A new potentially disease-causing Cystic Fibrosis mutation.a) .pdf
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A new potentially disease-causing \"Cystic Fibrosis\" mutation. a) Report the position of the mutation that the PCR reaction will detect. Describe which base is the one commonly found (also called wild-type) in the unaffected population and what it is changed to in people with Cystic Fibrosis. b) Explain where in the gene sequence this mutation is located and what is the predicted effect of having this mutation. Use the +1 position as a reference for counting bases. c) What can families learn from a genetic test that detects potential Cystic Fibrosis-causing mutations? d) Why is it useful to be able to test for genetic disease predisposition? e) What should parents know about Cystic Fibrosis? Solution b) Mutations at the 508th position (DF508) in the CFTR gene located on human chromosome 7 cause CF . The effects of having this mutation include affected liver, kidney, pancreas and intestine. Lung infections occur as the airways are clogged with mucus resulting in breathing problems. Mucus secreted in pancreas does not allow the release of the important digestive enzymes needed by the body to breakdown food and absorb vital nutrients. Other symptoms include clubbing of fingers and toes, affected growth, infection in sinus. d) Testing for genetic disease like CF beforehand determines the presence or absence of certain mutations in the gene that can cause CF. So, it is useful to be able to test for genetic disease predisposition. e) A child that has inherited 1 copy of mutated CF gene inherited from each parent suffers from Cystic Fibrosis. When any one of the parents is a carrier or have a family history of CF, they must be genetically tested. Parents should be aware about this and go though the test..
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The role genetics plays in the Cystic Fibrosis is.docx
Cystic fibrosis is a genetic disease caused by a mutation in the CFTR gene that results in a dysfunctional chloride channel protein. This protein normally regulates the movement of salt and water in and out of cells. In cystic fibrosis patients, thick mucus builds up in the lungs, pancreas, and other organs due to impaired chloride transport. Common symptoms include salty-tasting skin, digestive issues like poor growth and abdominal pain, and respiratory problems such as frequent lung infections. The disease is inherited in an autosomal recessive pattern and affects the epithelial cells throughout the body.
1- Calculate the frequency of the recessive and dominant allele in the.pdf
1. Calculate the frequency of the recessive and dominant allele in the population. (round
to nearest hundredth)
1. Calculate the frequency of the recessive and dominant allele in the population. (round
to nearest hundredth)
1. Calculate the frequency of the recessive and dominant allele in the population. (round to
nearest hundredth)
2. Calculate the percentage of heterozygous and homozygous dominant individuals in the
population.
please show all your work :)
thank you
Jse the following information: Every person has two copies of the cystic fibrosis transmembrane
conductance regulator (CFTR) gene. A person must inherit two mutated copies of the CFTR
gene (one copy from each parent) to have cystic fibrosis (CF). Cystic fibrosis is an example of a
recessive disease. That means a person must have a mutation in both copies of the CFTR gene to
have CF. People who inherit one copy of the CFTR gene that contains a mutation and one
normal copy are considered CF carriers. CF carriers do not have the disease but can pass their
copy of the defective gene on to their children. In people with CF, mutations in the CFTR gene
disrupt the normal production or functioning of the CFTR protein found in the cells of the lungs
and other parts of the body. This protein is responsible for regulating the flow of salt and fluids
in and out of the cells in different parts of the body. Mutations in the CFTR gene cause the CFTR
protein to malfunction or not be made at all, preventing normal movement of salt and fluids. This
leads to a buildup of thick mucus, which in turn leads to persistent lung infections, destruction of
the pancreas, and complications in other organs. Suppose you are a doctor researching CF in
North American populations. You determined in previous research studies that the typical allele
frequency of the mutant CF allele ( f ) among Caucasians is 0.025 , while the frequency of the
normal allele ( F ) is 0.975 . You sample a population of New York City residents, and you
determined that 4,810 individuals have a normal phenotype, while 190 individuals exhibit CF.
Answer the following questions..
Autosomal recessive diseases
This document provides information on autosomal recessive diseases and specifically discusses cystic fibrosis and hereditary hemochromatosis. It describes the inheritance patterns of autosomal recessive diseases and then goes into detail about the phenotypic expression, genetic basis, mutations, and clinical features of cystic fibrosis and hereditary hemochromatosis. Key points covered include that both diseases are autosomal recessive, caused by mutations in specific genes (CFTR and HFE), and can vary in severity depending on the mutations and other genetic/environmental factors. Diagnosis and management strategies are also summarized.
B2.7 genetic disorders
This document discusses several genetic disorders including polydactyly, cystic fibrosis, and Huntington's disease. It provides details on the inheritance patterns and characteristics of each disorder. Potential treatments and ethical issues related to genetic testing, gene therapy, cloning, and preimplantation genetic diagnosis are also examined.
Respond to your colleagues and respectfully agree or disagree with.docx
Respond
to your colleagues and respectfully agree or disagree with your colleague’s assessment and explain your reasoning. In your explanation, include why their explanations make physiological sense or why they do not
At least 2 references in each peer responses!
Cystic Fibrosis is an autosomal recessive disease that affects chromosome 7 on the DNA helix. The parents of the child with cystic fibrosis are both carriers of the disorder and likely have no symptoms and have no idea they are carriers. The disease is caused by a mutation in cystic fibrosis transmembrane regulator (CFTR). The CFTR regulates the flow of salt and fluids in and out of the cell. The CFTR protein provides instructions for the channel than transports negatively charged particles called chloride ions in and out of the cell and across the tissues. The lack of this channel causes the build-up of thick and sticky mucus because chloride helps with the movement of water across the tissues that assist with thinning the mucus. (CF Genetics: The Basics, 2020)
The organs that are affected most frequently are the lungs, digestive organs, pancreas, and reproductive organs. The thick mucus causes frequent lung infections and the cyst in the lungs. The thick mucus blocks the ducts of the pancreas and prevents the transport of digestive enzymes leading to malnutrition. The production of insulin is also affected by the thick mucus and cystic fibrosis patients can develop diabetes-related to this. Males with cystic fibrosis are infertile due to mucus plugging the vas deferens. Female with cystic fibrosis frequently have difficulty during pregnancy (Cystic Fibrosis, 2020).
Cystic fibrosis is a recessive disease and both parents must be carries to produce a child who has cystic fibrosis. The chances of two carriers having a child with cystic fibrosis are 25% and the chances that the child will have a 50% chance they are a carrier of the mutation and a 25% chance that the child will not be a carrier or have the disease. The person with cystic fibrosis has a child with a cystic fibrosis carrier then they have a 50% chance the child will have cystic fibrosis and a 50% chance they will be a carrier (Cystic Fibrosis, n.d.).
Cystic fibrosis is common in the Caucasian population with a frequency rate of 1 in 2500-3500 births. African American have a frequency rate of 1-17000 and Asian population have a frequency rate of 1-3100 births (CF Genetics: The Basics, 2020)
.
CYSTIC FIBROSIS KNOW IT NOW!
This document provides an overview of cystic fibrosis including:
- It is a genetic disease caused by mutations in the CFTR gene resulting in defective chloride channels.
- Diagnosis is based on clinical features and sweat chloride tests or genetic testing.
- Symptoms include chronic lung disease, poor growth, GI issues, and electrolyte imbalances.
