifies the rate of change of the resistance to flow. This can
also indicate disease severity and possibly be used to reduce the frequency of
vaso-occlusive crises.
For early diagnosis ofthis disorder, the micro fluidic platform recreates the
size, scale and pressures seen in the microvasculature in vivo, while
simultaneously control blood oxygen concentration.  The effects of
deoxygenation on hemoglobin polymerization can be studied through this micro
fluidic sickle cell chips.
 
 
MECHANISM OF THE SICKLE CELL CHIPS:

Sickle blood flows through a micro channel, roughly the size of an arteriole or
venule, under constant pressure drop. The micro channel is diffusively coupled
to a gas reservoir in which the oxygen concentration was controlled by a
custom-built gas mixer. The oxygen concentration in the gas reservoir was
measured in real time using a fiber optic oxygen sensor inserted into the outlet
of the gas reservoir, which was under constant flow. This allowed real-time
control for many parameters that mimic the physiological conditions that occur
during vaso-occlusion, including channel size, blood pressure, and oxygen
concentration.
To measure blood flow, a high-speed camera captured high frame rate video
sequences of flowing blood in real time. Cells in each video frame were
identified computationally based on morphologic criteria. Cell locations in
subsequent frames were linked to form trajectories using heuristics and machine
learning techniques. The velocity at each point in time as the median cell
velocity is calculated over a 32-frame video captured at higher than 200 frames
per second. Using the velocities computed from video tracking and the applied
pressures, the effective viscosity was calculated assuming Stokes flow through a
rectangular channel.
 A major innovation in diagnosis of this disease is the building of microchips
that actually show us what’s going on inside the human body. 
With these devices, blood flows just like it does in the human body and we can
reproduce the same kind of complications in the chips that people with sickle
cell disease experience.
This approach allows many independent experiments to be performed in series,
while providing a way for the cells' mechanical and biochemical environment to
be precisely controlled.  Since a small number of cells can be enclosed in one
droplet, this approach can serve as a general system to isolate and measure the
behavior of single cells, following changes in the environment or addition of
biochemical reagents. This work is a good example of new information that
may be obtained by combining clever optical techniques with confined
geometries. It to reduce sufferings of people who suffer from this deadly
disorder. This device will help shed new light on the mechanisms involved in
the disease and will provide a way to explore the effects of potential drugs on
sickle cells. 

PROMISING RESULTS OF SICKLE CELL CHIPS:

As oxygen concentration in the blood is reduced, blood velocity remains

constant until a critical concentration of oxygen is reached. Once the oxygen
concentration drops below this threshold, the velocity decreases significantly,
and at a lower oxygen threshold, the blood fully occludes the micro channel.
These oxygen thresholds indicate where rheological changes can be expected to
begin in the vasculature and where occlusions are most likely to occur. The
group also measured the rate of change in viscosity during an in vitro vaso-
occlusive event and found that these measurements correlated very well with
overall patient disease severity.
Just by measuring a sickle cell patient’s blood in the device, it can be monitored
how the patients doing clinically and whether they are at risk for complications.
In this technique instead of monitoring individual molecules the emphasis is
done on measuring the fluid mechanical properties of the blood, and that can be
used as biomarkers.” 
The idea of using micro devices to model human physiology is an exciting,
rapidly growing field with huge potential for treating a wide range of health
conditions.
2.LENTI GLOBIN:GENE THERAPY
A gene therapy called LentiGlobin could provide a permanent cure for sickle
cell disease. Patients treated with this therapy are beginning to show signs of
producing stable amounts of normal red blood cells containing hemoglobin. 
How the therapy works
In this therapy, we do not change or edit the gene that causes sickle cell disease.
Instead, they use a viral vector to deliver a new gene that will make a healthy
hemoglobin — a beta hemoglobin — into the stem cell. This is like coding new
instructions into the cell. The old instructions for hemoglobin S are still there,
but now the cell can make HbA and HbS. The vector can deliver more than one
copy of the instructions to each cell — usually between one and four copies —
so the cell can make more HbA than HbS.  
What is a vector?
A vector is part of a virus. In the process We take out the bad part of a virus and
leave the empty virus inside the body. We put a new gene with the right
instructions and send it into the stem cells. The viral parts of the vector are
removed so patients don’t get the virus itself — they only get the coding for the
new hemoglobin, called HbAT87Q.”
What is T87Q? 
T87Q is a special type of hemoglobin A which consist of amino acid and
threonine instead of glutamine at position 87 hence the name T87Q. It is slightly
different from regular hemoglobin A and has two advantages:
 The intentional change inserted (called T87Q) makes the hemoglobin even
less likely to cause sickling when it is near a hemoglobin S.
 The HbAT87Q can also be measured more accurately inside the cell which
allows doctors to know how much of the new hemoglobin a patient is making
compared to how much they get from a transfusion.
Pic of chart

3.Drugs
children and adults hospitalized for sickle pain were more likely to have
variations of the gene PKLR. 
This gene expresses production of the enzyme pyruvate kinase (PKR) in red
blood cells, which is a kind of protein that supports cellular health and
metabolism. This discovery led to us study how treatments that stimulate PKR
activity may prevent or alleviate severe pain crises. This is important, because
generally when people have a PKR deficiency, as caused by inherited mutations
in the PKLR gene, referred to as pyruvate kinase deficiencyexternal , their red
blood cells are very fragile and they have severe anemia. This drug was
originally developed for treating patients with inherited pyruvate kinase
deficiency and recently approved by the Food and Drug Administration in
February 2022. If activating PKR can improve red blood cell health, it will
make sickle cell disease milder and provide a new treatment strategy for
patients.
 What is unique about this treatment approach?    

This treatment approach is still in the early research phases, but it has the
potential to break new ground. Other anti-sickling therapies have targeted the
problem in conventional ways by looking at how to increase the size of red
blood cells, how to improve cell hydration, how to improve hemoglobin binding
of oxygen, and how to increase fetal hemoglobin. The goal of these therapies
has been to help cells deliver oxygen to tissues throughout the body. But we
started our research by studying characteristics of the patients themselves. Then,
we assessed how repurposing a drug developed for treating PKR deficiency
may help people with SCD.  
TOYS-A TOOL FOR SICKLE AWARENESS
We have designed a game based on the traditional ludo /snake-ladder game. The
game is designed for children of age group of 8 to 12 years.

The objective of the game is to:

1.spread awareness among children the cause of sickle cell anaemia
2.suggest preventive methods for it
3.spread knowledge regarding prevention and cure of the disease
4.identify the symptoms of the disease
5.adopt early diagnosis and curative methods for sickle cell

Pic of the game

CONCLUSION: 
If the new innovative method suggested by us is applied for the purpose of
diagnosis, then the life style of the infants can be regulated and monitored.
This can lead to fewer deaths and may contribute in reducing the sufferings of
people suffering through this disease. 

BIBLIOGRAPHY:

● wikipedia.org
● medicineandman.com
● youngscientist.org
● healthyheart.com
● journal-science today