- Treatments focus on airway clearance, antibiotics for infections, nutrition support, and management of complications.
Cystic fibrosis
Cystic fibrosis is a genetic disease that affects the lungs and digestive system. It causes a buildup of thick, sticky mucus in the lungs, pancreas, and other organs. Common symptoms include salty-tasting skin, persistent coughing, frequent lung infections, and difficulty gaining weight. While there is no cure, treatments aim to control symptoms and complications, and can help increase life expectancy. Managing cystic fibrosis requires medications, airway clearance techniques like chest physiotherapy, and following dietary recommendations.
Cystic Fibrosis
Cystic fibrosis is a genetic disorder caused by a mutation in the CFTR gene. It is a single-gene disorder that affects the lungs and digestive system by causing a buildup of thick mucus. Symptoms include difficulty breathing, coughing, lung infections, poor weight gain, and digestive issues. While there is no cure, treatments aim to clear mucus from the lungs, control infections with antibiotics, improve nutrition, and potentially replace the defective gene through experimental gene therapy.
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The role genetics plays in the Cystic Fibrosis is.docx
Cystic fibrosis is a genetic disease caused by a mutation in the CFTR gene that results in a dysfunctional chloride channel protein. This protein normally regulates the movement of salt and water in and out of cells. In cystic fibrosis patients, thick mucus builds up in the lungs, pancreas, and other organs due to impaired chloride transport. Common symptoms include salty-tasting skin, digestive issues like poor growth and abdominal pain, and respiratory problems such as frequent lung infections. The disease is inherited in an autosomal recessive pattern and affects the epithelial cells throughout the body.
1- Calculate the frequency of the recessive and dominant allele in the.pdf
1. Calculate the frequency of the recessive and dominant allele in the population. (round
to nearest hundredth)
1. Calculate the frequency of the recessive and dominant allele in the population. (round
to nearest hundredth)
1. Calculate the frequency of the recessive and dominant allele in the population. (round to
nearest hundredth)
2. Calculate the percentage of heterozygous and homozygous dominant individuals in the
population.
please show all your work :)
thank you
Jse the following information: Every person has two copies of the cystic fibrosis transmembrane
conductance regulator (CFTR) gene. A person must inherit two mutated copies of the CFTR
gene (one copy from each parent) to have cystic fibrosis (CF). Cystic fibrosis is an example of a
recessive disease. That means a person must have a mutation in both copies of the CFTR gene to
have CF. People who inherit one copy of the CFTR gene that contains a mutation and one
normal copy are considered CF carriers. CF carriers do not have the disease but can pass their
copy of the defective gene on to their children. In people with CF, mutations in the CFTR gene
disrupt the normal production or functioning of the CFTR protein found in the cells of the lungs
and other parts of the body. This protein is responsible for regulating the flow of salt and fluids
in and out of the cells in different parts of the body. Mutations in the CFTR gene cause the CFTR
protein to malfunction or not be made at all, preventing normal movement of salt and fluids. This
leads to a buildup of thick mucus, which in turn leads to persistent lung infections, destruction of
the pancreas, and complications in other organs. Suppose you are a doctor researching CF in
North American populations. You determined in previous research studies that the typical allele
frequency of the mutant CF allele ( f ) among Caucasians is 0.025 , while the frequency of the
normal allele ( F ) is 0.975 . You sample a population of New York City residents, and you
determined that 4,810 individuals have a normal phenotype, while 190 individuals exhibit CF.
Answer the following questions..
Autosomal recessive diseases
This document provides information on autosomal recessive diseases and specifically discusses cystic fibrosis and hereditary hemochromatosis. It describes the inheritance patterns of autosomal recessive diseases and then goes into detail about the phenotypic expression, genetic basis, mutations, and clinical features of cystic fibrosis and hereditary hemochromatosis. Key points covered include that both diseases are autosomal recessive, caused by mutations in specific genes (CFTR and HFE), and can vary in severity depending on the mutations and other genetic/environmental factors. Diagnosis and management strategies are also summarized.
B2.7 genetic disorders
This document discusses several genetic disorders including polydactyly, cystic fibrosis, and Huntington's disease. It provides details on the inheritance patterns and characteristics of each disorder. Potential treatments and ethical issues related to genetic testing, gene therapy, cloning, and preimplantation genetic diagnosis are also examined.
Respond to your colleagues and respectfully agree or disagree with.docx
Respond
to your colleagues and respectfully agree or disagree with your colleague’s assessment and explain your reasoning. In your explanation, include why their explanations make physiological sense or why they do not
At least 2 references in each peer responses!
Cystic Fibrosis is an autosomal recessive disease that affects chromosome 7 on the DNA helix. The parents of the child with cystic fibrosis are both carriers of the disorder and likely have no symptoms and have no idea they are carriers. The disease is caused by a mutation in cystic fibrosis transmembrane regulator (CFTR). The CFTR regulates the flow of salt and fluids in and out of the cell. The CFTR protein provides instructions for the channel than transports negatively charged particles called chloride ions in and out of the cell and across the tissues. The lack of this channel causes the build-up of thick and sticky mucus because chloride helps with the movement of water across the tissues that assist with thinning the mucus. (CF Genetics: The Basics, 2020)
The organs that are affected most frequently are the lungs, digestive organs, pancreas, and reproductive organs. The thick mucus causes frequent lung infections and the cyst in the lungs. The thick mucus blocks the ducts of the pancreas and prevents the transport of digestive enzymes leading to malnutrition. The production of insulin is also affected by the thick mucus and cystic fibrosis patients can develop diabetes-related to this. Males with cystic fibrosis are infertile due to mucus plugging the vas deferens. Female with cystic fibrosis frequently have difficulty during pregnancy (Cystic Fibrosis, 2020).
Cystic fibrosis is a recessive disease and both parents must be carries to produce a child who has cystic fibrosis. The chances of two carriers having a child with cystic fibrosis are 25% and the chances that the child will have a 50% chance they are a carrier of the mutation and a 25% chance that the child will not be a carrier or have the disease. The person with cystic fibrosis has a child with a cystic fibrosis carrier then they have a 50% chance the child will have cystic fibrosis and a 50% chance they will be a carrier (Cystic Fibrosis, n.d.).
Cystic fibrosis is common in the Caucasian population with a frequency rate of 1 in 2500-3500 births. African American have a frequency rate of 1-17000 and Asian population have a frequency rate of 1-3100 births (CF Genetics: The Basics, 2020)
.
CYSTIC FIBROSIS KNOW IT NOW!
This document provides an overview of cystic fibrosis including:
- It is a genetic disease caused by mutations in the CFTR gene resulting in defective chloride channels.
- Diagnosis is based on clinical features and sweat chloride tests or genetic testing.
- Symptoms include chronic lung disease, poor growth, GI issues, and electrolyte imbalances.
- Treatments focus on airway clearance, antibiotics for infections, nutrition support, and management of complications.
Cystic fibrosis
Cystic fibrosis is a genetic disease that affects the lungs and digestive system. It causes a buildup of thick, sticky mucus in the lungs, pancreas, and other organs. Common symptoms include salty-tasting skin, persistent coughing, frequent lung infections, and difficulty gaining weight. While there is no cure, treatments aim to control symptoms and complications, and can help increase life expectancy. Managing cystic fibrosis requires medications, airway clearance techniques like chest physiotherapy, and following dietary recommendations.
Cystic Fibrosis
Cystic fibrosis is a genetic disorder caused by a mutation in the CFTR gene. It is a single-gene disorder that affects the lungs and digestive system by causing a buildup of thick mucus. Symptoms include difficulty breathing, coughing, lung infections, poor weight gain, and digestive issues. While there is no cure, treatments aim to clear mucus from the lungs, control infections with antibiotics, improve nutrition, and potentially replace the defective gene through experimental gene therapy.
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Cystic fibrosis is a genetic disorder caused by a mutation in the CFTR gene. It is a single-gene disorder that affects the lungs and digestive system by causing a buildup of thick mucus. Symptoms include difficulty breathing, coughing, lung infections, poor weight gain, and digestive issues. Treatments include medications, chest physical therapy, nutritional supplements, and gene therapy, but currently there is no cure.
Cysticfibrosis
Cystic fibrosis is a genetic disease that affects the lungs and digestive system. It is caused by a defective gene that produces a thick, sticky mucus in the lungs and pancreas. Symptoms include persistent coughing, wheezing, shortness of breath, lung infections, and salty-tasting skin. There is no cure, but treatments aim to clear mucus from the lungs and aid digestion. Life expectancy has increased to around 37 years on average with advances in care and new therapies targeting the underlying genetic cause.
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Cystic fibrosis is a genetic disease that causes thick, sticky mucus to build up in the lungs and digestive tract. It is caused by mutations in the CFTR gene that result in defective or too few chloride channels. This leads to dehydrated mucus and chronic lung infections. Symptoms include difficulty breathing, coughing, weight loss, and excessive salt in sweat. Treatment focuses on clearing mucus from the lungs and controlling infections through antibiotics and airway clearance techniques. While there is no cure, managing symptoms has increased life expectancy to over 30 years on average.
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This document discusses cystic fibrosis, including its causes, symptoms, diagnosis, and treatment. It is a genetic disorder that causes thick mucus buildup in the lungs and digestive tract. The primary symptom is severe lung infections. It is caused by mutations in the CFTR gene and is usually diagnosed via sweat test. Treatments include antibiotics, mucus-thinning drugs, and lung therapies to help clear mucus and treat infections. Ongoing research is working to develop new diagnostic tests and find a cure.
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Respond to your colleagues and respectfully agree or disagree .docx
Respond
to your colleagues and respectfully agree or disagree with your colleague’s assessment and explain your reasoning. In your explanation, include why their explanations make physiological sense or why they do not
At least 2 references in each peer responses!
Cystic fibrosis (CF) is an inherited disease that affects mainly the gastrointestinal system, the reproductive system, and the lungs (McCance & Huether, 2019, pp 2171). The cystic fibrosis gene “is located on chromosome 7” with more than 2000 variants of the disease. They are divided into six classes, 1 through 3 being the more severe ones. The triad of Cystic fibrosis is “obstruction, infection, and inflammation that is evident throughout the gastrointestinal tract and within the airways” (McCance & Huether, 2019, pp 2871). The gastrointestinal problems are caused by the CF transmembrane regulator (CFTR) protein, “which is located on epithelial membranes and regulates chloride and sodium ion channels (McCance & Huether, 2019, pp 2870). You can find that protein through the airways, sweat glands, digestive tract, pancreas, hepatobiliary system, and reproductive system. The CFTR protein alters the reabsorption of sodium, chloride, and potassium (McCance & Huether, 2019, pp 2871), which gives kids skin a salty taste when parents kiss them because of the excessive salt they waste through sweat glands. It also interferes with the absorption of nutrients in those affected by the disease because it “leads to a dehydrated intestinal mucin layer and inspissated secretions” (Reed & Shores, 2020), which makes all the gut secretions thick and mucusy. This altered environment causes inflammation, pain, slow motility, and overgrowth of bacteria. Also, sixty-seven percent of CF kids may suffer from reflux due to “delayed gastric emptying and impaired gut motility” (Reed & Shores, 2020), among other reasons.
In terms of reproduction, if none of the parents have been diagnosed with CF and had children diagnosed with the disease, it means that both have to be carriers. The risk of knowing if they are going to have more kids with CF depends entirely on knowing their carrier’s status (Horsley, Cunningham, & Innes, 2015, pp147). In the case presented, to have a positive CF patient, both parents at least have to be carriers. The probability with parents being both carriers is 1:4 of having CF kids (Horsley, Cunningham, & Innes, 2015, pp 2).
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3. Cystic fibrosis is a hereditary disorder that is recessive affecting the lungs and digestive tract. People with cystic fibrosis have a mutation in the CFTR gene (transmembrane conductance regulator) that causes the CFTF protein to malfunction. Determine the genotypes of the parents and offspring for the following family scenarios in a and b below. Use ' C ' to indicate a dominant allele and ' C ' for a recessive allele). a. One parent with the recessive condition and the other parent who does not have the disorder have 2 children. Both children have Cystic fibrosis. 8 marks b. Two parents who do not have Cystic fibrosis have 4 children where 1 child has Cystic fibrosis. 10 marks NOTE: You must draw a Punnet square to determine the possible genotypes of the children. When two alternative genotypes are possible for an individual, indicate both.
.
CysticFibrosis.ppt
Cystic fibrosis is the most common autosomal recessive disease among people of Northern European descent, with an average life expectancy of 30 years. It is caused by mutations in the CFTR gene, which codes for a chloride channel protein. The most common mutation, ΔF508, causes a processing defect that results in reduced chloride transport. Over 1000 mutations in CFTR have been identified. While treatments aim to address symptoms, gene therapy may someday deliver a corrected version of the gene.
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This document provides information about cystic fibrosis (CF), including that it is a genetic disease that affects the lungs and digestive system, causing thick mucus production. It is caused by mutations in the CFTR gene. The document outlines symptoms of CF, including salty skin and lung infections, as well as treatments like medications and airway clearance. It discusses teaching strategies for students with CF, current research into treatments, and resources for support and information.
Write an equation for the height of the point P above the ground as .pdf
Write an equation for the height of the point P above the ground as a function of t, time in
seconds.
h(t) =
Hint: Start by thinking: What is the height of the point P above the center? How is the center
changing?
Solution
height of center at ant time = R + 7(sinA)t = 2 + 7(100/700)t = (2 + t) cm
now height of P wrt center = Rcos(x/2) where x = 7t
height of P = 2+ t + Rcos(7t/2)
= 2 + t + 2cos(7t/2)
7t/2 is value in radian. oon putting t in second
for t= 0,(starting point)
height = 2 + 2cos0 = 4 cm
at the end, at = 100 cm,
h = 2 + 100 + 2cos(350) = 101.433 cm.
Wild-type (WT) mice are irradiated, destroying all of their bone marr.pdf
Wild-type (WT) mice are irradiated, destroying all of their bone marrow cells including CD34+
hematopoietic stem cells (HSC). CD34+ HSC is isolated from (1) an untreated wild-type
syngeneic control mouse, and (2) various immune gene mutant (-/- null) donor mice. The CD34+
HSC from the different mouse genotypes is injected into the wild-type irradiated recipient mice.
Predict the reconstitution of the hematopoietic system in each of the recipient mice (+ or -).
Solution
Answer -
Hematopoietic cells reconstituted in recipient
CD34+HSC
Doner GenotypeErythrocytes macrophages T cells B cells
Wild Type mouse + + + +
CD19(-/-)mouse + + + -
Rag1/2(-/-)mouse + + - -
erythropoietin EPO(-/-) - + + +
AIRE(-/-)mouse + + + +
explaination -Wild type mouse has normal CD34+HSC which is responsible to diffentiate into
all type of immune cells in bone marrow. Whwn this CD34+HSC from wild type mouse injected
into recipient mouse its bone marrow produce all type of immune cells.
CD19 is a B cell lymphocyte antigen It is a protein which is coded by CD19 gene. it is found on
the surface of B cells and helps in its proliferation and differenciation.CD34+HSC from doner
who lack CD19 gene when injected into recipient mouse,It will be unable to produce B cell.
Rag 1/2 also known as recombination activating gene codes a protein which paly an important
role in recombination of the gene of immunoglobuline and T cell receptor marker.two gene
products of recombination activating gene are Rag 1 and Rag 2 protein.These two rag protein are
essential to the generation of mature Bcells and Tcells. .CD34+Hsc from doner who lack the
gene codes gor Rag1/2 protein when injected to the recipient mouse, recipient mousewill be
unable to produce mature B and T cells.
Erythropoietin EPO is a protein harmone secreated by kidney in responce to less
oxygen/Heamoglobine in blood.erythropoietin stimulates bone marrow to produce more Red
blood cells (erythrocytes) which contain Heamoglobine ( an Oxygen carrier) and supply required
amount of oxygen to the body by mean of blood flow through the body. when CD34+HSC from
doner lack the gene codes for Erythropoietin injected into recipient mouse,it bone marrow will
be unable to produce erythrocytes.
AIRE is an auto immune regulator protein encoded by AIRE gene.It controles a mechanism that
prevent T cells (an important cell for immune response) from attacking the self body antigen.T
cells recognizes antigen which are expresed on the surface of antigen presenting cell by T cell
receptors present on T cells and produce Immune responce against that antigen. In autoimmune
diseases T cell Recognize self antigen and produce immune response against self antigen which
leads to sever problem in self body.AIRE protein play an important role to controle these kind of
autoimmune disorders by the removel of T cell through apoptosis while T cells are still in
thymus.
When CD34+HSC from doner WHICh lake the gene for AIRE protein injected into recipient
mouse.Reci.
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Cystic fibrosis is a genetic disease that affects the lungs and digestive system. It is caused by a defective gene that produces a thick, sticky mucus in the lungs and pancreas. Symptoms include persistent coughing, wheezing, shortness of breath, lung infections, and salty-tasting skin. There is no cure, but treatments aim to clear mucus from the lungs and aid digestion. Life expectancy has increased to around 37 years on average with advances in care and new therapies targeting the underlying genetic cause.
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Cystic fibrosis is a genetic disease that causes thick, sticky mucus to build up in the lungs and digestive tract. It is caused by mutations in the CFTR gene that result in defective or too few chloride channels. This leads to dehydrated mucus and chronic lung infections. Symptoms include difficulty breathing, coughing, weight loss, and excessive salt in sweat. Treatment focuses on clearing mucus from the lungs and controlling infections through antibiotics and airway clearance techniques. While there is no cure, managing symptoms has increased life expectancy to over 30 years on average.
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This document discusses cystic fibrosis, including its causes, symptoms, diagnosis, and treatment. It is a genetic disorder that causes thick mucus buildup in the lungs and digestive tract. The primary symptom is severe lung infections. It is caused by mutations in the CFTR gene and is usually diagnosed via sweat test. Treatments include antibiotics, mucus-thinning drugs, and lung therapies to help clear mucus and treat infections. Ongoing research is working to develop new diagnostic tests and find a cure.
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Cystic fibrosis is a hereditary disease caused by a genetic mutation that causes thick mucus production in the lungs and digestive system. Symptoms often appear at birth and include salty skin, lung infections, and poor growth. Diagnosis involves sweat and genetic tests. No cure exists but treatments aim to thin mucus and fight infections through antibiotics and enzymes to improve life expectancy, which averages into the late 30s.
Little changes make a big difference case study
A case study designed for a first year undergraduate genetics course. Interrmittent iClicker questions enable students to recall information from previous slides and apply it through progression of the case study.
This case study was prepared as part of a pedagogical project to examine the effects of active learning versus passive learning. Animations included were independently designed using novice techniques in 3D MAX; as such they may contain inaccuracies and/or a few continuity errors.
Cystic fibrosis[1]
Cystic fibrosis is a genetic disease that affects the lungs and digestive system. It is caused by a mutation in the CFTR gene that causes thick, sticky mucus to build up in the lungs and pancreas. Symptoms often appear in childhood and can include persistent lung infections, digestive issues, and salty skin. Treatment focuses on airway clearance and medications to manage symptoms. While historically fatal in childhood, advances in care have improved life expectancy significantly in recent decades. However, it remains a serious condition currently without a cure.
X linked diseases-mitochondrial diseases
This document summarizes key information about X-linked diseases and mitochondrial DNA diseases. It discusses the X chromosome and genes located on it. It provides details on three specific X-linked diseases: hemophilia A, Duchenne muscular dystrophy, and fragile X syndrome. It describes the inheritance patterns, genetic causes, clinical features, and DNA testing approaches for each. It also provides a brief overview of the structure and function of mitochondrial DNA and its role in oxidative phosphorylation.
Respond to your colleagues and respectfully agree or disagree .docx
Respond
to your colleagues and respectfully agree or disagree with your colleague’s assessment and explain your reasoning. In your explanation, include why their explanations make physiological sense or why they do not
At least 2 references in each peer responses!
Cystic fibrosis (CF) is an inherited disease that affects mainly the gastrointestinal system, the reproductive system, and the lungs (McCance & Huether, 2019, pp 2171). The cystic fibrosis gene “is located on chromosome 7” with more than 2000 variants of the disease. They are divided into six classes, 1 through 3 being the more severe ones. The triad of Cystic fibrosis is “obstruction, infection, and inflammation that is evident throughout the gastrointestinal tract and within the airways” (McCance & Huether, 2019, pp 2871). The gastrointestinal problems are caused by the CF transmembrane regulator (CFTR) protein, “which is located on epithelial membranes and regulates chloride and sodium ion channels (McCance & Huether, 2019, pp 2870). You can find that protein through the airways, sweat glands, digestive tract, pancreas, hepatobiliary system, and reproductive system. The CFTR protein alters the reabsorption of sodium, chloride, and potassium (McCance & Huether, 2019, pp 2871), which gives kids skin a salty taste when parents kiss them because of the excessive salt they waste through sweat glands. It also interferes with the absorption of nutrients in those affected by the disease because it “leads to a dehydrated intestinal mucin layer and inspissated secretions” (Reed & Shores, 2020), which makes all the gut secretions thick and mucusy. This altered environment causes inflammation, pain, slow motility, and overgrowth of bacteria. Also, sixty-seven percent of CF kids may suffer from reflux due to “delayed gastric emptying and impaired gut motility” (Reed & Shores, 2020), among other reasons.
In terms of reproduction, if none of the parents have been diagnosed with CF and had children diagnosed with the disease, it means that both have to be carriers. The risk of knowing if they are going to have more kids with CF depends entirely on knowing their carrier’s status (Horsley, Cunningham, & Innes, 2015, pp147). In the case presented, to have a positive CF patient, both parents at least have to be carriers. The probability with parents being both carriers is 1:4 of having CF kids (Horsley, Cunningham, & Innes, 2015, pp 2).
.
IRF8 Mutations and Human Dendritic-Cell Immunodefiency
This study identified mutations in the IRF8 gene as the cause of immunodeficiency in patients who developed disseminated infections after receiving the BCG vaccine. Genetic and transcriptional analysis revealed two IRF8 variants, K108E and T80A, associated with autosomal recessive and dominant forms of the disease respectively. The IRF8 mutations were found to impair the development of dendritic cell subsets like myeloid dendritic cells and CD1c+ CD11c+ cells, providing insight into the molecular basis of this immunodeficiency.
Review Paper-Gene Therapy for the Treatment of Cystic Fibrosis
Cystic fibrosis is a genetic disease caused by mutations in the CFTR gene. Gene therapy aims to insert a normal copy of this gene to restore function. While conceptually simple, gene therapy for cystic fibrosis has proven difficult in practice due to biological barriers and challenges with delivery vectors. Early clinical trials used adenoviral vectors administered to the nose with limited success. Subsequent trials delivered vectors directly to the lungs but were also unsuccessful. Recent trials have focused on non-viral vectors which allow for repeated administration and show promise, though further development is still needed to achieve an effective treatment through gene therapy.
Cystic fibrosis.pdf
Welcome to this comprehensive exploration of cystic fibrosis (CF). This presentation delves into the intricate aspects of CF, a genetic disorder that impacts various organ systems, with a focus on the genetic basis, clinical manifestations, diagnosis, and advancements in research and treatment. Thank you for joining me on this journey to understand Cystic Fibrosis better. Together, let's contribute to raising awareness and supporting those affected by this condition.
Cystic Fibrosis - A Genetic Disorder.pptx
A comprehensive presentation about Cystic Fibrosis - a genetic and metabolic disorder. Made by Taha Haider, Roll No.# L1F22BSBC0004 (BS Biochemistry University of Central Punjab, Lahore)
3- Cystic fibrosis is a hereditary disorder that is recessive affectin (1).docx
3. Cystic fibrosis is a hereditary disorder that is recessive affecting the lungs and digestive tract. People with cystic fibrosis have a mutation in the CFTR gene (transmembrane conductance regulator) that causes the CFTF protein to malfunction. Determine the genotypes of the parents and offspring for the following family scenarios in a and b below. Use ' C ' to indicate a dominant allele and ' C ' for a recessive allele). a. One parent with the recessive condition and the other parent who does not have the disorder have 2 children. Both children have Cystic fibrosis. 8 marks b. Two parents who do not have Cystic fibrosis have 4 children where 1 child has Cystic fibrosis. 10 marks NOTE: You must draw a Punnet square to determine the possible genotypes of the children. When two alternative genotypes are possible for an individual, indicate both.
.
CysticFibrosis.ppt
Cystic fibrosis is the most common autosomal recessive disease among people of Northern European descent, with an average life expectancy of 30 years. It is caused by mutations in the CFTR gene, which codes for a chloride channel protein. The most common mutation, ΔF508, causes a processing defect that results in reduced chloride transport. Over 1000 mutations in CFTR have been identified. While treatments aim to address symptoms, gene therapy may someday deliver a corrected version of the gene.
Genetic Disorder
The document provides information about hereditary spherocytosis, an inherited blood disorder where red blood cells take on an abnormal spherical shape. It discusses how the condition is caused by defects in red blood cell membrane proteins and is diagnosed through blood tests and examination of red blood cell shape under a microscope. Signs and symptoms include anemia, jaundice, and an enlarged spleen. Treatment options include removing the spleen through surgery to prevent red blood cell destruction, or supplements for mild cases.
Cystic fibrosis- Ashley Verbeek
This document provides information about cystic fibrosis (CF), including that it is a genetic disease that affects the lungs and digestive system, causing thick mucus production. It is caused by mutations in the CFTR gene. The document outlines symptoms of CF, including salty skin and lung infections, as well as treatments like medications and airway clearance. It discusses teaching strategies for students with CF, current research into treatments, and resources for support and information.
Similar to A new potentially disease-causing Cystic Fibrosis mutation.a) .pdf (20)
#scichallenge2017 #scienceincypriotschools Cystic Fibrosis and gene therapy
#scichallenge2017 #scienceincypriotschools Cystic Fibrosis and gene therapy
Respond to your colleagues and respectfully agree or disagree .docx
Respond to your colleagues and respectfully agree or disagree .docx
IRF8 Mutations and Human Dendritic-Cell Immunodefiency
IRF8 Mutations and Human Dendritic-Cell Immunodefiency
Review Paper-Gene Therapy for the Treatment of Cystic Fibrosis
Review Paper-Gene Therapy for the Treatment of Cystic Fibrosis
3- Cystic fibrosis is a hereditary disorder that is recessive affectin (1).docx
3- Cystic fibrosis is a hereditary disorder that is recessive affectin (1).docx
More from herminaherman
Write an equation for the height of the point P above the ground as .pdf
Write an equation for the height of the point P above the ground as a function of t, time in
seconds.
h(t) =
Hint: Start by thinking: What is the height of the point P above the center? How is the center
changing?
Solution
height of center at ant time = R + 7(sinA)t = 2 + 7(100/700)t = (2 + t) cm
now height of P wrt center = Rcos(x/2) where x = 7t
height of P = 2+ t + Rcos(7t/2)
= 2 + t + 2cos(7t/2)
7t/2 is value in radian. oon putting t in second
for t= 0,(starting point)
height = 2 + 2cos0 = 4 cm
at the end, at = 100 cm,
h = 2 + 100 + 2cos(350) = 101.433 cm.
Wild-type (WT) mice are irradiated, destroying all of their bone marr.pdf
Wild-type (WT) mice are irradiated, destroying all of their bone marrow cells including CD34+
hematopoietic stem cells (HSC). CD34+ HSC is isolated from (1) an untreated wild-type
syngeneic control mouse, and (2) various immune gene mutant (-/- null) donor mice. The CD34+
HSC from the different mouse genotypes is injected into the wild-type irradiated recipient mice.
Predict the reconstitution of the hematopoietic system in each of the recipient mice (+ or -).
Solution
Answer -
Hematopoietic cells reconstituted in recipient
CD34+HSC
Doner GenotypeErythrocytes macrophages T cells B cells
Wild Type mouse + + + +
CD19(-/-)mouse + + + -
Rag1/2(-/-)mouse + + - -
erythropoietin EPO(-/-) - + + +
AIRE(-/-)mouse + + + +
explaination -Wild type mouse has normal CD34+HSC which is responsible to diffentiate into
all type of immune cells in bone marrow. Whwn this CD34+HSC from wild type mouse injected
into recipient mouse its bone marrow produce all type of immune cells.
CD19 is a B cell lymphocyte antigen It is a protein which is coded by CD19 gene. it is found on
the surface of B cells and helps in its proliferation and differenciation.CD34+HSC from doner
who lack CD19 gene when injected into recipient mouse,It will be unable to produce B cell.
Rag 1/2 also known as recombination activating gene codes a protein which paly an important
role in recombination of the gene of immunoglobuline and T cell receptor marker.two gene
products of recombination activating gene are Rag 1 and Rag 2 protein.These two rag protein are
essential to the generation of mature Bcells and Tcells. .CD34+Hsc from doner who lack the
gene codes gor Rag1/2 protein when injected to the recipient mouse, recipient mousewill be
unable to produce mature B and T cells.
Erythropoietin EPO is a protein harmone secreated by kidney in responce to less
oxygen/Heamoglobine in blood.erythropoietin stimulates bone marrow to produce more Red
blood cells (erythrocytes) which contain Heamoglobine ( an Oxygen carrier) and supply required
amount of oxygen to the body by mean of blood flow through the body. when CD34+HSC from
doner lack the gene codes for Erythropoietin injected into recipient mouse,it bone marrow will
be unable to produce erythrocytes.
AIRE is an auto immune regulator protein encoded by AIRE gene.It controles a mechanism that
prevent T cells (an important cell for immune response) from attacking the self body antigen.T
cells recognizes antigen which are expresed on the surface of antigen presenting cell by T cell
receptors present on T cells and produce Immune responce against that antigen. In autoimmune
diseases T cell Recognize self antigen and produce immune response against self antigen which
leads to sever problem in self body.AIRE protein play an important role to controle these kind of
autoimmune disorders by the removel of T cell through apoptosis while T cells are still in
thymus.
When CD34+HSC from doner WHICh lake the gene for AIRE protein injected into recipient
mouse.Reci.
Which of the following is considered to be a distributed denial of s.pdf
Which of the following is considered to be a distributed denial of service attack because it comes
from numerous sources?a.Smurf
Solution
The Distributed denial of service (DDOS) is an attack where the attacker repeatedly pings the
server from different computers/servers to restrict the server from handling the requests of the
legitimate users. This way all the requests of the authorized users will get be declined.
The SYN flood attack and the death ping send multiple requests to the server from a single
source and the sequence prediction attack is used to analyze the traffic to identify the data
packets.
The smurf attack uses a broadcast network to send multiple requests to the server from different
sources. Hence, the correct options is a. Smurf..
Which of the folllowing statements about the solubility of 1- propan.pdf
Which of the folllowing statements about the solubility of 1- propanol, ch3ch2ch2oh, and
ethanethiol, ch3ch2sh, are true?
A) Ethanethiol is more soluble in water because sulfer has agreater electronegativity value than
oxygen.
B) Ethanethiol is more soluble in water because it has a lower molecular mass than 1-propanol.
C) 1-propanol is more soluble in water because it has a greater molecular mass than ethanethiol.
D) 1-Propanol is more soluble in water because oxygen has a greater electronegativity value than
sulfer.
Solution
D) 1-Propanol is more soluble in water because oxygen has a greater electronegativity value
than sulfer.
\\\ eason
propanol has a hydrogen bonding by itself while ethanethiol does not have any hydrogen
bonding by itself that is why propanol is more soluble in water. because oxygen has a greater
electronegativity value than sulfer.
the more hydrogen bonding by itself the more soluble in water!.
What type of mutation that impacts splicing is a significant contrib.pdf
What type of mutation that impacts splicing is a significant contributor to human disease?
Solution
Disruptions in splicing are major contibutor of human diseases.Most genes in higher eukaryotes
are composed of introns (non coding segments) and exons (coding segments). The majority of
human intron removals ae catalyzed by a large and dynamic ribonucleoprotein (RNP) complex
called the spliceosome.This process involves two sequential transesterification reactions which
ligate the exons and release the intron as a lariat.
Alternate splicing which allows for the productioin of many proteins from a single genomic
locous.This greatly augments the repertorie of the protein.This greatly augments the repertoire of
proteins that can be produced by a given gene and plays an important role in
evolution,development and disease..
What data indicate that all three germ layers are specified in the b.pdf
What data indicate that all three germ layers are specified in the blastula? What are the
differences between dorsal and ventral mesodermal derivatives and what cellular interactions are
required for their specification?
Solution
Three germ layers of amphibians are specified in the blastula is determined by isolating these
tissues in vitro, and they are able to form into specific germ layers. The animal pole cap cells
make ectoderm, marginal region cells make mesoderm, and vegetal cells make endoderm.
Theyare specified but not determined. It is also interesting to note that if animal cap cells are
place co-cultured with vegetal cells, the animal cap cells with become mesoderm. This indicates
that vegetal cells induce other cells to form mesoderm. Experiment paired animal cap cells in 4
different sections of vegetal blastomeres to see if they induce different dorsal-ventral
mesodermal fates. Result showed that different sections of vegetal blastomere have specific
inductive capacities, which is crucial for dorsal-ventral mesoderm determination. Difference
between dorsal and ventral mesoderm derivatives: dorsal mesoderm is the notochord and somite.
In all bilaterian animals, the mesoderm is one of the three primary germ layers in the very early
embryo. The other two layers are the ectoderm (outside layer) and endoderm (inside layer), with
the mesoderm as the middle layer between them.
The mesoderm forms mesenchyme, mesothelium, non-epithelial blood cells and coelomocytes.
Some of the mesoderm derivatives include the muscle (smooth, cardiac and skeletal), the
muscles of the tongue (occipital somites), the pharyngeal arches muscle (muscles of mastication,
muscles of facial expressions), connective tissue, dermis and subcutaneous layer of the skin
At mid-blastula two signaling centers are present on the dorsal side: The prospective
neuroectoderm expresses bone morphogenetic protein (BMP) antagonists, and the future dorsal
endoderm secretes Nodal-related mesoderm-inducing factors. When dorsal mesoderm is formed
at gastrula, a cocktail of growth factor antagonists is secreted by the Spemann organizer and
further patterns the embryo. A ventral gastrula signaling center opposes the actions of the dorsal
organizer, and another set of secreted antagonists is produced ventrally under the control of
BMP4. The early dorsal -Catenin signal inhibits BMP expression at the transcriptional level and
promotes expression of secreted BMP antagonists in the prospective central nervous system
(CNS). In the absence of mesoderm, expression of Chordin and Noggin in ectoderm is required
for anterior CNS formation. FGF (fibroblast growth factor) and IGF (insulin-like growth factor)
signals are also potent neural inducers. Neural induction by anti-BMPs such as Chordin requires
mitogen-activated protein kinase (MAPK) activation mediated by FGF and IGF. These multiple
signals can be integrated at the level of Smad1. Phosphorylation by BMP receptor stimulates
Smad1 transcrip.
Unlike RNA, DNA containsA. adenine.B. uracil.C. phosphate grou.pdf
Unlike RNA, DNA contains
A. adenine.
B. uracil.
C. phosphate groups.
D. thymine.
Solution
Answer is: Thymine
Explanation:
Base Pairing in DNA: A-T (Adenine-Thymine), G-C (Guanine-Cytosine)
Base Pairing in RNA: A-U (Adenine-Uracil), G-C (Guanine-Cytosine)
The phosphate group is present in both RNA and DNA..
Use provided HTML file.Create JavaScript file to validate user i.pdf
Use provided HTML file.
Create *JavaScript file* to validate user input and process user input.
Show the conformation window for Valid Submission.
Title is required field.
Description is required field.
City is required field.
Rate this photo => positive numeric value 1 – 10
User must provide date and time.
User must accept the software license.
User must select “Creative Commons Type
Use JavaScript to display User information.
//HTML
Chapter 6Photo Details
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//CSS
/* general text formatting */
h1, h2, h3, nav, footer {
font-family: Georgia, Cambria, \"Times New Roman\", serif;
}
body {
font-family: \"Lucida Sans\", Verdana, Arial, sans-serif;
font-size: 85%;
}
table {
border: collapse;
border-spacing: 0;
width; 90%;
margin: 0 auto;
}
table tbody td{
/* border: 1pt solid #95BEF0; */
line-height: 1.5em;
vertical-align: top;
padding: 0.5em 0.75em;
}
legend {
background-color: #EBF4FB ;
margin: 0 auto;
width: 90%;
padding: 0.25em;
text-align: center;
font-weight: bold;
font-size: 100%;
}
fieldset {
margin: 1em auto;
background-color: #FAFCFF;
width: 60%;
}
form p {
margin-top: 0.5em;
}
.box {
border: 1pt solid #95BEF0;
padding: 0.5em;
margin-bottom: 0.4em;
}
.rectangle {
background-color: #EBF4FB;
padding: 0.5em;
}
.centered {
text-align: center;
}
.rounded, .rounded:hover {
border: 1px solid #172d6e;
border-bottom: 1px solid #0e1d45;
border-radius: 5px;
text-align: center;
color: white;
background-color: #8c9cbf;
padding: 0.5em 0 0.5em 0;
margin: 0.3em;
width: 7em;
-webkit-box-shadow: inset 0 1px 0 0 #72b9eb, 0 1px 4px 0 #b3b3b3;
box-shadow: inset 0 1px 0 0 #72b9eb, 0 1px 4px 0 #b3b3b3;
}
.rounded:hover {
background-color: #7f8dad;
}
Solution
script.js
/**************format.css**************************************/.
Two four-sided dice are rolled. One die has the letters A through D..pdf
Two four-sided dice are rolled. One die has the letters A through D. The other has the numbers 1
through 4.
Express the event “a roll of the dice will contain the letter A or B” as a set (show each of the
possible combinations).
What is the probability that a roll will contain an A or a B?
Solution
The set
S = { A1,A2,A3,A4,B1,B2,B3,B4,C1,C2,C3,C4,D1D,D3D4}
Let event M =a roll of the dice will contain the letter A or B
M = {A1,A2,A3,A4,B1,B2,B3,B4}
Probability = 8/16 = 1/2.
The job of a CODEC (CoderDecoder) is to Convert an analog voice si.pdf
The job of a CODEC (Coder/Decoder) is to: Convert an analog voice signal into a digital signal
Convert a digital signal into an analog voice signal Convert a computer signal into a voice signal
Both a and b
Solution
Option c is true, Since the job of a codec is to encode a stream of data a signal for storage and
transmission, possibly in encrypted form, and the process is revered in decoder function for
playback or editing. Codec are used in videoconferencing, streaming media, and video editing
applications..
Question 4 Constructive retirement is when A. P buys Ss common stoc.pdf
Question 4 Constructive retirement is when A. P buys S\'s common stock O B. P buys S\'s bonds
payable O C. P retires bonds payable. O D. P retires shares of its own stock.
Solution
If a company buys back its own share, which is treasury stock,and if the management of the
company decides to retire them permanently, its called constructive retirement.
So when P retires shares of its own stock, it results in constructive retirement .
Option D is correct..
Private and Public Health are working together through many program .pdf
Private and Public Health are working together through many program initiatives to promote
cost-effective, quality, and compassionate patient care and population health. Under the
Affordable Care Act (2010), and the patient-centered medical home model (PCMH) and
programs such as the All-Inclusive Care for the Elderly (PACE), how are health professionals in
both private and public health working together to meet the critical needs of the elderly
populations?
Solution
Let us start with PACE. It is a program helping people meet their healthcare needs without going
to a hospital or nursing home. A team of healthcare professionals work together to get this done.
PACE organizations work towards providing healthcare and services through their specialists so
that the needs of the elderly are met. the team of specialists come from different locations and
services. Some of them come from Public health organizations and some from private. However,
they all work together towards a common cause of serving the elderly. Thus PACE is an ideal
platform where both private and public health professionals work together to serve the elderly.
PCMH today is transforming the way primary care is managed and delivered. This model meets
a majority of each individual\'s health care needs in a comprehensive manner. Such a
comprehensive coverage would mean that a large team of specialists is involved including
doctors, nurses, pharmacists, assistants and so on. PCMH model is more relationship oriented. It
involves creating a relationship with the patient, understanding them and their families,
respecting their individual needs. This requires a lot of coordination across the healthcare
system, from hospitals to nursing homes to home health care. PCMH model delivers its services
around the clock. this requires the availability of services and specialist at every time. This is
possible through their pool of both private and public health professionals. Services are provided
in the shortest time by the available specialists, both private and public. Thus the PCMH model
also shows a way through which public and private health work together to serve the elderly.
Under the Affordable Care Act and programs like PACE and PCMH, a large pool of specialists
is created who jointly serve the elderly. Such a pool would not be possible if it is made by only
private or public healthcare professionals. Thus, the creation of these pools necessitates the
involvement of both private and public healthcare professionals. The creation of large pools acts
as a strong catalyst in bringing all types of health professionals towards the common goal of
serving the elderly and also the nation at large..
Name the two standards that are supported by major DBMSs for distrib.pdf
Name the two standards that are supported by major DBMSs for distributing data? Describe the
standard set of protocols developed by ISO and ANSI for remote access to database.
Solution
The two standards that are supported by major DBMS\'s Are ODMG 3.0 and JDO .
ODMG 3.0 stands for Object Data Management Group (ODMG) and JDO stands for java data
objects .
Remote database access (RDA) is the standard protocol for database access .
this standard has been developed by ISO and ANSI.
RDA provides protocol for eastablishing remote connection between database client and server.
The client is acting on behalf of an application program while the server is interfacing to a
process that controls data transfers to and from a database.
The RDA Communication Element converts RDA service requests into underlying ACSE and
TP service requests as part of an open systems interconnection..
Material Manufacturing Name 3 ways that the properties of thermosett.pdf
Material Manufacturing Name 3 ways that the properties of thermosetting polymers differ from
those of thermoplastics.
Solution
Thermoplastics can be melted and reshaped over and over again, while thermosetting plastics can
only be heated and shaped once
Thermoset are More resistant to high temperatures than thermoplastics
Thermoset have highly flexible design.
Mean can be computed for variables with ordinal-level measurements..pdf
Mean can be computed for variables with ordinal-level measurements.
True or False?
Solution
Sol)
False
Mean can not be computed for variables with ordinal-level measurements. we can find median
for ordinal measurement.
Ex: Gender, Intelligence and taste. These are qualitative variables so for these type of variables
we can not find mean. we use median.
Let u_1, u_2 be finite dimensional subspaces of a vector space V. Sho.pdf
Let u_1, u_2 be finite dimensional subspaces of a vector space V. Show that the sum u_1 + u_2
is direct if dim(u_1 +u_2) = dim(u_1) + dim (u_2)
Solution
we know that
dim(U1+U2)= dim(U1)+dim(U2)-dim(U1 intersection U2)
given that dim(U1+U2)= dim(U1)+dim(U2)
i.e dim(U1 intersection U2) =0
U1 intersection U2 = {0}
hence sum U1+U2 is direct.
IV. Which compound would have the higher water solubility, tetrahydro.pdf
IV. Which compound would have the higher water solubility, tetrahydropyran (THP) or ethyl
propyl ether? Explain using chemical drawings and no more than 2 sentences. (10 points) THP
ethyl propyl ether
Solution
Cyclic ether is miscible than acyclic ether because the oxygen atom of cyclic ether are more
exposed towards hydrogen bonding. Hence THP (cyclic) is more soluble than ethyl propyl ether
(acyclic)..
Interseting discussion topic,want to chime inDescribe a symbol .pdf
Interseting discussion topic,
want to chime in?
Describe a symbol in your life. It can be a religious one or not. But I want to know something in
your life that is communal (that is to say, it takes place with other people) or personal (you go
through it alone) that points \"beyond itself\". Especially good topics are symbols that you share
with friends, family, teams, scout troops, or whatever - just a meaningful group (important
places, annual parties, hand signs, code words, handshakes, etc).
I want you to deeply diagnose the thing - even if you never have before: What are the motions
involved? Do they have a significance? What is the connection between sign and symbolized?
What feeling or event is it meant to evoke? Just describe each and every element that is
consistently involved and explain its significance... Is there a \"mythology\" behind it? (that is to
say, a key founding story that\'s interpretive, rather than exact, history)
Solution
hand signs:
it involves acceptance, sometime ignorance, sometime victory, some time hapiness. Yes a lot. It
is beyond the language one speaks. It has grat power to communicate. I don\'t know of
mythology but yes its there..
IN JAVA Write a program to create a binary data file named RandomInt.pdf
IN JAVA Write a program to create a binary data file named RandomInt.dat that consists of 10
random integer numbers using DataOutputStream. Use DataInputStream to read the integers
from RandomInt.dat just created and print them on the console in the same program.
Solution
DataInputStreamTest.java
import java.io.DataInputStream;
import java.io.DataOutputStream;
import java.io.FileInputStream;
import java.io.FileNotFoundException;
import java.io.FileOutputStream;
import java.io.IOException;
import java.util.Random;
public class DataInputStreamTest {
public static void main(String[] args) {
String strFilePath = \"D:\\\\RandomInt.dat\";
Random r = new Random();
try
{
FileOutputStream outputStr = new FileOutputStream(strFilePath);
DataOutputStream outputStrData = new DataOutputStream(outputStr);
for(int i=0; i<10; i++){
outputStrData.writeInt(r.nextInt(100)+1);
outputStrData.writeChar(\'\\t\');
}
outputStrData.flush();
outputStrData.close();
outputStr.close();
FileInputStream inputStr = new FileInputStream(strFilePath);
DataInputStream inputStrData = new DataInputStream(inputStr);
int count = 0;
while(count<10){
int i = inputStrData.readInt();
inputStrData.readChar();
count++;
System.out.println( i);
}
outputStrData.flush();
inputStrData.close();
outputStrData.close();
}
catch(FileNotFoundException fe)
{
System.out.println(\"FileNotFoundException : \" + fe);
}
catch(IOException ioe)
{
System.out.println(\"IOException : \" + ioe);
}
}
}
Output:
65
8
95
69
1
77
16
97
85
1.
I wanna add the shape creator like rectangular , square , circle etc.pdf
I wanna add the shape creator like rectangular , square , circle etc shape creator in this program. I
tried many ways to do it but couldnt figure out the right way. Please help me do this. this is a
painter program and I want to add shape creator for an extra point.. Thanks..
//Painter.java
import java.awt.*;
import java.awt.event.*;
import java.util.ArrayList;
import javax.swing.*;
public class Painter extends JFrame
{
private JButton blueButton, redButton, greenButton,eraserButton,clearButton;
private Container myCP;
public Paint panel;
private JPanel mainContainer;
public Painter()
{
mainContainer = new JPanel(new BorderLayout());
mainContainer.setBackground(Color.WHITE);
JPanel panel2 = new JPanel();
panel2.setLayout(new FlowLayout());
blueButton = new JButton(\"Blue\");
blueButton.setPreferredSize(new Dimension(75,50));
panel2.add(blueButton);
blueButton.addActionListener(new
ButtonListener());
redButton = new JButton(\"Red\");
redButton.setPreferredSize(new Dimension(75,50));
panel2.add(redButton);
redButton.addActionListener(new ButtonListener());
greenButton = new JButton(\"Green\");
greenButton.setPreferredSize(new Dimension(75,50));
panel2.add(greenButton);
greenButton.addActionListener(new ButtonListener());
eraserButton = new JButton(\"Eraser\");
eraserButton.setPreferredSize(new Dimension(75,50));
panel2.add(eraserButton);
eraserButton.addActionListener(new ButtonListener());
clearButton = new JButton(\"Clear\");
clearButton.setPreferredSize(new Dimension(75,50));
panel2.add(clearButton);
clearButton.addActionListener(new ButtonListener());
panel = new Paint();
mainContainer.add(panel2, BorderLayout.NORTH);
mainContainer.add(panel, BorderLayout.CENTER);
add(mainContainer);
setVisible(true);
}
private class ButtonListener implements ActionListener
{
public void actionPerformed(ActionEvent e)
{
if (e.getSource() == blueButton)
{
panel.addCoordinateList(new ColorPoints(Color.BLUE,
new Point()));
}
if (e.getSource() == redButton)
{
panel.addCoordinateList(new ColorPoints(Color.RED,
new Point()));
}
if (e.getSource() == greenButton)
{
panel.addCoordinateList(new
ColorPoints(Color.GREEN,
new Point()));
}
if (e.getSource() == eraserButton)
{
panel.addCoordinateList(new ColorPoints(panel.getBackground(),
new Point()));
}
if (e.getSource() == clearButton)
{
panel.setCoordinateList(new ArrayList());
repaint();
}
}
}
public static void main(String args[])
{
Painter myAppF = new Painter();
myAppF.setTitle(\"Painter\");
myAppF.setVisible(true);
myAppF.setSize(500, 500);
myAppF.setDefaultCloseOperation(JFrame.EXIT_ON_CLOSE);
System.out.println(\"Programmed By Aashutosh Bajgain and Sujan Gautam!\");
}
}
//Paint.java
import java.awt.*;
import java.awt.event.*;
import java.util.ArrayList;
import javax.swing.*;
public class Paint extends JPanel
{
private boolean lineBeingDrawn;
private Point startingPoint;
private ArrayList coordinateList;
private Color selectedColor;
private ColorPoints pwc;
public Paint()
{
lineBeingDrawn = false;
startingPoint .
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